DHEA: 7.5 Range 1.4 - 12 ng/ml
ALDOSTERONE: 15 Range 4 - 31 ng/ml
IGF-1: 181 Range 117 - 328 ng/ml
ANTI DIURETIC HORMONE (VASOPRESSIN) 72.4
Reference Range: lower than 6.7 pg/ml !!!
Now i am wondering if it is wrong, i am going to call the lab or repeat the the vasopressin test, mine is 10 times above the limit.
Correiovip,
Have you had any other blood tests done on your T levels since Aug 25th? I noticed you had some other tests done, but I didn’t see any additional tests for Total T, Free T and SHBG.
I had a few blood tests done over a four month period and my Total T was dropping, but my free T was going up. I’m curious to know if the same is happening with you.
If a guys SHBG level is going down, then the Total T level should go down as well. Once this T is released of the SHBG (sex hormone binding globulin) Free T Should be increasing. I’m guessing this is what should be looking for.
Maybe Mew can let us know if this is correct or is it more complicated?
Bostonusa,
I test T and free T every six months or so. In the past three and half years, the rate T/free T has been stable on me. Even when my total T went down, my free T seemed to be high in percentage.
I have an appointment with Dr. Crisler on Thursday, November 5th, i talk to him about taking Tamoxifen and HGH.
oh ok, I did notice your free T didn’t look bad at all on your last test. Wow, so your traveling to the US to see Chrisler. Good luck, I hope he can get you going in the right direction. Do keep us posted on what treatments you end up trying.
I would be very interested to hear your results if you end up taking the HGH. That seems to be the trump card, if all else fails.
Could this be our solution? Did some research on it…some of us seem to have a low level of this…Read below…
Source: en.wikipedia.org/wiki/Vasopressin
Arginine vasopressin (AVP), also known as vasopressin, argipressin or antidiuretic hormone (ADH), is a hormone found in most mammals, including humans.[1] Vasopressin is a peptide hormone. It is derived from a preprohormone precursor that is synthesized in the hypothalamus and stored in vesicles at the posterior pituitary. Most of it is stored in the posterior pituitary to be released into the blood stream; however, some of it is also released directly into the brain.
Physiology
[edit] Function
One of the most important roles of AVP is to regulate the body’s retention of water; it is released when the body is dehydrated and causes the kidneys to conserve water, thus concentrating the urine, and reducing urine volume. In high concentrations, it also raises blood pressure by inducing moderate vasoconstriction. In addition, it has a variety of neurological effects on the brain, having been found, for example, to influence pair-bonding in voles.
A very similar substance, lysine vasopressin (LVP) or lypressin, has the same function in pigs and is often used in human therapy.
[edit] Kidney
Vasopressin has three effects by which it contributes to increased urine osmolarity (increased concentration), and decreased urine excretion. These are:
V2 receptors, G protein-coupled receptors coupled to Gs, on the basolateral membrane of the cells lining the distal convoluted tubules and conducting tubules (in the nephron) have an active site for AVP. The G protein, which is in contact with the V2 receptor inside the cell, move to adenylyl cyclase, triggering adenylyl cyclase to convert ATP into cAMP, plus 2 inorganic phosphates. The cAMP cascade then triggers the insertion of Aquaporin-2 water pores by exocytosis of storage vesicles.
The repressor protein that regulates the gene for protein kinase A (PKA) has a binding site for cAMP, causing the repressor protein to change its shape and leave the operator region of the gene. This allows for transcription of the gene for PKA. PKA then signals ATP to dephosphorylate, providing energy for vesicles (which contain aquaporin channel proteins in their membranes) to fuse with the apical membrane of the cell. Calcium ions may also be required in this process, therefore it may be possible that, PLC (phospholipase C- beta) has an associated role. It should be noted that PLC can be activated by a G-protein coupled receptor.
ADH’s second effect on the kidney is to increase the permeability of the papillary portion of the collecting duct to urea, allowing increased reabsorption of urea into the medullary interstitium, down the concentration gradient created from the removal of water in the cortical collecting duct.
The third effect that AVP has on the kidney is that it stimulates sodium reabsorption in the thick-ascending loop of Henle by increasing the activity of the Na±K±2Cl–cotransporter.
[edit] Cardiovascular system
Vasopressin increases peripheral vascular resistance and thus increases arterial blood pressure. This effect appears small in healthy individuals; however it becomes an important compensatory mechanism for restoring blood pressure in hypovolemic shock such as occurs during hemorrhage.
[edit] Central nervous system (CNS)
Vasopressin released within the brain has many actions:
It has been implicated in memory formation, including delayed reflexes, image, short- and long-term memory, though the mechanism remains unknown, and these findings are controversial. However, the synthetic vasopressin analogue desmopressin has come to interest as a likely nootropic.
Vasopressin is released into the brain in a circadian rhythm by neurons of the Supraoptic nucleus.
Vasopressin released from centrally-projecting hypothalamic neurons is involved in aggression, blood pressure regulation and temperature regulation.
In recent years there has been particular interest in the role of vasopressin in social behavior. It is thought that vasopressin, released into the brain during sexual activity, initiates and sustains patterns of activity that support the pair-bond between the sexual partners; in particular, vasopressin seems to induce the male to become aggressive towards other males.[2]
Evidence for this comes from experimental studies in several species, which indicate that the precise distribution of vasopressin and vasopressin receptors in the brain is associated with species-typical patterns of social behavior. In particular, there are consistent differences between monogamous species and promiscuous species in the distribution of AVP receptors, and sometimes in the distribution of vasopressin-containing axons, even when closely-related species are compared.[3] Moreover, studies involving either injecting AVP agonists into the brain, or blocking the actions of AVP, support the hypothesis that vasopressin is involved in aggression towards other males. There is also evidence that differences in the AVP receptor gene between individual members of a species might be predictive of differences in social behavior. One study has suggested that genetic variation in male humans effects pair-bonding behavior. The brain of males uses vasopressin as a reward for forming lasting bonds with a mate, and men with one or two of the genetic alleles are more likely to experience marital discord. The partners of the men with two of the alleles affecting vasopressin reception state disappointing levels of satisfaction, affection, and cohesion. [4]
[edit] Control
Vasopressin is secreted from the posterior pituitary gland in response to reductions in plasma volume, in response to increases in the plasma osmolality, and in response to cholecystokinin by the small intestine:
Secretion in response to reduced plasma volume is activated by pressure receptors in the veins, atria, and carotids.
Secretion in response to increases in plasma osmotic pressure is mediated by osmoreceptors in the hypothalamus.
Secretion in response to increases in plasma Cholecystokinin is mediated by an unknown pathway.
The neurons that make AVP, in the hypothalamic supraoptic nuclei (SON) and paraventricular nuclei (PVN), are themselves osmoreceptors, but they also receive synaptic input from other osmoreceptors located in regions adjacent to the anterior wall of the third ventricle. These regions include the organum vasculosum of the lamina terminalis and the subfornical organ.
Many factors influence the secretion of vasopressin:
Ethanol (alcohol) acts as an antagonist for AVP in the collecting ducts of the kidneys, which prevents aquaporins from binding to the collecting ducts, and prevents water reabsorption.
Angiotensin II may stimulate the secretion of AVP.[5]
[edit] Secretion
The main stimulus for secretion of vasopressin is increased osmolality of plasma. Reduced volume of extracellular fluid also has this effect, but is a less sensitive mechanism.
The AVP that is measured in peripheral blood is almost all derived from secretion from the posterior pituitary gland (except in cases of AVP-secreting tumours). However there are two other sources of AVP with important local effects:
Vasopressin is produced in the PVN and SON and travels down the axons through the infundibulum within neurosecretory granules that are found within Herring bodies, localized swellings of the axons and nerve terminals. These carry the peptide directly to the posterior pituitary gland, where it is stored until released into the blood.
Vasopressin is also released into the brain by several different populations of smaller neurons (see below).
The vasopressins are peptides consisting of nine amino acids (nonapeptides). (NB: the value in the table above of 164 amino acids is that obtained before the hormone is activated by cleavage). The amino acid sequence of arginine vasopressin is Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly, with the cysteine residues forming a sulfur bridge. Lysine vasopressin has a lysine in place of the arginine.
The structure of oxytocin is very similar to that of the vasopressins: it is also a nonapeptide with a disulfide bridge and its amino acid sequence differs at only two positions (see table below). The two genes are located on the same chromosome separated by a relatively small distance of less than 15,000 bases in most species. The magnocellular neurons that make vasopressin are adjacent to magnocellular neurons that make oxytocin, and are similar in many respects. The similarity of the two peptides can cause some cross-reactions: oxytocin has a slight antidiuretic function, and high levels of AVP can cause uterine contractions.
Here is a table showing the superfamily of vasopressin and oxytocin neuropeptides:
[edit] Pharmacology
[edit] Vasopressin analogues
Vasopressin agonists are used therapeutically in various conditions, and its long-acting synthetic analogue desmopressin is used in conditions featuring low vasopressin secretion, as well as for control of bleeding (in some forms of von Willebrand disease) and in extreme cases of bedwetting by children. Terlipressin and related analogues are used as vasoconstrictors in certain conditions. Use of vasopressin analogues for esophageal varices commenced in 1970.[13]
Vasopressin infusion has been used as a second line of management in septic shock patients not responding to high dose of inotropes (e.g., dopamine or norepinephrine). It had been shown to be more effective than epinephrine in asystolic cardiac arrest.[14] While not all studies are in agreement, a 2006 study of out-of hospital cardiac arrests has added to the evidence for the superiority of AVP in this situation, but these studies relied on sub-group analysis and better designed prospective studies show no benefit in ACLS.[15][16]
en.wikipedia.org/wiki/Tolvaptan
Tolvaptan (INN), also known as OPC-41061, is a selective, competitive arginine vasopressin receptor 2 antagonist used to treat hyponatremia (low blood sodium levels) associated with congestive heart failure, cirrhosis, and the syndrome of [b]inappropriate antidiuretic hormone /b. Tolvaptan was approved by the U.S. Food and Drug Administration on May 19, 2009, and is sold by Otsuka Pharmaceutical Co. under the trade name Samsca.
Tolvaptan is also in fast-track clinical trials[3] for polycystic kidney disease. In a 2004 trial, tolvaptan, when administered with traditional diuretics, was noted to increase excretion of excess fluids and improve blood sodium levels in patients with heart failure without producing side effects such as hypotension (low blood pressure) or hypokalemia (decreased blood levels of potassium) and without having an adverse effect on kidney function.[4
Annon1,
Vasopressin is part of the same issue we all probably have after propecia: a supressed pituitary. So far, i have found altered levels in four hormones directly released by pituitary: LH, FSH, Growth Hormone, and Vasopressin. To me it is clear enough that i have induced hipopituitarism. People are different, and the pituitary releases many hormones, so the symptoms may vary, but it is the same problem. Some might have 5 hormones affected, others 2 or 3, but we all need to take a close look at this. To me our problem is a supressed pituitary + 5 alpha reductase deficiency.
But as far as Vasopressin, my interpretation is that my body is trying to compensate for the lack of DHT and that is why my Vasopressin level is ten times the top range reference. I atribute to this hormone being so high the fact that i am able to have good erections when laying down. Also, my brain fog is not so severe and my blood pressure never changed from 12/8. The body is a wonderful machine and it finds ways of compensate some of the damage. Unfortunately, DHT s role is very important and the body can’t do miracles alone in our cases.
Bostonusa,
I am already in USA, it has been a week. I am in Boston too, and i am heading to Michigan tomorrow. I am going to spend a pretty long time in USA, as i plan to do my treatment here. I will keep you all informed, maybe i will start a recovery thread, to post like a journal how i am feeling with the medications.
correiovip,
I have noticed that pretty much every blood test I have seen posted on this board shows Low LH and Low FSH. Some guys have a normal total T and Low Free T others just opposite. I actually don’t think I have even seen one blood test where the LH and FSH levels are normal.
I am convinced a big part of the problem resides in the Pituitary gland and we need to get these hormones in check as well as T to get back to normal. I wonder if raised T levels would improve LH & FSH or if they operate more independently.
I hope you at least get some enjoyment in the US while your here.
I am scared it is not just pitutary but hypothalamus. GnRh is not coming down in sufficient quantity.
I am saying this because clomid or nolvadex has been uneffective to restart HPTA so far.
again Sawpalmetto or Fin no matter what you take , symptoms are the same. My LH dropped from 4 (1-9) to 1. so did my T-level and still declining.
spstriken,
When you say your T level is declining do you mean just your Total T or your Free and Total T are declining? My last three blood tests showed my Total T declining, but my Free T was going up.
I posed the question before, but no one answered. Is this what should be looking for? If we look at SHBG, Free & Total T. The SHBG is binded to total T, if the SHBG lowers some of the total T should free up and become Free T? I’m hoping one of the boar experts can answer this one.
I have been told by three doctors that Free T is not an accurate essay or a reliable indicator, yet we all know how important Free T is to our sexual well being.
Hey
You’re getting a bit confused here.
Our problem is not to do with pituitary suppression. If you want to test this, just take Tamoxifen or Clomid. Your pituitary will go into overdrive, LH and FSH will climb high, and T will get to the top of the range. And probably you won’t feel any better. Tamox sent my LH and FSH high and my T to the top of the range, and I felt no different.
There is widespread misunderstanding over interpretation of LH and FSH levels on this forum. LH is the signal that tells your testicles to produce testosterone: we all know that. In a healthy 18-year-old man, LH is likely to be very low and T will be high. Low LH and high T is the optimum situation: it means your testicles are working very efficiently, and they only require the smallest prompt from the pituitary to crank out a lot of testosterone.
As we age and the testicles become less efficient, LH tends to climb: now the testicles need more of a push in order to produce the same amount of testosterone. In men with primary hypogonadism - where the testicles don’t work at all - LH climbs very high, but still the testicles do not respond to it and so they produce nothing.
Our T is low not because the pituitary is suppressed.
Read the threads on androgen insensitivity to learn more about our best thinking on why T is low. At the moment you’re re-treading old ground. If this problem was about low LH and pituitary suppression, it would be easy to solve.
The vassopresin result is most likely a lab error.
You can still try Tamox to boost T as high as possible, to see if that helps. If it doesn’t and you still want to pursue treatment, try TRT.
Scaredmale,
I disagree with you. I think you felt no difference when you used tamox because we also are suffering from 5 alpha reductase deficiency. Because you did not feel any difference sexually, does not mean it did not benefit your metabolism. I know restoring my t levels to the upper limit is only part of the problem, the second part is finding a drug that will “turn on” 5 alpha reductase again.
What i expect from using tamox is to improve the insulin resistance i developed i the past year, feel a little more energy, prevent bone loss and other problems. By any means i am expecting to restore my sexual function completely using only tamox.
Feeling a difference or not, i don’t agree it is healthy to live with 75 y.o. T levels. You might not feel a difference, but i am sure it benefited you, even if in the long run.
About pituitary supression, read this quote please:
“Generally, the finding of a combination of a low pituitary hormone together with a low hormone from the effector gland is indicative of hypopituitarism.[11] Occasionally, the pituitary hormone may be normal but the effector gland hormone decreased; in this case, the pituitary is not responding appropriately, and the combination of findings is still suggestive of hypopituitarism”
Well, in my case i have low FSH, low LH and low growth hormone. The effect gland hormone (testosterone) is decreased.
About the vasopressin test, we can not affirm it is an error. I’ve been using this same lab for 3 years, and results are very consistent. We can only say it is an error if i test it again and it shows a big difference.
My total and free both declining.Total T within range but at lower end while free T below the range.
When I tried Agel I felt alot of energy for first few weeks that tells my or our problem is purely T-level
4 months back my LH was 4 (scale 1-9) and free T was 31 (scale 25-80)
now my free T is 24 (25-80) and LH is 1. What is it telling now? free T is lowering with lowering LH.
Hi Corriovip
Look up Awor’s post on why a dysfunction of the 5AR II enzyme does not do a very good job of explaining our condition. In brief: if this were a problem about conversion of T to DHT, we would still be able to feel the benefits of T. But many of us raise T higher, and feel no benefit: not even the benefit that we’d expect from T quite apart from DHT. People who suffer from 5AR II deficiency have no problem building muscle, because T is the primary muscle builder. So if 5AR II deficiency is our problem, why is muscle wasting a part of our condition?
Tamox took my T from bottom of the range to top of the range. Not only did I not feel any sexual response, I felt no response whatsoever. If our problem were about T to DHT conversion, I’d expect at least to feel some more energy from the higher T, and increased muscle mass. Also, there were no measurable effects on my body from the increase in T on my body. I have a very low red blood count. As you know, T stimulates production of red blood cells in normal men: whenever you increase T, red blood cell count should climb. Mine did not change at all. What does this indicate? It seems to indicate that we are simply not responding to T in the normal way: our bodies cannot use it any more. Given this, I doubt that higher T was doing the other things we usually expect: stimulating bone maintenance, etc.
Of course it is not healthy for a normal man to live with low T levels. But we are faced with a greater problem that simply low T. We are faced with the problem of insensitivity to T. That means we face all the health problems associated with low T, but raising T makes little difference.
But you don’t have to take my word for it: take the Tamox and see if you feel more energy, if you become less insulin resistant, etc. It may be that it does help. But that will be because you have raised T high enough to partially overcome your insensitivity to T, not because you have overcome pituitary suppression. We are not pituitary suppressed.
If you do feel better on Tamox, or on TRT, then you’ve come as close to treating this problem as we can get at the moment. Taking TRT, feeling much better, and then deciding to stop because you don’t feel like taking it any more, like SpStriken did, is insane.
If our 5ar2 isn’t working, how come we still lose hair? I don’t believe the drug can switch the enzyme off.
I am not losing my hair at the same pace, i still have a head full of hair.
Scaredmale,
Have you tested 3 adiol-G?
Androstenadiol Glucoronide (3 adiol-G) is a product of DHT conversion by 5 alpha reductase II. My test result is 2.44 ng/dl (range: 3.5 to 22.00 ng/dl) To me this is a clear indication that i have a 5 alpha reductase II deficiency (3 adiol G blood test is very precise).
5 alpha reductase II deficiency involves a lot more than conversion from T to DHT. What about conversion from DHT to 3 adiol G? What about conversion from Progesterone to Allopregnanolone? I never said it was a matter of T/dht conversion or insuficient dht, i said it is 5 alpha reductase II deficiency, there is a lot more involved. There seems to be a role of 5 alpha in the CNS. Science does not know how it works… Why discard this theory if we have a blood test that indicates we are 5 alpha II deficient?
Have you ever heard of pollycistic ovary syndrome that some women have? These women develop some masculine characteristics, like facial hair among other problems. What stands out on their blood test? Elevated Androstenadiol Glucoronide.
My point is, if we already confirmed there is an issue with 5 alpha reductase, why not pursue a drug that can activate it? Can you absolutely guarantee that this problem is not the culprit of our disease? Can anybody here garantee that if we correct the 3 adiol G this will not solve our symptoms? Can we say, for sure, that 3 adiol G is not the substance missing to allow us to feel the androgen power again? I think we are not in a position to discard any theories, specially if there is a blood test backing it.
You re talking about Androgen Insensitivity. Funny enough, 3 adiol G is the most active form of androgen in the male body. We are talking about the same problem… Of course you re going to feel very little difference if you bump your T up, because 5 alpha will still not be converting DHT to 3 adiol G, besides other roles 5 alpha II might have that science doesn’t even know. 5 alpha reductase II deficiency could very weell be what is causing androgen insensitivity
Now, about my case, the reason i am going to take tamox is because i was much better untill June 2009. I had to take prednisone (corticoids) against a severe allergie reaction and lung inflammation (never had this prior to propecia). Since June my T dropped from around 650 to 470 in the same scale. And i have been feeling much worse. My intention is to feel like i was feeling before June, i know Tamox by itself is not a cure.
Correiovip,
Please let us know how your apt goes with the dr this week. I can’ t remember if you were going to see Shippen or Chrisler, but I am real curious to hear what he has to say. I am also curious to see how he reacts to your idea about wanting to go on HGH.
I have had no luck with any drs wanting to prescribe anything for me and I know how controversial HGH is. I am going to see one of these drs if things don’t improve for me in the next two months with my blood tests.