There is something funky going on in my abdominal region and they should be able to see or find it somehow. And I was never tested for allergic reaction to finasteride, it would seem intutive that they test all of us right off the bat for this.
I get the bloating too… it’s all the time whether I fast or not.
Yeah man me to my digestive system is sideways at the moment. Let me know
How you go
I eat half a sandwich and it feels like I ate a entire steer.
Do u guys get muscle twitches my legs r going crazy
Not anymore… For the first 10 months off yes really bad.
yes must go and please let us know. We should look at all possiblities. Maybe someone comes up with the real cause.
bloating is common among all pfs sufferers and yet anyone who think out of the DHT box get heavily discredited. There is something funky that goes in my abdomen too. Continuous bloating and it is not because of estrogen because my estrogen is within range. My liver functions are fine with the exception of slightly elevated liver enzyme. What could be causing this?
That study along with the appetite issues, digestive issues, and the consistency of my stools should be enough evidence for then to think something is going on.
I mean this “mass” in my abdominal area is coming from something if its fluid or actual tissue, I guess we’ll see.
In my opinion, it seems like just because estrogen is “in range”, it does mean that it is not the dominating hormonal force in our bodies. In other words, if androgens do not work properly in us, it might make sense that estrogen, even if it is “in range”, it can still be the dominating hormone in us. My body, based on gyno, female fat patterns etc., is over run with estrogen. Last I checked it though, it was well within range if I remember correctly.
Obviously, I have nothing to base this on other than my own drawn up conclusions, but it does seem possible
if Androgens are not working, then your beard hair would not grow
my beard does grow, but much, much thinner and lighter than before
Is your bloating in any one location?
I have some distention on the left side of my abdomen. This is actually the opposite side to where the liver is.
I think this is due to an enlarged Spleen (medicinenet.com/enlarged_spleen_splenomegaly/article.htm). This usually has no symptoms but can cause loss of appetite and bloating.
Seems to be the entire upper abdomen… Left and right side bloating. Loss of appetite as well as liver pain.
Get your saliva cortisol checked throughout the day.
For what purpose?
Well it’s just another way of checking things. Urine, Blood, Saliva measure active hormones you might find some answers. I know my blood cortisol was average, test was low, estrogen was average. Saliva was cortisol was extremely low, test low, and estrogen extremely high. I also had extremely low Aldosterone.
[Size=4]“Your adrenal glands, located just above your kidneys, are responsible for the “fight or flight” response during an emergency. This is caused by the hormone adrenaline, also called epinephrine. The adrenal cortex is the outer portion of your adrenal gland responsible for making two steroid hormones. Cortisol and aldosterone affect your blood pressure and response to stress. Sometimes the adrenal glands make insufficient levels of cortisol. Certain vitamins can have an impact on the symptoms of this condition.”[/size]
I think Cortisol plays a huge role! in this.
Fatigue
A lack of cortisol can make a person extremely tired and weak, according to the National Institutes of Health. Cortisol is produced as a response to the normal functioning of the pituitary glands. When the pituitary glands do not function properly, many of the body’s functions become abnormal. Fatigue is a common symptom of many of these disorders, including glucose management, immune system response and thyroid hormone production.
Gastrointestinal Effects
Addison’s disease is an adrenal gland disorder that may be indicated when a person’s cortisol levels are low. The adrenal glands produce hormones that regulate glucose, potassium and sodium levels within the body and help the body respond appropriately to stress. People with Addison’s disease do not produce enough hormones to oversee these functions. Gastrointestinal symptoms may be the marker of low cortisol in these cases, and include chronic diarrhea, vomiting, a loss of appetite and weight loss.
Low Blood Pressure
People who have low cortisol may also suffer from low blood pressure in response to the systemic lack of hormones. Low blood pressure can be a dangerous medical condition. People who have low blood pressure often feel lightheaded and dizzy and may injure themselves when suffering from falls relating to their health condition. Blood pressure levels more often than not revert to normal readings once cortisol is restored to the body.
Reproductive Effects
Low cortisol levels that are caused by hypopituitarism, the underproduction of hormones by the pituitary gland, can lead to a host of sexual dysfunction and reproductive problems. The NIH reports that some of the common symptoms of hypopituitarism are a lack of sex drive in men and women and amenorrhea (lack of periods) in women of childbearing age. Women who are nursing and show a drop in cortisol may see a decrease in milk production. Infertility can be the result of low cortisol if hormone levels are not supplemented with medication.
When i quit propecia my Cortisol was extremely over range!
Common Causes
Some of the most common causes of adrenal gland overload include: physical stress from illness or disease, emotional stress, chronic infections, underproduction of cortisol, general hormonal imbalance and a weak immune system. Stress in the body can cause inflammation and pain that makes the adrenaline glands work harder than usual, resulting in an increased demand for more cortisol. When this demand is not met, the result is adrenal overload.
Identification
Common symptoms of adrenal gland overload include difficulty sleeping, difficulty concentrating, poor memory, chronic fatigue, lack of energy in the morning, unexplained pain, especially in the upper back, decreased sex drive, depression, nausea, constipation and diarrhea, unexplained hair loss, food cravings, low blood pressure, low blood sugar and weight gain around the waist.
In addition to reviewing basic symptoms of adrenal gland overload, a doctor can conduct several tests to determine any hormonal imbalances or nutritional deficiencies that may be the root of the problem. An Adrenal Function Test (AFT) measures the amount of DHEA and cortisol in the body; the DHEA-S measures levels of DHEA in the saliva; the ACTH test measures the concentration of adrenocorticotropic hormone (ACTH) in the body, which can be an indicator of adrenal gland dysfunction; a basic cortisol test measures the amount of cortisol in the blood to determine if inflammation or a poorly functioning metabolism are to blame.
I’m getting muscle twitching recently. Could that be the affects of low aldotesterone, yes! low aldo = potassium intake is low.
low potassium = anxiety, depression, insomnia, constipation, high blood pressure, heart disease, kidney stones, hyperthyroidism, arthritis, obesity, headaches, pain in the eyes, muscle spasms, “restless leg syndrome,” fatigue, or muscle tension
WHAT IS ALDOSTERONE? Aldosterone is the principal of a group of mineralocorticoids. It helps regulate levels of sodium and potassium in your body–i.e. it helps you retain needed salt, which in turn helps control your blood pressure, the distribution of fluids in the body, and the balance of electrolytes in your blood. Aldosterone also helps remove excess potassium, keeping those levels balanced.
WHAT HAPPENS IF ALDOSTERONE GETS TOO HIGH OR LOW? When aldosterone gets too high, your blood pressure also gets too high and your potassium levels become too low. You can have muscle cramps, muscle weakness, and numbness or tingling in your extremities.
Again, I’m not here to prove i’m right. I’m just starting a discussion. I really think i’m onto something.
Why do I have low testoterone?
Androgens
The adrenal cortex secretes precursors to androgens such as testosterone.
In sexually-mature males, this source is so much lower than that of the testes that it is probably of little physiological significance. However, excessive production of adrenal androgens can cause premature puberty in young boys.
In females, the adrenal cortex is a major source of androgens. Their hypersecretion may produce a masculine pattern of body hair and cessation of menstruation.
[Size=4]Bottom line. Corticosteroids are required as anti-inflammatory. Probably why your having kidney or liver pains.[/size]
simple, because fin blocks 5AR2 and 3 and sometimes 1. This is depending on the tissue and where the damge on the cells is set. as Fin mostly blocks 5AR2 be got mostly sexual sides, for those, where 5AR3 is also blocked highly they get also other Problems, for those where even 5AR1 was blocked away, thes get also menatl sides. We are are very individual. This goes to a point, when the cells shut down. for some it even can be that its short for the point and the cell are not so hypersensitiv to Androgens and they get some benefit. here is a guy, whos muscels grow extremly for a other guy his dick grow. Like i said its going to a point, and if the signaling gets to high the cells shuts down. This also depending on the tissue and where the 5AR is expressed and blocked away. even the gut and the neves have Androgenrezeptors. Some get oily skin more than before, because the cells get hypersensitiv until a point when the cells shut down.
The reason could be, that cells still work and do not need androgens? Our dick and our balls did not fall off, also.
My beard is growing not as fast as it did before.
Though couldn’t the hypothalamus be responsible?
What is it?
Anatomy
The hypothalamus is an integral part of the substance of the brain. A small cone-shaped structure, it projects downward, ending in the pituitary (infundibular) stalk, a tubular connection to the pituitary gland. The round bony cavity containing the pituitary gland is called the sella turcica. The posterior portion of the hypothalamus, called the median eminence, contains many neurosecretory cells. Important adjacent structures include the mammillary bodies, the third ventricle, and the optic chiasm, the last being of particular concern to physicians because pressure from expanding tumours or inflammations in the hypothalamus or pituitary gland may result in severe visual defects or total blindness. Above the hypothalamus is the thalamus. (For discussion of the function of these surrounding structures, see the nervous system.)
Regulation of hormone secretion
The hypothalamus regulates homeostasis. It has regulatory areas for thirst, hunger, body temperature, water balance, and blood pressure, and links the nervous system to the endocrine system.
The hypothalamus, like the rest of the brain, consists of interconnecting nerve cells ( neurons) with a rich blood supply. To understand hypothalamic function it is necessary to define the various forms of neurosecretion. First, there is neurotransmission, which occurs throughout the brain and is the process by which one nerve cell communicates with another at an intimate intermingling of projections from the two cells (a synapse). This transmission of an electrical impulse from one cell to another requires the secretion of a chemical substance from a long projection from one nerve cell body (the axon) into the synaptic space. The chemical substance that is secreted is called a neurotransmitter. The process of synthesis and secretion of neurotransmitters is similar to that shown in Figure 1 with the exception that neurosecretory granules migrate through lengths of the axon before being discharged into the synaptic space.
Figure 1: Intracellular structure of a typical endocrine cell.
Neurologists have long been aware of four classical neurotransmitters: epinephrine, norepinephrine, serotonin, and acetylcholine, but recently there have emerged a large number of additional neurotransmitters, of which an important group is the neuropeptides. While bioamines and neuropeptides function as neurotransmitters, some of them also perform the role of neuromodulators; they do not act directly as neurotransmitters but rather as inhibitors or stimulators of neurotransmission. Well-known examples are the opioids (for example, enkephalins), so named because they are the naturally occurring peptides with a strong affinity to the receptors that bind opiate drugs such as morphine and heroin. In effect, they are the body’s opiates.
Thus the brain, and indeed the entire central nervous system, consists of an extraordinary network of neurons interconnected by neurotransmitters. The secretion of specific neurotransmitters, modified by neuromodulators, lends an organized, directed function to the overall system. These neural connections extend upward from the hypothalamus into other key areas, including the cerebral cortex. The result is that intellectual and functional activities as well as external influences, including stresses, can be funneled into the hypothalamus and thence to the endocrine system, from which they may exert effects on the body.
In addition to secreting neurotransmitters and neuromodulators, the hypothalamus synthesizes and secretes a number of neurohormones. The neurons secreting neurohormones are true endocrine (neurohemal) cells in the classical sense since secretory granules containing neurohormones travel from the cell body through the axon to be extruded, where they enter directly a capillary network, thence to be transported through the hypophyseal-portal circulation to the anterior pituitary gland.
Finally, the neurohypophysis, or posterior lobe of the pituitary gland, provides the classical example of neurohormonal activity. The secretory products, mainly vasopressin and oxytocin, are extruded into a capillary network, which feeds directly into the general circulation.
The existence of hormones of the hypothalamus was predicted well before they were detected and chemically characterized, and they have been studied intensively by many investigators. Two groups of American investigators, led by Andrew Schally and Roger Guillemin, respectively, shared the Nobel Prize for Physiology or Medicine for 1977 for their research on pituitary hormones.
These neurohormones are known as releasing hormones because the major function generally is to stimulate the secretion of hormones originating in the anterior pituitary gland. They consist of simple peptides (chains of amino acids) ranging in size from only three amino acids (thyrotropin-releasing hormone) to 44 amino acids (growth hormone-releasing hormone).
Hormones
Thyrotropin-releasing hormone
Thyrotropin-releasing hormone (TRH), a neurohormone, is the simplest of the hypothalamic neuropeptides. It consists essentially of three amino acids in the sequence glutamic acid–histidine–proline. The simplicity of this structure is deceiving for TRH is involved in an extraordinary array of functions. Not only is it a neurohormone that stimulates the secretion of thyroid-stimulating hormone from the pituitary, and, quite independently, the secretion of another pituitary hormone called prolactin, but it also subserves other central nervous system activities because it is a widespread neurotransmitter or neuromodulator within the brain and spinal cord. There is evidence that TRH is involved in the control of body temperature and that it has psychological and behavioral effects, at least in animals. It may also have therapeutic value. There are studies suggesting that it mitigates the damage induced by spinal cord injury and that it leads to some improvement in the nervous disease known as amyotrophic lateral sclerosis (Lou Gehrig’s disease).
These multiple effects are less surprising when it is considered that TRH appeared very early in the evolutionary scale of vertebrates and that, while the concentration of TRH is greatest in the hypothalamus, the total amount of TRH in the remainder of the brain far exceeds that of the hypothalamus. The TRH-secreting cells are subject to stimulatory and inhibitory influences from higher centres in the brain and they also are inhibited by circulating thyroid hormone. In this way TRH forms the topmost segment of the hypothalamic-pituitary-thyroid axis.
Gonadotropin-releasing hormone
Gonadotropin-releasing hormone (GnRH), a neurohormone also known as luteinizing hormone-releasing hormone (LHRH), is a peptide chain of 10 amino acids. It stimulates the synthesis and release of the two pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). While some investigators hold that there are two types of GnRH, most evidence supports the conclusion that only one type of neuropeptide stimulates the release of the two gonadotropins and that the variations in levels of both gonadotropins in the circulation are due to other modulating factors.
Characteristic of all releasing hormones and most striking in the case of GnRH is the phenomenon of pulsatile secretion. In normal individuals, GnRH is released in spurts at intervals of about 80 minutes. The pulsatile administration of GnRH in large doses results in an ever-increasing concentration of gonadotropins in the blood. In striking contrast, the constant infusion of GnRH suppresses gonadotropin secretion. This phenomenon is advantageous for persons for whom suppression is important. Such persons include children with precocious puberty, and elderly men with cancer of the prostate. On the other hand, pulsatile administration of GnRH is efficacious in men or women in whom deficiency of gonadal function is due to impaired secretion of GnRH. A potential application of this phenomenon is the synthetic modifications of GnRH as a male as well as a female contraceptive.
Neurons that secrete GnRH have connections to an area of the brain known as the limbic system, which is heavily involved in the control of emotions and sexual activity. Studies in rats deprived of pituitary glands and ovaries but maintained on physiological amounts of female hormone (estrogen) have demonstrated that the injection of GnRH results in complex and striking changes in posture characteristic of the receptive female stance for sexual intercourse.
Some individuals have hypogonadism (in which the functional activity of the gonads is decreased and sexual development is inhibited) due to a congenital deficiency of GnRH, which responds to treatment with GnRH. Most of these people also suffer from hypothalamic disease and are deficient in other releasing hormones as well, but there are also individuals in whom GnRH deficiency is isolated and associated with a loss of the sense of smell (anosmia). Abnormalities in the pulses of GnRH secretion result in subnormal fertility, abnormal or absent menstruation, and possibly cystic disease of the ovary or even ovarian cancer
Corticotropin-releasing hormone
Corticotropin-releasing hormone (CRH), a neurohormone, is a large peptide consisting of a single chain of 41 amino acids. It stimulates not only secretion of corticotropin in the pituitary gland but also the synthesis of corticotropin in the corticotropin-producing cells (corticotrophs) of the anterior lobe of the pituitary gland. Many factors, both neurogenic and hormonal, regulate the secretion of CRH, since CRH is the final common element directing the body’s response to all forms of stress, whether physical or emotional, external or internal. (This key role of CRH in the hypothalamic-pituitary-adrenal axis is discussed below in connection with the adrenal gland.) Among the hormones that play an important role in modulating the influence of CRH is cortisol, the major hormone secreted by the adrenal cortex, which, as part of the negative feedback servomechanism (exerting control over another system through negative feedback), blocks the secretion of CRH. Vasopressin, the major regulator of the body’s excretion of water, has an additional ancillary role in stimulating the secretion of CRH.
Excessive secretion of CRH leads to an increase in the size and number of corticotrophs in the pituitary gland, often resulting in a pituitary tumour. This, in turn, leads to excessive stimulation of the adrenal cortex, resulting in high circulating levels of adrenocortical hormones, the clinical manifestations of which are known as Cushing’s syndrome. Conversely, a deficiency of CRH-producing cells can, by a lack of stimulation of the pituitary and adrenal cortical cells, result in adrenocortical deficiency. (These conditions are discussed below.
Growth hormone-releasing hormone
Like CRH, growth hormone-releasing hormone (GHRH) is a large peptide. A number of forms have been described that differ from one another only in minor detail and in the number of amino acids (varying from 37 to 44). Unlike the other neurohormones, GHRH is not widely distributed in other parts of the brain. It is stimulated by stresses, including physical exercise, and secretion is blocked by a powerful inhibitor called somatostatin (see below Somatostatin). Negative feedback control of GHRH secretion is mediated largely through compounds called somatomedins, growth-promoting hormones that are generated when tissues are exposed to growth hormone itself.
An excess of circulating growth hormone in adults leads to a condition called acromegaly. Rarely, a benign tumour, called a hamartoma, located in the hypothalamus may produce excessive amounts of GHRH, leading to acromegaly. Equally rare are tumours arising in the islets of Langerhans of the pancreas that may secrete excessive quantities of GHRH. Indeed, GHRH was first successfully isolated and analyzed from such an ectopic (abnormally positioned) hormone-producing tumour. Isolated deficiency of GHRH (in which there is normal functioning of the hypothalamus except for this deficiency) may be the cause of one form of dwarfism, a general term applied to all individuals with abnormally small stature.
Somatostatin
Somatostatin refers to a number of polypeptides consisting of chains of 14 to 28 amino acids. The name was coined when its discoverers found that an extract of the hypothalamus strongly inhibited the release of growth hormone from the pituitary gland. Somatostatin is also a powerful inhibitor of pituitary TSH secretion. Somatostatin, like TRH, is widely distributed in the central nervous system and in other tissues. It serves an important paracrine function in the islets of Langerhans, by blocking the secretion of both insulin and glucagon from adjacent cells. Somatostatin has emerged not only as a powerful blocker of the secretion of GH, insulin, glucagon, and other hormones but also as a potent inhibitor of many functions of the gastrointestinal tract, including the secretion of stomach acid, the secretion of pancreatic enzymes, and the process of intestinal absorption. Despite these multiple, widespread actions, the term somatostatin has persisted because of its major role as a regulator of GH secretion, and impaired somatostatin secretion may cause some forms of hypersecretion of growth hormone.
No examples of somatostatin deficiency have been found, but a tumour called a somatostatinoma has been well characterized in a number of patients. Persons with a somatostatinoma have cramping abdominal pain, persistent diarrhea, a mild elevation of blood glucose levels, and sudden flushing of the skin.
Prolactin-inhibiting and releasing hormones
The hypothalamic regulation of prolactin secretion from the pituitary is different from the hypothalamic regulation of other pituitary hormones in two respects. First, the hypothalamus primarily inhibits rather than stimulates the release of prolactin from the pituitary (the hypothalamus stimulates the release of all other pituitary hormones). Thus, if pituitary cells are removed from the influence of the hypothalamus, few or none of the pituitary hormones are secreted, except for prolactin, which continues to be secreted by the prolactin-secreting cells (lactotrophs). Second, this major inhibiting factor is not a neuropeptide, but rather the neurotransmitter dopamine, a fact exploited in afflicted persons by physicians who are able to reduce abnormally high concentrations of prolactin by using drugs that mimic the prolactin-inhibiting effects of dopamine. Another prolactin-inhibiting factor (PRF) comes into play primarily during pregnancy and lactation. Prolactin-stimulating factors also exist, among them TRH.
Prolactin deficiency is known to occur, but only rarely. Excessive prolactin production (hyperprolactinemia) is a common endocrine abnormality, and the prolactinoma is the most frequently encountered pituitary tumour.
Gastrointestinal neuropeptides
Although modern endocrinology began with the discovery that a substance, secretin, secreted into the blood from the cells lining the gastrointestinal tract stimulates the secretion of pancreatic juices, little attention was subsequently paid to gastrointestinal hormones. When investigators began to examine the distribution of neuropeptides within the body, however, there emerged a bewildering variety of these hormones, not only within the brain but also in the lining of the gastrointestinal tract and in other organs. The list includes glucagon, the enkephalins, secretin, cholecystokinin, gastrin, calcitonin, angiotensin, substance P, pancreatic polypeptide, neuropeptide Y (a human variant of a peptide called bombesin), delta-sleep-inducing peptide, and vasoactive intestinal peptide. The actions and interactions of these hormones both in the intestinal tract and in the brain are complex and are the subject of continuing investigations. Briefly, these peptides play important roles in the transmission and inhibition of pain stimuli, in eating and drinking behaviour, in memory and learning, in the regulation of body temperature, in the induction of sleep, and in sexual behaviour.
Study
Identification of Specific Sites of Hormonal Regulation in Spermatogenesis in Rats, Monkeys, and Man
rphr.endojournals.org/cgi/content/full/57/1/149
