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angelic8956 · 5 years

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Post cycle therapy

Introduction to post-cycle therapy

Post cycle therapy (PCT) may be the most important aspect when using anabolic steroids. The concept of PCT did not exist before the late 1980s and early 1990s because the understanding of the mechanisms by which anabolic steroids affected the body was not fully understood in the 1950s, 1960s, and 1970s. During this time, doctors, scientists, and users of anabolic steroids were only just beginning to learn about the dynamics of anabolic steroids and their effects on the endocrine system. It has been understood since the start of anabolic steroid use that the exogenous administration of anabolic steroids would result in the body's negative feedback loop for the HPTA (Hypothalamic Pituitary Testicular Axis) being triggered and consequently the endogenous testosterone production would be suppressed and / or reduced turn off.

Today it is a very different story in which the scientific and medical understanding of the use of anabolic steroids has grown exponentially since the old days of bodybuilding and the use of anabolic steroids in athletics. Thanks to numerous developments of active ingredients for hormone restoration after taking anabolic steroids and the increasing scientific and medical knowledge, taking anabolic steroids and the associated disorders of the endocrine system has become much safer than ever before. With the right knowledge of how to properly and efficiently restore HPTA and the body's hormonal system through post-cycle therapy (PCT), people can not only emerge from their anabolic steroid cycles,

After using exogenous anabolic steroids, the majority of users will experience what is referred to as a "hormonal crash" or "post-cycle crash". This is an endogenous environment in which important hormones are important for maintaining the newly formed muscle mass that has been suppressed or shut down. The key hormones in question are LH (luteinizing hormone), FSH (follicle-stimulating hormone) and then (and most importantly) testosterone. LH and FSH are known as gonadotropins. These are hormones that signal the gonads (testes) to start or increase the production and secretion of testosterone. In addition to low levels of these hormones, the overall balance of total hormones is essentially disturbed, causing testosterone levels to be low and most (depending on many factors), Estrogen levels and cortisol levels are higher (a steroid hormone that destroys muscle tissue) will be at normal levels. If the testosterone level is low and the cortisol level is in the normal (or high) range, cortisol now becomes a threat to the newly created muscle that was formed during the recent steroid cycle (testosterone properly suppresses and counteracts cortisol's catabolic effects on muscle tissue) . SHBG (sex hormone-binding globulin) is also a problem here, which is a protein that binds to sex hormones (testosterone) and makes them inactive, essentially handcuffing them and preventing them from working.

Normally, the human body restores this hormone imbalance and restores its endogenous testosterone level over time. However, studies have shown that this happens over a period of 1 to 4 months without the action of testosterone-stimulating active ingredients. Obviously, this is enough time for the hormonal imbalance to devastate the body and cause everyone to lose most or all of the new muscle gained during that time. Therefore, all users of anabolic steroids should strive for the fastest possible hormone recovery, which is supported and promoted through the correct use of a testosterone stimulating compounds. In addition, trying to allow the body to recover on its own represents a very high probability of long-term endocrine damage to HPTA over time, causing the individual to develop hypogonadism induced by anabolic steroids (the inability to produce the correct testosterone levels for the drug) for the rest of their lives). It is therefore of the utmost importance that a proper onePost-cycle therapy This involves using multiple recovery connections to not only bring HPTA function back to normal as quickly as possible but also to avoid any permanent damage that takes precedence over preserving recently gained muscle mass to have.

Which post cycle therapy protocol is to be used?

There are many different types of PCT protocols that have been developed over the years, and at first glance, everyone will be extremely confused as to how many different opinions exist among the anabolic steroids that the community uses and how many different ones established PCT protocols are in existence. This article presents the best possible and most efficient post-cycle therapy protocol based on valid scientific data and logical considerations. This article will also dispel various myths related to PCT and outline which PCT protocols should not be followed due to recent advanced developments, as well as newer better scientific and medical knowledge about them, how an appropriate post-cycle therapy protocol should work. At this point in time, there are still very outdated - and consequently ineffective - PCT protocols that are still used by many users of anabolic steroids, and this poses a serious danger, not only to the person who unknowingly is outdated Post cycle therapy program used but also for people who observe, learn and collect ideas from that person.

Without a proper understanding of what is going on in the endocrine system during these crucial weeks, and without understanding what connections to use, what each connection does, and how to use them correctly, serious problems can arise.

The HPTA: how it works

The HPTA is the hypothalamic-pituitary-testicular axis, an axis of interconnected endocrine glands in the body that deal with and control testosterone production.

A HPTA diagram is shown above. The HPTA regulates how much testosterone is produced at a given time and how much testosterone circulates in the body. Each individual is essentially programmed through their genetics (DNA) on how much maximum testosterone they will produce, and this is the most important determining factor. There are other factors that determine how much testosterone a person will produce, and these include age, diet, body composition, lifestyle, and physical activity. All of these factors play a role in how much testosterone a person will produce overall.

The HPTA works under the so-called negative feedback loop, whereby the body reduces its production and secretion of testosterone if too much testosterone circulates in the body, and also adapt if too little testosterone is detected. This detection and adjustment, known as a negative feedback loop, is controlled by the hypothalamus, which is essentially the main gland for all endocrine and hormonal functions in the body. The negative feedback loop is ultimately the body's attempt to maintain hormonal homeostasis, which involves regulating a system (in this case, the body's internal systems) to maintain stable and consistently favorable conditions. All endocrine glands work in one way or another and to different degrees through the negative feedback loop. In the case of post-cycle therapy The main problem lies in the negative feedback loop of the HPTA.

Within the HPTA, the concern during PCT is the restoration and regulation of the following 5 hormones for homeostasis:

- GnRH (gonadotropin-releasing hormone)

- LH (luteinizing hormone)

- FSH (follicle-stimulating hormone)

- testosterone

The HPTA starts with the first axis point, the hypothalamus, which recognizes that the human body has to produce more testosterone and releases different amounts of GnRH. GnRH is a hormone that signals the next axis point, the pituitary, to start producing and releasing two important gonadotropins: LH and FSH. LH and FSH are two hormones that work to signal the point on the third axis, the testes, and to start the production and secretion of testosterone. This is the final stage of testosterone production in the HPTA.

There are two primary hormonal factors that are used to inhibit, reduce, suppress, or stop testosterone production in the HPTA:

- Excess testosterone - Excess estrogen

Although there are other hormones that work to inhibit and suppress HPTA function (like progestins and prolactin), these are the two primary conditional hormones that are of concern. If the hypothalamus detects too high levels of testosterone and / or estrogen in the body (either through the use of exogenous androgens in an anabolic steroid cycle or otherwise), the hypothalamus tries to restore balance by doing essentially the opposite of that what was previously described. The hypothalamus reduces or stops the production of GnRH, which stops the production of LH and FSH, which ultimately reduces or stops the production of testosterone. As long as the ideal hormonal environment of the hypothalamus is not restored, The production of the various signaling hormones within the HPTA does not begin, and it will often take months for the body to do this alone without the intervention of testosterone stimulants. The reason why the recovery of the HPTA naturally takes so long should be very clear due to the described functioning of the HPTA.

This basic understanding of the mechanisms of HPTA and the negative feedback loop described above is essential to understand how and why a proper PCT needs to be developed and used after an anabolic steroid cycle.

Decisive factors in restoring HPTA

When using anabolic steroids, there are several key factors that determine how difficult it is for a person to restore their HPTA and endogenous testosterone function during PCT. These are the following factors, which are not important in any particular order:

1. Individual answer

2. Type of anabolic steroid used

3. Cycle duration (degree of testicular desensitization)

1. Individual response: Every individual reacts to a chemical, compound, anabolic steroid, food or drug in different ways. While some people may not experience HPTA suppression or shutdown at all, others may experience severe HPTA suppression and shutdown to the extent that they may take significantly longer periods of time to ensure full recovery than most others. Like everything else, this is a spectrum in which there are the very “happy” people who recover very quickly and easily at one end of the spectrum and the “unhappy” people who have a hard time recovering after the cycle can. In between is the average.

2. Type of anabolic steroids used (the anabolic steroids used): All anabolic steroids have HPTA suppression or shut down by the negative feedback loop mechanisms, and there are no exceptions to this. Various anabolic steroids are known to be mildly suppressive, while others are known to be strongly suppressive. It all depends on several reasons, many of which are not discussed here. In any case, no matter how mild or hard an anabolic steroid exerts HPTA suppression, all anabolic steroids when used for typical cycle lengths of weeks at a time, will eventually result in the HPTA shutting down or at least strongly suppressing their hormonal signaling processes.

3. Cycle time (degree of desensitization of the testes): this is possibly the most important and influential factor. As anabolic steroids continue to be used, the majority of testicular Leydig cells remain dormant and inactive, and the longer these interstitial cells remain dormant and inactive, the greater the difficulty of essentially getting these cells onto the React stimulus from LH and FSH again. Studies have found that the problem of restoring Leydig cells after using anabolic steroids is not due to a deficiency in LH, but to the desensitization of Leydig cells to LH. In a study in which male test subjects were given exogenous testosterone for 21 weeks, LH levels were suppressed shortly after the start of administration. At the end of the 21-week period, however, it was observed that LH levels rose within 3 weeks once exogenous testosterone administration ceased, but testosterone levels did not arise until many weeks later in most subjects.

The three primary testosterone stimulants for HPTA recovery during PCT

Before you look at the three different types of testosterone stimulating substances for hormone recovery during post-cycle therapy, it is very important for individuals to understand that the use of a single compound with the exception of one or two selected substances for the Hormone restoration is inadequate during PCT. Ideally, all post-cycle therapy programs should be a multi-component PCT program that contains several different compounds that work together to achieve the most effective and fastest possible HPTA recovery after an anabolic steroid cycle.

The three categories of connections are (in order of importance):

1. SERMs (Selective Estrogen Receptor Modulators)

2. Aromatase Inhibitors

3. HCG (Human Chorionic Gonadotropin)

SERMs: The active substance classes in the SERM category include: Nolvadex (tamoxifen citrate), Clomid (clomiphene citrate), Raloxifene and Fareston (toremifene citrate). The nature of a SERM is that it shows the mixed effects of estrogen agonists and estrogen antagonists on the body. This means that while a SERM can block the effects of estrogen at the cellular level in certain tissues, it can increase the effects of estrogen in other areas of the body. These can be both positive and negative effects. For example, Nolvadex shows estrogenic agonistic effects in the liver, which have a positive effect in every respect, since their effects lead to a positive change in the cholesterol profiles (which is desired by many). All SERMs act to varying degrees as estrogen antagonists in this area to mitigate the effects of estrogen on breast tissue and to reduce or block the side effects of gynecomastia. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. to mitigate the effects of estrogen on breast tissue and reduce or block the side effects of gynecomastia. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. to mitigate the effects of estrogen on breast tissue and reduce or block the side effects of gynecomastia. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. With regard to the effect of SERMs on endogenous testosterone stimulation, they serve as an estrogen antagonist on the pituitary gland and thereby trigger the release of LH and FSH. Increased estrogen levels in men can and can suppress the production of endogenous testosterone via the negative feedback loop, which leads to hypogonadism. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs. SERMs for this purpose are an essential addition to any PCT protocol and must under no circumstances be excluded. Regardless, the sole focus should not be on SERMs.

Aromatase inhibitors: These are compounds such as Aromasin (exemestane), Arimidex (Anastrozole) and Letrozole (Femara). Instead of blocking the activity of estrogen at the cellular level in different tissues, aromatase inhibitors (AIs) serve to lower the total circulating level of estrogen in the body by inhibiting the aromatase enzyme, which is the enzyme responsible for converting androgens to estrogen is. Converting androgens to estrogen results in an excess of estrogen, which, as explained earlier in this article, triggers the negative feedback loop that leads to the suppression of testosterone production. By reducing the total amount of circulating blood plasma estrogen, the negative feedback loop is activated in a positive way and LH and FSH are released, to produce and secrete more testosterone. This is largely due to the hypothalamus, which detects that estrogen levels are in the bloodstream also low and will try to increase testosterone levels in the bloodstream so that part of the excreted testosterone is able to be flavored in estrogen to restore hormonal balance. The other meaning of aromatase inhibitors is the ability to mitigate the estrogenic effects of HCG, which will be explained shortly. However, it is important to note that the majority of aromatase inhibitors do not match SERMs such as Nolvadex very well and that very specific decisions regarding the use of AI should be made PCT.

HCG: Human chorionic gonadotropin is mostly synthetic LH. It is a protein hormone that is produced in large quantities by pregnant women and contains a protein subunit that is 100% identical to LH. Therefore, when administered to men, it mimics the effects of LH in target tissues such as the testicles. The result is an increase in testosterone production by stimulating Leydig cells with HCG. HCG should never be used alone because its nature as a gonadotropin itself triggers a negative feedback loop, causing the pituitary gland to stop producing LH after using HCG until the use of HCG is discontinued. Therefore, HCG must be used together with a SERM and especially an aromatase inhibitor, since HCG has been shown to increase aromatase activity in the testes,

Put everything together

Readers may be wondering which compounds to choose from the three categories listed and how to use them correctly. The answer is to understand the characteristics of everyone and to use these characteristics efficiently and appropriately.

HCG

The first item to be examined is HCG. The majority of anabolic steroid users from the 1960s - mid-1980s did not even use compounds for hormone recovery purposes, and the term PCT did not even exist at that time. As the use of HCG became more popular (around 1980), it was the only compound used. Since then, medical and scientific understanding of such things has increased exponentially, and there should be no reason for an informed and properly trained person to use HCG for PCT alone. In connection with one of the other two connection categories (AI and SERM), the dynamics change considerably.

It has previously been mentioned that much of the difficulty in obtaining HPTA after an anabolic steroid cycle is the result of the desensitization of Leydig cells. HCG is essentially an analog of LH, and the testes after a long cycle of anabolic steroids would be as insensitive to HCG as to LH. However, the human body itself produces LH levels that are far too inefficient for proper and rapid testosterone production. The body's own increase in LH and FSH after an anabolic steroid cycle is also not a rapid climax, but a very slow and steady increase, as can be seen from the aforementioned study, in which it only started after 3 weeks to reach the LH values normal physiological measurements after discontinuation of exogenous testosterone.

HCG, which is used in a dose of 100 - 1,500 IU every 2 days in the first 1-2 weeks of PCT in a specific way, enables the patient to supply the testicles with a high dose to give them a “shock” - To give effect and maintain this shock effect on the Leydig cells of the testicles for a longer period of the first 1-2 weeks after the cycle therapy. Indeed, studies have shown the incredible effectiveness of HCG for this purpose, and it is even clinically suggested to use HCG to treat hypogonadism induced by anabolic steroids. After this consideration, the other two compounds (the SERM and the AI) should be used as supporting compounds for the use of HCG in this period of 1 to 2 weeks,

Despite the good news regarding HCG's ability to support hormone recovery, two questions remain to be resolved:

- The fact that HCG causes an increased production of aromatase, which leads to increased estrogen levels.

- After stopping HCG, the body has only a very low endogenous LH and FSH production due to the exogenous administration of HCG.

Aromatase inhibitor: Aromasin (exemestane) above all

The first of the two remaining problems that need to be addressed is that HCG triggers an increase in testicular aromatase expression and an increase in estrogen in the body. It should also be noted that there is an increase in the level of progesterone in the testicles. Of course, an increase in estrogen during PCT is undesirable, since it has already been explained that estrogen triggers the suppression of endogenous testosterone production, and there is no doubt that everyone wants to have estrogenic side effects during PCT.

Therefore, there is an option to include an aromatase inhibitor. However, there is a major problem with the other two of the three main aromatase inhibitors (Arimidex and Letrozole). The problem is the fact that Arimidex and Letrozole have direct negative interactions with Nolvadex in a PCT program involving the use of SERMs like Nolvadex and Clomid, which are known to be absolutely essential components of a PCT program. The problem here is that Arimidex (or Letrozole) and Nolvadex both work directly against each other. One study showed that Nolvadex, when used with Arimidex, reduces the blood plasma level of Arimidex (as well as letrozole, another commonly used aromatase inhibitor). The conclusion here is that using Arimidex or Letrozole with Nolvadex together is a very bad idea and can be counterproductive when used together in a PCT protocol. Aromasin completely bypasses this problem because it has been proven that there are no interactions with Nolvadex, unlike the other two aromatase inhibitors mentioned above. In one study, Aromasin did not show such reduced efficacy or decreased blood plasma levels when using Nolvadex.

The other advantage of choosing Aromasin over all other AIs is that Aromasin has been shown in several studies to have a far less negative effect on cholesterol profiles than other aromatase inhibitors that used Aromasin for 24 weeks in a particular study in cancer patients Exemestane administration did not affect cholesterol profiles, and some other studies have also shown that using Aromasin has no effect on cholesterol profiles, although there have been some studies that have shown negative effects on cholesterol profiles due to the use of Aromasin, it is apparent that there is no significant or negative effect of Aromasin on cholesterol than other aromatase inhibitors.

In addition to these benefits of Aromasin, it is very clear that Aromasin is able to increase testosterone levels in men, as studies have shown. For example, in a particularly noteworthy study, 12 healthy young male volunteers were selected who were randomly given aroma doses of 25 mg and 50 mg over a period of 10 days and who not only had significant estrogen suppression (38%) but also testosterone levels It was observed that the test subjects gained an incredible 60%.

According to this information, Aromasin would be the best possible aromatase inhibitor of choice to counteract the increased aromatase activity caused by HCG. Therefore, Aromasin would be used at a full daily dose of 25 mg and only if HCG was used. As soon as HCG is discontinued, Aromasin should also be discontinued.

The only issue that needs to be addressed now is to stimulate and maintain proper endogenous LH release to drive recovery until the body can become self-sufficient.

SERMs: Nolvadex and Clomid

The question is often asked among the anabolic steroids that the community uses: Clomid or Nolvadex? Which one for PCT?

Zuallererst ist die bestmögliche Zugabe zu HCG in einem PCT-Protokoll Nolvadex (Tamoxifen Citrate), da Studien gezeigt haben, dass HCG und Nolvadex zusammen einen bemerkenswerten synergistischen Effekt in Bezug auf die Stimulierung der endogenen Testosteronproduktion gezeigt haben und Nolvadex tatsächlich arbeiten, um den Desensibilisierungseffekt auf die Leydig-Zellen der Hoden zu blockieren, der durch hohe Dosen von HCG verursacht wird. Dies ist sehr wichtig, da eine zu geringe LH-Sekretion über längere Zeiträume eine Desensibilisierung der Gonadotropine bewirken kann, eine zu starke Gonadotropinstimulation (in Form von HCG oder auf andere Weise) ebenfalls eine Desensibilisierungswirkung hervorruft.

Second, mg for mg, Nolvadex is far more effective than Clomid in stimulating endogenous testosterone production and a cheaper choice than Clomid itself. Studies have shown that 150 mg Clomid (Clomiphene Citrate) administered daily reduced endogenous testosterone levels of 10 healthy men increased approximately 150%, while 20 mg Nolvadex (Tamoxifen Citrate) increased endogenous testosterone levels by the same amount daily. It is very obvious here that Clomid is very effective for this purpose, but Nolvadex appears to be a cheaper choice since it is more effective than Clomid compared to mg for mg. The advantages of Nolvadex compared to Clomid do not end here - although Clomid shows estrogen antagonist effects on the pituitary gland like Nolvadex, however, shows estrogen agonist effects there too. This means that Clomid actually acts to varying degrees as a pituitary estrogen, triggers the negative feedback loop, and reduces testosterone-stimulating gonadotropin (LH and FSH) emissions. This is a very serious problem during post-cycle therapy, where people try to restore their HPTA function rather than stopping it. Ideally, you want a SERM that has an almost 100% estrogen-antagonistic effect on the pituitary gland, and Nolvadex is the perfect choice for it. This is a very serious problem during post-cycle therapy, where people try to restore their HPTA function rather than stopping it. Ideally, you want a SERM that has an almost 100% estrogen-antagonistic effect on the pituitary gland, and Nolvadex is the perfect choice for it. This is a very serious problem during post-cycle therapy, where people try to restore their HPTA function rather than stopping it. Ideally, you want a SERM that has an almost 100% estrogen-antagonistic effect on the pituitary gland, and Nolvadex is the perfect choice for it.

When it comes to dosing Nolvadex, the standard dose for PCT and to stimulate the release of GnRH (Gonadotropin-Releasing Hormone), LH, FSH and ultimately testosterone is the same as a simple Nolvadex dose of 20-40 mg daily. In all studies with Nolvadex doses to stimulate endogenous testosterone production, only 20 to 40 mg Nolvadex were used per day, and it was actually shown that doubling the dose to 40 mg or more did not produce a significant difference in endogenous testosterone secretion. The only reason why many choose to use Nolvadex 40 mg daily for the first 1-2 weeks of a PCT program is to achieve optimal peak plasma levels faster to ensure faster HPTA recovery.

The final layout

The ideal post-cycle therapy protocol should then be as follows:

4 - 6 weeks total PCT time (depending on the individual's ability to recover )

Week 1 - 2:

- HCG at 1000iu / E2D

- Aromasin (exemestane) at 25 mg / day

- Nolvadex (tamoxifen citrate) at 40 mg / day

week 2 - 6:

- Nolvadex (tamoxifen citrate) at 20 mg / day

Additional optional components (vitamins / supplements / compounds) to support PCT

Apart from the main components that are being discussed, there are various other components that are largely optional but are still very effective for hormonal restoration of HPTA during the weeks after cycle therapy.

Vitamin D (Cholecalciferol): There is ample evidence backed by studies that the legalization of Vitamin D (Cholecalciferol) has a significant effect on increasing testosterone levels in men and also has a significant ability to suppress SHBG levels in the body. Indeed, one of the best PCT supplements is vitamin D. There are a plethora of clinical studies showing that low levels of vitamin D correspond to low endogenous testosterone production (especially in the winter months for obvious reasons). In a study carried out in Austria, in which around 200 subjects were involved in a group with 3332iu vitamin D and a placebo group daily, the results showed that those men with sufficient vitamin D levels had significantly higher testosterone levels and significantly lower SHBG levels when compared to the D-deficient subjects. Androgen levels and vitamin D levels are associated with men and show a consistent seasonal variation. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D. if compared to the D-deficient subjects. Androgen levels and vitamin D levels are associated with men and show a consistent seasonal variation. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D. if compared to the D-deficient subjects. Androgen levels and vitamin D levels are associated with men and show a consistent seasonal variation. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D. Similar results have been reported in several other studies, in which subjects who were given higher amounts of vitamin D over time showed a sharp increase in total testosterone levels and a decrease in SHBG. Anecdotes from people who have taken vitamin D and receive regular blood tests from their doctors report a sharp increase in their total and free testosterone levels about 1 - 2 months after taking vitamin D.

#sports #steroid #bodybuilding #fitness

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mcatmemoranda · 5 years

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Opioids: Morphine, hydromorphone, oxymorphone, meperidine, methadone, codeine. They are Mu receptor agonists. Effects/toxicity: respiratory depression, nausea/vomiting, constipation, itching, hypotension, bronchoconstriction, miosis, biliary colic, increased prolactin release, inhibition of luteinizing hormone release, increased intracranial pressure, emesis, tolerance, withdrawal, physical dependence, addiction. Activation of opioid receptors results in inhibition of synaptic neurotransmission in the central nervous system (CNS) and peripheral nervous system (PNS). This occurs through an inhibitory G protein mechanism. The physiologic effects of opioids are mediated principally through the mu and kappa opioid receptors in the CNS and PNS. Mu receptor effects include analgesia, euphoria, respiratory depression, constipation, and miosis. Morphine is a full mu receptor agonist with potent analgesic and anxiolytic effects, as well as hemodynamic effects, that are potentially beneficial in persons with unstable angina. Morphine causes vasodilation and can produce modest reductions in heart rate through increased vagal tone, and in systolic blood pressure to further reduce myocardial oxygen demand. While this effect on cardiovascular status can benefit the patient presented in this vignette, a lowering of blood pressure can be potentiated in those with existing hypotension. Bottom Line: Morphine-induced vasodilation can induce hypotension.

#morphine #opioids #pharm

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hemprepublic · 2 years

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Hemp Hearts Nutrition Facts and Health Benefits

Hemp seeds are a good source of healthy fats. They’re high in omega-3 fatty acids and gamma-linolenic acid, both of which have been shown to reduce prolactin levels, a hormone linked to premenstrual syndrome. Hemp Heart Nutrition can be consumed whole or crushed into flour for use in baking. The hemp seed oil also has a high amount of important fatty acids.

Hemp seeds provide all of the essential amino acids. Essential amino acids cannot be synthesized by the body, They are mostly obtained through an animal source. These essential amino acids are found in hemp seeds.

Hemp seeds are an excellent vegetarian source of protein for your body.

Hemp seeds provide a lot of protein and are a good source of fibre. They have 33 per cent of the daily protein allowance.

Hemp seeds are also high in essential fats like omega-3 and omega-6, which the body cannot produce.

They are high in vitamins and minerals and assist to control inflammation in the body. For a variety of reasons, hemp seeds are a fantastic addition to your diet. You’ll be glad you took the time to do so!

They include alpha-linolenic acid, which promotes heart health and brain development. They’re also high in Omega 6 fatty acids, which are an important component of a healthy diet. Hemp seeds are high in fibre as well. Hemp seeds are very low in calories and provide a wonderful source of energy. Hemp seeds are an excellent supplement to a ketogenic or paleo diet.

Hemp seeds are a nutritious and delicious crunchy snack that can be added to any cuisine. They get along with practically everyone and go well with almost anything. Smoothies and smoothie bowls. They can be used as bread crumbs or added to baked dishes.

Here Are the Hemp Seed Benefits You Should Know!

Despite the fact that cannabis was used therapeutically for its proven therapeutic properties decades ago, fears of abuse led to prohibitions on its usage in the United States in the 1930s and 1940s. However, following Dr Rafael Mechoulam’s pioneering study, hemp in the form of medical cannabis, commonly referred to as cannabidiol or CBD, has once again been the topic of medical research and clinical studies.

In human physiognomy, Dr Mechoulam developed the Endo-Cannabinoid System, which revealed that humans contain CBD receptors in their bodies, resulting in a cascade of homeostasis (health stability) throughout the central nervous system and immune system.

The two most major active chemical components found in hemp are THC (tetrahydrocannabinol) and CBD (cannabidiol). THC is psychoactive and causes a high, whereas CBD is a nutritional supplement that is incredibly useful to humans and does not induce a high. Patients will find CBD-dominant marijuana strains to be non-addictive because they contain little or no THC.

In this article, we will look at how medical cannabis can help treat a variety of diseases that are often crippling and can be fatal.

Hemp Can Treat a Variety of Diseases and Conditions

Since the time medical cannabis was legalised in several states in the United States and was clinically administered to patients, it has been a miracle drug in treating several acute symptoms of major diseases that affect millions of people.

Some examples are as follows:

1) Insomnia: Studies show that CBD improves sleep, particularly when anxiety is present.

2) Nausea: Nausea is a common side effect of chemotherapy and cancer treatments.

3) Anxiety and depression: CBD oil has shown remarkable results in the treatment of depression, anxiety, and panic attacks. CBD has an excellent ability to act on our brain’s receptors to release the serotonin neurotransmitter, which becomes severely depleted in patients suffering from mental illnesses, making them feel “low” and enervated.

4) PTSD: One of the most promising areas of medical marijuana research is in the treatment of war veterans with PTSD, with miraculous and drastic improvements after hemp administration. Whereas pharmaceutical drugs such as benzodiazepines are highly addictive and can even lead to substance abuse, CBD does not.

5) Glaucoma: It has also been reported to aid in the treatment of Glaucoma, an eye condition that can lead to blindness, though the results are debatable.

6) Epilepsy: One particular type of epilepsy in kids, known as the Dravet Syndrome, is practically impossible to manage but responds to CBD miraculously. This CBD-dominant strain is also popularly known as Charlotte’s Web. (3)Epilepsy also comes with muscle spasms, stiffness, and chronic pain, all of which are significantly reduced with the use of cannabidiol.

7) Muscle Spasticity: caused by multiple sclerosis or arthritis, as well as several neurological illnesses that cause chronic pain and tremors, responds remarkably to CBD. Sativex, an oral spray that contains both CBD and THC, is both helpful and safe in relieving these symptoms. Marijuana does wonders for nerve pain and multiple sclerosis. While there are various pharmacological medicines available to treat these disorders, such as Lyrica and Neurontin, the patients are heavily sedated. Patients who use CBD report feeling significantly more relaxed when they return to their usual routines.

8) Parkinson’s disease: CBD is a unique treatment for tremors produced by Parkinson’s disease since it functions as a muscle relaxant.

9) Chronic pain: CBD interacts with and releases neurotransmitters naturally present in the human body to alleviate acute pain and inflammation.

10) Alzheimer’s disease: CBD oil can effectively reduce inflammation, which is one of the leading causes of Alzheimer’s symptoms. CBD has also been proven in clinical trials to be effective in reversing, postponing, and even avoiding the deleterious effects of Alzheimer’s disease.

11) ALS: CBD oil is an effective treatment for ALS since it slows the course of symptoms like stiffness and increases patient longevity due to its neuroprotective properties.

12) Anorexia Nervosa: is a serious eating and psychiatric illness characterised by a loss of appetite and severe anorexia. Whereas anti-depressants and anti-anxiety medications are commonly used for anorexics, they have significant side effects that make patients drowsy, while research reveals that CBD contains orexigenic (an appetite stimulant/hormone) properties that can control and boost appetite.

13) AIDS and cancer symptoms: While many people suffer from the anguish of weight gain or obesity, many others, especially those with AIDS or cancer, find it incredibly difficult to gain weight. Dronabinol, a synthetic THC popularly referred to as Marinol, is medically approved for usage in patients, and its effects have always been beneficial, with persistent improvements in appetite, nausea, and vomiting in cancer and AIDS patients. Wasting Syndrome, an AIDS-related illness characterised by a slow, painful loss of muscle mass and a progressive decline in health, has also shown promising results in lowering symptoms.

14) Endometriosis, Fibromyalgia, Migraine, and Interstitial cystitis (all of which cause chronic pain and inflammation) are some of the key ailments whose symptoms are efficiently reduced by hemp oil use.

The most popular application of medical marijuana is to treat chronic pain. It is extremely safe, as there is no risk of overdose, and it is non-addictive. It can take the place of NSAIDs (non-steroidal anti-inflammatory drug(s)), which are not suitable for those with kidney issues, GERD, or ulcers. While pharmaceutical drugs function at the symptom level, they don’t work at the system level, thus they don’t provide a “cure,” which puts an immense burden on the human physiology

The list isn’t exhaustive; rather, it’s a sampling of the various ailments for which medical marijuana can be used and has previously shown to be successful.

In the grand scheme of things, no one in today’s urban society is immune to an inflamed immune and central nervous system, owing to environmental toxins and our inflammatory diet (which contains far too much sugar), both of which contribute to an inflamed immune system and symptoms of brain inflammation.

CBD’s potential to manage and relieve these symptoms is obvious, necessitating increased use and understanding of cannabinoids.

Credits: https://hempfoundation.net/top-14-diseases-that-can-be-cured-by-hemp/

#Hemp Heart Nutrition

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thewaltzy · 7 years

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Bipolar Disorder

Bipolar disorder is a mental health disorder characterised by periods of depression and periods of mania.

Potential symptoms of mania include:-

Erratic, impulsive behaviour

Rapid, uninterruptible speech

Poor decisions based on unrealistic ideas

Short attention span

Reduced sleep

Racing thoughts

Elevated mood

Irritability

To be classifed as mania, the symptoms need to be present for at least 1 week and must impair an individual’s ability to work and/or socialise.

There are 4 types of Bipolar DIsorder.

Cyclothymic

Sequential periods of minor depression and hypomania

Hard to diagnose as patient may not realise they are having an episode

Bipolar II

Sequential periods of depression and hypomania

Easily mistaken for depression due to less obvious manic symptoms

Bipolar I

Sequential period of depression and mania

Mixed Affective

Simultaneous depression and mania

Low mood from depression combined with impulsiveness from mania leads to a greatly increased risk of suicide.

Bipolar Disorder is difficult to diagnose as there are no chemical markers. Tests can be done to rule out other possible conditions, but diagnosis generally relies on history taking by the patient and friends/family. The first symptoms that present are usually depressive symptoms so it can easily misdiagnosed as depression.

Aetiology

Bipolar Disorder has both genetic and environmental factors that may contribute to its cause. However, it is not fully understood how these are linked.

Genetic Factors

60% to 80% of patients are related to someone with Bipolar Disorder

~67% chance of developing Bipolar Disorder if identical twin has Bipolar Disorder

~19% chance of developing Bipolar Disorder if non-identical twice has Bipolar Disorder

There are some candidate risk genes that are thought to increase someone’s chance of having Bipolar DIsorder

Environmental Factors

Early life stress such as trauma or abuse may increase a person’s chance of having Bipolar Disorder

Kindling Hypothesis

The Kindling Hypothesis suggests that whenever someone with a genetic predisposition to Bipolar Disorder experiences a stressful event, the stress threshold at which their mood changes is gradually decreased until episodes can start spontaneously

Pathophysiology

Neuroanatomy

Enlarged Lateral and 3rd Ventricles

Decreased brain size

Smaller hippocampi

Decreased grey matter

Neurotransmitters

Increased activity/levels of Noradrenaline, Serotonin and Dopamine

Neurotrophic Factors

Biological elements that direct growth/maturation

Decreased levels of Brain-Derived Neurotrophic Factors

Treatment

Therapies for Bipolar Disorder include Lithium, Anticonvulsants, Antipsychotics, Cognitive Behavioural Therapy and Electroconvulsive Therapy.

Pharmacological

Lithium

Mechanism of action not fully understood, but it decreases Noradrenaline release and induces the synthesis of Serotonin

Important side effects include:-

Nephrotoxicity

Teratogenic

Hypothyroidism

Dehydration

Does not induce mania in non-bipolar patients

Anticonvulsants

Called mood stabilisers when used in Bipolar Disorder

e.g., Carbamazepine

Causes a blockade of Voltage-Gated Sodium Channels

Can only treat the episodes of Mania

Can cause Agranulocytosis

e.g., Sodium Valproate

Thought to cause a blockade of Voltage-Gated Sodium Channels

Thought to increase levels of GABA

Can only treat the episodes of Mania

Teratogenic

e.g., Lamotrigine

Causes a blockade of Voltage-Gated Sodium Channels

Causes a blockade of Voltage-Gated Calcium Channels

Antagonise 5-HT3 receptors

Can be used to treat both the Manic and Depressive episodes

Teratogenic

Antipsychotics

Only the Atypicals (2nd Generation) can be used as the Typicals (1st Generation) are more anti-mania rather mood stabilisers and so may worsen depressive episodes

e.g., Clozapine, Olanzapine, Risperidone, Aripriprazole

Olanzapine most commonly prescribed

Antagonise D2 and 5-HT2A receptors

Side effects include:-

Extrapyramidal side effects

Extrapyramidal tracts act to modulate and regulate movement

Controlled by the nigrostriatal pathway in the basal ganglia

Slow movement, and slow initiation of movement

Spasms of neck and face muscles

Motor restlessness

Antipsychotic Malignant Syndrome

Life threatening

Muscles cramps

Tremor

Fever

Unstable autonomic nervous system

Increased prolactin secretion

Prolactin promotes milk production

Blockade of tuberohypophyseal pathway

Breast swelling

Lactation

Period cessation

Weight gain

May antagonise H1 receptors

Increase appetite via stimulating production of AMP-activated protein kinase

Decreased lipolysis

Decreased thermogenesis

Sedation

May occur due to D2 receptor antagonism in the mesocortical pathway

May occur due to central H1 receptor antagonism

Hypotension

May antagonise α1 adrenoreceptor

Vasodilation

Anticholinergic effects

May antagonise muscarinic acetylcholine receptors

Dry mouth

Blurred vision

Constipation

Urinary Retention

Cognitive Behavioural Therapy

Based on the concept that thoughts, feelings, physical sensations and actions are interconnected, and that negative thoughts and feelings can create a vicious cycle.

Help deal with overwhelming problems in a more positive way by breaking them down into smaller parts.

Looks for practical ways to improve your state of mind on a daily basis.

Electroconvulsive Therapy

‘Restarts’ the brain

Only used in severe cases where symptoms are debilitating and other treatments have not worked.

#bipolar #mental health #medicine #treatment #health #bipolar disorder #psychology #depression #mania #hypomania #Bipolar I #cyclothymia #Bipolar II #uni #mental disorder

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siva3155 · 5 years

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300+ TOP GYNAECOLOGY Objective Questions and Answers

GYNAECOLOGY Multiple Choice Questions :-

1. A 48-year-old woman presents with intermenstrual bleeding for two months and episodes of bleeding occurring any time in the cycle. There is no associated pain. Differential diagnosis for intermenstrual bleeding does not include: a. endocervical polyp b. cervical malignancy c. endometrial polyp d. ovarian teratoma e. atrophic vaginitis. Ans: d 3. All of the following are effects of premature menopause, apart from: a. decreased cardiovascular risk b. infertility c. osteoporosis d. vasomotor symptoms e. vaginal dryness. Ans: a 4. A 32-year-old woman presents to the gynaecology clinic with infrequent periods. A hormone profi le is done and all of the following are consistent with polycystic ovarian syndrome, apart from: a. increased androgen levels b. normal FSH c. normal oestradiol d. decreased LH e. low progesterone levels. Ans: d 5. A 28-year-old woman attends the colposcopy clinic after an abnormal smear test. The smear is reported as severe dyskaryosis and she has an intrauterine contraceptive device in situ. All of the following statements are likely to be true, apart from: a. the cervix is macroscopically normal b. acetic acid is applied and an irregular white area is apparent to the left of the cervical os c. Lugol’s iodine is applied and the same area stains dark brown while the rest of the cervix stains pale d. a biopsy is taken e. the IUCD can stay, as it will not aggravate the cervical abnormality. Ans: c 6. A 24-year-old woman presents with the absence of periods for nine months. She started her periods at the age of 13 years and had a regular 28-day cycle until 18 months ago. The periods then became irregular, occurring every two to three months until they stopped completely. The following are all included in the differential diagnosis of secondary amenorrhoea, apart from: a. excessive exercise b. hyperprolactinaemia c. hyperthyroidism d. premature ovarian failure e. signifi cant weight loss Ans: c 7. The following statements regarding adenomyosis are true, apart from one. a. It tends to occur in women over 35 years. b. Risk factors include increased parity, termination and quick labours. c. The condition commonly occurs in association with endometriosis. d. With each period, bleeding occurs from the endometrial tissue into the smooth muscle. e. The diagnosis can be made by ultrasound or magnetic resonance imaging scan. Ans: b 8. A 20-year-old woman is referred with a problem of post-coital bleeding. Over the past two months it has occurred on six occasions and there has been a small amount of bright red blood noticed after intercourse. There is no associated pain. The following investigations should initially be performed, apart from: a. cervical smear b. endocervical swab for chlamydia c. colposcopy d. endocervical swab for gonorrhoea e. speculum examination to observe the cervix. Ans: c 9 The following are all consistent with the diagnosis of antiphospholipid syndrome except: a hydatidiform mole b severe early-onset pre-eclampsia c arterial or venous thrombosis d mid-trimester fetal loss e placental abruption. Ans: a 10. The following are all causes of recurrent miscarriage, apart from: a. parental chromosomal abnormality b. activated protein C-resistance c. uncontrolled hypothyroidism d. chlamydia infection e. submucosal fi broids. Ans: d

GYNAECOLOGY MCQs 11. Which one of the following statements about pituitary tumours is true? a. Weight loss is a common feature of pituitary failure (hypopituitarism) due to a pituitary tumour. b. Visual fi eld loss in female patients with prolactin-secreting pituitary tumours (prolactinoma) is usual. c. Adrenocorticotrophic hormone (ACTH) secreting pituitary tumours cause a syndrome of cortisol excess that can lead to exaggerated vertical growth in adolescence. d. Growth hormone defi ciency is a recognised feature in adult patients presenting with acromegaly due to a pituitary macroadenoma. e. A low testosterone level is more common than a low thyroxine level in men with non-functioning gonads. Ans: e 12. Which of the following statements concerning the anterior pituitary is true? a. It develops in the embryo from a down-growth of the hypothalamus. b. It secretes antidiuretic hormone (ADH). c. It is regulated by hypothalamic-releasing hormones. d. It secretes its hormones into the pituitary portal system. e. It is down-regulated by low oestrogen levels. Ans: c 13. Which one of the following statements about the implantation of the human embryo is true? a. It will occur at any time over a period of about 14 days. b. It will occur whether or not the zona pellucida is present. c. It will occur when the cytotrophoblast contacts the endometrial epithelium and begins to invade the maternal tissue. d. It will occur with the inner cell mass closest to the endometrium. e. It will occur even if there is only cytotrophoblast present. Ans: d 14. Which one of the following statements about puberty is true? a. Puberty is preceded by falling plasma levels of adrenal androgens. b. The fi rst menstrual period is called the adrenarche. c. The pubertal growth spurt is the fi rst sign of puberty. d. Pubic hair growth is stimulated in girls by oestrogen. e. Spermatogenesis starts at puberty. Ans: a 15. Which is the most appropriate statement concerning pulmonary embolism? a. It is now rarely fatal, with the introduction of modern diagnostic tests and treatments. b. It gives an area of lung which is unventilated on a ventilationperfusion scan. c. It does not usually show up on a CT pulmonary angiogram. d. It is likely that the patient has symptoms of deep-vein thrombosis. e. It may give symptoms similar to pneumonia. Ans: e 16. One of the following is true. It is recognised that the positive predictive value of initial mammography for breast cancer within the national screening programme in the UK is 16%. This means that: a. 16% of people who have breast cancer are detected on initial mammography b. 84% of people without breast cancer have a normal mammogram c. 16% of initial mammograms are abnormal d. a patient with an abnormal initial mammogram has a 16% chance of having breast cancer e. out of every 100 patients with an abnormal mammogram, Ans: d 17. One of the following is true. Successful fertilisation and subsequent normal embryonic development: a. require at least two spermatozoa b. require the retention of the cortical granules in the oocyte c. are most likely when the oocytes have been ovulated in an immature stage d. require exclusion of the second polar body e. often occur when the oocyte has lost its zona pellucida. Ans: d 18. One of the following is true. The increase in maternal blood volume in pregnancy occurs as a result of: a. peripheral vasoconstriction b. a reduction in progesterone c. decreased synthesis of vasopressin d. increased aldosterone synthesis e. reduced renin activity. Ans: d 19. One of the following is true. Decreased peripheral resistance in pregnancy has been attributed to an increase in synthesis of: a. angiotensin b. endothelin c. nitric oxide d. renin e. thromboxane. Ans: c 20. A 25-year-old woman on liver enzyme inducers is requesting contraceptive advice. The method providing her with the most reliable form of contraception would be: a. combined oral contraceptive pill b. Depo-Provera injection c. diaphragm d. male condom e. progesterone-only pill. Ans: b 21. A 35-year-old woman comes requesting long-term reversible contraception. You advise that the method that can provide the longest protection is: a. contraceptive implant b. copper intrauterine device c. Depo-Provera injection d. intrauterine hormonal system (IUS) e. laparoscopic sterilisation. Ans: b 22. Regarding cervical cancer, which is the true statement? a. HPV types 6 and 12 are high risk for developing cervical cancer. b. The new vaccines can prevent invasive carcinoma but not CIN. c. As soon as the new vaccination is introduced, cervical screening programmes can cease. d. HPV types 16 and 18 account for the majority of cervical cancer in the UK. e. HPV is an oncogenic virus for squamous cell but not adenocarcinoma of the cervix. Ans: d 23. Regarding the menstrual cycle, which is the true statement? a. Menstruation occurs with vasodilation of the spiral arteries. b. The LH surge triggers menstruation. c. The Graafi an follicle develops during the luteal phase. d. Both the follicle and the corpus luteum secrete oestradiol. e. Progesterone levels fall after the onset of menstruation. Ans: d 24. Regarding Müllerian duct abnormalities which is the true statement? a. occur about 1 in 500 b. the commonest uterine abnormality is septate uterus c. occur not infrequently with gastrointestinal abnormalities d. surgical correction of a septate uterus is followed by fetal salvage in Read the full article

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medicomunicare · 3 years

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Il ruolo biologico della prolattina nel tumore al seno

I ruoli della prolattina nella fisiologia e nel tumore mammario È noto da tempo che l’ormone prolattina svolge un ruolo vitale nella crescita e nello sviluppo del seno e nella produzione di latte durante la gravidanza. La prolattina (PRL) è un ormone polipeptidico prodotto principalmente da cellule note come lattotrofi, che si trovano nella ghiandola pituitaria anteriore di tutti i vertebrati.…

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#carcinoma mammario #cromatina #espressione genica #estradiolo #estrogeni #fattore di crescita #fattore di trascrizione #fibronectina #ghiandola mammaria #istone deacetilasi #matrice extracellulare #metastasi #progesterone #prolactin-induced protein #prolattina #protein kinase #recettore #tumore al seno

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supplier-of-peptidesz · 5 years

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Muscle Gain and Weight Loss Peptides

If you're looking for the best bodybuilding supplement for muscle gain and weight loss, Somatropin will be your preferential choice due to its good quality and excellent effect that can help you to achieve. Human Growth Hormone is also known as a direct and fast supplement for bodybuilders. For GHRP(Growth Hormone Release Peptide) category includes GHRP-6, GHRP-2, Hexarelin and Ipamorelin, GHRH(Growth Hormone Release Hormone) category includes CJC1295 DAC or NO DAC and Sermorelin, they work most commonly to increase GH production. If products from these two categories can be used in combination, they will release the most potent effect on your goals.

1. Somatropin HGH191aa Human Growth hormone (GH or HGH), also known as somatotropin or somatropin which has 191 amino acids, is a peptide hormone that stimulates growth hormone cell reproduction and regeneration in humans. It is a type of mitogen which is specific only to certain kinds of cells. It also stimulates the production of IGF-1. HGH is used as a prescription drug in medicine to treat children's growth disorders and adult growth hormone deficiency. It does great help to muscle gain, fat loss, better sleep, reducing wrinkles, grow hair and nails faster, it's also called Fountain of Youth, the natural human hormone supplement.

2. CJC-1295 with DAC CJC-1295 with DAC is a peptide which is known to help in promoting muscle gain, muscle strength, lean body mass and improve overall physical performance. It is considered as a long-acting analog of growth hormone-releasing hormone (GHRH) through its drug affinity complex (DAC) lengthens its life span considerably as compared to other growth hormones. Hence, CJC-1295 with DAC is able to exert its beneficial effects with infrequent dosing as compared to your standard synthetic growth hormone injections. Most benefits associated with the use of CJC 1295 with DAC have been associated with muscle development. It is able to do so because of its ability to increase muscle tissue growth and improve protein synthesis. Hence, most of its users include fitness buffs, athletes and bodybuilders. Clinical trials and anecdotal evidence have shown that I can considerably improve one’s physical performance. It is also thought to increase muscle strength, promote overall body mass whilst increase muscle gain. Benefits of CJC 1295 with DAC has also been associated with cell growth stimulation, skin, internal organ mass, and immunity improvement as well as improved sleep. Anecdotal evidence has shown that it promotes faster recovery from muscle injuries and improvement of mental well-being.

3. IGF-1 Lr3

IGF-1 plays a significant role in muscle regeneration. Although IGF-1 induces differentiation to a much greater degree, it stimulates both proliferation and differentiation of stem cells in an autocrine-paracrine manner. When IGF-1 is injected locally, it increases satellite cell activity, muscle DNA, muscle protein content, muscle weight, and muscle cross-sectional area. The importance of IGF-1 lies in the fact that all of its apparent functions act to induce muscle growth with or without overload although it really shines as a growth promoter when combined with physical loading of the muscle.

IGF-1 also acts as an endocrine growth factor having an anabolic effect on distant tissues once released into the bloodstream by the liver. IGF-1 possesses the insulin-like property of inhibiting degradation, in addition, it stimulates protein synthesis. The insulin-like effects are probably because of the similarity of the signaling pathways between insulin and IGF-1 following ligand binding at the receptors.

4. GHRP-2

GHRP-2, like its brother GHRP-6, is a hexapeptide that is a pure growth hormone secretagogue. In addition, GHRP-2 is a synthetic agonist of ghrelin. Unlike GHRP-6, this peptide does not bring on the heavy hunger side effects; however, some users will notice slight increases in hunger, in this case, users may increase their appetite to a certain extent. Somewhere in between GHRP-6 and Ipamorelin, this hexapeptide has the ability to be a serious contender when considering which GHRP to use with your GHRH. If you are looking for anti-aging properties or for the ability to increase lean body mass gains on cycle/off cycle, GHRP-2 will help you on that. It is a very potent growth hormone-releasing peptide. As always, it's advised that while it comes with some side effects, GHRP-2 will not shut down your natural production of growth hormone. With a proper diet and training, users can utilize GHRP-2 along with a GHRH as a tool that is safe and effective for athletes and bodybuilders alike.

5. GHRP-6

GHRP-6, also known as growth hormone-releasing hexapeptide, is an injectable peptide of growth hormone-releasing peptides, or GHRP’s. The most common use of these peptides is to increase GH production. Other peptides in this category include GHRP-2, Hexarelin, and ipamorelin. In relation to increasing GH, all of them work similarly, and there is no need or advantage to combining them. Instead, the one most suited for the particular case is chosen. The principal use of GHRP-6 is to provide increased GH levels, which also results in increased IGF-1 levels. This aids fat loss and under certain conditions, it aids muscle gain as well. Generally, GHRP use is chosen as an alternative to GH use and only rarely is combined with GH. Reasons to prefer GHRP-6 over other GHRP’s are its side effect on increasing appetite (which also can be a disadvantage), and its demonstrated value in reducing inflammation and helping to heal injury, especially tendinitis.

6. HGH Fragment 176-191 AOD 9604

HGH Fragment 176-191 is an injectable drug which is a stabilized analog of the growth hormone-releasing factor (GRF) that induces growth hormone (GH) in a specific and physiological manner. It is a part of the Growth Hormone molecule responsible for fat burning. The main effect of this compound is to reduce abdominal fat (mainly visceral fat), without compromising blood glucose levels and increases muscle mass. Other positive features of HGH Fragment 176-191 include protein synthesis, vascularity from increased nitrogen retention, increased bone mineral density, better sleep, and increased strength through hyperplasia. Many studies have shown the fact that the HGH Fragment 176-191 is an effective treatment for obesity and fat loss, and much safer than its Human Growth Hormone counterpart. The average dosage of the compound is 2-6 IU or (500-1000 mcg) per day split into two or three doses. Studies show that the use of HGH Fragment 176-191 during 30 days produced a considerable reduction of body fat. In most studies, no adverse side effects were reported with continuous use in the rational dosage limits.

7. Hexarelin

Hexarelin (HEX) is a synthetic growth-hormone-releasing peptides(GHRP), structurally similar to GHRP-6, in the factor family which stimulates the release of growth hormone (GH). It can medically be used to treat GH deficiency. Hexarelin is getting more popular to be used as a performance enhancement drug. Because the ability of Hexarelin to increase secretion of natural growth hormone, most of its effects are similar to those of synthetic GH. Effects of it include: increase in strength, growth of new muscle fibers, increase in the size of already existing muscle fibers, neural protection, joint rejuvenation, protection, and healing. Also, with Hexarelin use the GH receptors in adipose (fat) tissue allow for potential fat reduction. Hexarelin use causes levels of Insulin-Like Growth Factor (IGF-1) to rise in the liver. IGF-1 is the prime cause of muscle growth in response to GH stimulation.

8. Ipamorelin

Ipamorelin is a penta-peptides hormone. It has similar properties of GHRP-2, it does not have ghrelin's lipogenic properties and does not promote hunger. Ipamorelin acts synergistically when applied during a Releasing Hormone (GHRH) pulse or when it is used along with a GHRH such as Sermorelin or Modified GRF 1-29 (growth releasing factor, amino 1-29). The synergy comes both due to the suppression of somatostatin and the fact that ipamorelin increases GH release per-somatotrope, while GHRH increases the number of somatotropes releasing GH. On the other hand, Ipamorelin is similar to GHRP-6 in that they both release GH at a very similar strength minus the side effects that of GHRP-6. Both GHRP-2 and GHRP-6 cause a release and an increase in cortisol and prolactin levels, however, Ipamorelin only selectively releases GH at any dose. Ipamorelin shares similar function to Hexarelin and compared to other peptides, it is a much more steady form of ghrelin and has longer half-life periods of at least two hours long and causes secondary effect by making neurons to become excited.

9. Sermorelin

Sermorelin Acetate stimulates the pituitary gland to naturally produce human growth hormone. It is a truncated analog of a growth hormone-releasing factor that is naturally produced by the brain to stimulate pituitary production of human growth hormone. The increased volume of human growth hormone (HGH) produced by the pituitary gland causes an increase in the production of the liver.

10. Synthetic EPO Erythropoietin Injection

EPO is a protein hormone produced by the kidney. It binds with receptors in the bone marrow after being released into the bloodstream and stimulates the production of red blood cells (erythrocytes).EPO is produced by interstitial fibroblasts in the kidney closely associated with peritubular capillary and tubular epithelial tubule and it's also derived from perisinusoidal cells in the liver. Although liver production predominating during fetal and perinatal period, renal production is predominant during adulthood. Except for erythropoiesis, erythropoietin also has other known biological functions. For instance, it plays an essential role in the brain's response to neuronal injury. EPO is also well known for its wound-healing ability.

11. Gonadorelin

Gonadorelin is a medicine that is the same as gonadotropin-releasing hormone (GnRH) that is naturally released from the hypothalamus gland.GnRH is responsible for the release of follicle stimulating hormone and luteinizing hormone from the anterior pituitary.Gonadorelin is used to test how well the hypothalamus and the pituitary glands are working. It is also used to cause ovulation in women who do not have regular ovulation and menstrual periods because the hypothalamus gland does not release enough GnRH. Gonadorelin is used for the treatment of amenorrhea, delayed puberty, and infertility the administration of gonadorelin is used to simulate the physiologic release of GnRH from the hypothalamus in treatment of delayed puberty, treatment of infertility caused by hypogonadotropic hypogonadism, and induction of ovulation in those women with hypothalamic amenorrhea.

#health & fitness #fitness #muscle gain #muscle #weight loss #lose weight #fat #peptides #bodybuilding

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garden-of-everything · 7 years

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ABIM: Endocrinology

ABIM syllabus can be found here Let me know if you find any errors Sources: UWorld, MKSAP 16/17, Rizk Review Course, Louisville Lectures, Knowmedge (free version)

Adrenal Disorders

Primary aldosteronism and mineralocorticoid excess: - Sx: HYPERNATREMIA, hypokalemia, metabolic alkalosis, HTN - Dx: aldosterone:renin >20 (aldosterone >15 with low renin levels), salt challenge fails to decrease aldosterone levels --> get CT scan - Tx: thiazide for BP control, spironolactone for hyperplasia, surgery for adenoma Adrenal insufficiency: - Addison’s = primary: tan, orthostatic HTN, hyponatremia, hyperkalemia, hypoglycemia, prolonged QTc - Dx: morning cortisol levels --> cosyntropin stimulation test <18mcg/dL = adrenal insufficiency --> check morning ACTH levels (if decreased ACTH, MRI brain; if increased ACTH, CT adrenals) - acute Tx: dexamethasone - chronic Tx: hydrocortisone +/- fludrocortisone only if primary - x2-10 dose of steroids during stress Pheochromocytoma: - associated with MENIIa and IIb (increased calcitonin/medullary thyroid cancer is also associated with both MENII’s; if IIa: hypercalcemia/parathyroid, if IIb: Marfan’s/neuromas) - Dx: serum or 24 hour urine metanephrines --> MRI/CT ab --> if negative: T-MIBG Tx: surgery: - pre-op BP control with phenoxybenzamine/doxazosin/nicardipine - intra-op HTN crisis: nitroprusside or phentolamine Incidentaloma: - if <4cm, f/u CT; if >6cm, surgery - Dx with 1mg overnight dex suppression test (Cushings) + urine metanephrines (PCC) +/i if hypertensive: aldosterone:renin ratio (hyperaldosteronism if elevated)

Thyroid Disorders

Hyperthyroidism: - Grave’s: anti-TSHR Ab - associated with vitiligo - Tx: Methimazole (AE: sore throat/agranulocytosis, hepatotoxicity) > PTU (for first trimester; AE: hepatotoxicity) Hypothyroidism: - Hashimoto’s: anti-TPO antibodies - associated with primary thyroid lymphoma - Tx if TSH>10 or planning pregnancy or symptomatic *FYI: increase Synthroid dose in pregnancy and in CELIAC DISEASE Thyroiditis: 1. subacute/DeQuervain’s: PAINFUL, Tx with NSAIDs only 2. Peripartum: painless, autoimmune 3. amiodarone-induced *subclinical presentation (decreased TSH, normal T4): repeat TFT in 4-6mo Thyroid nodules: - if <1cm and doesn’t look cancerous, repeat US in 3-6 months - if >1cm, FNA > Sx Euthyroid sick syndrome: transient and mild, weird TSH/T3/T4 levels during illness without prior thyroid issues; usually T3 is decreased while TSH/T4 is normal - Tx underlying illness only (no need for Synthroid) Thyroid storm: fever, HF, psych changes/coma; Tx: PTU, propranolol/BB, steroids (vs. Myxedema coma from hypothyroidism: hypothermia/hypotension/bradycardia/bradypnea, desaturation, AMS, hyponatremia, hypoglycemia; Tx with Synthroid + hydrocortisone) *if TSH/T3/T4 are all weirdly increased or decreased, cause is likely a pituitary tumor *suspect toxic multinodular goiter when patient experiences hyperthyroid symptoms after receiving IV iodine contrast

Hypertension

Hyperaldosteronism: - hypernatremia, hypokalemia, metabolic alkalosis (basically the opposite of RTA type 4) - Tx with thiazide Renal artery stenosis: Tx with ACEi Cushing’s Disease: - round and squishy - Dx: elevated 24 hour urine cortisol, 1mg dexamethasone suppression test (positive if fails to bring cortisol <5), elevated late salivary cortisol

Lipid disorders

- start screening every 5 years in >35yoM, >45yoF; or >20 if +CAD risk - goals: LDL<160, Cholesterol <190; pretty much decrease both goals by 30 for every additional CAD risk up to 3 times - diet > exercise - offer Orlistat if BMI>30 - offer Bariatric surgery if BMI >40 OR >35 with obesity-related condition

Ovarian disorders and female reproductive health

Polycystic ovary syndrome: - amenorrhea and virilization - Dx: bleeds with progesterone challenge, has elevated LH - Tx hirsuitism with OCP --> if fails: spirnolactone; use clomiphene if wants babies Amenorrhea: 1. primary ovarian insufficiency: elevated FSH = menopause --> if normal: check karyotype to r/o Turner’s (obtain cardiac imagining and kidney US for all patients with Turner’s) *if amenorrheic because of super athleticism: screen for bulimia 2. hypothalamic cause: functional/tumor/lymphoma; has decreased FSH and NO withdrawal bleed after progesterone challenge 3. anatomic cause/Asherman syndrome: adhesions basically retain periods; also has no withdrawal bleeding --> Tx: surgery Ovarian cancer: - hyperandrogenism; normal DHEA levels but elevated total testosterone levels >200 in a woman = ovarian cancer until proven otherwise - Dx: TVUS --> adrenal CT

Testes and male reproductive health

Male hypogonadism: total testosterone <200 +: - increased LH/FSH = primary testicular failure (Klinefelter’s, Mumps orchitis, XRT, autoimmune) - normal/decreased LH/FSH, elevated prolactin = secondary cause (prolactinoma --> MRI brain, opiates, steroids) --> obtain iron study to rule out hemochromatosis* *Hemochromatosis presents as tan Diabetes with elevated transaminases, and hypogonadism; has OA symptoms and is associated with CPPD/Pseudogout Male infertility: - Cystic Fibrosis is associated with azospermia, bilateral absence of vas deferens Gynecomastia: associated with anabolic steroids, marijuana, spironolactone - if elevated estradiol --> check testicular ultrasound to r/o neoplasm --> chest/adrenal CT to r/o choriocarcinoma (elevated beta hCG, lung infiltrates, hemoptysis) - if elevated LH, decreased testosterone --> check karyotype to r/o Klinefelters (associated with increased risk of breast cancer) *testosterone therapy can worsen OSA, erythrocytosis, and increases risk of clots

Diabetes mellitus

Type I: - associated with other autoimmune diseases (Celiac, vitiligo, thyroid) - DKA Type II: - Dx with two of the following on separate days: (1) fasting >126, (2) A1c >6.5%, (3) random >200, or just one of this: (4) 2 hour gtt >200 *if a health-seeming patient >35yo with h/o CAD or 2 CAD risk factors wants to do a vigorous exercise program --> do an exercise stress test first Diabetes mellitus and pregnancy: STOP ACE/ARB/statin (teratogenic!) - obtain eye exam once/trimester - BP control with methyldopa, BB (labetalol), CCB, Hydralazine - goal: preprandial BG <90, 1 hour postprandial <120 using NPH and short-acting insulin (NOT long-acting insulin or orals) - require annual DM screening after delivery Diabetes goals: - BP <140/90: use ACEi - start statin regardless of LDL if cholesterol >135 and check yearly - cholesterol goal <135 > LDL goal <100 - annual eye exam with Q3-5 year dilated eye exam - urine albumin excretion <30; if >30, start ACEi/ARB Indications for continuous BG monitoring: (1) postprandial hyperglycemia (2) Dawn phenomenon: morning hyperglycemia (vs. Somogyi = rebound hyperglycemia) (3) overnight hypoglycemia Diabetes complications: - acute mononeuropathy: spontaneously resolves, no Tx - gastroparesis: Tx: small meals, Reglan/Erythromycin (vs. Rifaximin for Scleroderma-related bacterial overgrowth that presents similarly as bloating) - orthostatic hypotension: Tx with compression stockings +/- fludrocortisone - peripheral neuropathy: BG control --> DULOXETINE > pregabalin - HHS: plasma osm >320, BG >600-1000, normal pH/ketones; Tx with NS --> insulin --> when BG<200 and tolerating PO --> SQ insulin - DKA: pH <7.3, bicarb <15, BG >250, elevated ketones elevated AG vs. Diabetes insipidus: excessive thirst for cold water, can’t concentrate urine - r/o DM, hypercalcemia - Dx: water deprivation test --> if urine osm still <200 --> desmopressin challenge: (1) can concentrate after challenge = positive test --> brain MRI; Tx intranasal or PO desmo/vasopressin (2) still can’t concentrate after desmo: negative test --> kidney ultrasound; Tx sodium restriction and thiazide *if Lithium-induced: Tx Amiloride

Disorders of calcium metabolism and bone

Hypercalcemia: - hyperparathyroidism associated with MEN I and IIa (increased PTH or normal PTH with increased calcium and decreased phos), chondrocalcinosis, bone cyst --> Dx: Sestamibi scan --> Surgery *Indications for parathyroidectomy: (1) Age <50yo (2) Ca >12 or 1 above baseline (3) GFR<60 (4) 24 hour urine Ca >400 (5) symptoms of hypercalcemia - drug-induced hypercalcemia: lithium, thiazide - sarcoidosis: increased calcitriol = active Vit D = 1, 25 Vit D - cancer / multiple myeloma: CRAB, difference in urine vs dipstick protein due to presence of undetected light chain, hypervitaminosis D - Dx: check ionized calcium first --> r/o decreased TSH --> PTH/Ca/Phos/25Vit D levels --> decreased urine calcium ( = familial hypocalciuric hypercalcemia --> Dx: CASR mutation, urine Ca;Cr ratio <0.01) Hypocalcemia: check ionized level, because may be due to hypoalbuminemia - associated with DiGeorge - symptoms include circumoral paresthesia, Chvostek cheek tap, Trousseau BP cuff Hyperphosphatemia: - CKD (increased PTH, decreased Vit D) --> Tx: Calcitriol/1,25VitD - hypoparathyroid (decreased PTH) - pseudohypoparathyroid (increased PTH, normal Vit D) Hypophosphatemia: - bone tenderness due to vitamin deficiency Paget’s: - hat size changes, bone pains, fractures, femur/tibia bowing, cranial nerve compressions; heart failure - elevated alk phos --> bone scan - Tx: bisphosphonate Osteoporosis: T-score<-2.5 (ignore age-adjusted Z-score) - get DEXA every 10 years (if normal) in woman >65 OR younger if FRAX >9.3% (they smoke, have h/o hip fx, steroid use, etc) Vitamin D deficiency and osteomalacia: - proximal muscle weakness/falls (especially in elderly), bone pain - decreased calcium, phosphate; increased alk phos - associated with Celiac disease, liver disease, kidney disease - Dx: bone marrow biopsy (BMB) - Tx: ergocalciferol/Vit D2 Renal osteodystrophy: ESRD pt w decreased Ca, Vit D; increased Phos, PTH; chondrocalcinosis at knees and pubic symphysis

Anterior pituitary disorders

Pituitary tumors: MRI (order first if mass effect) - associated with MEN I, pregnancy, and check TSH! (1) Prolactinoma: prolactin >500, galactorrhea/amenorrhea/erectile dysfunction; Tx: Cabergoline (2) Acromegaly: Dx: IgF1 or oral glucose tolerance test that fails to decrease GH; Tx: surgery (3) Cushing’s: HTN, DM, proximal muscle weakness; Dx: 24 hour urine cortisol, elevated late night salivary cortisol --> elevated morning ACTH = pituitary tumor --> Tx: surgery > XRT - incidental pituitary tumors: f/u repeat MRI with prolactin levels - Rx (TCA, CCB, Reglan, opiates) and pregnancy can cause elevated prolactin! Hypopituitarism: (1) apoplexy: sudden HA, vision change, AMS; Tx: steroids (2) Sheehans (after pregnancy): amenorrhea, no lactation (3) lymphocytic hypophysitis (occurs peripregnancy): sellar mass with anti-pituitary antibody; Tx: steroids OR if vision changes, surgery

Posterior pituitary and water metabolism

Hypernatremia: DI: polyuria, inability to concentrate urine; Dx: water deprivation --> desmopressin: (1) concentrates urine (urine osms goes up) = MRI brain and Tx w desmo/vasopressin; (2) still doesn’t concentrate (urine osms stay low) = kidney ultrasound and Tx with salt restriction, thiazide Hyponatremia: SIADH: urine osm > serum osm, urine osm >500, euvolemic (vs. psychogenic polydipsia where decreased serum AND urine osm)

Endocrine tumors and endocrine manifestations of tumors

Pancreatic tumors associated with MENI (hypercalcemia/hyperparathyroid, prolactinoma/pituitary tumor): - Insulinoma: Dx 72 hour fast (BG<45, insulin >5) --> CT abdomen --> still not detected?: check endoscopic ultrasound - VIPOMA: watery diarrhea - Gastrinoma/Zollinger-Ellison syndrome: severe dyspepsia; Dx: gastrin levels --> secretin stimulation test causing increased gastrin >200 - Glucagonoma: hyperglycemia, pustular rash, diarrhea, DVTs - Carcinoid: flushing, N/V/D/AP; Dx: 24 hour urine 5-HIAA Malignancy-associated hypercalcemia (squamous cell): decreased PTH, normal/decreased phosphate, increased PTHrpeptide Ectopic ACTH (Cushing’s) due to tumor: associated with small cell, medullary thyroid cancer (elevated calcitonin), bronchial carcinoid (flushing, wheezing) SIADH from tumor: associated with small cell; hyponatremia and euvolemia; urine osm >500

Hypoglycemia

- most commonly after gastrectomy/gastric bypass - insulin use: decreased C-peptide - sulfonylurea: increased C-peptide --> check for medication in urine - insulinoma: seen in MEN I with hypercalcemia/hyperparathyroid, prolactinoma/pituitary adenoma; Dx with 72 hour fast: if BG <45 and insulin >5 --> CT abdomen - exercise-induced delayed hypoglycemia: Tx: complex carbs

Polyglandular disorders

MENI (”3P’s”): (1) Pituitary: prolactinoma, acromegaly, Cushings (2) Pancreas: insulinoma hypoglycemia, VIPoma diarrhea, gastrinoma GERD, carcinoid flushing, glucagonoma hyperglycemia (3) Parathyroid: hypercalcemia MENIIa: (1) Parathyroid: hypercalcemia (2) PCC: hypertension (3) Medullary thyroid cancer: elevated calcitonin MENIIb: (1) Marfan’s/neuromas (2) PCC: hypertension (3) Medullary thyroid cancer: elevated calcitonin

#me #endocrinology #abim #internal medicine #im #exam #test #diabetes #metabolism #medical #medicine #study #notes

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dogdata · 5 years

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Understanding Skin and hairs in dogs and why you need to GROOM

If your dog have a good coat it could mean your dog is healthy because the skin and coat reflects a good health. It is important for you to maintain it.

The primary function of the dog’s hair is is to protect and also to insulate

Shiny hair, that is an is indicator of overall health like i said before.

In contrast, a dull coat that lacks luster is an indicator that the dog is not healthy.

Having a healthy coat promotes increased contact between a dog and its owner, with frequent contact ultimately strengthening the human-animal bond. With a good coat you could touch your dog frequently and also let him embrace you. Some owners are very sensitive to the feel and beauty of their dogs and to the “social status” that comes from owning a dog with a beautiful and/or unusual haircoat.

Changes in the texture or appearance of a dog’s coat are an indicator of something going amiss within, but haircoat changes are not specific for any one disease or condition anyway.

Dull or brittle hair can be caused by a dietary imbalance, or it may be due to diseases of digestive, hepatic, renal, thyroidal, immune, or parasitic infection.

If your dog has a bad hair coat as a result of dietary supplement then it would take about four or more weeks before a dietary supplement will have any positive effects on the quality of the hair.

The shine attributed to a healthy dog’s coat is largely due to a complex provide protection from sunlight, moisture; b) “secondary” hairs (also known as fur or wool hairs, or the undercoat) that form the inner coat of an animal and provide insulation; and c) tactile hairs (whiskers) that provide sensory functions.

All adult dogs have longer primary hairs and shorter secondary hairs, but the ratio of each type of hair differs by age and especially breed. Some breeds have almost no undercoat and relatively short and thin primary hair. These “single coated” dogs include Boxers, Dalmatians, and Greyhounds. Yorkshire Terriers, too, don’t have much of an undercoat, but their primary coat is long and silky. So-called “double-coated” breeds have significant undercoats and dense primary coats. The Labrador has a short but very dense coat of coarse primary hairs, and a thick undercoat of softer, insulating secondary hairs. The Bearded Collie has a soft, close undercoat and a shaggy outer coat.

Puppies are born with short, soft secondary hairs only. Sometimes the puppy’s coat color is similar to the adult’s; in other instances, the coat darkens or spots as the puppy matures. Dalmatian puppies are born with a pure white coat that develops black spots as the puppy grows.

Most dogs have full, adult coats by six to eight months of age. The dog’s environment (length of day, average temperature), diet, and hormone levels can influence his coat development.

Dog hair is made of a hard substance called keratin, an insoluble protein that contains high amounts of sulfur (as the amino acid cystine) and lesser amounts of the amino acids tyrosine and leucine. Hair emerges from follicles, just below the outermost layer of skin. In humans, each hair grows from a single follicle. Dogs have single and compound hair follicles; a central follicle that produces the primary hair or guard hair may have two or more lateral follicles that produce 5 to 25 secondary hairs each. Healthy hair relies on the balance of the diet: proteins (and especially the sulfur-rich amino acids such as cystine, as well as tyrosine and methionine), essential fatty acids, copper, and B vitamins. Up to 30 percent of the daily protein requirement of an adult dog can be used for the renewal of the skin and the hair.

Hormonal factors can also interfere with proper hair growth: thyroid and growth hormone stimulate the activity of the hair follicles, whereas corticoids and sexual hormones slow it down. When prolactin (a hormone produced by lactating females) levels stay high in the blood, the coat looks like the summer one, rather thin and sparse. Everybody sheds Breeds and individuals within every breed shed and regrow hair at varying rates. Dogs who live indoors, with little exposure to natural light or cold temperatures, tend to shed in a more or less continuous fashion.

In contrast, dogs who live outside, exposed to natural light and cold temperatures, are more likely to shed for several weeks

Some believe that there are dogs that do not shed but that’s wrong as all dogs shed there is no such thing as a dog who does not shed, there are only dogs who shed a lot less.

Each hair shaft produced by a hair follicle will eventually die and become dislodged from the skin (shed) and be replaced by a new hair shaft produced by that hair follicle.

However, there are some breeds whose hair grows for a much longer period before it dies and is shed. The growth of the new hair pushes the old hair out of the skin.

Finally, any stress such as anesthesia, disease, pregnancy, or administration of certain drugs is likely to put most of the follicles into a resting phase. About two to three months after the stressful event, when the follicles start to be active again, abnormal shedding will often be observed.

A dog’s coat color is determined by his genes. That said, a variety of environmental factors can somewhat alter the color of his hair. Specific nutrients may be involved in hair color. Cystine, methionine, arginine, tyrosine, and phenylalanine deficiencies are reported to induce hair discoloration.

Protein malnutrition induces disturbances in hair growth and quality.

Other trace elements such as iron and iodine can also affect hair color, as well as vitamins A, B-2, and B-6, pantothenic, folic, and nicotinic acids, and biotin. Too much exposure to sunlight can make the hair brittle and cause a black coat to redden or turn brown. After a dog has been clipped, the color of its hair is noticeably lighter, and scars often leave a mark of hair that remains white throughout the rest of the dog’s life.

In aged dogs, hair color tends to fade. As a dog ages, his hair turns gray, especially on the head, beginning with the muzzle.

Hair loss in dogs

The common causes of hair loss in dogs, along with the basics of the appropriate natural remedies, are summarized below. Most are primarily problems of the skin

1. Flea-associated dermatitis A dog with flea infestation typically has a brittle, broken hair coat, especially in the area just in front of the tail head where fleas prefer to reside.

Natural flea control always involves a multi-pronged approach.

You have to remove larvae and pupae from your dog’s home and eliminating places where the flea eggs can develop.

Accomplishing this requires what’s called an “integrated pest management” program.

2. Canine atopy This is an allergic itching syndrome along with subsequent loss of hair that is thought to be genetic in origin. Natural care will involve enhancing the immune system with supplements. Natural anti-itch and antianxiety herbal remedies, acupuncture, or homeopathic therapy may also be helpful.

3. Pyotraumatic dermatitis (hot spots) Hot spots involve intense itching in one or two isolated area of the trunk or limbs of the body. The involved areas may become inflamed and raw within a matter of hours. Stress may be a factor in its onset.

4. Mange Demodectic mange is caused when a parasite, Demodex canis, which lives a natural life in the hair and oil glands of the skin of most healthy dogs, starts multiplying rapidly. This tends to occur in young animals with an unhealthy immune system. It may have a genetic basis, as it tends to run in certain lines of dogs and seems to be more common in certain breeds. It doesn’t cause itching, but the involved areas are subject to secondary bacterial infection.

Sarcoptic mange is due to a transmissible parasite that burrows through the layers of the skin causing intense itching. It passes from pet to pet through contact, and can pass to humans, too.

Topical remedies can help decrease infections and minimize parasite numbers. Topical and internal anti-itch remedies may also help.

5. Ringworm Ringworm is a fungal disease that creates a round or oval non-itchy area of hair loss. Hair is lost because the fungus weakens the hair shaft and causes it to break off. Iodine preparations, used topically, may be helpful, and once again, energizing the immune system may be beneficial.

6. Stress-induced dermatitis This “disease” typically affects “Nervous Nellies” who cannot sit still. Affected dogs simply chew on themselves if they can’t find anything else interesting to do. The primary cure for this condition is to provide plenty of exercise and plenty of challenging tasks for the dog to do. Training games, food-dispensing toys, and frequent changes of activity can help distract and engage the dog in more healthful patterns.

Many of these dogs have an itch caused by a misaligned vertebrae and they chew or dig at it. Chiropractic adjustments have helped a lot of these animals.

7. Food allergies While food allergies may be the cause of some itchy dogs, research would indicate that skin cases are not often related to food allergies. In dogs, the primary signs of food allergies are most often related to gastrointestinal upset.

8. Miscellaneous conditions Pyoderma, excessive numbers of bacteria in the hair follicle, may cause circular areas of alopecia or generalized excessive shedding. Natural treatment for pyoderma includes the use of topical and oral herbal remedies with antibiotic activity. Some breeds, like the Chow-Chow, may have an arrest in the hair growth after clipping. This resolves spontaneously after several months of a lack of hair regrowth. Many diseases are associated with hair cycle abnormalities, including endocrine diseases such as hypothyroidism and Cushing’s syndrome, hereditary alopecia and hypotrichosis (the presence of less than normal amounts of hair); and familial zinc-responsive dermatopathy.

Identifying and Treating Skin Conditions that can Affect Your Dog early is very important.

Why you need to groom your dog.

Grooming is not just about maintaining your dog’s level of cleanliness, and it is not just about keeping your dog good-looking. Grooming is about maintaining both your dog’s physical health as well as his appearance.

To do this you must begin training your dog to endure grooming while he is still a puppy. Some dogs would not want to bath and some cannot sit for you to brush their hairs. If you introduce this when they are still puppies then it helps them greatly.

If you wait too long to begin the grooming sessions, your puppy may not be agreeable to it later on, especially when it comes to ear cleaning and nail clipping.

This is especially important for long-haired dogs, which require more intense grooming sessions as compared to short-haired dogs. It takes more time to brush their long fur and they need to get used to staying still for this starting at an early age. That is not to say dogs with short, clipped fur do not require grooming.

Brushing for example, is beneficial for all kinds of dogs no matter what breed they are, helping to remove dead hair, dirt, and dandruff.

Regular brushing also helps to bring out the natural oils in the dog’s fur. As you brush, the natural oils are spread all over your puppy’s fur giving the coat a healthy sheen.

You can begin grooming a puppy when he is as young as three weeks old. Experienced breeders will even begin acquainting their puppies with grooming before they go to their new homes so that by the time they are picked up by their owners, they are already used to it.

Another benefit of grooming is that it allows you to check your dog for any abnormalities. This includes skin problems such as ticks, fleas and dry patches, or issues with their nails, teeth, ears, and eyes such as infection or inflammation. When found at an early stage, these problems can be treated right away, before they have a chance to become more serious.

Simply put, grooming helps keep your dog happy and healthy, gives you and your dog a time that is set aside just for the two of you, and helps you to save on veterinary bills. So don’t delay, start grooming your puppy early.

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shotgunstrength · 4 years

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The Whey To Weight Loss (Part II)

Effects on serotonin, blood sugar regulation, and more!

Although the above would probably be the major mechanisms by which whey could help the dieter, there are several secondary effects of whey that may assist in weight loss. For example, whey’s effects on serotonin levels. Serotonin is probably the most studied neurotransmitter since it has been found to be involved in a wide range of psychological and biological functions. Serotonin ( also called 5-hydroxytryptamine or 5-HT) is involved with mood, anxiety, and appetite.

Elevated levels of serotonin can cause relaxation and reduced anxiety. Low serotonin levels are associated with low mood, increased anxiety (hence the current popularity of the SSRI drugs such as Prozac and others), and poor appetite control. This is an extremely abbreviated description of all the functions serotonin performs in the human body – many of which have yet to be fully elucidated – but a full explanation is beyond the scope of this article.

Needless to say, Increased brain serotonin levels are associated with an improved ability of people to cope with stress, whereas a decline in serotonin activity is associated with depression and anxiety. Elevated levels of serotonin in the body often result in the relief of depression, as well as substantial reduction in pain sensitivity, anxiety and stress. It has also been theorized that a diet-induced increase in tryptophan will increase brain serotonin levels, while a diet designed for weight loss (e.g., a diet that reduces calories) may lead to a reduction of brain serotonin levels due to reduced substrate for production and a reduction in carbohydrates.

Many people on a reduced calorie intake in an attempt to lose weight find they are often ill tempered and more anxious. Reductions in serotonin may be partially to blame here. One recent study (The bovine protein alpha-lactalbumin increases the plasma ratio of tryptophan to the other large neutral amino acids, and in vulnerable subjects raises brain serotonin activity, reduces cortisol concentration, and improves mood under stress. Am J Clin Nutr 2000 Jun;71(6):1536-1544) examined whether alpha-lactalbumin – a major sub fraction found in whey which has an especially high tryptophan content – would increase plasma Tryptophan levels as well reduce depression and cortisol concentrations in subjects under acute stress considered to be vulnerable to stress.

The researchers examined twenty-nine “highly stress-vulnerable subjects” and 29 “relatively stress-invulnerable” subjects using a double blind, placebo-controlled study design. The study participants were exposed to experimental stress after eating a diet enriched with either alpha-lactalbumin (found in whey) or sodium-caseinate, another milk based protein. They researchers looked at:

* Diet-induced changes in the plasma Tryptophan and its ratio to other large neutral amino acids.

* Prolactin levels.

* Changes in mood and pulse rate.

* Cortisol levels (which were assessed before and after the stressor).

Amazingly, the ratio of plasma Tryptophan to the other amino acids tested was 48% higher after the alpha-lactalbumin diet than after the casein diet! This was accompanied by a decrease in cortisol levels and higher prolactin concentration. Perhaps most important and relevant to the average person reading this article, they found “reduced depressive feelings” when test subjects were put under stress.

They concluded that the “Consumption of a dietary protein enriched in tryptophan increased the plasma Trp-LNAA ratio and, in stress-vulnerable subjects, improved coping ability, probably through alterations in brain serotonin.” This effect was not seen in the sodium-caseinate group. If other studies can confirm these findings, whey may turn out to be yet another safe and effective supplement in the battle against depression and stress, as well as reduced serotonin levels due to dieting.

Although there is a long list of hormones involved in appetite regulation, some of which have been mentioned above, serotonin appears to be a key player in the game. In general, experiments find increased serotonin availability or activity = reduced food consumption and decreased serotonin = increase food consumption. If whey can selectively increase serotonin levels above that of other proteins, it could be very helpful to the dieter.

Other possible advantages whey may confer to the dieter is improved blood sugar regulation (Frid AH, Nilsson M, Holst JJ, Bjorck IM. Effect of whey on blood glucose and insulin responses to composite breakfast and lunch meals in type 2 diabetic subjects. Am J Clin Nutr. 2005 Jul;82(1):69-75.) which is yet another key area in controlling appetite and metabolism.

Finally, calcium from dairy products has been found to be associated with a reduction in bodyweight and fat mass. Calcium is thought to influence energy metabolism as intracellular calcium regulates fat cell (adipocyte) lipid metabolism as well as triglyceride storage. It’s been demonstrated in several studies the superiority of dairy versus non-dairy sources of calcium for improving body composition, and the whey fraction of dairy maybe the key.

The mechanism responsible for increased fat loss found with dairy-based calcium versus nondairy calcium has not is not fully understood but researchers looking at the issue theorized “… dairy sources of calcium markedly attenuate weight and fat gain and accelerate fat loss to a greater degree than do supplemental sources of calcium. This augmented effect of dairy products relative to supplemental calcium is likely due to additional bioactive compounds, including the angiotensin-converting enzyme inhibitors and the rich concentration of branched-chain amino acids in whey, which act synergistically with calcium to attenuate adiposity.”

It appears components in whey – some of which have been mentioned above – are thought to act synergistically with calcium to improve body composition (Zemel MB. Role of calcium and dairy products in energy partitioning and weight management. Am J Clin Nutr. 2004 May;79(5):907S-912S.).

Conclusion

Taken in isolation, none of these studies are so compelling that people should run out and use whey as some form of weight loss nirvana. However, taken as a total picture, the bulk of the research seems to conclude that whey may in fact have some unique effects for weight loss and should be of great use to the dieter. More studies are clearly needed however.

So what is the practical application of all this information and how does the dieter put it to good use? Being the appetite suppressing effects of whey appear to last approximately 2-3 hours, it would seem best to stagger the intake throughout the day. For example, breakfast might be 1-2 scoops of whey and a bowl of oatmeal, and perhaps a few scoops of whey taken between lunch and dinner.

If whey does what the data suggests it does in the above, that should be the most effective method for maximizing the effects of whey on food (calorie) intake on subsequent meals as well as the other metabolic effects covered. If working out, the schedule may be different however and people should follow the pre and post nutrition recommendations made in my ebook “Muscle Building Nutrition” or advice easily found on the ‘net via the many sports nutrition and bodybuilding related web sites.

source https://www.shotgunstrength.com/the-whey-to-weight-loss-part-ii/

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howellrichard · 4 years

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Can Gluten Affect Your Hormones?

How Gluten Affects Your Hormones

Hormones are chemicals produced by various glands throughout your body and released to regulate specific functions. For example, your thyroid hormone helps regulate your metabolism. Estrogen, a sex hormone, helps regulate menstruation in women. And cortisol, a stress hormone, helps regulate blood pressure. Thus, hormones play many vital roles, which means any imbalances can lead to dysfunction and disease.

Symptoms of Hormonal Imbalances

A hormone imbalance occurs when there’s too much or not enough of a specific hormone circulating in your bloodstream at a specific time. For example, estrogen rises and falls twice throughout your menstrual cycle. And insulin rises after you eat and falls hours later.

Sadly, hormonal imbalances are prevalent in today’s modern world. Common symptoms include (but are not limited to):

Painful and/or irregular periods

Infertility

Low libido

Headaches

Fatigue

Weight gain

Mood swings and irritability

Insomnia

Skin rashes, dry skin, and acne

Brain fog

Hair loss

Anxiety and depression

Hot flashes

Muscle aches and stiffness

Constipation or diarrhea

And while these symptoms are common, they’re not normal. These are signs that something isn’t quite right.

Causes of Hormonal Imbalances

There are many avenues to explore when it comes to hormonal imbalances. Stress, environmental toxins, disease, medications, and physical injuries to glands. But one that often gets overlooked is nutrition. And gluten alone can cause a wide range of hormonal problems.

Nutrition and Your Hormones

Your diet plays a significant role in hormone health. For example, your body needs certain nutrients to synthesize hormones. Steroid hormones, such as estrogen and testosterone, are made from cholesterol. And insulin is made from protein.

Vitamins and minerals also regulate the synthesis of hormones. For instance, in the absence of iodine, your thyroid hormone production decreases. Therefore, an iodine deficiency can lead to hypothyroidism (a.k.a. under active or low thyroid).

This is relevant because those with gluten sensitivity often experience nutrient deficiencies. Essentially, gluten irritates and damages the lining of the small intestine. And the small intestine is responsible for a significant portion of digestion and nutrient absorption.

Plus, grain-based foods, such as bread, pasta, crackers, and sweets, are heavily processed and void of essential nutrients.

Gluten is an Endocrine Disruptor

An endocrine disruptor is a substance that can mimic your hormones and lead to imbalances, dysfunction, and disease. For instance, they can bind to hormone receptors on your cells and trigger a response. Sometimes the response may be too strong, not strong enough, or different than desired.

Gluten itself can act as an endocrine disruptor. More specifically, gluten proteins may cross-react with antigens on your cells and trigger an inflammatory immune response. This helps explain why several common abnormalities among those with celiac disease are hormonal in nature, including delayed puberty, type 1 diabetes, low thyroid, and low cortisol.

Wheat is also sprayed with an herbicide known as glyphosate before harvesting to help speed up the drying process. And glyphosate is a known hormone disruptor in human cells. Plus, it’s toxic effects can also damage your DNA.

In addition, some pesticides used to grow grains can also have endocrine-disrupting effects. And studies have shown they can alter the synthesis or action of a wide range of hormones, including estrogen, testosterone, thyroid hormone, cortisol, progesterone, and prolactin.

Gluten and Cortisol Imbalances

As previously mentioned, cortisol is a stress hormone produced and secreted by your adrenal glands. Cortisol naturally rises and falls throughout the day. At normal levels, cortisol helps regulate your metabolism, blood pressure, and blood sugar. It also helps reduce inflammation.

However, when under stress, a cascade of events triggers your adrenal glands to release adrenaline and increase the output of cortisol to support your body’s “fight or flight” response.

This response is necessary to combat acute stress. For example, cortisol raises your blood sugar to ensure you have the energy you need to overcome the threat at hand. However, many people today are under constant stress, whether it be emotional, physical, or often a combination of both.

Chronic inflammation caused by gluten is a form of physical stress, which can raise your cortisol levels. If untreated, the consequences are far-reaching. For example, elevated cortisol hinders digestion, growth, and reproduction as well as immune function. There’s even a connection to a region in the brain that controls your mood.

Thus, symptoms associated with high cortisol include anxiety, depression, weight gain, digestive dysfunction, poor sleep, muscle weakness, and lack of focus among others. High cortisol is also associated with high blood pressure, heart disease, diabetes, hirsutism in women (excessive growth of dark, thick hair), and osteoporosis.

On the other hand, celiac disease is associated with Addison’s disease, an autoimmune condition that attacks your adrenal glands and causes low cortisol (a.k.a. adrenal insufficiency).

An animal study found that glyphosate directly influenced the adrenal glands, which led to abnormally low levels of cortisol. The symptoms mimicked adrenal insufficiency, which caused fatigue, anxiety, sweating, and weight loss. Other symptoms of adrenal insufficiency include low blood sugar, dehydration, and low blood pressure.

In addition, nutrient deficiencies caused by gluten can play a role in the development of Addison’s disease. For example, vitamin D appears to be involved in regulating genes responsible for the synthesis of cortisol.

Gluten and Sex Hormone Imbalances

The three sex hormones are estrogen, progesterone, and testosterone. They play a role in the development of sex distinguishing features as well as reproduction. Thus, common abnormalities and conditions associated with sex hormone imbalances include:

Infertility

Premenstrual syndrome (PMS)

Headaches

Irregular or missing periods

Polycystic ovary syndrome (PCOS)

Low libido

Your sex hormones may be affected by endocrine disruptors as I mentioned above. Gluten-induced inflammation, an overactive immune system, other hormonal imbalances (e.g., cortisol, thyroid hormone, prolactin), and nutrient deficiencies are also potential problems. This may help explain why those with celiac disease and gluten sensitivity are prone to the abnormalities listed above.

Science tells us that women with celiac disease are more likely to experience infertility and menstrual abnormalities than the general population. And these conditions are commonly linked to low progesterone, low thyroid hormone, and high prolactin.

If untreated, celiac disease also appears to increase a woman’s risk of abnormal fetal growth, unexplained miscarriage, and preterm birth.

A study comparing pregnancy outcomes of mothers with celiac disease on a gluten-free diet versus untreated mothers found the following:

The relative risk of miscarriage was 8.9 times higher in the untreated group

The relative risk of low birth weight was 5.84 times higher in the untreated group

The duration of breastfeeding was 2.54 times shorter in the untreated group

These are significant consequences. However, the same researchers also found that these outcomes were corrected with a gluten-free diet.

The exact mechanisms behind these correlations are not fully understood yet. But researchers believe an overactive immune system plays a role.

For example, one study found that celiac disease autoantibodies were binding to the placenta and causing dysfunction. And it’s worth noting that once established, the placenta is responsible for producing both progesterone and estrogen.

Another study analyzed the placentas from 32 full-term births of mothers with celiac disease. Of the mothers with untreated cases, researchers found large concentrations of gliadin, a gluten protein, in the cells of the placenta. And the birth weights of the babies in these cases were lower. This may suggest that gluten proteins interact unfavorably with the placenta in genetically susceptible women.

Gluten and Thyroid Hormone

Hypothyroidism is a condition in which your thyroid gland fails to produce enough thyroid hormone, which can cause most of the symptoms I listed in the introduction of this article. This is possible because your thyroid hormone helps regulate many functions, including your metabolism, brain development, protein synthesis, and bone growth to name a few.

There are four main causes of thyroid hormone dysfunction, which include:

Autoimmune disease (a.k.a. Hashimoto’s)

Nutrient deficiencies that affect the production, regulation, and/or activation of thyroid hormone

Chemical exposures/endocrine disruptors (e.g., glyphosate)

Physical damage to the thyroid gland

Autoimmune Thyroid Disease

Celiac disease is associated with many other autoimmune diseases, including Hashimoto’s. Essentially, damage to the lining of the gut leads to inflammation, over stimulation of the immune system, and cross-reactivity of gluten proteins with antigens on the thyroid gland. If unchecked, Hashimoto’s is likely to develop.

Science has shown that women with autoimmune thyroid disease that were put on a gluten-free diet experienced a reduction in antibodies that attack the thyroid as well as an increase in thyroid hormone and vitamin D. However, women in a control group that kept gluten in their diet didn’t experience any of these clinical changes.

Another study evaluated a diet without gluten and found that it significantly reduced markers associated with inflammation and immune system activation in women with Hashimoto’s. Plus, the women in the study experienced a reduction in related symptoms.

Nutrient Deficiencies and Thyroid Hormone

As previously mentioned, gluten can cause nutrient deficiencies. One nutrient specifically that greatly affects the thyroid is selenium. It’s necessary for the production and activity of thyroid hormone. Selenium also acts as an antioxidant and helps protect the thyroid gland from damage. Thus, gluten-induced selenium deficiency is believed to lead to thyroid dysfunction.

Other common nutrient deficiencies caused by gluten that are necessary for optimal thyroid function include magnesium, zinc, vitamin D, and vitamin B12.

Gluten and Insulin

When you eat a diet rich in heavily processed gluten-rich foods, it has a negative impact on your metabolic hormones. Because these foods contain high amounts of quickly digested starch and sugar, which spikes your insulin and can lead to chronically high insulin levels over time.

Insulin is a fat-storing hormone secreted by your pancreas. It pushes all sources of energy into your cells and excess energy gets stored as fat. It also prevents your body from burning stored fat.

If unchecked, insulin resistance, obesity, and type 2 diabetes are likely to develop. All of these conditions are inflammatory. Insulin resistance is also closely linked to polycystic ovarian syndrome (PCOS), which is characterized by elevated testosterone in women that causes infertility, hirsutism, and abnormal periods.

Gluten and Prolactin

The last hormone I want to discuss is prolactin–a hormone secreted by your pituitary gland that works with estrogen and progesterone to develop breast tissue and prepare for lactation.

There’s evidence that a compound in gluten acts as an opioid compound in the brain, which leads to an excess of prolactin. Researchers also suggest inflammation associated with gluten can contribute to elevated prolactin levels, which can cause low libido, irregular periods, infertility, bone loss, and erectile dysfunction.

Can Gluten Affect Your Hormones?

Hormonal balance is essential for optimal health. And gluten can affect many hormones throughout your body as well as trigger a cascade of hormone-related problems. Thus, if you’re experiencing any hormonal imbalance symptoms, don’t rule gluten out as a contributing factor. A gluten-free diet may be what your body needs most.

Have you recovered hormone function after going gluten free? Chime in below.

The post Can Gluten Affect Your Hormones? appeared first on Gluten-Free Society.

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