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Leptin Hormone Guide: The Effects of the Satiety Hormone


Leptin Hormone Guide

What is Leptin?

Leptin is a hormone that has many purposes, but primarily it is responsible for the full sensation that we get after the body decides that we've had enough to eat. It is frequently referred to as the “satiety hormone.” Leptin is released by fat cells in an effort to control the way that our body stores fat. In addition to suppressing hunger, leptin also alters the way that our body uses energy.

The fat cells release leptin when they have stored a certain level of fat converted from the calories from the food that we eat. When leptin is released, it enters the blood stream and passes through the body. Leptin travels through the cardiovascular system to the hypothalamus, where it activates special receptors in the arcuate nucleus.

When leptin receptors are activated, it causes the body to increase metabolism, while also reducing signals for hunger. Although this is primarily affected through the brain, there are targets throughout the body which are also responsible for increasing metabolism.

The two hormones, Leptin and Ghrelin, have opposite, component effects upon the body. Whereas leptin controls the feeling of satiation, Ghrelin controls the sensation of hunger. Leptin and Ghrelin receptors are actually located on the same cells, and are two vital hormones responsible for the way that our body both stores and expends energy.

Leptin has a number of different purposes in the body, but the most important of these is considered the regulation of the way that the body stores fat. Our knowledge of how Leptin works is far from complete, but leptin is produced not only by fat cells, but by other organs as well.

Where is Leptin Produced?

The majority of leptin is secreted by white adipose fat tissue by organelles known as adipocytes. Leptin is also secreted from other locations, including the liver, pituitary, bone marrow, epithelial cells, stomach, skeletal muscle, ovaries, placenta, and brown adipose fat tissue.

What Causes Leptin Levels to Fluctuate?

Like other hormones such as Testosterone, Leptin flows through the blood stream both locked into a carrier protein and freely. Because body fat produces leptin, the more body fat that a person carries, the more leptin that they will produce. Perhaps surprisingly, the amount of leptin produced by body fat increases exponentially with the volume of body fat that a person carries.

Leptin concentrations also follow the circadian rhythm under normal circumstances. From around 12am to some point in the early morning, leptin levels remain quite high, which is believed to prevent hunger and promote sleep. Although this is the normal pattern of leptin release and circulation, if a person eats at odd times, such as in the middle of the night, this alters the rhythm of leptin release.

There are many ways that Leptin production is unrelated to body fat as well:

  • Fasting for one to three days leads to a drop in Leptin production, even if body fat remains the same. Related to this, Leptin levels also drop as a response to starvation, encouraging hunger even when the body still has a large amount of body fat. This is actually one reason why crash diets don't work effectively. Starving yourself will eventually cause you to lose weight, but once you lose the weight, your body will not be able to effectively send signals for satiation, causing you to eat more than your body needs and experience hunger even though you are eating a healthy diet.

  • Psychological stress increases Leptin Production.

  • Leptin is affected significantly by sex hormone concentrations in the body. Testosterone is associated with reduced leptin, whereas estrogen is associated with increased leptin. Some hormones released in response to stress, including dexamethasone, also increase leptin secretion.

  • Physical training will cause leptin levels to drop for the duration of time that a person engages in a healthy exercise routine. This makes sense, because physical exercise stimulates metabolism and increases the need for calories to maintain a certain weight.

  • The more insulin that your body produces, the more leptin that your body will produce.

  • For complex reasons, obesity actually leads to an increase in Leptin production.

  • Overweight individuals with obstructive sleep apnea experience increased leptin levels, but CPAP treatment can bring leptin production back to more normalized levels. Short-term sleep deprivation can lead to a reduction in Leptin production, but long term issues with sleep deprivation, such as sleep apnea, can increase leptin concentrations.

Effects of Leptin

After Leptin is released by body fat and other cells, it suppresses hunger primarily through three mechanisms:

  • Encourages the production of α-MSH, which suppresses hunger.

  • Blocks the activity of anandamide, a hormone which encourages hunger via the same mechanism as THC present in marijuana.

  • Blocks the activity of Neuropeptide Y, a molecule released by the hypothalamus and the stomach which encourages hunger.

In spite of the fact that leptin is the hormone that we most associate with hunger, it is actually only responsible for long-term appetite control. Other hormones are responsible for short term and intermediate hunger:

  • PYY3-36 is the reason why we don't feel hungry between meals. This hormone encourages us to eat our meals during single sittings.

  • Cholecystokinin is the hormone which is produced as we eat which inhibits hunger signals. This hormone helps us know when we are full at a particular meal.

Of course, leptin does play a role in the way that these hormones function. Animal research involving leptin clearly shows how the hormone contributes to diet control, as animals which have their ability to produce leptin removed gain weight uncontrollably as a result of a loss of their ability to become full.

Caloric restriction and fasting both have an inhibitive effect upon the production of Leptin. In addition to this, the body is more reactive to the absence of food, rather than its overabundance, so Leptin production will change faster and more dramatically when the body is not getting enough food. This also means that once food access is restored, hunger response won't return to normal as quickly as it was first altered.

Changes in leptin production resulting from abrupt changes in food access appear to be correlated with changes in food intake and diet rather than the energy available that is locked in body fat. This means that leptin suppression due to hunger is not mitigated by existing body fat.

How Does Leptin Control Diet?

Leptin encourages eating and changes in metabolism by triggering receptors in the mediobasal hypothalamus. It used to be believed that blood sugar directly controlled metabolism and eating patterns, but it is clear today that leptin is the mediator of this process.

As we mentioned earlier, Neuropeptide Y activity encourages hunger. There are neurons which produce this hormone in the arcuate nucleus, and as leptin passes through the body, it binds to these neurons, preventing the release of this potent hunger hormone, promoting a disinterest in food. There is also evidence that when Leptin levels are in balance, this makes it easier to eat a healthy diet and not be tempted by the allure of calorie-dense foods.

Prior research has shown that Neuropeptide Y plays an important role in the way that animals eat, including humans. When Neuropeptide Y is artificially introduced to the brain, it automatically triggers the animal to seek out food. The opposite is also true. If the neurons which produce Neuropeptide Y are destroyed, the mice ill become disinterested in eating and become drastically underweight.

Leptin also encourages the release of a peptide known as α-MSH which promotes the feeling of satiety, and genetic abnormalities which limit α-MSH have been shown to increase hunger response and increase the risk of obesity considerably.

Melatonin Affects Leptin Production

In a vacuum, elevated melatonin leads directly to reduced production of leptin. On the other hand, if insulin is in circulation, melatonin leads to an increase in leptin production. This interaction is important because it prevents us from becoming hungry while we are asleep, which can disturb sleeping patterns.

This is why it is generally encouraged to eat a healthy dinner a few hours before bed. This way, your stomach isn't full while you are asleep, but your digestive system is still somewhat active, which means that you have insulin and melatonin in your blood stream, which encourages healthy sleep.

By the end of the night, when insulin levels drop, Leptin levels start to fall as well, as melatonin levels are still elevated. This, in combination with an increase in cortisol and other factors, helps set the stage for you to wake up refreshed and hungry.

Leptin and Diabetes

Preliminary animal research shows that combining leptin with insulin improves metabolism and stabilizes blood sugar more effectively. This combination also helped promote healthier body composition while also balancing cholesterol.

Leptin and the Cardiovascular System

Leptin has an impact on the activity of T-Cells in the immune system. Leptin promotes the health of the heart tissue and healthy leptin levels reduce the inflammatory activity which promotes atherosclerosis. There is also evidence that elevated Leptin levels can help control blood pressure if prescribed medically.

Leptin and the Reproductive System

Leptin does not play any predominant role in human fertility, but it is important and necessary to create the conditions which promote fertility. The regularity of the menstrual cycle depends upon proper metabolism, and is dependent upon the normalized flow of energy through the body, which leptin plays a part in regulating.

If a woman frequently enters a state of starvation, whether purposefully or unintentionally, the menstrual cycle will go into dormancy. Also, if a woman engages in heavy exercise, they also risk entering this state, even if they consume enough calories to meet the demands of their body. On the other hand, menstruation is only affected by low body mass in extreme cases.

In both sexes, Leptin encourages the hypothalamus to produce Gonadotropin-Releasing Hormone, the precursor to Luteinizing Hormone and Follicle-Stimulating Hormone necessary to encourage both sex hormone production as well as sperm production.

Leptin and Pregnancy

During pregnancy, leptin is produced by the placenta, and it continues to be produced in greater concentration throughout pregnancy before returning to baseline after the child is born. This is because leptin has an inhibitory effect upon contractions, allowing the child to develop within the womb. When leptin levels fall, this encourages contractions and helps to stimulate childbirth. Elevated leptin levels also contribute to the condition of morning sickness that commonly takes place during pregnancy.

Leptin and Puberty

There are two hormones which determine when an individual enters puberty: kisspeptin and leptin. In the period just before puberty, leptin levels start to rise, and once they reach a certain point, puberty is triggered. Childhood obesity can lead to early puberty, because adipose fat cells produce leptin, and cause leptin levels to reach the triggering point much faster than in children with normal levels of body fat. There is also evidence that girls that enter puberty early don't grow as tall as their peers, because the increase in estrogen production promotes the closure of the growth plates.

Leptin and Bone Mineral Density

Leptin also appears to help promote healthy bone mineral density. When the brain receives sufficient satiation signals, it then signals the bones to undergo metabolic changes which promote cortical bone growth and inhibit cancellous bone. Cancellous bone is the softer tissue in the core of the bone, and cortical bone is the hard casing which covers the cancellous bone. Thus, leptin plays a role in bone maturation during puberty because the bones become thicker and harder, allowing them to carry more weight.

After puberty, leptin still plays a role in bone metabolism, because once it activates at its receptor sites on the hypothalamus, is alters the production of a number of other hormones and peptides associated with the regulation of bone mineral density. There is also some evidence that Leptin directly contributes to increased bone mineral density by playing an intermediary role between metabolism and the release and activation of Insulin-Like Growth Factor-One. As a result of this connection, there may be treatments in the future which utilize leptin in order to enhance the natural healing processes of bone tissue after breaks and fractures.

Leptin and the Brain

Although the primary trigger point for leptin is the hypothalamus, there are also receptors for the hormone at other locations within the brain. One of the largest receptor sites outside of the hypothalamus is the hippocampus.

Research has clearly shown that Leptin Deficiency has a negative impact on the normal function of neurons as well as brain proteins. In animal studies, normal neurological function in this instance can be restored by providing injections of leptin.

In humans, Leptin Deficiency is associated with neurological and cognitive changes that are associated with HIV, depression, and anorexia. There is even evidence in rats that leptin deficiency may play a role in Alzheimer's, and that providing leptin therapy may be able to increase cognitive ability and reduce the negative effects of the disease by limiting the concentrations of hyperphosphorylated tau and b-amyloid, which are two of the main factors which make Alzheimer's such a devastating neurological disorder.

Leptin and the Immune System

Leptin is intricately related to the immune system response of inflammation, and leptin has a regulatory effect upon a number of factors which affect immune health, including body fat, caloric restriction, stress, sleep, and Testosterone levels. It is hypothesized that the primary mechanism which links Leptin to immune health is that Leptin helps control the activity of cytokines released by adipose tissue.

Leptin is actually structurally similar to cytokines both in function and its molecular composition. There is evidence that Leptin plays an active role in the way that the body handles and manages stress, but the direct mechanisms are not completely understood. There is also a positive correlation between white blood cell count and leptin levels.

Diseases Associated with High Leptin Levels

There are a number of medical conditions which are associated with abnormally high leptin levels, especially those associated with inflammation. Among these are cardiovascular disease, chronic fatigue, and hypertension.

Elevated levels of leptin are correlated with overeating, the mass of adipose fat cells, and overall body composition, but leptin is not connected in any way to physical activity. Exercise does not stimulate or suppress the production of leptin directly. For this reason, it is hypothesized that leptin is designed to activate only with regard to inflammation related to adipose fat. Leptin promotes the formation of new blood vessels, promotes inflammation, and encourages cellular metabolism.

Based on these factors, it is believed that the elevation of leptin levels due to overeating is a mechanism designed to limit the stress on fat cells caused by abrupt changes related to increased caloric intake. When the fat cells no longer have enough room to absorb all the calories being delivered, this causes the body to begin to store fat in the muscles, arteries, and organs, which is dangerous.

So in this sense, leptin triggers satiation in order to prevent the body from eating so much that the fat cells can no longer make room for it all, but obesity causes the body to produce too much of the hormone, which can have negative effects. Like other inflammatory/stress hormones, the body needs leptin, but there are serious issues which can result when the hormone is allowed to remain at abnormally high levels for too long.

References:

The Facts on Leptin: FAQ - The Truth about the Hormone Leptin and Obesity

http://www.webmd.com/diet/features/the-facts-on-leptin-faq

Serum Leptin Levels in Males with Delayed Puberty during Short-Term Pulsatile GnRH Administration.

http://www.ncbi.nlm.nih.gov/pubmed/10090130

Wikipedia: Leptin

http://en.wikipedia.org/wiki/Leptin

19 August 2014

Enclomiphene Citrate Andropause Treatment Up for FDA Approval

Enclomiphene Citrate May Treat Andropause More Effectively than Bio-Identical Testosterone

Bio-Identical Testosterone has been used for decades in order to treat Low-T caused by Hypogonadism and Andropause. There is a drug currently undergoing Clinical Evaluation which is likely to reach the open market in just a matter of years, known as Enclomiphene Citrate.

Medications similar to Enclomiphene Citrate have long been used as fertility treatments for women, but studies indicate that the treatment can also provide men with a potent boost of Testosterone without a risk of overdose.

Enclomiphene Citrate Affects Men and Women Differently

In women, Enclomiphene Citrate encourages the process of ovulation, but in men, it encourages the release of precursor hormones which stimulate the production of both natural, endogenous Testosterone and sperm.

In fact, these trials provide evidence that Enclomiphene Citrate is even better than Testosterone Injections and Creams at restoring natural Testosterone Levels, all the while promoting healthier hormone balance and circulation in other ways.

How Does Testosterone Replacement Treat Low-T?

Bio-Identical Testosterone Therapy simply replaces the Testosterone that the body no longer produces at sufficient concentrations to sustain male health. Testosterone Therapy can bring Testosterone Levels back to normal, but it comes with side-effects, both inherent in the treatment and related to accidental overdose. Because Testosterone Therapy provides an outside source of Testosterone, the treatment suppresses the body's production of Testosterone Precursors that are responsible for healthy testicles, which leads to fertility issues as well as Testicular shrinkage.

Enclomiphene Citrate is Cheaper than Testosterone

Enclomiphene Citrate is also cheaper than Testosterone, meaning that, if the treatment is found to be effective and gains FDA Approval, and it appears likely that this will be the case, countless men will flock from Bio-Identical Testosterone to Enclomiphene Citrate in order to get more cost effective care that is easier to administer. Unlike Testosterone, which is generally delivered via injection or topical formulation, Enclomiphene Citrate is a simple pill.

Enclomiphene Citrate Clinical Research Study

At this point, Enclomiphene Citrate for Men is in the second stage of its clinical trial, after showing incredible promise in the initial stage of research. The details regarding this second phase will be published in the academic publication Fertility and Sterility.

Of course, the process for FDA Approval is a four stage process, but, based on off-label usage of similar medications, and the effectiveness of the treatment in the first two stages, it seems clear that Enclomiphene Citrate for Andropause and Male Infertility will almost certainly obtain FDA Approval.

Testosterone Deficiency Prevalent in American Society

Low-T, also known as Andropause or Age-Related Hypogonadism, is a prevalent condition among men in the United States. Millions of American males suffer from the condition, and studies suggest that the condition is still under-diagnosed, due to a number of different factors.

Testosterone Deficiency is most well-known for its impact on sexual health, but Low-T affects male health and longevity in a number of different ways. Aside from Low Libido, Infertility, and Erectile Dysfunction, other symptoms of Andropause include depression, anxiety, changes in body composition, loss of Bone Mineral Density, muscle atrophy, and lack of energy.

Low-T is a natural aspect of the process of aging, but not everything that is natural is healthy. Study after study shows that men with naturally high Testosterone tend to be both healthier and more well-adjusted than their peers that have lower levels of Testosterone.

When Does Testosterone Production Peak?

Biologically, our Testosterone Levels peak while we are in our teens and twenties, and start to fall off beginning in the thirties. Every man is impacted by Low-T in their own way, and some experience symptoms more quickly and more severely than others. Testosterone Deficiency is associated with a number of chronic medical conditions, from cardiovascular disease to diabetes to obesity.

The State of Modern Testosterone Therapy

One issue with Testosterone Deficiency as it is treated today is that there are no definite thresholds regarding how low Testosterone Concentrations must fall before a patient is ultimately diagnosed. This is partially because there is still ongoing research regarding Testosterone for Andropause, but also because each patient has his own personal genetic profile as well as their own set of unique lifestyle choices.

This means that part of diagnosing Low-T is up to the discretion of the prescribing physician, because it is up to his or her expertise to determine if the severity of the symptoms and the underlying hormone levels warrant therapy.

This also means that Testosterone Therapy is prescribed to meet our standards for what healthy Testosterone Levels should be, rather than the body's natural processes to provide youthful Testosterone. This is where Enclomiphene Citrate can be both useful and perhaps even superior to Testosterone Therapy for many patients.

Enclomiphene Citrate and Andropause

Andropause is a form of Secondary Hypogonadism, meaning that the testes are still fully capable of producing their own Testosterone, they just aren't receiving the same signals that they did when the patient was younger. Enclomiphene Citrate restores this youthful signaling, allowing the body to make just as much Testosterone as it needs to meet the needs of the body. Enclomiphene Citrate encourages youthful production of Testosterone, without the risk of overdose (or under-dose) that is sometimes associated with Testosterone Treatment.

Why is Enclomiphene Citrate Superior to Testosterone?

Bio-Identical Low-T Treatments restore Testosterone quite capably, but they do so without taking into account the other hormones and processes of the male body which depend upon Luteinizing Hormone, Follicle-Stimulating Hormone, and Gonadotropin-Releasing Hormone to take place.

When Bio-Identical Testosterone is administered, the body fully absorbs and utilizes the Testosterone, but the three precursors listed above, LH, FSH, and GnRH, no longer get produced in sufficient quantities. This condition does not have a significant impact on health and wellness, but it has a tremendous impact on both male fertility and the condition of the testes themselves.

Doctors Often Prescribe Testosterone to Men that Want Children

Many men take Testosterone without realizing the fertility risk associated with Standard Testosterone Therapy. This is because many general practitioners prescribe Testosterone for Low-T without fully recognizing the downsides associated with the treatment, and thus, they don't relay that information effectively to their patients.

Often, we think of Testosterone Treatment as a therapy for men in the latter stages of their life, but Age-Related Low-T can affect male health even as soon as the early thirties, and many men start taking Testosterone while they are still interested in having children, without recognizing the suppressive effect that the treatment has on a man's ability to produce sufficient sperm for conception.

This lack of knowledge on the part of many physicians is not anecdote, there are studies to back it up. A recent poll by the American Urological Association discovered that fully a quarter of urological specialists were not aware that Testosterone inhibited fertility, and would prescribe Bio-Identical Testosterone Treatments like Axiron to men that were vocally interested in having children in the near future.

Fertility Suppression Due to Low-T Treatment Temporary

Luckily, the fertility risks associated with Bio-Identical Testosterone are short-term, and fertility returns to pre-treatment levels after therapy is suspended, but this still means that many men that would greatly benefit from Testosterone Therapy don't get the opportunity for treatment because of their desire for children.

Clomid vs. Enclomiphene Citrate

In the very near future, there will be a new option available for these men, so they can protect their health and their sexual function while also promoting the healthy production of sperm. Enclomiphene Citrate is a component of a medical treatment that has long been on the market in generic form known as Clomiphene Citrate.

This treatment is also available under the brand name Clomid. The treatment was originally designed to improve fertility in women, but also shows some effectiveness at restoring Testosterone Levels in males. In women, Clomid and Enclomiphene encourage the production of female sex hormones, but in men, the medical treatments encourage the production of Testosterone and sperm.

Clomid is a combination of two active compounds, Enclomiphene Citrate and Zuclomiphene. The benefits of Clomid on Male Sexual Health are primarily the result of the Enclomiphene component of the medication.

The issue with Off-Label prescription of Clomid is that Zuclomiphene does increase the level of Estrogen in the body by a slight amount, meaning that the ideal form of the medication would omit Zuclomiphene entirely. Because of the Estrogenic effects of Zuclomiphene, Clomid is often prescribed in combination with Arimadex in order to counteract those effects and optimize treatment.

Enclomiphene Shown to Be Effective in Stage-2 FDA Trial

In the second stage of clinical research for Enclomiphene Citrate, medical specialists from the Houston campus of the Baylor College of Medicine and Repros Therapeutrics provided 73 male patients with Enclomiphene Citrate for the treatment of Low-T caused by inhibited stimulation of the testes. This is most commonly the result of natural aging, but there are other factors which can impede the release of precursors from the pituitary and hypothalamus as well.

The study went according to the hypotheses supported by Off-Label use of the medication. The researchers found that Enclomiphene Citrate was incredibly effective at increasing Free and Total Testosterone to youthful levels, as well as LH and FSH Levels, which are necessary for proper sexual function.

As a result, Enclomiphene Citrate had no inhibitive effect upon the production of sperm, and perhaps even improved fertility among patients, though this is unclear.

Enclomiphene Works Better Than Clomid for Men

The lead researcher of the study, Dr. Ron Wiehle, explains that Enclomiphene Citrate works via the same mechanism as Clomid, which is prescribed Off-Label, but appears to do so with improved consistency. Further research could prove or disprove that notion, but because Clomid is no longer under patent, there is no financial incentive to study its effects.

On the other hand, Enclomiphene Citrate is still under patent, and is potentially effective for a greater subset of the male population, which provides the motivation for funding and research by private pharmaceutical manufacturers such as Repros Therapeutrics.

Enclomiphene Slightly Reduces IGF-1 Levels

Prior research shows that Enclomiphene Citrate does have a slight suppressive effect upon IGF-1 Production in men. This means that Enclomiphene is likely not a good option for men that simulataneously suffer from significant HGH Deficiency and Testosterone Deficiency simultaneously. This does mean, however, that Enclomiphene Citrate is safer for the prostate than Testosterone Therapy. Further study is needed to elucidate the impact of Enclomiphene upon IGF-1.

Enclomiphene to Be Marketed as Androxal

Although Enclomiphene Citrate is not available on the open market quite yet, the plans are to sell and distribute the medication under the brand name Androxal. Androxal will be specially formulated for male use, to provide the optimal amount of medication to restore the youthful cascade of male hormones necessary to restore vitality and sexual potency.

One reason why there is so much interest in Enclomiphene Citrate is that men in America are choosing to have children later and later in the lifespan, meaning that the segment of the population that experiences symptoms related to Low-T while also being interested in having children continues to grow.

Interested in Enclomiphene Now? Talk to Your Doctor About Clomid!

Although Enclomiphene Citrate is not currently on the market, you can still talk to your doctor about Clomid (Clomiphene Citrate), and find out if you are a candidate for treatment. Clomid is designed and certified for use by women, but there are many physicians all across the country that are highly experienced with the treatment regimen. Clomid may never gain enough traction for FDA-Approval, but the treatment has been used effectively for decades.

28 September 2015

Human Growth Hormone Deficiency Impact On Sleeping Habits


How Does Human Growth Hormone Deficiency Impact Sleeping Habits: A Clinical Study

Researchers have long been aware that HGH Deficiency is strongly correlated with an increased incidence of sleeping problems, and in recent years, more time and effort have gone into exploring that correlation.

How Were Patients Selected for this HGH Sleep Study?

One study, published in 2010, analyzed thirty patients with Abnormally Low Growth Hormone Levels from four different University medical centers: the University of Pisa, Italy, the University of Liege in Belgium, the Free University of Brussels, and the University of Chicago. Patients were diagnosed with Human Growth Hormone Deficiency using a method known as the Insulin Tolerance Test. Patients were selected for this study if they showed less than three micrograms per liter after drinking Glucose Solution. Twenty-four of the patients suffered from Adult-Onset Hypopituitarism, while six were diagnosed early in life with Childhood-Onset Hypopituitarism.

Patients that were selected for study had not taken Bio-Identical HGH Injections for a minimum of six months before they were selected, and some participants had never used Bio-Identical Human Growth Hormone Injections. Subjects were screened for a number of conditions, and were turned away if they showed any signs of Diabetes, Hyperprolactinemia, Psychiatric/Neurological Disease, chronic infection, heart problems, kidney problems, liver disease, or drug/alcohol abuse.

Also, patients that had traveled three time zones or more in the previous two weeks were excluded, as were people that were shift workers in the prior three months. Finally, participants had to be off of sleeping medications for a minimum of 90 days.

Adult-Onset HGH Deficiency Causes

The source of Hypogonadism varied from patient to patient. In twelve of the thirty patients, Adult-Onset Hypopituitarism was the result of a pituitary issue that did not involve other parts of the endocrine system. Ten patients had their pituitary removed via surgery. One patient experienced the death of a pituitary tumor which suppressed HGH Levels, and one patient suffered from the same issue, but from the stalk of the pituitary. None of these patients suffered from Diabetes Insipidus.

The second group of patients had pituitary issues that could have been partially the result of hypothalamic insufficiency. Two patients had a tumor removed from the pituitary and suffered from Diabetes Insipidus. One patient received radiation therapy to remove a pituitary tumor. Two patients experienced HGH Deficiency as a result of Craniopharyngioma. One patient had a pituitary tumor break down while also suffering from Diabetes Insipidus. There were two patients that had lesions both of the hypothalamus and the pituitary, resulting from histiocytosis and neurosarcoidosis, respectively.

Childhood-Onset HGH Deficiency Causes

In the Childhood-Onset Hypopituitarism group, six of the ten patients experienced their deficiency as a result of a known genetic predisposition to HGH Deficiency. One patient suffered from Hypothalamic Insufficiency that led to HGH Deficiency. Three others suffered from Hypopituitarism resulting from the appearance or removal of tumors from the Pineal Gland, the Olfactory Duct, and a Brain Tumor, respectively. Finally, the tenth participant suffered from HGH Deficiency resulting from Brain Thrombosis.

More HGH Patient Information

Among the thirty patients, 28 of them had received Bio-Identical Hormone Deficiency Treatment in the past for their Pituitary Insufficiency. There were 24 male patients and 6 female patients in the study. Each female HGH Deficiency subject was taking Estrogen Replacement Therapy, with 4 of those 6 taking progesterone as well.

Sixteen of the patients were simultaneously suffering from Testosterone Deficiency, and were either replacing their Testosterone with Intramuscular Testosterone Injections, or Topical Testosterone Products.

Twenty-one patients were taking Thyroxine for Thyroid Deficiency and twenty-four were taking cortisone acetate or hydrocortisone for adrenal hormone deficiency. Finally, seven patients were taking desmopressin.

HGH Deficiency: Experimental vs. Control

Every patient in this Hypopituitarism Sleep Study had their own personal control with normal HGH Levels. Experimental Group Patients averaged around 72 micrograms per deciliter, whereas control patients had an average of 194 micrograms per deciliter. All experimental patients had normal levels of potassium, sodium, and glucose. Overall, patients had Thyroxine Levels which averaged 86% of normal.


Each patient was matched with a control based upon Body Mass Index, Age, and Gender. The results of this study indicate that Human Growth Hormone Deficiency is strongly associated with daytime fatigue, inhibited sleep quality, and too much high-intensity Slow Wave Sleep. Strangely enough, this increased level of Slow Wave Sleep is not normally associated with most sleeping disorders, which are the result of inhibited Slow Wave Sleep.


There are a number of mechanisms by which this abnormal sleeping condition could lead to issues with sleep health and quality. There is evidence that Growth Hormone-Releasing Hormone enhances Delta Activity, because in healthy brains, HGH and IGF-1 serve as a negative feedback mechanism to limit Human Growth Hormone Production. There is animal research which supports this theory.


How Did HGH Deficiency Effect the Sleeping Patterns of Younger Patients?


Researchers also hypothesize that the hormone imbalance caused by the overproduction of Growth Hormone-Releasing Hormone could cause the body to continue to release signals for Slow Wave Sleep even while awake, which could lead to issues with daytime tiredness. This is especially pronounced among the youngest patients, as those with elevated levels of Slow Wave Sleep were more tired during the day than their counterparts. Among the thirty participants, exhaustion was the single complaint most reported in Self-Reported Quality of Life Scales.



How Did HGH Deficiency Effect the Sleep of Older Patients?

Among older Hypopituitarism patients, the most significant issue appeared to be a lack of sufficient REM Sleep, which is strongly correlated with Human Growth Hormone Deficiency. Lack of REM-Sleep is associated with a number of medical issues, including issues with memory. In this study, older patients with Human Growth Hormone Deficiency were more likely than their control counterparts to suffer from memory issues. As the body of research continues to grow, it becomes increasingly clear that memory is strongly correlated with sufficient REM-Sleep in adult patients.

Another issue that Older Adult Hypopituitarism Patients experienced was that they slept less than their control counterparts, and also slept less soundly and experienced a higher level of sleep fragmentation. It is true that older men and women experience less REM sleep as they grow older, as well as shorter sleep, and more frequent rousing from sleep, but experimental patients experienced these sleep issues at a rate higher than their control peers, and HGH Deficiency appears to be a powerful mechanism which inhibits healthy sleep among these patients.

Older Adult HGH Deficiency patients simultaneously experienced Slow Wave Sleep of high intensity and long duration earlier in the sleep cycle, and had more issues staying asleep later in the sleep cycle. This is a strange issue, because enhanced Slow Wave Sleep is usually correlated with longer, steadier sleep.

Pituitary Insufficiency Vs. Combination Hypothalamic-Pituitary Insufficiency

So, for patients that only experienced pituitary issues with no hormone imbalance resulting from hypothalamic insufficiency, Slow Wave Sleep was longer, but didn't provide sleep benefits for other reasons. This was not the case for patients that were suffering from Hypothalamic issues in addition to Pituitary Insufficiency. Patients that had diminished GH-RH response had issues with Non-REM Sleep, not reaching a sufficient depth of sleep for optimal health. There is significant evidence from other studies that shows that GH-RH Deficiency is associated with an inability to sleep deeply.

For participants that were suffering from Pituitary issues in which Hypothalamic Insufficiency was not ruled out, the results were a mix between the two classes of Hormone Deficiency.

How Did this HGH Sleep Study Compare to Previous Studies?

Interestingly enough, the results of this study were different from another study released twenty years previously, which studied patients with Isolated Growth Hormone Deficiency. There are a number of reasons for this, however. In the older study, participants were controlled on age and sex, but not with regard to Body Mass Index.

There were other aspects which were insufficiently controlled as well. Patients were not monitored for how long they slept, nor when they went to sleep. The earlier study also allowed for naps, and patients were not limited in their activity in the previous study.

In this earlier study, patients slept much longer, ranging from 7:45 of sleep to 11:44 among the eight patients. Increased need for naps and longer periods of sleep are generally associated with fitful sleep which is not sufficiently deep. Because of these various differences, the results in the newer study were different.

Another older study found no significant difference between patients with Adult-Onset Human Growth Hormone Deficiency and otherwise healthy patients, but the patients were not matched to their controls with regard to sleeping habits, age, gender, and other characteristics, which led the study to be unable to register sleep differences between HGH Deficiency patients and healthy patients.

Could Other Hormone Deficiencies Have Impacted Sleep Quality?

Almost all of the patients in this Growth Hormone Deficiency Study received some form of Hormone Replacement Treatment, such as Estrogen, Testosterone, Thyroxine, Cortisone, or Hydrocortisone, although none of the patients were receiving Growth Hormone Therapy.

There is no way to rule out that any of these treatments or other underlying hormone deficiencies could have an impact on their sleeping patterns and habits as well. In spite of this, the fact that older patients experienced greater issues with sleep than their younger counterparts does provide strong evidence that HGH / GH-RH Deficiency do have a powerful impact on sleep quality.

HGH Study Conclusion

Based on the results of this study, there is strong evidence that Human Growth Hormone Deficiency impacts health in a number of ways related to sleep, including increased feelings of exhaustion and sleepiness during the day, caused by inhibited sleep quality during the night.

The mechanism by which Human Growth Hormone Deficiency impacts sleep quality depends on multiple variables, and the age of the patient and the cause of HGH Deficiency both seem to be very important signifiers.

How Does This Study Relate to Age-Related Hypopituitarism and Somatopause?

It's important to note that this study almost universally involved patients with damaged or otherwise non-functional Somatotrophs. Age-Related HGH Deficiency is most commonly the result of an underlying GH-RH Deficiency.

Patients in this study that were unable to produce sufficient GH-RH experienced issues with their ability to achieve deep sleep, which is in line with the experiences of patients that suffer from HGH Deficiency resulting from the aging process.

06 July 2014

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