There could have been an underlying condition
or something along these lines.
There is no way a grown man with a good diet and supplementing zinc should fail this test. Even Mew said that 
[Size=4]THE EFFECTS OF DIETARY ZINC DEFICIENCY ON THE REPRODUCTIVE SYSTEM OF MALE RATS[/size]
M. J. Millar, M. I. Fischer, P. V. Elcoate, and C. A. Mawson
Abstract: Dietary zinc deficiency produced by feeding a zinc-poor diet (0.5 Îźg. zinc per g.) to weanling rats for 8 weeks [Size=4]caused marked retardation in body growth, depressed growth and development of testes, epididymes, accessory sex organs, and pituitary glands, and in many cases severe atrophy of testicular germinal epithelium. The zinc concentration of dorsolateral prostates, testes, epididymes, and bone was reduced in zinc-deficient rats compared with controls receiving the zinc-poor diet plus 100 Îźg. zinc daily.[/size] Restricted feeding of the zinc-supplemented diet to produce body weights comparable to those in zinc-deficient rats [Size=4]caused a reduction in pituitary gland and accessory sex organ size which was similar to that observed in zinc-deficient rats. [/size]Testis growth and development were normal in the restricted controls and did not differ from controls fed ad libitum. The zinc concentration of dorsolateral prostates was reduced in restricted controls but exceeded that in the zinc-deficient rats. [Size=4]All the observed changes produced by zinc deficiency except the testicular atrophy were reversed when zinc was replaced in the diet. If testicular atrophy had occurred, neither testis nor epididymis regained normal size, function, or zinc concentration.[/size]
[Size=4]Comparative absorption of zinc picolinate, zinc citrate and zinc gluconate in humans.[/size]
Barrie SA, Wright JV, Pizzorno JE, Kutter E, Barron PC.
Abstract
The comparative absorption of zinc after oral administration of three different complexed forms was studied in 15 healthy human volunteers in a double-blind four-period crossover trial. The individuals were randomly divided into four groups. Each group rotated for four week periods through a random sequence of oral supplementation including: zinc picolinate, zinc citrate, and zinc gluconate (equivalent to 50 mg elemental zinc per day) and placebo. Zinc was measured in hair, urine, erythrocyte and serum before and after each period. [Size=4]At the end of four weeks hair, urine and erythrocyte zinc levels rose significantly (p less than 0.005, p less than 0.001, and p less than 0.001) during zinc picolinate administration. There was no significant change in any of these parameters from zinc gluconate, zinc citrate or placebo administration. [/size]There was a small, insignificant rise in serum zinc during zinc picolinate, zinc citrate and placebo supplementation. The results of this study suggest that zinc absorption in humans can be improved by complexing zinc with picolinic acid.
[Size=4]Acute Zn deficiency impairs electrophysiology [/size]and behavior of rats (Hesse 1979 , Hesse et al. 1979 ). Zn deficiency during early brain development causes malformations (Hurley and Swenerton 1966 ). Zn deficiency during later brain development impairs neuronal growth and synaptogenesis (Dvergsten 1984 ), and causes behavioral sequellae (Golub et al. 1995 , Halas and Eberhardt 1987 , Strobel and Sandstead 1984 ).
Yes, this is my line of thinking as well. Namely gut dysbosis and perhaps not enough bile. Leaky gut syndrome, perhaps gluten and wheat sensitivity, giving a celiac type response meaning you dont absorb vitamins and minerals properly.
If some of us had this (I know I had gut dysbosis), then that could have predisposed us to both zinc defeciency and copper toxicity (the candle burnt at both ends).
Potential magic bullet :
Zinc Picolinate 50mg p/d (I had to get from compound pharmacy in new zealand, maybe different in other countries.)
Vitamin b6 liquid form( every time with zinc)
If no results in reasonable time period above conditions listed by j899 must be considered.
Of note fellas zinc citrate, zinc sulphate, zinc gluconate have poor absorbtion rates and a history of side effects such as muscle pains, stomach upsets, nausia.
I have already posted this study but this one gives an idea of time frames
Experimental zinc deficiency in man. Effect on testicular function.
Abbasi AA, Prasad AS, Rabbani P, DuMouchelle E.
Abstract
Dietary zinc intake was restricted (2.7 to 5.0 mg daily) for 24 to 40 weeks in five male volunteers. Their mean age was 57 years. Oligospermia (total sperm count less than 40 million per ejaculate) was induced in four out of five subjects. A decrease in the sperm count occurred during zinc restricion and the early phase of zinc repletion before body stores of zinc were restored to normal. The duration of oligospermia in the four subjects ranged from 6 to 14 months. [Size=4]Oligospermia was reversed after zinc supplementation in physiologic amounts[/size]. The baseline sperm concentration and total sperm count per ejaculate in all five subjects dropped significantly (p < 0.05) after zinc restriction and returned to [Size=4]normal 6 to 12 months[/size] after zinc supplementation. The decrease in sperm count coincided with decline in Leydig cell function and was reversed after zinc supplementation in low doses. [Size=4]Our study has demonstrated that dietary restriction of zinc can affect testicular function adversely. This effect of zinc deficiency, however, is a reversible process and can be corrected by proper supplementation with zinc.[/size]
Gives hope
J899 this could be the one we are after brother
[Size=4]Infertility, obstetric and gynaecological problems in coeliac sprue[/size].
Sher KS, Jayanthi V, Probert CS, Stewart CR, Mayberry JF.
Leicester General Hospital, UK.
Abstract
There is now substantial evidence that coeliac sprue is associated with infertility both in men and women. In women it can also lead to delayed menarche, amenorrhoea, early menopause, recurrent abortions, and a reduced pregnancy rate. [Size=4]In men it can cause hypogonadism, immature secondary sex characteristics and reduce semen quality.[/size] The real mechanism by which coeliac sprue produces these changes is unclear, but factors such as malnutrition, iron, folate and [Size=4]zinc deficiencies [/size]have all been implicated. [Size=4]In addition in men gonadal dysfunction is believed to be due to reduced conversion of testosterone to dihydrotestosterone caused by low levels of 5 alpha-reductase in coeliac sprue. This leads to derangement of the hypothalamic-pituitary axis[/size]. Hyperprolactinaemia is seen in 25% of coeliac patients, which causes impotence and loss of libido. [Size=4]Gluten withdrawal and correction of deficient dietary elements can lead to a return of fertility both in men and women.[/size]
[Size=4]Further more from [/size]http://www.celiac.com/articles/22095/1/-Celiac-Disease-and-Zinc-Deficiency/Page1.html
All patients received a 20 milligram dose of elemental zinc supplementation for 4 weeks. Plasma zinc levels were compared at baseline and also at 4 weeks to determine zinc deficiency. Patients found to be deficient in zinc levels were randomly divided into two groups, Group G and Group G+Z. Group G treatments included a gluten-free diet without zinc supplementation. Group G+Z received a gluten-free diet with zinc supplementation.
The results of this study showed that plasma zinc levels had a significant rise in Group G and Group G+Z regardless of zinc supplementation. However, a gluten-free diet alone showed a profound increase in plasma zinc levels, even when compared to gluten-free diet with zinc supplements; thereby indicating that zinc supplementation combined with a gluten-free diet gives no additional benefits to plasma zinc levels. In fact, all celiac patients that maintained a gluten-free diet for this study showed that their ability to absorb zinc had significantly improved. [Size=4]Therefore, it can be concluded that zinc levels rise with a gluten-free diet regardless of zinc supplementation, proving that a completely gluten-free diet is the cure to poor zinc absorption in celiac patients. [/size]
[Size=4]No more gluten, now im pissed [/size] 
New potential magic bullet
Zinc picolinate
B6 liquid
Vitamin d to rebuild stores
Gluten free diet
(Resolving copper toxicity may have to be considered if you were on fin for a significant period)
Ok j899 heres my theoryâŚfin has triggered an acute zinc loss due to 5ar2 supression, supressing 5ar2 has made us take a big step towards becoming woman. So the body has dumped some zinc at a âtipping pointâ seems to be after men stop taking the drug for me it was one day for others its two weeks, i suspect 5ar2/aromatase activity is the scale in which the tipping point is measured. Us all losing hair could be evidence we had very active 5ar pre fin, which would probably mean we all had low aromatase rates, so fin fucked this up big timeâŚlet me guess the most of us pre fin had quite respectable body shapes, not much fat. I know i do.
I suspect the reason why men are zinc dominant is because zinc is a potent inhibitor of the aromatase enzyme(its in one of my above posts)letting t go to dht via 5ar. Woman are copper dominant, with a very suppressed 5ar, so im wondering if 5ar controls the mineral balance here, copper is said to be positively corrilated with estrogen which in theory would increase aromatase activity.
The low zinc has then triggered celiacs disease, which could have been, not certainly an underlying condition in some men, waiting to happen if not already happening, i must admit i had suspicions years before fin but was never going to give up the âgood lifeâ of gluten.
Some men quite the drug, crash(due to zinc loss) then get better, no celiacs (they can easily restore thier zinc levels.
Some dont get better because the cant absorb zinc to replenish thier depleted reserves due to celiacs.
[Size=4]The liver in celiac disease.[/size]
Rubio-Tapia A, Murray JA.
Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN, USA.
Abstract
Celiac disease is a common (1% prevalence) chronic immune-mediated disorder of the small intestine induced by dietary wheat, barley, and rye. Several hepatic disorders have been described in association with celiac disease. Isolated hypertransaminasemia with nonspecific histologic changes in a liver biopsy is the commonest hepatic presentation of celiac disease. A gluten-free diet normalizes liver enzymes and histologic changes in most patients. Moreover, celiac disease can coexist with autoimmune liver disorders such as autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis. Celiac disease has increasingly been reported with a variety of other liver diseases. Thus, the hepatologist needs to consider celiac disease in the differential of abnormal liver blood tests and to be aware of the clinical implications of this frequent disease in patients with liver disorders. The possible mechanisms of liver injury and those common factors that explain the association of celiac disease with liver disorders are discussed. The aims of this article are (1) to review the spectrum and pathogenesis of liver injury related to celiac disease and (2) to provide direction to those caring for patients with chronic liver diseases regarding the detection and effective treatment of celiac disease.
Experiments with animals, as well as clinical observations in
humans, have shown that prostatic zinc is under hormonal
control. [Size=4]Administration of estrogen or castration decreases
normal prostatic zinc levels, whereas administration of testos
terone increases the concentration of zinc in the prostate gland[/size]
(11, 28). Further, reports have demonstrated that the concen
tration of free zinc in prostatic cells influences the metabolism
of testosterone to DHT (33). Since zinc levels are depleted in
carcinoma of the prostate, there may be a relationship between
zinc and the abnormal testosterone levels.
Cant get the zinc cause of celiacs
If you are somehow implying we are all suffering from celiac disease because of Finasteride, you are becoming delusional my friend.
In the future, there will surely be published articles on the Post-Finasteride Syndrome that will discuss potential mechanisms, as written by medical professionals and research scientists â and Iâm sorry to say, but all of the efforts you are currently undertaking to research & convince yourself the post-Fin hypogonadism, lack of response to androgenic treatments, gynecomastia, penile shrinkage, loss of nocturnal/morning/spontaneous erections etc are going to be attributable to âzinc deficiencyâ, âceliac diseaseâ, âcopper toxicityâ or whatever other concepts have been mentioned around here, will be in vain.
You are wasting your time following this path â and I donât say that to spite you or others latching onto naturopathy as a cure, but to give you some real objective perspective. I can 99.99% guarantee that whatever is published in a scientific journal on this problem will have nothing to do with what you currently think it does, and are so busy trying to convince others as âthe cureâ.
When the real articles on this problem come out and are published in scientific journals, as authored by researchers with PHDs who have the knowledge to understand the issues at a level beyond anyone on this site, all the speculating on this forum and related nonsense will be put to an end â we will finally have something we can use with doctors, generate real awareness with, and start real investigations to find a cure.
Until then, this is all just speculation and opinion, much of it based on nothing but blind faith⌠which is sad, considering everyone on this forum can draw from the scientific articles describing how Finasteride operates here viewforum.php?f=8 , so we can all at least be on the same page when discussing this problem and the drugâs mechanisms of action.
When did i imply fin caused?
I implyed it was aquired via a zinc def. or it was and underlying condition.
You are sad mew, i am happy. But whatever.
Interestingly enough i found out my sister is gluten intolerant last night. Im one hell of a brother.
Go get your zinc levels done and celiac tests done, see how you go Mew, shut me up good and proper, if you got the balls.
You said it yourself: âCant get the zinc cause of celiacsâ, therby implying we have Zinc deficiency and that we cannot absorb Zinc due to Celiac disease.
You implied Finasteride as the root cause of this based on nothing but your own personal theory which is not backed by anything remotely scientific:
"So when our estrogen gets to a point/or when our 5ar2 gets stopped it must prompt a âzinc dumpâ.
Whereâs the studies showing Finasteride causes a âzinc dumpâ and that Finasteride use leads to celiac disease? Oh thatâs right, there is no such thing because youâve just created something out of thin air, based on nothing but your own personal thoughts, and there is no research that substantiates such claims.
Another blanket statement based on nothing, completely unproven unless everyone on this forum were to have such tests done that came back deficient. You are extrapolating your personal opinion and test results and applying them to everyone else when you in fact might be the odd man out.
âbody wants to be copper dominantâ⌠again, your personal theory based on nothing but opinion and belief. And even if you are âcopper dominantâ, so what? That doesnât mean Finasteride caused your issue.
Maybe youâve been drinking tap water for years that has large amount of copper, maybe you take a multivitamin that has contributed to excess copper levels, maybe you eat copper fortified foods⌠you are looking for scapegoats for your Finasteride related problems and have simply decided to choose copper as your basis.
And you base this statement on what scientific research or mechanism that this is even plausible? Because right now itâs simply personal opinion.
Honestly, a confrontational attitude and disrespectful language is not cool and will not be tolerated. Weâre here to work together, share info and try and help each other as best we can⌠so if the whole forum gets tested and turns out to be Zinc deficient or closet celiacs, it will just be another pattern weâve identified.
As for âshutting you up good and properâ, donât worry â Iâll let the scientific researchers who publish their papers on our problem in the future take care of that. It will be interesting to see what they propose as the mechanism for our issues, and a breath of fresh air to get rid of all these red herrings and grasping for straws that some people around here tend to do.
Mew i respect you with all my heart for what you have done for the cause and i would almost go to the point of saying with out you i would probably be dead. I dont know you but i would gladly go into battle with you. That is what i think of you and i dont want to get into a slugging match with you, which is a bit hypocritical considering the agression in my last post.
I would like to leave this as i gotta do what i gotta do and you gotta do what you gotta do and as always i will keep the board informed in my progress.
[Size=4]Androgen receptors in ventral prostate glands of zinc deficient rats.[/size]
Chung KW, Kim SY, Chan WY, Rennert OM.
Abstract
Androgen binding has been studied in the prostate cytosol of zinc deficient rats by charcoal assays. Rats were housed individually in plastic cages and maintained on a zinc deficient diet for 3 months. The cytosol fraction of prostate gland was incubated with various concentrations of tritiated methyltrienolone (3H-R1881, a synthetic androgen) alone or in the presence of 500-fold excess of radioinert R1881. [Size=4]Scatchard analysis of the data revealed that the number of androgen binding sites in the cytosol fraction of the zinc deficient rat prostate was 31 +/- 5.2 fmol/mg cytosol protein. This was significantly lower than that (84 +/- 11.5 fmol/mg protein) of the controls. [/size]Their dissociation constant (Kd = 1.6 +/- 0.6 nM) on the other hand was not different from that (1.7 +/- 0.7 nM) of control animals. [Size=4]This decrease in the concentration of cytosol receptor sites in the zinc deficient state suggests that this metal is involved in the androgen-binding process in the target cells.[/size]
[Size=4]Complete androgen insensitivity due to deletion of exon C of the androgen receptor gene highlights the functional importance of the second zinc finger of the androgen receptor in vivo.[/size]
Quigley CA, Evans BA, Simental JA, Marschke KB, Sar M, Lubahn DB, Davies P, Hughes IA, Wilson EM, French FS.
Department of Pediatrics, University of North Carolina, Chapel Hill 27599-7500.
Abstract
Androgen-dependent gene transcription is mediated by the androgen receptor (AR) through interaction of its central zinc finger region with specific DNA sequences on target genes. Failure of this receptor-mediated gene transcription results in end organ resistance to androgens-the androgen insensitivity syndromes. In a pair of siblings with complete androgen insensitivity who had supranormal levels of androgen binding in genital skin fibroblasts, polymerase chain reaction and Southern blot analysis of the androgen receptor gene confirmed by polymerase chain reaction and sequence analysis of AR cDNA, revealed an in-frame deletion of exon C encoding the second zinc finger of the receptor. The mutant receptor in cultured genital skin fibroblasts had normal androgen binding affinity and was localized in the nucleus but had markedly reduced DNA-binding affinity. When recreated in vitro and tested in a cotransfection assay system the mutant receptor failed to activate transcription of an androgen-responsive reporter gene. This naturally occurring mutation highlights the functional dependence of the AR upon its second zinc finger in vivo and explains the complete insensitivity to androgen manifest by the affected individuals despite increased androgen binding. The elevated AR levels in the subjectsâ genital skin fibroblasts further suggests a possible role for the second zinc finger in autoregulation of receptor levels in vivo.
j899 failed zinc test aswell, so im not the lone wolf. To my knowledge we are the only two to have them.
[Size=4]Vitamin B12 deficiency in untreated celiac disease.[/size]Dahele A, Ghosh S.
Department of Medical Sciences, University of Edinburgh, Western General Hospital, Scotland.
Abstract
OBJECTIVES: Iron and folate malabsorption are common in untreated celiac disease as the proximal small intestine is predominantly affected. Vitamin B12 deficiency is thought to be uncommon, as the terminal ileum is relatively spared. This study aims to investigate the prevalence of vitamin B12, deficiency in patients with untreated celiac disease.
METHODS: Prospective study of 39 consecutive biopsy-proven celiac disease patients (32 women, seven men; median age 48 yr, range 22-77 yr) between September 1997 and February 1999. The full blood count, serum vitamin B12, red blood cell folate, and celiac autoantibodies (IgA antigliadin and IgA antiendomysium antibodies) were measured before and after a median of 4 months (range 2-13 months) of treatment with a gluten-free diet. In vitamin B12-deficient patients, intrinsic factor antibodies and a Schilling test, part 1, were performed.
RESULTS: A total of 16 (41%) patients were vitamin B12 deficient (<220 ng/L) and 16 (41%) patients (11 women and live men) were anemic. Concomitant folate deficiency was present in only 5/16 (31%) of the vitamin B12 patients. The Schilling test, performed in 10 of the vitamin B12-deficient patients, showed five low and five normal results. Although only five patients received parenteral vitamin B12, at follow-up the vitamin B12 results had normalized in all patients. Acral paraesthesia at presentation in three vitamin B12-deficient patients resolved after vitamin B12 replacement.
CONCLUSIONS: [Size=4]Vitamin B12 deficiency is common in untreated celiac disease, and concentrations should be measured routinely before hematinic replacement. Vitamin B12 concentrations normalize on a gluten-free diet alone, but symptomatic patients may require supplementation.[/size]