Dietary zinc deficiency alters 5 alpha-reduction

Dietary zinc deficiency alters 5 alpha-reduction and aromatization of testosterone and androgen and estrogen receptors in rat liver.
Om AS, Chung KW.

Department of Food and Nutrition, College of Home Economics, Hanyang University, Seoul, Korea.

Abstract
We studied the effects of zinc deficiency on hepatic androgen metabolism and aromatization, androgen and estrogen receptor binding, and circulating levels of reproductive hormones in freely fed, pair-fed and zinc deficient rats. Hepatic conversion of testosterone to dihydrotestosterone was significantly less, but formation of estradiol from testosterone was significantly greater in rats fed the zinc-deficient diet compared with freely fed and pair-fed control rats. There were significantly lower serum concentrations of luteinizing hormone, estradiol and testosterone in rats fed the zinc-deficient diet. No difference in the concentration of serum follicle-stimulating hormone was observed between the zinc-deficient group and either control group. Scatchard analyses of the receptor binding data showed a significantly higher level of estrogen receptor in zinc-deficient rats (36.6 +/- 3.4 fmol/mg protein) than in pair-fed controls (23.3 +/- 2.2 fmol/mg protein) and a significantly lower level of androgen binding sites in rats fed the zinc-deficient diet (6.7 +/- 0.7 fmol/mg protein) than in pair-fed control rats (11.3 +/- 1.2 fmol/mg protein). There were no differences in hepatic androgen and estrogen receptor levels between freely fed and pair-fed controls. These findings indicate that zinc deficiency reduces circulating luteinizing hormone and testosterone concentrations, alters hepatic steroid metabolism, and modifies sex steroid hormone receptor levels, thereby contributing to the pathogenesis of male reproductive dysfunction.

ncbi.nlm.nih.gov/pubmed/8613886

[Size=4]This below study is huge for us, you must read it. Im not shitting you guys. Ive posted some shit this week forget that and read this[/size]

jn.nutrition.org/cgi/reprint/126/4/842.pdf

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Im wondering if the chosen few on propecia help had a pre-existing zinc deficiency or we have some issue absorbing zinc…cause some people just get better :exclamation:…like the user manual says :angry:

Zinc sulfate is the most frequently used supplement. This is the least expensive form, but it is the least easily absorbed and may cause stomach upset. …

66.148.0.6/zinc1.htm

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[Size=4]Effect of zinc deficiency on the protein expression of vitamin D receptor and calcium binding protein in growth-stage rats duodenal mucosa][/size]
[Article in Chinese]

Yu XD, Yan CH, Yu XG, Gao Y, Xu J, Shen XM.

Xin Hua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai Institute of Pediatric Research, Shanghai 200092, China.

Abstract
OBJECTIVE: To study the effect of zinc deficiency on the protein expression of vitamin D receptor (VDR) and calcium binding protein (CaBP) in growth-term rats duodenal mucosa and to clarify the mechanism of zinc deficiency affecting the calcium absorption by gene transcription.

METHODS: Thirty weaning male rats were randomly divided into three groups: zinc deficiency (ZD), paired-fed (PF) and zinc adequation (ZA). The ZA group received a diet containing 29.5 microg/g diet ad libitum; the ZD group received a diet containing less than 0.4 microg zinc/g diet ad libitum. To eliminate the effect of zinc deficiency on appetite, the PF group received a zinc-adequate diet restricted to the quantity of food consumed the previous day by the ZD rats. After 15 days feeding, duodenal mucosa was taken to measure expression of the protein of VDR and of CaBP by immunohistochemistry and Western-blotting.

RESULTS: [Size=4]Immunohistochemistry demonstrated that the intestinal mucosal expression of both VDR protein and CaBP protein in ZD rats significantly decreased. Analysis of the photographs showed that the number of cells expressed VDR protein in ZD rats was significantly less than that of the PF and ZA rats [/size](P < 0.001). The number of cells which expressed VDR protein in ZD, PF, and ZA groups was 52, 162, and 220, and the number of cells which expressed CaBP protein was 169, 240 and 280 (F = 132 and 22, P < 0.001). Western-blotting showed similar results.

CONCLUSIONS: [Size=4]Zinc deficiency, by changing the activity of VDR, changes the protein expression of VDR,[/size] and thus affects the transcription of the target gene CaBP, resulting in the absorption of calcium that causes allo-osteogenesis.

ncbi.nlm.nih.gov/pubmed/16623997

Minerals for Mental Health
Some essential elements can act as brain boosters, working as preventive medicine against mental illness.
Of the minerals that can help to protect the nervous system, the most important are zinc and magnesium. [Size=4]Zinc is
essential to the synthesis of RNA, DNA and protein, and to the maintenance of vitamin A levels in the blood. A
zinc deficiency can cause confusion and difficulties with taste and smell.[/size] When older people are not eating properly,
zinc deficiency may be at fault since food is less appetizing when the senses of smell and taste are reduced.
In the 1950s, the late Carl Pfeiffer, Ph.D., M.D., former director of the Brain Bio Center in Princeton, New Jersey,
found that trace metal imbalances, for example copper and zinc, can contribute to mental disorders. William Walsh,
Ph.D., a former research scientist at Argonne National Laboratories and a colleague of Dr. Pfeiffer estimates that
95 percent of violent individuals suffer from mineral imbalances that predispose them to bad behavior.”
Dr. Walsh discovered that violent individuals often had an imbalance of copper to zinc and low levels of sodium,
potassium and manganese. He found people who were delinquent, impulsive and irritable were low in all the trace
minerals including calcium and magnesium.
An article in Biological Psychiatry reported that of patients hospitalized with major depression or schizophrenia,
magnesium was significantly lower in those who made suicide attempts. The authors believe magnesium has a role
in regulating serotonin levels of the brain.”
[Size=4]Remember, you’re not what you put into your mouth, you’re what you absorb and digest and deliver to cells. A
vitamin or mineral tablet is only one to five percent absorbable. Since the process of digestion is a process of
liquefaction, your body has to take a hard rock tablet and turn it into solution. This may not be possible due to a
number of factors, such as inadequate stomach acid, food allergies and intestinal problems. [/size]This is why it is so
important that when you decide to supplement, you target minerals in solution. Look for a good, easily absorbable,
derived-from-nature mineral blend in solution. Formulations in solution help provide the maximum absorption
ratios.

enterhisrest.org/articles/mental_illness.pdf

Do we have any vitamin A tests in the house?..I’ll tack it on today, how bout that

[Size=4]In terms of zinc and thyroid function, Morley et al. (1980) and Kralik et al. (1996) reported that zinc deficiency significantly reduced serum T3 concentrations in rats. In a zinc depletion-repletion study conducted in humans, Wada and King (1986) observed that circulating TSH, total T4 and free T4 tended to decrease during the depletion phase, returning to control levels after zinc repletion.[/size]

jn.nutrition.org/cgi/content/ful … 74#Results

OMG did our body’s dump all the zinc while on fin because it deemed it unneccessary…and for some reason now doesnt absorb it via the GI tract…holy fuck…whos piss was filthy dirty and stinky and frothy when on or coming off fin…holy fucken shit…sorry about the language mew

Can someone who is just coming off fin do a 24 hour urine test…please please please

Heres your adrenal problems

[Size=4]Zinc deficiency affects the composition of the rat adrenal gland.[/size]
Rothman RJ, Leure-duPree AE, Fosmire GJ.

Abstract
The response of the adrenal gland to zinc deficiency was examined in male weanling rats. In comparison with decapsulated adrenals from ad libitum fed controls, glands from zinc deficient rats had greater relative weight (mg/g body wt), DNA concentration, and total lipid and cholesterol concentrations as well as a smaller protein/DNA ratio. Several of these differences (protein/DNA and cholesterol concentration) could be attributed to the inanition accompanying zinc deficiency, as zinc deficient values were similar to those of pair fed controls. Values for total DNA and protein concentration were similar for all groups. Electron micrographs of the zona fasciculata showed a small number of lipid droplets in the adrenals from ad libitum fed controls, an increase in lipid droplets from pair fed controls, and an even more striking increase in lipid droplets from the zinc deficient adrenals. The increased adrenal lipid composition in the zinc deficient group may be secondary to enhanced steroidogenesis or a zinc deficiency-induced defect of lipid metabolism.

ncbi.nlm.nih.gov/pubmed/3714717

Shit guys…10 years of sufferering…

These are a bit spamish but they all say the same thing…[Size=4]vitamin d deficiency causes cracking joints[/size]
thestudentroom.co.uk/showthr … ?t=1028157
wiki.answers.com/Q/My_Joints_are … _a_vitamin
healthproductreviewers.com/s … sh-it.html
vegtalk.org/health-forum/joi … t1571.html
eatmoveimprove.com/2010/03/c … ing-oh-my/

and so on

[Size=4]The effects of severe zinc deficiency on skeletal muscle are well defined (32). Rats fed diets very low in zinc exhibit reduced muscle growth and decreased muscle DNA concentrations.

Animal experiments have shown the importance of zinc for skeletal muscle performance and resistance to fatigue [/size]

ajcn.org/cgi/content/full/72/2/585S#SEC6

[Size=4]Zinc deficiency and tinnitus☆[/size]

Kentaro Ochi, Hirotsugu Kinoshita, Mutsumi Kenmochi, Hirohito Nishino, Toru Ohashi

Abstract
Objective: To determine if there is a correlation between serum zinc levels and audiometric performance in tinnitus patients. Methods: Seventy-three patients participated in this study. Patient’s age was restricted to 20–59 years. All patients were examined at the otolaryngology outpatient clinic of the St. Marianna University Toyoko Hospital. The control group consisted of 38 age- and sex-matched healthy volunteers. A blood sample was taken to measure serum zinc levels. Hypozincemia was set at a level of the mean minus one S.D. in the control group. An average hearing sensitivity was calculated as the mean value of hearing thresholds at five frequencies: 250, 500, 1000, 2000, and 4000 Hz. Normal hearing was indicated when the hearing threshold at each of these frequencies was within 20 dB of normal thresholds. Results: There was no significant difference in serum zinc levels between patients with tinnitus and controls. However, patients with tinnitus who had normal hearing had significantly lower serum zinc levels compared to controls. In contrast, no significant difference in serum zinc levels was found between patients with tinnitus who had hearing loss, and controls. A significant correlation between average hearing sensitivity and serum zinc level was observed. Conclusions: [Size=4]These findings suggest that zinc is involved in the generation of tinnitus, especially in patients whose hearing is relatively normal.[/size]

aurisnasuslarynx.com/article/S0385-8146(0200145-1/abstract

Function

Numerous aspects of cellular metabolism are zinc-dependent. Zinc plays important roles in growth and development, the immune response, neurological function, and reproduction. On the cellular level, the function of zinc can be divided into three categories: 1) catalytic, 2) structural, and 3) regulatory (3).

Catalytic role

Nearly 100 different enzymes depend on zinc for their ability to catalyze vital chemical reactions. Zinc-dependent enzymes can be found in all known classes of enzymes (4).

Structural role

Zinc plays an important role in the structure of proteins and cell membranes. A finger-like structure, known as a zinc finger motif, stabilizes the structure of a number of proteins. For example, copper provides the catalytic activity for the antioxidant enzyme copper-zinc superoxide dismutase (CuZnSOD), while zinc plays a critical structural role (4, 5). The structure and function of cell membranes are also affected by zinc. Loss of zinc from biological membranes increases their susceptibility to oxidative damage and impairs their function (6).

Regulatory role

Zinc finger proteins have been found to regulate gene expression by acting as transcription factors (binding to DNA and influencing the transcription of specific genes). Zinc also plays a role in cell signaling and has been found to influence hormone release and nerve impulse transmission. Recently, zinc has been found to play a role in apoptosis (gene-directed cell death), a critical cellular regulatory process with implications for growth and development, as well as a number of chronic diseases (7).

[Size=4]Brain fog[/size]

ABSTRACT

Zinc (Zn) is essential for synthesis of coenzymes that mediate biogenic-amine synthesis and metabolism. Zn from vesicles in presynaptic terminals of certain glutaminergic neurons modulates postsynaptic N-methyl-D-aspartate (NMDA) receptors for glutamate. Large amounts of Zn released from vesicles by seizures or ischemia can kill postsynaptic neurons. Acute Zn deficiency impairs brain function of experimental animals and humans. [Size=4]Zn deficiency in experimental animals during early brain development causes malformations, whereas deficiency later in brain development causes microscopic abnormalities and impairs subsequent function. A limited number of studies suggest that similar phenomena can occur in humans.[/size]

jn.nutrition.org/cgi/content/full/130/2/496S#ABS

Theres more studies out there on this guys i just picked the first one.

Hence:

Abstract
[Size=4]The effect of nutritional zinc deficiency on the zinc concentrations of various brain regions was studied in the pig. Only the cerebellum showed a statistically significant decrease in zinc concentration suggesting that the cerebellum is particularly sensitive to zinc depletion.[/size]
sciencedirect.com/science?_o … archtype=a

[Size=4]Cerebellum[/size]

According to wiki

[Size=4]The cerebellum (Latin for little brain) is a region of the brain that plays an important role in motor control. It is also involved in some cognitive functions such as attention and language, and probably in some emotional functions such as regulating fear and pleasure responses,[1] but it is its function in movement that is most clearly understood. The cerebellum does not initiate movement, but it contributes to coordination, precision, and accurate timing[/size].[Size=4]DING DING DING [/size]It receives input from sensory systems and from other parts of the brain and spinal cord, and integrates these inputs to fine tune motor activity.[2] Because of this fine-tuning function, damage to the cerebellum does not cause paralysis, but instead produces disorders in fine movement, equilibrium, posture, and motor learning.

en.wikipedia.org/wiki/Cerebellum

[Size=4]Dental problems[/size]

The effects of graded levels of dietary zinc on the development and mineralization of teeth and bones and on the susceptibility of teeth to dental caries were studied in young growing rats. Thirty-six weanling male Sprague-Dawley rats were randomly assigned to four dietary treatments: 1) zinc-deficient, less than 1 ppm; 2) 12 ppm zinc; 3) 36 ppm zinc, and 4) 108 ppm zinc. For treatments 2, 3 and 4, rats were pair-fed the quantity of feed consumed by their individual counterparts fed the zinc-deficient diet. After 4 weeks of treatment, growth retardation along with other clinical zinc deficiency signs were observed in rats fed the zinc-deficient diet. The zinc levels in bones and teeth of zinc-deficient rats were lower than those for rats fed supplemental zinc. Increased dietary zinc resulted in greater levels of zinc in bones and teeth, but the levels of calcium decreased. [Size=4]Greater incidences of enamel lesions in mandibular molars were observed in rats fed the zinc-deficient diet than in rats pair-fed zinc-supplemented diets. Furthermore, the effect of zinc deficiency on dental caries of young rats was predominantly at the smooth surfaces of the molars.[/size] Dietary zinc may be an important trace mineral in the process of post-eruptive mineralization of the enamel and may reduce the susceptibility of teeth to caries

biomedsearch.com/nih/Effects … 73428.html

Sorry to crash your party but most of the western world is not deficient in zinc, and nowhere has Finasteride usage been linked to influencing zinc metabolism. Not to mention if one eats a healthy diet or takes multivitamins this is a non-issue, and does not cause penile shrinkage overnight, gynecomastia, or complete loss of libido.

While interesting material from a general health perspective, it’s important to keep things in perspective as they relate to Finasteride’s true mechanisms of action. That’s just my opinion but you are free to believe what you choose.

Sure thing Mew, I respect your opinion. We will see

Finasteride will do this, the inhibition of 5ar2, increased aromatasing of testosterone we know that, im not even concerned about what happens to people who are taking the drug, im concerned about why people dont get better when they stop.
When our hormone panal changes our bodys must be programmed to change our mineral balance, for example woman are copper dominant, men are zinc dominant. So when our estrogen gets to a point/or when our 5ar2 gets stopped it must prompt a “zinc dump” i wish i had have done a urine sample when my piss was at its dirtiest and stinkyiest, because i was definantley expelling something out of my body.

For some reason we are not absorbing zinc, and this is the part that scares me, have we been permanantly changed, idk the only way to find out is get zinc directly into the blood stream.
I have taken a test that shows if zinc is being absorbed and it came back 9 (1-10) which suggests im not doing it very well, they suggested that i supplement heavy with zinc for 6 weeks and retest. Of note i was not supplementing zinc before the first test and im a vegetarian.

Yes when the 5ar2 enzyme is deactivated the body is changed, starting a chain reaction in the body, why it takes such a short time for some men and a long time for others idk. Could be to do with how strongly fin inhibitits the enzyme for each individual and how long it takes for estrogen to rise.

When your 5ar2 isn’t working your not a man, therefore your body doesn’t need zinc and removes it because it thinks your a women and wants to be copper dominant, evidence of this is my copper blood 20.9 and 20.2 (12.3-17.3) respectively. My zincs going to have to be mighty high to make me zinc dominant.

I got my zinc bloods tested today along with vitamin A, and im seeing the doctor tomorrow.
Im a big enough man to admit when im wrong, all going well i wont have to.

I would dare to say that the reason why we have not got better is because our zinc has flat lined and for some reason we are not absorbing or storing the incoming zinc from vitamins and food(via the GI tract) in our bodies. Could be dealing with acute zinc deficiency here. It must also be considered that if you were on fin for a decent amount of time you may have high copper levels in your body. I was on fin for 1 month and my numbers are elevated.

[Size=4]Experimental zinc deficiency in man. Effect on testicular function.[/size]
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. Oligospermia was reversed after zinc supplementation in physiologic amounts. [Size=4]The baseline sperm concentration and total sperm count per ejaculate in all five subjects dropped significantly (p < 0.05) after zinc restriction [/size]and returned to normal 6 to 12 months after zinc supplementation. The decrease in sperm count coincided with decline in Leydig cell function and was reversed after zinc supplementation in low doses. 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.

ncbi.nlm.nih.gov/pubmed/6772723

Why would you have a sex drive if your not producing sperm?

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[Size=4]Hypogonadism in the zinc-deficient rat: localization of the functional abnormalities.[/size]
McClain CJ, Gavaler JS, Van Thiel DH.

Abstract
Hypogonadism is a major manifestation of zinc deficiency in humans and animals, but the mechanisms responsible for this hypogonadism are unclear. We evaluated the pituitary gonadal axis of zinc-deficient rats with basal testosterone, follicle-stimulating hormone, and luteinizing hormone measurements and both luteinizing hormone releasing hormone (GnRH) and human chorionic gonadotropin (HCG) stimulation tests, and we utilized pair-fed (isocalorically fed to zinc deficient), weight-restricted (fed to weigh the same as zinc deficient), and ad libitum-fed controls. Basal testosterone levels were significantly decreased in rats with zinc deficiency (0.6 +/- 0.2 ng/ml) and weight-restricted rats (0.6 +/- 0.1 ng/ml) compared with pair-fed rats (1.2 +/- 0.2 ng/ml) and ad libitum-fed rats (1.6 +/- 0.2 ng/ml, p less than 0.01). Appropriate pituitary response to GnRH were noted in each group of rats. In a final study, zinc-deficient and weight-restricted rats were given injections of 1 U HCG for 5 days. Weight-restricted rats demonstrated a highly significant increase in stimulated testosterone (7.6 +/- 0.9 ng/ml) compared with zinc-deficient rats (2.1 +/- 0.3 ng/ml, p less than 0.0005). [Size=4]We conclude: (1) hypogonadism occurs in both zinc-deficient and weight-restricted rats compared with pair-fed and ad libitum-fed controls; (2) pituitary reserve is intact in zinc-deficient rats; (3) HCG stimulation demonstrates Leydig cell failure in zinc-deficient but not weight-restricted hypogonadal rats; and (4) the hypogonadism in zinc-deficient rats results mainly from Leydig cell failure.[/size]
ncbi.nlm.nih.gov/pubmed/6438259

[Size=4]Improvement of scotopic electroretinograms and night blindness with recovery of serum zinc levels.[/size]Mochizuki K, Murase H, Imose M, Kawakami H, Sawada A.

Department of Ophthalmology, JA Gifu Koseren, Chuno General Hospital, Gifu, Japan. mochi-gif@umin.ac.jp

Abstract
BACKGROUND: We sought to determine the cause of reduced scotopic and photopic electroretinograms (ERGs) and night blindness in a 46-year-old man with liver dysfunction but no history of alcoholism.

CASE: A 46-year-old Japanese man with a complaint of visual difficulties in dim light for 1 month.

OBSERVATIONS: By electrophysiological investigation, the patient was found to have low levels of serum zinc and vitamin A on admission. The rod b wave was unrecordable, and the bright-flash ERGs were reduced, with the a wave > b wave. The amplitudes of the cone and 30-Hz flicker responses were also reduced, and their implicit times were prolonged. Three weeks after admission, the patient’s serum zinc level recovered to normal levels, but his serum vitamin A level was still low. The symptoms of night blindness were gone, and the rod ERGs and single bright-flash responses were within normal limits. However, the cone ERGs and 30-Hz flicker responses were still depressed.

CONCLUSIONS: [Size=4]The recovery of scotopic function together with the recovery of zinc but not vitamin A levels suggests that the ERG changes were most likely related to low zinc levels.[/size]

Tim, what makes you say we cant absorb zinc properly? I get that copper toxicity would be interfering with zinc absorbtion but are you saying you think we simply cant absorb zinc full stop and if so why?

This is interesting because I am still failing a zinc taste test after taking quite a lot of zinc.