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Natural Hormone Replacement Treatment | eHow

Posted on April 16, 2014 by Prof Baldwin

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Erin Morris

Erin Morris is a freelance and professional writer who has been writing and editing since 2004. She worked as a copywriter for an Internet marketing firm for more than four years before attaining a copywriter position with "The Buffalo News." Morris holds a Bachelor of Arts in professional writing.

Menopause can be a very difficult transition for many women. Symptoms of menopause range from hot flashes and mood swings to sleep disorders, depression, hair loss and wrinkles. On top of that, many women start to feel a sense of worthlessness because their child-bearing years have come to a close. Natural hormone-replacement treatment is a way to supplement natural hormones in order to feel more balanced. Menopause halts the production of certain hormones in females, but hormone replacement can make you feel like you again.

The idea is to supply the body with natural hormones like estrogen and progesterone when the body stops producing them naturally. Menopausal symptoms can sometimes begin as much as five to seven years before menopause occurs. Natural hormone-replacement treatments allow women to minimize menopause symptoms for a more normal life.

Replacement hormones can be administered in one of several ways. Women can administer estrogen by way of oral pills, subcutaneous pellets, intramuscular injections, transdermal patches and vaginal hormonal creams. Progesterone can be administered by way of vaginal suppositories, injections or oil.

Before you begin natural hormone-replacement therapy, it is important to know all the facts. Hormone-replacement therapy may not work for everyone, and if it does work, may work in only varying degrees. However, many women have found a significant reduction in menopausal symptoms when undergoing hormone-replacement therapy. When you visit your physician for a menopausal diagnosis, discuss all of your options.

While hormone-replacement therapy has been very beneficial for many women, there are still some controversial risks that are associated with continual therapy. The most severe include uterine and breast cancer, blood clots, liver disease and hypertension.

Natural hormone-replacement treatment provides a significant improvement in quality of life. Menopausal symptoms can hit some women hard. By replacing hormones naturally, you can create a healthier state of body and mind.

A hysterectomy involves the removal of a woman's reproductive organs. A hysterectomy can be partial (such as removal of the upper-part of...

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Natural Hormone Replacement Treatment | eHow

Hormone Replacement Treatment | eHow

Posted on April 16, 2014 by Prof Baldwin

Browse Articles & Videos By Category

Marcia Frost

Marcia Frost is a writer covering topics such as travel, food, wine/spirits, health and fitness. She is the content editor for Cocktails and Joints and writes regularly for many on- and offline publications, including "Michigan Avenue," "Gotham," "Aspen Peak," "Los Angeles Confidential" and "Hamptons Magazines." She has a B.A. in journalism from Long Island University.

There has been much controversy in recent years about hormone replacement therapy. The treatment of women with hormones has been proven to dramatically reduce the symptoms of menopause. On the other hand, there have been studies that have shown an increase in conditions such as heart disease and breast cancer with hormone therapy.

Hormone replacement treatment, also known as hormone replacement therapy or HRT, is the administration of estrogen or a combination of estrogen or progesterone.

Women who go through hormone replacement treatment are usually looking for relief of severe symptoms from menopause. These can include hot flashes, night sweats, difficulty sleeping, cognitive disturbances and anxiety.

A study by the NIH-sponsored Women's Health Initiative showed an increased risk of heart attack, stroke and breast cancer with long term use of hormone replacement treatment. Additional studies of HRT have not been totally conclusive.

In time, symptoms of menopause will naturally disappear without hormone replacement treatment. There are also a number of homeopathic remedies to treat the symptoms.

Hormone replacement treatment has proven useful in controlling women's symptoms and possibly protecting bones from osteoporosis. Its benefits and risks should be weighed carefully by patient and physician.

Menopause can be a very difficult transition for many women. Symptoms of menopause range from hot flashes and mood swings to sleep...

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Hormone Replacement Treatment | eHow

Retarding Aging: Injectable Growth Hormone (HGH)

Posted on July 6, 2015 by Prof Baldwin

Since Dr. Rudmans initial findings, a number of studies have supported the fact that HGH will retard aging, but also reverses the process as well.

Even though called Growth Hormone, the effects are not that it causes you to grow after the age of 20, but to repair and heal.

Despite comments made, Growth hormone is not used to make people muscular, but to cause a lean appearance as well as to provide recovery and healing.

Also there is a tremendous amount of confusion that Growth Hormone is a steroid. It is not a steroid, but is a chain of 191 amino acids.

And because those amino acids are readily available and can cause a secretogogue response (something that allows and encourages more growth hormone to be produced in the pituitary) we have excellent alternatives to increase growth hormone production versus using actual growth hormone therapy.

Benefits of increasing Growth hormone levels include consistent increase in lean muscle mass, loss of the belly fat, improved cardiovascular risk profile, more energy, improved memory, improved sleep and just feeling good. HGH affects almost every cell in our body and it helps to regenerate skin, bones, heart, lungs, liver and kidneys to their more youthful function.

Because HGH reduces inflammation and improves lipid profiles, the heart attack and stroke factors are diminished.

I believe that healing and repairing is the main function of HGH after the age of 20 and with aging when the HGH levels drop to critically low and dangerous values bringing those levels of IGF-1 ( best way of monitoring HGH levels and production) down to below 200, we move into a programmed annihilation mode.

And that doesnt sound very good!

Increasing HGH levels to more healthy levels will begin to restore, recover and heal our aging body. With healthy HGH levels, osteoporosis is blocked, hair growth is increased, and, and skin integrity, once healthy and now injured resulting in the aging appearance of skin with wrinkling and loss of texture, is restored to a healthy appearance.

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Retarding Aging: Injectable Growth Hormone (HGH)

Growth Hormone IGF-1 Cancer – Trans-D Tropin

Posted on November 24, 2016 by Prof Baldwin

Growth Hormone IGF-1 cancer

Rashid A Buttar D.O. Visiting Scientist, North Carolina State University As published in "Anti-Aging Medical Therapies, Volume 5"

ABSTRACT

The benefits of growth hormone (GH, also known as human growth hormone or hGH) have received increasing attention from not only the media but the medical profession as well, as a result of studies indicating GH may have the ability to restore a more youthful physiology and enhance the quality of life. However, there is controversy centered on the possibility that maintaining youthful GH levels may actually be harmful in the long run and may result in shortening life span by inducing cancer.

The first foundational objective essential to gaining an insight into these issues is to clearly understand the hypothalamic-pituitary axis. More often than not, we forget the physiological safety mechanisms designed within our systems to protect us. In this case, we refer to the negative inhibitory feedback loop designed to decrease or stop the release of endogenous GH when levels exceed the physiological range. This inhibitory feed back loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using growth hormone releasing hormone (GHRH) to increase endogenous GH as opposed to using exogenous GH.

This will lead to the discussion of why assessing increases in insulin-like growth factor type1 (IGF-1) as a marker of GH efficacy may not only be unreliable, but a compelling argument will be presented that the practice may be nothing more than the perpetuation of a medical myth. In fact, conclusive data from multiple sources showing that increases in IGF-1 are conducive to the propagation of oncogenesis will be presented and then supported by general physiological concepts, scientific observation and published research.

Finally, the inter-relationship of GH, GHRH, and IGF-1, as well as how each individual component correlates with incidence of cancer, will be thoroughly explained.

Keywords: Growth Hormo ne ; IGF-1; Cancer; Trans-D Tropin; Geref; GHRH analog

INTRODUCTION

Intuitively, it is obvious that naturally occurring endogenous GH released within physiological parameters itself could not possibly cause cancer. The reasoning for this statement is actually quite simple because all mammalian species achieve the maximum level of GH levels when reaching late adolescence and young adulthood. If endogenous GH were actually a cause of cancer, then all mammalian species including man would have the highest incidence of cancer during late adolescence and young adulthood. However, as we all know, this is not what occurs.

So, what then causes cancer? The answer unfortunately, is more than a little involved. We know that a minimum of 75% of all cancers have been shown to have environmental etiologies. In addition, there are certain factors that predispose individuals to have a higher propensity to develop uncontrolled cellular proliferation and induce the suppression of apoptosis, leading to oncogenesis or the formation of cancer. In addition, we know that the incidence of cancer generally occurs later in life as opposed to late adolescence and young adulthood when we have the highest levels of GH.

This will lead to the discussion of why assessing increases in insulin-like growth factor type1 (IGF-1) as a marker of GH efficacy may not only be unreliable, but a compelling argument will be presented that the practice may be nothing more than the perpetuation of a medical myth. In fact, conclusive data from multiple sources showing that increases in IGF-1 are conducive to the propagation of oncogenesis will be presented and then supported by published research. This conclusion is very well supported by scientific observation, clinical data, and published research, as well as being supported by general physiological concepts - all of which will be presented later in this chapter.

Finally, the inter-relationship between GH, GHRH, and IGF-1, as well as how each individual component correlates with incidence of cancer, will be thoroughly explained. It is important however, to first discuss the common characteristics of cancer and the various treatment options available so that all readers have the same foundational knowledge essential to understanding and conceptually comprehending the material being presented.

CANCER CHARACTERISTICS

The vast majority of cancers exhibit certain common characteristics including, but not limited to, uncontrolled cellular proliferation, suppression of apoptosis, and anaerobic metabolism. They also require a specific environmental state within the biological system. Cancer is also characterized as being an opportunistic process, inflammatory in nature, an obligate glucose feeder, and is associated at least in the early stages with a hyperinsulinemic state.

Despite the traditional methods of fighting cancer which include surgery, chemotherapy, and radiation, as well as the non-traditional treatments including nutrition, supplementation, herbs, lifestyle changes, detoxification, metabolism optimization, IV treatments, hyperthermia, immune modulation using peptides, insulin potentiation techniques, and the hundreds of other methods which can not be listed due to space constraints, the best defensive strategy against cancer remains maintaining a good offensive stance. What exactly do we mean by this statement? Remember, the process of oncogenesis begins not weeks or months before it manifests itself as cancer, but actually starts years before the cancer reaches a point where it can be diagnosed.

What this means is that it is essential to be proactive earlier in the game prior to the cancer being diagnosed. This strategy is most evident in the cardiovascular model where physicians intervene prior to the manifestation of heart disease, by managing hypertension and hypertriglyceridemia while encouraging life style changes such as reducing body fat, increasing exercise, and facilitating smoking cessation. Despite the trillions of dollars spent in the war against cancer, the mortality rate from cancer is secondary only to cardiac disease, with the incidence steadily rising. Therefore, the key to solving the issue of cancer, just as in cardiovascular disease, is prevention.

METHODS OF INCREASING GROWTH HORMONE

Extensive research to further the understanding of the aging process is currently being conducted at a number of leading institutions. Some of the findings from these studies show that as we age, GH levels steadily decline. The numerous potential benefits associated with GH treatments to stem this decline have generated an incredible plethora of products claiming to increase GH and IGF-1 levels. The studies necessary to validate these various anti-aging treatments as a result of this marketing surge unfortunately have not followed suit.

The answer that we seek as clinicians is how to effectively inhibit, or at least slow down the aging process and thus prevent the associated debilitating limitations, which are accepted by society as being inevitable as we grow older. The benefits of GH have increasingly received attention as a result of the ability of GH to restore a more youthful physiology and enhance the quality of life. However, controversy has centered on the possibility that maintaining youthful growth hormone levels may actually be harmful in the long run, actually shortening life span by promoting cancer. The topic of GH and cancer will be discussed in detail later but it is now becoming clear that in the quest for a longer life, we may possibly be hurting our patients by contributing to the increased incidence of cancer. We must be ever vigilant of the first rule of medicine as epitomized by Hippocrates, to Do No Harm.

Currently, there are only two clinically documented methods of increasing GH. The first method is by injecting recombinant, synthetic GH (a 198 amino acid peptide with a terminal end). There are a number of choices available to physicians who choose to pursue this method of increasing GH in their patients. The pitfalls of this choice will be clearly delineated. Tosimply summarize, the physiological safety mechanism, namely the negative, inhibitory feedback loop between the hypothalamus and pituitary is violated, leading to many potentially serious consequences.

The increased attention to the benefits attributed to GH has also given rise to hundreds of products that reportedly claim to increase GH levels. This second method of increasing GH levels is achieved by stimulating the pituitary to increase endogenous levels of GH. This technique of simulating the action of growth hormone releasing hormone (GHRH) has rapidly become a popular method, although the vast majority of products claiming to achieve these results have no scientific validity, having failed medical scrutiny.

The first foundational objective is to clearly understand the hypothalamic-pituitary axis (Figure 1). More often than not, we forget the physiological safety mechanisms designed within the biological system to protect us. In the case of GH, the reference is being made to the negative inhibitory feedback loop designed to decrease or stop the release of GH if the levels being released are beyond physiological range. This inhibitory feedback loop plays a significant role in the hypothalamic-pituitary axis and realizing its significance is vital to understanding the advantages of using GHRH manipulation to increase endogenous GH as opposed to simply injecting exogenous GH.

Although the GH injections and secretagogues (substances that cause the release of GH, including GHRH and other substances like GHRH) do offer many benefits to counteract the limitations associated with aging, the need for a safer and more effective modality of therapy has long been warranted. The necessity for a therapy offering a greater spectrum of results while providing an accelerated and rapid onset of subjective and objectively measurable efficacy, with a safer profile, a more efficient delivery mechanism, and an ease of administration leading to better patient compliance has led to the advent of many innovative and promising therapeutics. One among these has been uni que due to having created some interesting controversy as a result of going against the current fundamental understanding of the relationship between GH and IGF-1.

Figure 1. The hypothalamic-pituitary axis.

To date, there are only two GHRH analog products that have been clinically validated and scientifically studied. Both are available only via prescription. The first is Geref (NDC # 44087- 4010-1), which is marketed by Serono Laboratories, one of the largest producers of injectable growth hormone. Their product, Geref, is a 22 amino acid analog of GHRH, administered via subcutaneous injection. The second GHRH analog on the market is Trans-D Tropin (NDC # 65448-2115-1) marketed by a European company named Balance Dermaceuticals. Compared to Geref, Trans-D Tropin has the uniqueness of being the first and only GHRH analog that is administered transdermally (TD-GHRH-A). Trans-D Tropin is a polypeptide combinant, consisting of four different naturally conjugated amino acid sequences that are not recombinant in nature. Although not animal derived, these peptide combinants are also not synthetically sequenced. Rather, they are sequenced in a natural proprietary manner most easily explained as being as close to the in vivo process as we currently understand.

In an editorial review appearing in the Journal of Clinical Endocrinology (1999;50:547-556) Scott Chappel, PhD of Serono Laboratories wrote:

"Long-term stimulation of pituitary cells with GHRH will shift the GHRH/somatostatin tone by exogenous [injection] therapy to increase GHRH responsivity and pituitary GH stores. It is predicted that this therapy will reverse the chronic inhibitory state induced by long-term somatostatin domination and create an environment now responsive to the endogenous GHRH toneand allow for the normal [physiological] pulsatile GH release to reappear. This would produce a greater therapeutic benefit and a better safety profile compared with once daily injections of a bolus of recombinant GH...[the need for] repeated stimulation of GHRH receptors is required in a patient friendly formatefforts are ongoing"

From a long-term efficacy, safety, physiological, functional, and compliance standpoint, Trans-D Tropin (henceforth referred to as the trans-dermal GHRH analog or TD-GHRH-A in this chapter), appears to accomplish the goals that Chappel delineates. But some further interesting additional observations were noted during the clinical studies conducted on this TD-GHRH-A by the author, shedding light on a subject that is of great importance to any physician considering manipulation of their patient's hypothalamic-pituitary axis and vital for any patient who may be considering GH therapy as a treatment option.

It was during the initial clinical testing of this TD-GHRH-A, while undergoing the characteristic rigid scrutiny used for medical therapeutics, where the observation was made of IGF-1 deviating from the expected trend. Later, during subsequent clinical studies, the same observations were reproduced with findings being confirmed not only by other independently conducted studies but also found to be well documented within the published medical literature.

At the same time, other clinicians and researchers studying IGF-1 independent of the author, began observing and documenting similar findings. When these scientists began to report their findings starting in 1999, they enabled a greater understanding of the actual nature of IGF-1.

STUDY SHOWS INCREASED GROWTH HORMONE WITH DECREASED IGF-1

In 1998, we conducted a subjective study based upon the SF-36 patient outcome based research model, evaluating 30 patients taking the TD-GHRH-A. The study, which was published in published in the Journal of Integrative Medicine (2000;4:51-61), measured 22 subjective life style criteria and 5 objective criteria including overall strength, endurance, and IGF-1. Although every patient reported significant improvement in most criteria being monitored, a departure from the expected trend of IGF-1 was noted.

The observation of decreasing levels of IGF-1 prompted a second small study, this time to evaluate endogenous GH by drawing serum GH radioimmunoassays and comparing the response to changes measured in IGF-1. A total of 53 sets of serum GH levels were drawn before and after treatment, and analyzed using radioimmunoassays. IGF-1 levels were also collected at baseline and again at three weeks post treatment with the TD-GHRH-A.

Endogenous GH levels measured 90 minutes post treatment showed a 631.46% increase compared to baseline levels (Figure 2). The data was then re-evaluated using the first set of blood drawn and compared to the second set of blood drawn two weeks later in order to assess if changes in GH levels were only dose dependent or if the response were transitory in nature (Figure 3). There was also a concern that the response measured in GH would decrease after a few weeks due to desensitization or acclimatization to the TD-GHRH-A. The results were again diametrically opposed to what was expected. There was actually an improvement in GH release measured after two weeks of treatment with the TD-GHRH-A compared to first time usage. The results indicated an actual increase in sensitization or improvement in pituitary responsivity with continuous usage. This subject will be addressed in greater detail later in this chapter.

Figure 2. Effect of TD-GHRH treatment on endogenous growth hormone levels.

One of the criticisms when this data was presented was regarding the amount of change that was measured in GH levels. The increases in GH levels were felt to be insignificant since they were less than 5 ng/ml. However, the opposing argument questioned how an increase of greater than 600% within a two-week period could be considered insignificant. This argument can only be settled by defining what level of GH increase is necessary in order to achieve therapeutic benefit.

Endocrinology and physiology textbooks indicate that an absolute level of GH above 5 ng/ml is needed before efficacy can be attained. However, the "efficacy" being referred to is a "diagnostic" response (for purposes of diagnosis), not a "therapeutic" response. The "diagnostic" response would be defined as a change to elicit a response far beyond the normal physiological range by taxing and overloading the system. An example of this would be seen in the insulin and dopamine challenges done by endocrinologists to determine GH deficiency.

Figure 3. Comparison of growth hormone levels after initial treatment and after two weeks of treatment.

However, a "therapeutic" response would simply elicit a subtle response well within the normal physiological range in order to achieve a "therapeutic" effect. Although the average range of GH levels measured during this study was well below the 5 ng/ml level defining the diagnostic criteria, an increase in endogenous GH levels greater than 600% compared to baseline measurements is clinically and statistically significant. Furthermore, by keeping the levels of GH below 5 ng/ml, we experience a more physiological increase in endogenous GH as opposed to exceeding the physiological parameters achieved by exogenous, recombinant, injectable GH.

The interesting component of this study was the relationship of "increasing endogenous GH' to a concomitant measurable "decrease in IGF-1 levels' (ng/ml) on a consistent basis. TD-GHRH- A caused not only an increase in endogenous GH but also a decrease in IGF-1. If IGF-1 is an active metabolite of GH and is known to be converted in the liver from GH to one of the many growth factors responsible for normal growth, then why would IGF-1 levels decrease when the GH levels are increasing? Before discussing this important question, let's first discuss the data.

Figure 4. Serum IGF-1 levels at baseline and at three weeks post treatment with TD-GHRH-A

The IGF-1 levels reported in Figure 4 were drawn at baseline and three weeks post treatment with the TD-GHRH-A. There was over a 14% drop measured in IGF-1 levels in the males participating in the study. The female participants showed a greater drop in IGF-1 exceeding a 26% drop. The overall drop in IGF-1 was over a 20% decline in IGF-1 levels compared to baseline measurements over the three-week period. The evidence based on this study seemed to show an inverse correlation between IGF-1 and GH levels. Upon reviewing the published literature, it became clearly evident that IGF-1 and GH have at best, an unreliable correlation.

DOUBLE BLIND STUDY CONFIRMS DECREASING IGF-1

Eventually, the above mentioned data showing the increase in endogenous GH and decrease in IGF-1 became the pilot for a larger, more definitive study to determine not only the correlation between GH and IGF-1 but also to evaluate the effect the TD-GHRH-A had on cortisol, glucose, chemistry, and lipid parameters. The preliminary results of this multi-centered, double blind, placebo controlled, crossover study evaluating endogenous GH levels with serial GH radioimmunoassay levels after TD-GHRH-A administration showed some very interesting results and reinforced the earlier findings of the smaller previous studies.

The requirements for this study were stringent due to the transitory nature of serum GH so all data collection was tightly regulated in order to insure accuracy of the information collected. Patient selection criteria was simple, with age over 30 and non-gravid state being the only absolute exclusion criteria. The primary end point was eight weeks post treatment when the placebo group was scheduled to crossover into the treated group with the secondary endpoint being 16 weeks after the initiation of either treatment or placebo. The placebo (control) was completely indistinguishable from the TD-GHRH-A (treatment) with both utilizing the exact same carrier, with the same consistency, smell, color, and appearance, and with the packaging kept identical.

All control and treatment bottles were labeled with a numerical code and randomly distributed among the patient population selected for the study. The numerical codes facilitated the double blind component with supervising physicians unaware of which patients received placebo versus treatment . Study participants were scheduled for blood draws at very specific time intervals. If a study patient did not present as scheduled for blood draws, the patient was eliminated from the study. Out of 25 centers selected for participation, only eight centers completed the study, with 117 patients out of 317 patients reaching the stated endpoints without deviances from the testing schedule.

All study patients had blood drawn at specified intervals, starting with baseline GH radio- immunoassay levels as well as IGF-1, cortisol, lipid panels, and basic chemistry panels, followed immediately by administration of either the placebo in the control group or the TD-GHRH-A in the treated group. All study patients then had to have repeat blood draws at 30, 60, and 90 minutes after treatment administration. Each of these subsequent blood draws consisted of all the above mentioned serum parameters, with each set of blood draws obtained at a very specific weekly interval. If a study participant did not present at the specified time for a scheduled blood draw, they were eliminated from the study. This was the primary reason why only 117 patients completed the study.

The blood specimen analysis schedule for the treated group (on the TD-GHRH-A) was at the onset of the study, followed up again at the end of the second week, the fifth week and finally on the eighth week after study initiation. The blood specimen analysis schedule for the control group (on placebo) was at the onset of the study and then repeated at eight weeks after the initiation of the study. The blood specimens obtained during the second and fifth week blood draws in the placebo group were discarded, primarily due to the study's financial constraints but also because no significant change was anticipated in the placebo group. Only the start and the endpoint specimens, prior to the crossover point, were analyzed in the control (placebo) group. However, the blood had to be drawn in both placebo and treatment groups at the same time in order to preserve the double blind component of the study.

The percent change measured in endogenous GH levels as measured by GH radioimmunoassay in the 117 patients that completed the study were statistically significant. The change from the baseline blood draw to the blood drawn 90 minutes after the TD-GHRH-A treatment showed a 462.39% increase upon first time usage. At the end of two weeks after using the TD-GHRH-A, an increase of 815.59% in endogenous GH levels was noted, compared to baseline base line levels drawn 90 minutes earlier. By the fifth week, an increase of 1754.22% in endogenous GH was measured from baseline to 90 minutes post treatment with the TD-GHRH-A. However, by the eighth week, there was actually a drop in GH levels when compared to the fifth week, but overall, endogenous GH levels still increased over 609% over a 90 minute period compared to baseline.

The statistical analysis of the data was conducted by an independent source, showing a baseline mean of 0.295918367 with a 90-minute mean of 2.213636364 and a P value < 0.001. The baseline standard deviation was 0.464112 with the 90-minute standard deviation being 2.673173, establishing that the increase s in endogenous GH levels observed in this study were statistically significant. The most dramatic increases in endogenous GH release were measured between the 60 and 90 minute time periods post treatment, regardless of what weekly interval in the study the serum GH samples were drawn. All four time periods (initial baseline, second week, fifth week, and eighth week) clearly showed the time interval between 60 and 90 minutes as the most significant for endogenous GH release.

Figure 5. The change in endogenous growth hormone levels from baseline to 90 minutes after TD-GHRH-A treatment over an eight week period.

Although an increase in endogenous GH levels was clearly established, the decrease in GH levels at week eight compared to week five (Figure 5) was initially confusing. However, referring back to basic physiological principals, it became evident that there were only two possible postulates explaining the reason for a decrease in GH levels during the eight week of usage of the TD-GHRH-A.

The first possibility revolved around somatostatin. An increase of over 1750% in endogenous GH levels by the fifth week is a very significant increase. It would therefore logically follow that with such a tremendous increase in GH from baseline in such a short period, the negative inhibitory feedback loops would be initiated, causing the release of somatostatin from the hypothalamus in order to inhibit the release of GH by the pituitary. An increase in somatostatin (GH antagonist) would result in decreased levels of endogenous GH being released. This hypothesis based on clinical observation will be confirmed or refuted in future studies. The second postulate involves the issue of pituitary reserves. The pituitary gland holds only a limited amount of GH in store, releasing it in a pulsatile manner. Due to the effectiveness of the TD- GHRH-A, the pituitary reserves of GH may have been rapidly depleted and by the eight week, required additional time necessary for the pituitary to replenish its GH stores.

Figure 6. Serum cortisol levels obtained at baseline and 90-minutes after TD-GHRH-A administration.

As the possibilities were being entertained regarding the drop in GH observed at the eighth week compared to the fifth week in the TD-GHRH-A treated group, the placebo data was also being analyzed. The increase in GH in the treated group was measured at 1754 % at the fifth week interval but in the placebo group, although the blood was drawn, the samples were not analyzed as previously mentioned because the placebo group had the second and fifth weeks blood draws discarded. Therefore, a comparison of the fifth week data in the treated versus the placebo group could not be made. However, the data for the eighth week for both the treated group (on the TD-GHRH-A) and the control group (on placebo) were analyzed. Although this comparison did not allow for an explanation for the relative drop in GH from the fifth week to the eighth week in the treated group, it did give additional confirmation to previously conducted research unrelated to this study, further intriguing the study investigators.

The eighth week data for the treated group on the TD-GHRH-A showed 609.04 % increase in endogenous GH. However, surprisingly, the placebo group showed an increase of endogenous GH of 118.13% during the same time period. Although initially unexpected, this increase in GH in the placebo group validated previous research regarding the effect of diet and exercise on GH release. Life style modifications that all study patients were instructed to follow while participating in the study included a specific combination of aerobic and resistance exercise, as well as a high protein, low carbohydrate diet.

These findings validate some earlier independent studies showing that even without medical intervention, one can significantly increase endogenous GH levels by simple lifestyle modifications in diet and exercise. All patients in this study were crossed over into the treated group at the eighth week and subjectively followed for another eight weeks. Subjective improvements reported by patients were recorded in the form of a detailed questionnaire based upon the SF-36 patient outcome based research model, answered every two weeks by all study participants. Results correlated well with the objective data collected.

The most significant changes noted were in renal function, with bilirubin dropping 34.56% and creatinine dropping 22.23%. In addition, significant decreases were noted in serum glucose, serum cortisol and IGF-1 levels.

Figure 7. Percentage drop in serum cortisol levels over the 8-week study period.

Serum cortisol levels dropped significantly within a 90-minute interval on each consecutive blood draw (Figure 6). With the exception of a slight increase in baseline cortisol measured during the second week, all cortisol levels drawn decreased in a consistent manner. As depicted in Figure 7, cortisol levels not only dropped from baseline blood draw to the 90-minute blood draw during every occasion, but were also observed to consistently decrease throughout the study period as well. These changes in cortisol were significant for a number of reasons.

First, subjective improvements in attitude, depression, anxiety, sense of well being, ability to focus, concentration and ability to handle periods of stress were reported by a large number of patients participating in this study. These changes were reported later in the course of treatment, usually experienced by the third or fourth month of therapy. The steadily decreasing levels of cortisol correlate with the subjective response reported by patients in their patient self-assessment forms. Second, cortisol, being commonly referred to as the stress hormone, is known to have a significant inflammatory component and contributes to increased rate of aging. Reduction in any inflammatory component may have a substantial effect by reducing oxidative stress on the physiology and improving the "peak and trough" nature of cortisol, as opposed to chronically elevated levels. Reduction in serum cortisol levels was pronounced and consistent.

In addition, IGF-1 and serum Glucose levels were also noted to consistently drop (Figure 8).

Figure 8. Effect of TD-GHRH-A on serum IGF-1 and glucose levels.

The TD-GHRH-A appears to have a distinct "euglycemic" effect on serum glucose. Glucose level modulation was evidenced by glucose levels below 75 mg/dl trending up to approximately the 100 mg/dl levels while the levels above 150 mg/dl trending down to approximately the 110 mg/dl levels. Patients with Insulin-dependent diabetes mellitus (IDDM) experienced 50 to 70 mg/dl drops in serum glucose levels within 90 minutes after using the TD-GHRH-A. The IGF-1 levels were expected to drop based upon the earlier pilot study results, and were observed to drop on a consistent basis as expected.

Figure 9. Response in serum IGF-1 levels to TD-GHRH-A treatment.

The response in serum IGF-1 levels in the treated group showed a consistent and significant drop while on the TD-GHRH-A, dropping acutely within 90 minutes of administration of the TD- GHRH-A compared to baseline levels, and overall throughout the study period intervals as well. Despite endogenous GH levels increasing over 1750% by the 5 week, the mean serum IGF-1 t h levels dropped over 60 ng/ml in the treated group on the TD-GHRH-A. Figure 9 shows the consistently decreasing IGF-1 levels as the study progressed. This was the final indication that an increase in IGF-1 levels was not an appropriate method of monitoring efficacy of GH therapy.

In fact, an inverse correlation between IGF-1 and GH efficacy seemed to be established based on this data, which upon further review was well supported in published literature, current research, and in clinical observation. But further investigation revealed another component of IGF-1 that seemed to have been ignored despite extensive documentation in the medical literature. It was during this study and resulting subsequent inquiry into the IGF-1 controversy that led to the following observations, conclusions, and discovery regarding the correlation between IGF-1 and cancer. The evidence of this correlation is overwhelmingly clear and well supported.

THE NEW PARADIGM IN UNDERSTANDING IGF-1

IGF-1 insulin-like growth factor type is regarded as the most important metabolite of growth hormone, an anabolic hormone that promotes tissue growth. IGF-1 has a structure highly similar in morphology and function to that of insulin, while the receptor site of IGF-1 is indistinguishable from the insulin receptor site. Many of the effects attributed to IGF-1 are also attributable to, and overlap with, those of insulin.

Figure 10. Molecular Structure of IGF-1

The traditional view is that growth hormone is "translated" in the liver into IGF-1, and expresses its activity through IGF-1, even though it has been documented that low levels of IGF-1 are not a reliable indicator of growth hormone deficiency. Yet, many clinicians continue to use IGF-1 as a monitor of efficacy for GH treatment. The problem however is that numerous studies have shown IGF-1 to be modulated by factors completely independent from GH levels.

Many in the research arena have long felt that the chief culprits responsible for reducing life expectancy are likely to be excessive levels of insulin as well as IGF-1. In fact, excessive insulin and IGF-1 are precisely the type of pathological endocrine profiles that are observed in sedentary, obese patients. This has been reported in a number of studies, and recently confirmed in a massive National Institute of Aging study, which singled out low insulin as the best predictor of longevity in men.

All physicians treating patients with any modality used to manipulate growth hormone levels should make themselves familiar with the research on the extraordinary longevity of dwarf mice, which are deficient in IGF-1. Dr A Bartke, one of the chief investigators involved in the dwarf mouse research, was interviewed by Ivy Greenwell for the consumer oriented periodical LifeExtention Magazine (February 2001). When questioned regarding his opinion on the controversy of IGF-1, Bartke expressed that it is high IGF-1 that is likely to be harmful. Low IGF-1 correlates with longevity and is "virtually absent" from the serum of the long-lived dwarf mice according to Bartke. He stated that aiming at high IGF-1 levels might not be desirable not only in terms of life expectancy but also in those of cancer susceptibility as well. However, Bartke points out that the confusion regarding this issue is in great part, due to the difficulty and trouble with separating the effects of GH itself from those of its metabolites, specifically IGF-1. There is growing consensus that IGF-1 levels are indeed not related to GH levels. In a study published in the Journal of Metabolism Research (1999;10:576-579) , Inuki et al found that thyroid hormone modulates IGF-1 and IGF-BP3, without mediation by GH. Just a few months later, Janssen et al, published a study in the Journal of Clinical Endocrinology and Metabolism (2000:85:464-466), where the authors reported finding a direct relationship between serum levels of estradiol and IGF-1 levels, completely independent of GH levels.

Both these studies have set precedence in developing new strategies in treating cancer patients, which will be discussed in detail later in this chapter. However, before delving into the topic of IGF-1 and its relationship to cancer, it is important to review a few fundamental physiological concepts that may enhance the understanding of the nature of IGF-1.

Review of General Physiological Principals

When considering basic science physiological principals, the nature of IGF-1 becomes easier to understand and the controversy surrounding IGF-1 is removed. In order to accomplish this goal, the reader is asked to consider the following two questions and answer them before continuing to read. By answering these two questions, a logical explanation for the decrease in IGF-1 levels witnessed in the aforementioned studies will become self-evident.

Question 1: EXERCISE AND INSULIN SENSITIVITY Do sedentary people or athletes have lower glucose levels?

Exercise leads to an increase in insulin sensitivity. In other words, an increase in exercise leads to the body becoming more "sensitive" to the effects of insulin, thus requiring less insulin to accomplish the same task. The function of insulin is to drive glucose into the cell. Since exercise sensitizes the cells of the body to the effects of insulin, the body needs less insulin to drive the same amount of glucose into the cell. Thus, exercise leads to lower insulin levels by increasing insulin sensitivity.

There is also a higher efficiency in the use of glucose in individuals who exercise. This is due to a number of reasons. First, individuals who exercise have a higher metabolism because they have a greater lean body mass compared to sedentary individuals. Since it takes more energy (glucose) to maintain a greater lean body mass, i ndividuals who exercise have lower levels of circulating gl ucose. This is due to higher fuel consumption as a result of higher levels of activity, as well as a higher requirement to maintain an increased resting metabolism. The higher lean body mass plus higher levels of activity lead to more glucose usage.

Using a car as an analogy, an individual who exercises (exerciser) is like a racecar. The racecar (exerciser) has a larger engine (more lean body mass) and travels greater distances in a shorter period of time (more activity due to exercise), which leads to lower fuel levels due to increased consumption (lower glucose levels due to increased utilization). This in turn, reduces the need for a fuel injector that pushes fuel into the engine (insulin). A decrease in insulin requirements is referred to as becoming insulin sensitive.

This basic physiological concept is evidenced in clinical medicine every day. Individuals who exercise regularly have lower circulating glucose levels, and as a result require less insulin. The sedentary, obese, non-exercising patients have higher glucose levels, eventually having to increase their insulin requirements due to becoming insulin resistant. Insulin resistance is more commonly referred to as non insulin-dependent diabetes (NIDDM). Our obvious goal as clinicians should be to drive the physiology of our patients towards that of the exercising, athletic patient with lower insulin levels.

Question 2: EXERCISE AND YOUNGER PHYSIOLOGY Are people who exercise, biologically (physiologically) younger or older?

Exercise has always been considered a natural form of anti-aging or longevity therapy. From the study on the TD-GHRH-A, we know the placebo group was able to increase GH levels simply by lifestyle modifications including exercise. Other studies have also shown that exercise will increase GH. However, exercise will increase other hormones as well, including testosterone. In fact, exercise has been shown to improve the overall hormonal response within the entire biological system.

Exercise causes a decrease in blood pressure, heart rate, respiratory rate, and peripheral vascular resistance, making the system more efficient and allowing the "engine" to idle at a lower threshold. Exercise increases endorphin release, lean body mass, immunity, range of motion, endurance, stamina, libido, etc. These physiological changes induced by exercise are well established and extensively documented in the medical literature. All these responses are evidence of a younger physiology and are characteristics of younger individuals. Therefore, exercise leads to the physiology of a younger state. This is one of the primary reasons that exercise has long been recommended for better health.

EXPLANATION OF DECREASING IGF-1 LEVELS

The answers to our two questions at this point should be clear. The answer to the first question is that athletes have lower serum glucose levels secondary to an increase in insulin sensitivity. The answer to the second question is that exercise leads to a younger physiological age, i.e., increase in lean body mass, increase in insulin sensitivity (decrease in insulin levels), increase in GH, etc.

Now lets look at IGF-1 versus insulin. First, why is the molecule commonly referred to as IGF-1, named "Insulin-like growth factor type 1?" Insulin-like growth factor type 1 is just one of many growth factors. The polypeptide sequence of the general class of molecules referred to as IGF overall are very similar to the insulin molecule. The fact that IGF-1 is an acronym for "insulin-like growth factor type 1" should be the first indication that insulin and IGF-1 may be highly similar molecules. In fact, insulin and IGF-1 are extremely similar and have many of the same morphological characteristics, appearing to share many of the same properties and traits as one another much more so than the other insulin like growth factors

Figure 11. The Insulin-like growth factors, their receptors, and their binding proteins. SOURCE: The International Society for IGF Research website, http://www.igf-society.org

In Figure 11, note that the receptor site for insulin and the receptor site for IGF-1 are morphologically identical. Also note the significant difference in IGF-1 and insulin receptor sites compared to that of the IGF-2 receptor site. IGF-1 and insulin receptors appear to be completely interchangeable. Therefore, any molecule that binds to these receptor sites could also be interchangeable, indicating that insulin and IGF-1 should be able to interchangeably bind to either receptor site. All evidence indicates this theory to be correct with the findings appearing to be well confirmed on a clinical basis as well as confirmed within the didactic and research communities.

GENERAL PHYSIOLOGICAL PRINCIPALS

Based upon the answers to the two questions asked earlier, we can now support the conclusion that athletes have lower insulin levels and are biologically younger compared to their counterparts who do not exercise. As an example, a 79 year-old patient who exercises regularly is biologically younger than his 79 year-old sedentary counterparts. Based on this supposition, we can now logically conclude that exercise equates to a slowing down of the aging process or, a form of "anti-aging" therapy. Put another way, exercise promotes longevity.

Recognizing that exercise creates a physiological situation that results in an increase in lean body mass, an increase in GH levels, an overall increase in hormonal levels, an increase in insulin sensitivity, a decrease in physiological age and a decrease in insulin levels, we can now understand why exercise equals "anti-aging". These physiological changes represent the goal all physicians desire to achieve in all their patients. These biological parameters are what doctors strive to accomplish, regardless of a patient seeking to simply optimize their health and live a longer life or facing a life threatening chronic illness such as diabetes, heart disease, or cancer.

If we recognize that all the above-mentioned desired physiological parameters are a consequence of exercise, then it would follow that as physicians, we would want to embrace any treatment modality for our patients that would recreate the same physiological parameters achieved by exercising, i.e., creating lower glucose levels, leading to insulin sensitivity and resulting in lower insulin levels as observed in young athletes. Conversely, we would want to refrain from any treatment modality that would oppose the effects of exercise, i.e., creating higher glucose levels, leading to insulin resistance and resulting in higher insulin levels as observed in sedentary, obese, diabetic patients. As previously discussed, the problem is that IGF-1 and insulin are very similar to one another morphologically. Even more importantly, IGF-1 and insulin receptor sites are virtually identical and interchangeable.

If lower insulin levels, such as those found in young athletes, are desirable from a longevity standpoint, then wouldn't we expect IGF-1 to also be lower in young athletes? The answer of course is "yes'. This is due to one simple reason that as a result of IGF-1 and insulin being morphologically identical, these two substances generally cannot be opposed in a normally functioning biological system. If IGF-1 is high, then the insulin levels will also be high.

IGF-1 should be lower in young athletes, just as insulin levels are lower in athletes. And in fact, this is exactly what is clinically observed! The same observation is noted when insulin begins to drop in individuals who begin to exercise. We tested this basic physiological principal and applied it clinically. The above conclusions were easily verified in a small clinical study, demonstrating IGF-1 to be demonstratively lower in athletes.

IGF-1 IN ATHLETES VS. SEDENTARY PATIENTS

In a small, outcome based study to assess IGF-1 levels in un-manipulated patients (patients who had no hormonal manipulation), the true nature of IGF-1 was clearly elucidated (Figure 12). The aged, inactive, obese subjects (sedentary group) had very high levels of IGF-1 when compared to the younger, active subjects (athletic group) who had levels as low as 88 ng/ml.

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National Organization for Rare Disorders Gives Batten Disease Community a Voice in Washington – Batten Disease News

Posted on August 3, 2017 by Prof Baldwin

Even by the standards of rare illnesses, Batten disease is extremely uncommon, affecting only two to four of every 100,000 births in the United States. That translates into 20 or so American babies born each year with the hereditary illness.

Yet no disease is too insignificant for the National Organization for Rare Disorders, or NORD, which represents those with 7,000 rare conditions that together affect an estimated 30 million Americans.

In April, the U.S. Food and Drug Administration approved Brineura (cerliponase alfa) as a treatment for children 3 and older with a Batten disease.BioMarin Pharmaceuticalsenzyme replacement therapy is for a version of the disease known aslate infantile neuronal ceroid lipofuscinosis type 2 (CLN2). Another name for the condition is tripeptidyl peptidase-1 (TPP1) deficiency.

We were excited to learn of the FDAs approval of the very first treatment for Batten disease, Paul Melmeyer, the National Organization for Rare Disorders director of federal policy, said in an interview in Washington. Yet as we understand it, it will be effective in only a small portion of those with Batten a specific genetic subset of 150 or so patients.

BioMarin said its therapy costs $27,000 per biweekly infusion, or just over $700,000 a year, to treat each of the few children born with the condition. This makes Brineura one of the worlds most expensive drugs.

While Brineura doesnt cure the condition, clinical trials have shown that it delays major symptoms. Those treated with it are able to continue walking and talking until around 6 years of age.

Now that theres an innovative treatment for a genetic subtype, we also want to be sure that the rest of the population with Batten disease will have access to therapies which may be coming down the pipeline over the next couple of years, Melmeyer said.

The suggested dose of Brineura is 300 mg, administered once every other week by intraventricular infusion into the cerebrospinal fluid, followed by an infusion of electrolytes. The whole process lasts about four and a half hours. The FDA recommends pre-treatment of patients with antihistamines with our without antipyretics [to prevent fever] or corticosteroids 30 to 60 minutes before starting the infusion.

Orphan therapies [those for rare diseases] do run the gamut of medical technologies and routes of administration, Melmeyer said. Many therapies are infused, many are blood products delivered through plasma, many are standard pills, and many are medical foods. Theres a whole lot of innovative ways to get effective treatment to individuals with rare diseases. Theyre unique and complex and the developers of these therapies have to get very creative.

The patient organizations and advocates who lobbied for passage of the Orphan Drug Act founded the National Organization for Rare Disorders in 1983. The law facilitates the development of treatments for rare diseases.

Ever since then, our role has been to support the rare disease patient organizations and act as a union of those associations, Melmeyer told Batten Disease News.

The organization operates from the fifth floor of a Dupont Circle office building that also houses the Pulitzer Center, the Carnegie Endowment for International Peace and the Embassy of Papua New Guinea.

Its 260 or so member organizations include the Batten Disease Support and Research Association.The voluntary nonprofit group, based in Columbus, Ohio, promotes the civil and human rights of people with Batten disease.

Established in 1987, the association offers referral services so that families with Batten disease can secure benefits available by law. It also maintains a database of people with Batten disease by state, nationally and internationally. And it functions as a national registry for researchers worldwide who are studying the disease.

We did a survey showing that 70 percent of our member organizations have fewer than five full-time employees, Melmeyer said. Many of them may have only one or two staffers or volunteers. Thats indicative of the level of resources, that only a handful of people are paying attention to them.

On the wall of his office are posters marking The Orphan Drug Hall of Fame drugs that has become successful therapies against rare diseases. One is for Norditropin, an injectable growth hormone that the FDA approved in August 2006. Another is for Revlimid, a multiple myeloma therapy approved in December 2005. And still another for Cystadane, an oral powder to treat homocystinuria that was approved in May 1994.

BioMarin, which is based in San Rafael, California, said most patients with CLN2 are on federal medical assistance programs such as Medicaid. The mandatory discounts the government demands drop the price by about a third, from $700,000 a year to $486,000, it said.

Weve been hearing from a lot of patients who are frustrated by the cost of these therapies, and also a lot from advocates who want us to focus more on ensuring innovation and less on what the end-stage cost is, Melmeyer told us. We see both sides of those arguments.

He added: We have been very public in our advocacy [for rare diseases insurance coverage] over the last couple of months, ever since efforts to repeal and replace the Affordable Care Act started last year. We understood it was going to take a very large effort on our part to protect our patients.

Tiny organizations such as the Batten association pay $50 a year to belong to the National Organization for Rare Disorders, while larger ones pay a few hundred dollars. The rare disease organization sometimes offers research grants, partnering with a specific disease community.

We are seeing patient organizations starting to get more and more into investing in companies, Melmeyer said. Organizations also take stakes in compounds that are being developed in return for a portion of the compounds sales when theyre approved.

For example, the Cystic Fibrosis Foundation invested from start to finish in Vertexs development of Kalydeco and Orkambi.

Melmeyer said 80 percent of rare diseases are genetic, like Batten disease, and that half the patients who have them are children.

Those who donate to the National Association for Rare Disorders are mostly individuals and foundations, with some money coming from pharmaceutical companies. The organization has a grant from the FDA to work on family history registries.

Last year, over 40 percent of the therapies the FDA approved were orphan drugs. Were very happy that is the case, Melmeyer said. Back in the 80s, wed see one, two, maybe three approved each year. In the 90s, that increased very slightly, but it didnt get to over 10 a year. Really, its only within the last 10 years or so that weve seen a substantial increase in the development and approval of rare drugs for diseases.

Melmeyer said his organization doesnt take positions on drug pricing, including what an appropriate price should be for Brineura or any other therapy.

When we look at the drug pricing debate, we are constantly weighing the two sides, he said. On one side, we need to encourage innovations for individuals with rare diseases, while, on the other, ensuring these same therapies are accessible. Its such a delicate balancing act.

He added: We have drawn a line in the sand for ourselves to not get involved. Once we do, in the interest of consistency, wed have to do that for any drug.

Melmeyer, a native of Pittsburgh, did an internship with the office of Pennsylvania Democratic Sen. Bob Casey before working on health policy issues at the Center for American Progress. He took the National Association for Rare Disorders in February 2013 as associate director of public policy. Hes been in the directors job for five months.

We believe pharmaceutical companies want to ensure that patients with the disease can access their therapy, he said. There are publicity benefits for doing so, especially for kids with a very serious disease. It looks good. But we want it because our patients dont have any other options. Many of these orphan drugs will substantially improve the quality of their lives, which is why we hope the insurance companies will see the value of these therapies.

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National Organization for Rare Disorders Gives Batten Disease Community a Voice in Washington - Batten Disease News

HGH A Natural Cure for Boomer Belly and Reversal of Somatopause – Fitcommerce

Posted on December 7, 2019 by Prof Baldwin

Stimulating the bodys own HGH production can reverse Somatopause, remove fat, add muscle, and take years off your appearance, and perhaps extend longevity because its natures way, its safe.

Capsule: For you boomers, imagine one day a drug that will make you look 20 years younger, remove 15 lbs. of body fat, add lean muscle mass, increase your cognitive functions including memory, give you a healthier heart, increase your bone density, and elevate both your mood and your libido. Well, actually that drug is here now and its called, human growth hormone (HGH). The injecting of HGH is popular among the Hollywood cognoscenti but its expensive and risky. However, there is a way tap into this amazing fountain of youth naturally

The Long Steady Decline

O.K., so youre 60-years old and have been sedentary your whole adult life, but you weigh only 15 pounds more than you did at age 30 so youre O.K. right? Wrong.

Meet HGH, a powerful hormone that keeps us lean, young and strong and keeps all our biomarkers in the healthy range. With enough of it you can stay young and vital long into your elder years.

Unfortunately theres a pivot point right around age 30 where there is a marked drop in your bodys natural production of HGH which, if unabated, will continue to decline for the rest of your life. This condition is called somatopause.

This precipitous drop in HGH leads to a severe drop in lean muscle mass and an increase in adipose tissue especially in the belly. On average, without proper exercise people will lose 10 lbs. of lean muscle mass per decade after the age of 30.

So, the aforementioned 60-year-old may only weigh 15 more pounds, but in actuality he/she lost 30 lbs. of muscle! Add that onto the gain of 15 lbs. and he/she actually has 45 lbs. more visceral fat not a healthy condition.

Dont be depressed, there are positive actions you can take to reverse this trend of HGH loss, read on.

From Hollywood to Main Street

If you want to know whats truly hot and fashionable, look to Hollywood. Many aging actors have been regularly taking human growth hormones for years to remain thin and attractive for their careers. This was originally made known in a March 2012 article in Vanity Fair.

Although far from being a mainstream phenomenon, it is estimated that about 30,000 Americans are shooting up with HGH, a rapid rise from the estimated 2,000 that were doing so in the mid-1990s.

One of the reasons is that HGH is more readily available now that biotech companies have learned to synthesize it through recombinant DNA technology; previously the only source was natural HGH from human cadavers, an obviously rare and expensive supply.

Somatopause The Boomer Belly

Older people face a double whammy. Although they work out at the gym regularly and seem to be constantly dieting, as they age they lose more muscle mass and gain more body fat especially around the middle. Those long cardio sessions cant seem to get the midriff reduced past a certain point.

This malady is called somatopause (So-MAT-a-pause). Somatopause is signified by energy decline, weight-gain (usually around the middle, and hips), loss of muscle, and wrinkled skin. Other symptoms include energy decline, a rise in LDL cholesterol and a lowering of the good HDL.

Somatopause is related directly to the decline of HGH being produced by the body by the pituitary gland as we age. It is an extrapolation of the term menopause and applies to both men and women whose natural production of HGH started a steady gradual decline since age 30 and continues to decline for the rest of their lives.

So, it begs the question, if somatopause is caused by the bodys natural decline of HGH, what if we were to increase the HGH in our system, would that reverse its effects? By most observations, the answer appears to be yes.

It All began With a 1990 Journal of Medicine Article

The late Dr. Daniel Rudman of Madison Wisconsin along with a team of researchers made a startling discovery in July 1990. They performed experiments on men age 61 to 81 to determine if HGH could cause a reversal in symptoms were succumb to during aging.

One group was given subcutaneous injections of HGH while the control group was not. HGH cannot be measured directly because it is detectable in the blood for only a few minutes; therefore they measured a byproduct called IGF-1 (Insulin Like Growth Factor). The more IGF-1 in the system, the more HGH is there as well.

At the start, both groups averaged less than 350 U per liter of IGF-1. After 6 months, the group given the HGH injections had levels of IGF-1 in the range of 500 to 1500 U per liter, a level found at a much youthful age, while the control group still remained at the original 350 level.

What was more astonishing was that with no other variables, there was: An 8.8% increase in lean body mass A 14.4% decrease in adipose tissue, aka body fat A 1.6% increase in vertebral bone density.

It was concluded that the drop in natural HGH levels is directly responsible for much of the observable effects we call aging. And furthermore, that agings effects could be reversed if the level of HGH could be maintained at a higher elevation. This is the finding that launched a thousand ships and explains why today you get all those spam e-mails trying to sell you HGH and HGH releasers over the web. Who doesnt want the fountain of youth?

The Vanity Medicine

There are roughly 74 million baby boomers in the U.S. alone and in contrast to previous generations that have reached older age, this generation is determined to remain young and vigorous. They seem to be looking for that magic bullet, or pill they can take to keep their looks and vitality. Should that magic pill be regular subcutaneous injections of HGH cost anywhere from $500 to $1,000 per month and carry unknown health risks?

Risks of Artificial HGH

If taking a pill, or in this case an injection, for prolonged youth seems too good to be true, well, youre probably right.

A respected source about anti-aging is Dr. Nicolas Perricone, a Yale affiliated dermatologist. In his book, The Perricone Prescription, he clarified the findings of the original Rudman studies as follows:

As exciting as these results were, there was a downside. Subsequent studies using injectable growth hormone at similar doses to the first study found unacceptable side effects . . . The studies were extended to a period of a year or longer and researchers realized that prolonged supplementation could induce diabetes, arthritis or carpal tunnel syndrome, making the results very disappointingSupplementation with injectable human growth hormone is still very experimental and we have not accumulated enough data to assure its safety.

He goes on to explain that HGH is basically good, its the means of injecting high doses of HGH that causes health risks, therefore, its best to mimic our own bodys production of HGH.

Dr. Perricone goes on to say: Another very new and exciting strategy for growth hormone supplementation is to use amino acids or small peptides to trigger the bodys own release of HGH from our pituitary. This is a much safer method because we have normal feedback mechanisms and controls over a hormone when it is being produced by our own bodies.

Read our post:

The Promise of Successful Aging An Interview with Superstar Dermatologist/Nutritionist Dr. Nicolas Perricone

Luckily, there are alternative ways of raising the HGH levels without costly injections and one of those is the neighborhood gym.

Look Younger and Lose Weight with HGH The Natural Way

It is widely believed that certain forms of exercise will stimulate the bodys natural production of HGH in older adults. Since the body seldom produces compounds that will be harmful to itself, what better way to enjoy the benefits of HGH invoked youth without the health risks?

According to Phil Campbell, author of a fitness book, Ready, Set, GO! Synergy Fitness, natural HGH production can indeed be stimulated to produce outstanding physical results. He cites 160 biomedical research studies in his book.

Read our post on how to boost HGH naturally:

Stay Youthful by Biohacking Your HGH through Sprinting

His presents a new regimen which focuses on high-intensity training (HIIT). Such training, combined with proper sleep and diet, can spur the pituitary glands pulsing output of HGH. Campbell calls such HGH goosing a natural anti-aging regimen. And he stresses natural.

Anaerobic Exercise Should Be a Part of Every Fitness Routine

The focus is not on endless hours of aerobic exercise, but on the incredible benefits of anaerobic exercise on the bodys hormone release system.

Short bursts lasting 10 to 30 seconds of intense activity can induce your body to naturally release HGH growth hormone by 530%, which is the substance that keeps you looking and feeling young.

The reason older professional athletes keep playing beyond their time, is due to the anaerobic exercise that they perform during practice. Anaerobic exercise the hard and fast, sprinting types of exercise is shown by medical researchers to make the body produce significant amounts anti-aging growth hormone, says Campbell, and this keeps older players strong, lean and muscular.

Growth hormone is given to children with clinical stature growth problems to help them grow normally, says Campbell, however, it does not make adults grow taller, but it does reverse several measurable clinical factors of the middle-age spread, which has been named the somatopause by researchers.

Anaerobic exercise should be a part of every fitness routine, However, he cautions that physician clearance and a progressive build-up of the high-intensity exercise is necessary to prevent injury.

Conclusion

Youth and fitness are an associated pair. Conversely, pharmacology is closely associated with disease. Nature should always be preferred over drugs. Mankinds quest for the fountain of youth may lie not in a bottle or in a syringe, but in the grunts and groans of intense exercise.

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HGH A Natural Cure for Boomer Belly and Reversal of Somatopause - Fitcommerce

Aytu BioScience Announces Fiscal Q4 2020 Net Revenue of $14.9 Million, an Increase of 82% Sequentially, and 766% Year-Over-Year – BioSpace

Posted on October 8, 2020 by Prof Baldwin

ENGLEWOOD, CO / ACCESSWIRE / October 6, 2020 / Aytu BioScience, Inc. (NASDAQ:AYTU), a specialty pharmaceutical company (the "Company") focused on commercializing novel products that address significant patient needs today reported financial results for its fiscal fourth quarter 2020, for the three month period ending June 30, 2020.

Fourth Quarter Fiscal 2020 Financial Highlights

Commenting on the fourth quarter of fiscal 2020, Josh Disbrow, Chief Executive Officer of Aytu BioScience, stated "Revenue increased exponentially in Q4 2020, to $14.9 million, compared to $1.7 million for Q4 2019. It is important to note that this was the first full quarter of revenue from the combined Aytu and Innovus businesses, along with the Cerecor assets. Turning to the bottom line, adjusted EBITDA loss was reduced to just $1.7 million for Q4 2020, compared to a $3.7 million adjusted EBITDA loss for Q4 2019. On the balance sheet, with approximately $48.3 million in cash, cash equivalents and restricted cash after paying $15 million to fully extinguish the Deerfield balloon payment previously due January 2021, we have less than $1 million of debt, and at current spending levels, we believe we have sufficient runway to reach profitability."

Mr. Disbrow continued, "Taking a closer look at the top line, both of our revenue streams, from the Consumer Health and Rx segments, performed well. On the Consumer Health side, we generated $6.9 million in revenue, an increase compared to Q3. Contributing to those results was organic growth within our core Consumer Health product lines of diabetes care, sexual wellness and bladder health. Additionally, we strengthened our e-commerce business for Consumer Health. Furthermore, our newly launched Consumer Health product, Regoxidine, an over-the-counter foam formulation of minoxidil for hair regrowth, is on track to contribute revenue in excess of seven figures in its first twelve months from launch."

Mr. Disbrow added, "On the Rx side, revenue was $7.9 million, a significant increase compared to Q3. Contributing to Rx revenue was solid contribution from the pediatric franchise. Additional value was created with Natesto gaining preferred status on Express Scripts' national formulary and the Natesto spermatogenesis study results published in the Journal of Urology, both of which we expect to drive prescription growth in the coming quarters. Organic Rx growth was fueled by a relatively balanced contribution across our key products and improved sales execution. Despite the impact COVID has had on physician office access, Q4 represented a record revenue quarter for our Rx business and significant growth over the previous quarters. This is a strong statement about our field execution and clinical value of our products, and I'm pleased to see our call levels now picking back up to near normal in the current quarter to further drive prescription growth."

Mr. Disbrow concluded, "At $14.9 million in record quarterly revenue, with a narrowed Adjusted EBITDA loss, $48.3 million of cash, cash equivalents and restricted cash on the balance sheet, the addition of the Healight opportunity for COVID-19 and future potential non-COVID-19 applications, and our addition to the Russell 2000, we have strong momentum to grow shareholder value in fiscal 2021 and onward."

Conference Call Information

The company will host a live conference call at 4:30 p.m. ET today. The conference call can be accessed by dialing either:

877-407-9124 (toll-free)

201-689-8584 (international)

The webcast will be accessible live at https://www.webcaster4.com/Webcast/Page/2142/37506 and archived on Aytu BioScience's website, within the Investors section under Events & Presentations, at aytubio.com, for 90 days.

A replay of the call will be available for fourteen days. Access the replay by calling 1-877-481-4010 (toll-free) or 919-882-2331 (international) and using the replay access code 37506.

About Aytu BioScience, Inc.

Aytu BioScience is a commercial-stage specialty pharmaceutical company focused on commercializing novel products that address significant patient needs. The company currently markets a portfolio of prescription products addressing large primary care and pediatric markets. The primary care portfolio includes (i) Natesto, the only FDA-approved nasal formulation of testosterone for men with hypogonadism (low testosterone, or "Low T"), (ii) ZolpiMist, the only FDA-approved oral spray prescription sleep aid, and (iii) Tuzistra XR, the only FDA-approved 12-hour codeine-based antitussive syrup. The recently acquired Pediatric Portfolio includes (i) Cefaclor, a second-generation cephalosporin antibiotic suspension; (ii) Karbinal ER, an extended-release carbinoxamine (antihistamine) suspension indicated to treat numerous allergic conditions; and (iii) Poly-Vi-Flor and Tri-Vi-Flor, two complementary prescription fluoride-based supplement product lines containing combinations of fluoride and vitamins in various for infants and children with fluoride deficiency. Aytu also distributes a COVID-19 IgG/IgM rapid test. This antibody test is a solid phase immunochromatographic assay used in the rapid, qualitative and differential detection of IgG and IgM antibodies to the 2019 Novel Coronavirus in human whole blood, serum or plasma. Aytu has also licensed the Healight Platform Technology. Healight is a pre-clinical investigational device being studied as a potential treatment for COVID-19 in severely ill, intubated patients and potentially other respiratory illnesses.

Aytu also operates a consumer health subsidiary, Innovus Pharmaceuticals, Inc. ("Innovus"), a specialty pharmaceutical company licensing, developing, and commercializing safe and effective consumer healthcare products designed to improve health and vitality. Innovus commercializes over twenty consumer health products competing in large healthcare categories including diabetes, men's health, sexual wellness and respiratory health. The Innovus product portfolio is commercialized through direct-to-consumer marketing channels utilizing the company's proprietary Beyond Human marketing and sales platform.

Aytu's strategy is to continue building its portfolio of revenue-generating Rx and consumer health products, leveraging its focused commercial team and expertise to build leading brands within large therapeutic markets. For more information visit aytubio.com and visit innovuspharma.com to learn about the company's consumer healthcare products.

Forward-Looking Statement

This press release includes forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, or the Exchange Act. All statements other than statements of historical facts contained in this presentation, are forward-looking statements. Forward-looking statements are generally written in the future tense and/or are preceded by words such as ''may,'' ''will,'' ''should,'' ''forecast,'' ''could,'' ''expect,'' ''suggest,'' ''believe,'' ''estimate,'' ''continue,'' ''anticipate,'' ''intend,'' ''plan,'' or similar words, or the negatives of such terms or other variations on such terms or comparable terminology. These statements are just predictions and are subject to risks and uncertainties that could cause the actual events or results to differ materially. These risks and uncertainties include, among others: market and other conditions, our ability to successfully commercialize Healight Platform Technology, our ability to obtain FDA approval for the Healight Platform Technology, the effectiveness of the Healight Platform Technology in treating patients with COVID-19 or other illnesses, our ability to adequately protect the intellectual property associated with the Healight Platform Technology, regulatory delays, the reliability of the Healight Platform Technology in killing viruses and bacteria, market acceptance of UV based medical devices, the regulatory and commercial risks associated with introducing the COVID-19 rapid tests, any delays in shipment that may impact our ability to distribute the COVID-19 rapid tests, any reputational harm we may incur if there are delays in receiving the shipment of the COVID-19 rapid tests, our ability to enforce the exclusivity provisions of the distribution agreements, the reliability of serological testing in detecting COVID-19, shipping delays and their impact on our ability to introduce the COVID-19 rapid tests, the ability of the COVID-19 rapid tests to accurately and reliably test for COVID-19, the manufacturers of the COVID-19 rapid tests' ability to manufacture such testing kits on a high volume scale, manufacturing problems or delays related to the COVID-19 rapid tests, our ability to satisfy any labelling conditions or other FDA or other regulatory conditions to sell the COVID-19 rapid test kits, the demand or lack thereof for the COVID-19 rapid test kits, our ability to obtain additional COVID-19 rapid tests to meet demand, our ability to secure additional tests if the manufacturers of the COVID-19 rapid tests are unable to meet demand, the effects of the business combination of Aytu and the Pediatric Portfolio and the recently completed merger ("Merger") with Innovus Pharmaceuticals, including the combined company's future financial condition, results of operations, strategy and plans, the ability of the combined company to realize anticipated synergies in the timeframe expected or at all, changes in capital markets and the ability of the combined company to finance operations in the manner expected, the diversion of management time on Merger-related issues and integration of the Pediatric Portfolio, the ultimate timing, outcome and results of integrating the operations the Pediatric Portfolio and Innovus with Aytu's existing operations, risks relating to gaining market acceptance of our products, obtaining or maintaining reimbursement by third-party payors for our prescription products, the potential future commercialization.

Contact for Media and Investors:

James CarbonaraHayden IR(646) 755-7412james@haydenir.com

Non-GAAP Financial Information

This press release contains a financial measure that does not comply with U.S. generally accepted accounting principles (GAAP), Non-GAAP Adjusted EBITDA. Non-GAAP Adjusted EBITDA excludes (i) amortization, (ii) depreciation, (iii) stock-based compensation, (iv) other expenses comprising net interest expense, (v) non-cash gains and/or losses recognized in the quarter or year due to changes in the fair value of certain of Aytu's financial liabilities, such as contingent consideration, derivative warrant liability, or certain exchanges of debt, (vi) bad debt expense, (vii) impairment of certain long-lived assets; (viii) one-time transaction costs and (ix) costs associated with the Company's Healight technology. Management believes these measures are useful to supplement its GAAP financial statements with this non-GAAP information because management uses such information internally for its operating, budgeting and financial planning purposes. In addition, Aytu believes these non-GAAP financial measures are useful to investors because they allow for greater transparency into the indicators used by management as a basis for its financial and operational decision making. Non-GAAP information is not prepared under a comprehensive set of accounting rules and therefore, should only be read in conjunction with financial information reported under U.S. GAAP when understanding Aytu's operating performance. A reconciliation between GAAP and non-GAAP financial information is provided in the financial statement tables below.

AYTU BIOSCIENCE, INC. AND SUBSIDIARIESConsolidated Statements of Operations

(Unaudited)

Three Months Ended June 30,

Revenues

Product revenue, net

License revenue, net

Total product revenue

Operating expenses

Cost of sales

Research and development

Selling, general and administrative

Selling, general and administrative - related party

Impairment of intangible assets

Amortization of intangible assets

Total operating expenses

Loss from operations

Other (expense) income

Other (expense), net

(Loss) / gain from change in fair value of contingent consideration

(Loss) on extinguishment of debt

Gain from warrant derivative liability

Total other (expense) income

Net loss

Weighted average number of shares outstanding ofcommon shares outstanding

Basic and diluted net loss per common share

AYTU BIOSCIENCE, INC. AND SUBSIDIARIESConsolidated Balance Sheets

Assets

Current assets

Cash and cash equivalents

Restricted cash

Accounts receivable, net

Inventory, net

Prepaid expenses and other

Other current assets

Total current assets

Fixed assets, net

Right-of-use asset

Licensed assets, net

Patents and tradenames, net

Product technology rights, net

Deposits

Goodwill

Total long-term assets

Total assets

AYTU BIOSCIENCE, INC. AND SUBSIDIARIESConsolidated Balance Sheets, Cont'd

Liabilities

Current liabilities

Accounts payable and other

Accrued liabilities

Accrued compensation

Debt

Contract liability

Current lease liability

Current portion of fixed payment arrangements

Current portion of CVR liabilities

Current portion of contingent consideration

Total current liabilities

Long-term contingent consideration, net of current portion

Long-term lease liability, net of current portion

Long-term fixed payment arrangements, net of current portion

Long-term CVR liabilities, net of current portion

Warrant derivative liability

Total liabilities

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Aytu BioScience Announces Fiscal Q4 2020 Net Revenue of $14.9 Million, an Increase of 82% Sequentially, and 766% Year-Over-Year - BioSpace

How low T increase risk of severe COVID-19 in men – The Southern Maryland Chronicle

Posted on June 28, 2021 by Prof Baldwin

Research recently conducted connects diminished blood concentrations of testosterone in men with more severe presentations of COVID-19.

This data completely debunks popularly brandished myths and presumptions suggesting that higher testosterone levels explained why men stood at greater risk of developing severer cases of the illness than their female counterparts.

That said, as the pandemic has progressed, data put forth by healthcare providers has concluded that men seem to develop worse cases than women.

One initial theory supporting the hypothesis that hormonal differences seen in the genders might make men more vulnerable to the pathogens most serious impacts. Researchers continued to suggest that testosterone correlates with aggressive behavior, as mens bodies contain much more testosterone than women. Early speculation centered around such factoids being the reason men seemed to fare worse.

However, newer findings might suggest that, in actuality, the opposite is true. That said, this research didnt provide any data unequivocally linking low T levels to serious cases of the COVID-19. Researchers emphasize that such outcomes could be related to other underlying factors.

That said, these same medical professionals strongly caution the efficacy and safety of clinical trials of drugs used to lower testosterone or heighten estrogen levels as therapeutic protocols for men diagnosed with COVID-19.

In a fresh study Association of Circulating Sex Hormones With Inflammation and Disease Severity in Patients With COVID-19, doctor Abhinav Diwan, who also serves as a professor of medicine at Saint Louiss Washington University School of Medicine, said that the pandemic has created a prevailing belief amongst medical community members that testosterone fuels COVIDs fire.

The physician continued that the reality is quite the opposite. On average, men who possessed diminished systemic concentrations of testosterone upon entering the hospital actually had a higher risk of developing severe COVID-related manifestations or even death than men with higher internal levels of the hormone.

Moreover, researchers found that, if men with already low testosterone levels experienced further systemic declines, their risk for significant complications rose even greater.

Study overseers examined the blood samples of 90 men and 62 women who visited the Barnes-Jewish Hospital presenting with confirmed cases. Of the 143 patients ultimately admitted, researchers again sampled their blood after 3, 7, 14, and 28 days. In addition to testosterone, researchers measured systemic levels of several other notable hormones.

Examiners found that, in women, no appreciable links between hormonal levels and disease severity could be found. Amongst men, no other substances but testosterone revealed any notable findings.

Blood concentrations of testosterone are considered low if the numbers fall below 250 nanograms per deciliter. At admission, men with serious COVID-19 presentations averaged readings of 53 nanograms per deciliter. However, men with milder cases averaged 153 nanograms per deciliter.

Moreover, the results produced by the sickest subjects continued to decline as time progressed. By their third day in the hospital, readings dropped to an average of 19 nanograms per deciliter.

Researchers emphasize that other factors are known to induce more severe illness. Such as high blood pressure, diabetes, older age, and obesity are also connected to low testosterone.

Also, they discovered that men with low T who were not terribly ill at first were more likely to require placement in intensive care or intubation in the immediate days that followed.

Such data, inspired endocrinologist and study author, Dr. Sandeep Dhindsa to confidently opine that lower T levels seemed to be a significant predicting factor in which patients would grow significantly ill.

Additionally, this team of researchers is examining if these findings might suggest links between reproductive hormones and post-Covid cardiovascular concerns. Diwan, who is a cardiologist by trade, opined that when symptoms lingered on for months after initial infection, such issues could arise.

The doctor also stated that men stricken with severe cases or lingering manifestations might benefit from testosterone therapy. For some time, this therapeutic protocol has been employed as a treatment for men coping with low T levels and experiencing the physical and emotional symptoms of said occurrence.

The study was conducted in collaboration with Washington Universitys biorepository and the academic institutions Institute of Clinical and Translational Sciences.

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How low T increase risk of severe COVID-19 in men - The Southern Maryland Chronicle

New Osteoporosis Recommendations From AACE Help Therapy Selection – Medscape

Posted on July 23, 2020 by Prof Baldwin

Recommendations on use of the new dual-action anabolic agent romosozumab (Evenity, Amgen)and how to safely transition between osteoporosis agents are two of the issues addressed in the latest clinical practice guidelines for the diagnosis and treatment of postmenopausal osteoporosis from the American Association of Clinical Endocrinologists (AACE) and American College of Endocrinology (ACE).

"This guideline is a practical tool for endocrinologists, physicians in general, regulatory bodies, health-related organizations, and interested laypersons regarding the diagnosis, evaluation, and treatment of postmenopausal osteoporosis," the authors say.

The guidelines focus on 12 key clinical questions related to postmenopausal osteoporosis, with 52 specific recommendations, each graded according to the level of evidence.

They also include a treatment algorithm to help guide choice of therapy.

Among key updates is an emphasis on the role of the Fracture Risk Assessment Tool (FRAX) in the diagnosis of osteoporosis in patients with osteopenia.

While patients have traditionally been diagnosed with osteoporosis based on the presence of low bone mineral density (BMD) in the absence of fracture, the updated guidelines indicate that osteoporosis may be diagnosed in patients with osteopenia and an increased fracture risk using FRAX.

"The use of FRAX and osteopenia to diagnosis osteoporosis was first proposed by the National Bone Health Alliance years ago, and in the 2016 guideline, we agreed with it," Pauline M. Camacho, MD, co-chair of the guidelines task force, told Medscape Medical News.

"We reiterate in the 2020 guideline that we feel this is a valid diagnostic criteria," said Camacho, professor of medicine and director of the Osteoporosis and Metabolic Bone Disease Center, Loyola University, in Maywood, Illinois.

"It makes sense because when the thresholds are met by FRAX in patients with osteopenia, treatment is recommended. Therefore, why would they not fulfill treatment criteria for diagnosing osteoporosis?"

An increased risk of fracture based on a FRAX score may also be used to determine pharmacologic therapy, as can other traditional factors such as a low T-score or a fragility fracture, the guidelines state.

Another key update is the clarification of the risk stratification of patients who are high risk versus very high risk, which is key in determining the initial choice of agents and duration of therapy.

Specifically, patients should be consideredat a very high fracture risk if they have the following criteria: a recent fracture (eg, within the past 12 months), fractures while on approved osteoporosis therapy, multiple fractures, fractures while on drugs causing skeletal harm (eg, long-term glucocorticoids), very low T-score (eg, less than 3.0), a high risk for falls or history of injurious falls, and a very high fracture probability by FRAX (eg, major osteoporosis fracture > 30%, hip fracture > 4.5%) or other validated fracture risk algorithm.

Meanwhile, patients should be considered at high risk if they have been diagnosed with osteoporosis but do not meet the criteria for very high fracture risk.

Another important update provides information on the role of one of the newest osteoporosis agents on the market, the anabolic drug romosozumab, a monoclonal antibody directed against sclerostin.

The drug's approval by the US Food and Drug Administration (FDA) in 2019 for postmenopausal women at high risk of fracture was based on two large trials that showed dramatic increases in bone density through modeling as well as remodeling.

Those studies specifically showed significant reductions in radiographic vertebral fractures with romosozumab compared to placebo and alendronate.

Camacho noted that romosozumab "will likely be for the very high risk group and those who have maxed out on teriparatide or abaloparatide."

Romosozumab can safely be used in patients with prior radiation exposure, the guidelines note.

Importantly, due to reports of a higher risk of serious cardiovascular events with romosozumab compared to alendronate, romosozumab comes with a black box warning that it should not be used in patients at high risk for cardiovascular events or who have had a recent myocardial infarction or stroke.

"Unfortunately, the very high risk group is often the older patients,"Camacho notes.

"The drug should not be given if there is a history of myocardial infarction or stroke in the past year," she emphasized. "Clinical judgement is needed to decide who is at risk for cardiovascular complications."

Notably, teriparatide and abaloparatide have black box warnings of their own regardingrisk for osteosarcoma.

Reflecting the evolving data on osteoporosis drug holidays, the guidelines also address the issue and the clinical challenges of switching therapies.

"In 2016, we said drug holidays are not recommended, and the treatment can be continued indefinitely, [however] in 2020, we felt that if some patients are no longer high risk, they can be transitioned off the drug," Camacho said.

For teriparatide and abaloparatide, the FDA recommends treatment be limited to no more than 2 years, and for romosozumab, 1 year.

The updated guidelines recommend that upon discontinuation of an anabolic agent (eg, abaloparatide, romosozumab, or teriparatide), a switch to therapy with an antiresorptive agent, such as denosumab or bisphosphonates, should be implemented to prevent loss of BMD and fracture efficacy.

Discontinuation of denosumab, however, can have notably negative effects. Clinical trials show rapid decreases in BMD when denosumab treatment is stopped after 2 or 8 years, as well as rapid loss of protection from vertebral fractures.

Therefore, if denosumab is going to be discontinued, there should be a proper transition to an antiresorptive agent for a limited time, such as one infusion of the bisphosphonate zoledronate.

The authors underscore that in addition to communicating the potential risk and expected benefits of osteoporosis treatments, clinicians should make sure patients fully appreciate the risk of fractures and their consequences, such as pain, disability, loss of independence, and death, when no treatment is given.

"It is incumbent on the clinician to provide this information to each patient in a manner that is fully understood, and it is equally important to learn from the patient about cultural beliefs, previous treatment experiences, fears, and concerns," they write.

And in estimating patients' fracture risk, T-score must be combined with clinical risk factors, particularly advanced age and previous fracture, and clinicians should recognize that the absolute fracture risk is more useful than a risk ratio in developing treatment plans.

"Treatment recommendations may be quite different; an early postmenopausal woman with a T-score of 2.5 has osteoporosis, although fracture risk is much lower than an 80-year-old woman with the same T-score," the authors explain.

Camacho has reported financial relationships with Amgen and Shire. Disclosures for other task force members are detailed in the guidelines.

AACE/ACE Guidelines 2020 Update. Full text

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New Osteoporosis Recommendations From AACE Help Therapy Selection - Medscape

Equipping the Immune System to Fight Against COVID-19 – BioSpace

Posted on August 28, 2020 by Prof Baldwin

The coronavirus that causes COVID-19 has one major advantage over us it is a new human virus. Most people have not encountered the virus before, meaning their immune system is not primed and ready to fight it. When someone gets sick with COVID-19, there is a lag in an efficient immune response, giving the virus time to do significant damage before the immune system can reign in the infection.

It essentially becomes a race between how fast your immune system can clear the virus and how quickly the virus can replicate and induce damage, Agustin Melian, MD, Chief Medical Officer and Head of Global Medical Sciences at AlloVir, told BioSpace.

To develop an effective treatment or vaccine for COVID-19, scientists must understand how the immune system is impacted during the disease. One type of immune cell that is particularly important in the bodys response to COVID-19 is T-cells. T-cells perform many functions, including recognizing invading viruses such as the coronavirus that causes COVID-19.

Multiple studies from Wuhan, China reported that COVID-19 patients had very low T-cell counts; the sicker the patient, the lower their T-cell count. Lower T-cell counts were correlated with poorer outcomes (including higher risk of death) and T-cells isolated from COVID-19 patients also showed signs of exhaustion.

The elderly, patients with low T-cell numbers, and patients who express exhaustion markers on their T-cells are high risk groups in which nave cell responses (responses against a virus they have never seen before) may be deficient or delayed, thus allowing the virus to induce a large amount of damage, Dr. Melian explained. These patients may, therefore, benefit from AlloVirs approach which is designed to restore natural T-cell immunity in high risk patients.

Could giving high-risk COVID-19 patients functional T-cells against the coronavirus boost their immune system and help them recover? This is the question AlloVir aims to answer.

AlloVir creates allogeneic (off-the-shelf) virus-specific T-cells designed to treat common and devastating viral-associated diseases in vulnerable patients, such as those who are immunocompromised or patients who received an organ or stem cell transplant. Now, they are expanding their anti-viral T-cell arsenal and taking aim at COVID-19.

We believe AlloVirs technology is well positioned to treat patients with COVID-19 because our technology is designed to provide SARS-CoV-2 specific T-cell immunity while leaving non-infected cells intact, Dr. Melian commented. Our virus-specific T-cell candidates have been used to treat more than 275 immunocompromised patients with life-threatening viral infections and diseases and we believe it our approach may also have promise in treating COVID-19.

Fighting viruses with T-cells in immunocompromised patients

When you get infected with a virus, your immune system responds to the foreign threat by making specific T-cells that can recognize the virus. These specific T-cells prompt your immune system to destroy any cells infected by the virus.

However, if you have a T-cell deficiency, your immune system cannot robustly protect you. This is a major problem because an otherwise innocuous virus can become a serious infection, causing complications, and possibly even be life-threatening.

That is where AlloVir comes in. They address the underlying problem the weakened immune system. A weakened immune system can be beefed up by giving patients with T-cell deficiencies off-the-shelf virus-specific T-cells (VSTs) originally taken from healthy people. This restores their natural T-cell immunity and helps their immune system fight off the viruses.

At AlloVir, we are a leading innovator in discovering and developing allogeneic, virus-specific T-cell immunotherapies, Dr. Melian said. We are now excited to be applying our capabilities in discovering and developing SARS-CoV-2 specific T-cells to join the fight in developing a COVID-19 program for patients at high risk of severe and devastating disease.

AlloVirs virus-specific T-cell platform

To create AlloVirs T-cell therapies, the target virus is first studied carefully to identify its specific antigens (unique molecules on the outside of each virus that are specific to the virus and alert the immune system). The best antigens those that induce a strong T-cell response are used to create the therapy.

Next, blood is taken from healthy donors who have been exposed to the virus of interest and T-cells are isolated from the blood. The T-cells are activated in the lab they are trained to recognize the identified viral antigens, enabling the T-cells to selectively recognize only the desired virus.

After the T-cells have learned to recognize the specific virus, they are expanded to generate multitudes of cells. Once the activated, specific T-cells are created, they can be cryopreserved and kept for a long time, making them readily available as soon as a patient needs them. The entire process, from antigen selection to donor to ready-to-go T-cell treatment, can be completed in a matter of weeks. This process can be seen in the visual below.

Source: AlloVir

Patients are matched using the companys proprietary human leukocyte antigen (HLA)-matching formula. HLAs are proteins on the surface of cells that regulate the immune system.

Our proprietary donor selection algorithm, known as Cytokin enables us to cover >95 percent of patients in our target population from cells derived from a small number of donors, Dr. Melian said. This proprietary process of prospectively manufacturing cells for off-the-shelf use enables us to study our allogeneic cell therapies in large numbers of patients that suffer from global health crises, like seasonal influenza and, as we are discussing, the COVID-19 pandemic.

These T-cells are advantageous because they are active against a single virus or multiple viruses, are not patient-specific (so they are readily available) and are a single treatment that provides lasting protection. The biggest bonus is the immediate off-the-shelf use for time-sensitive infections in vulnerable populations, added Dr. Melian.

In addition to developing their COVID-19 therapy (called ALVR109), AlloVir has two other multi-virus specific T-cell therapies in development: Viralym-M (ALVR105) and ALVR106. Both therapies focus on treating viral diseases common to stem cell and solid organ transplant patients and other vulnerable populations.

Viralym-M targets six common viruses: BK virus (BKV), cytomegalovirus (CMV), adenovirus (AdV), Epstein-Barr virus (EBV, also called human herpesvirus 4), human herpesvirus 6, and JC virus (also called human polyomavirus 2). Although these viruses are widespread and infect most people, they only cause severe problems in people with weakened immune systems due to age, organ or stem cell transplant, or disease (such as diabetes or AIDS). In a Phase 2 study, 93 percent of 38 allogeneic stem cell transplant patients had a clinical response to Viralym-M treatment and functional Viralym-M cells lasted up to 12 weeks in the patients.

ALVR106 targets four common respiratory viruses: influenza, parainfluenza virus, respiratory syncytial virus (RSV), and human meta-pneumovirus (HMPV). While these viruses tend to cause mild to moderate respiratory illnesses, they can cause severe, life-threatening illness, especially in people with weakened immune systems. ALVR106 is still in preclinical development but clinical trials are expected to begin this year. Overall, AlloVir expects to have three new proof-of-concept (POC) Phase 1b/2 and three pivotal Phase 3 studies started over the next 6-18 months.

Off-the-shelf T-cells against COVID-19

While AlloVir originally designed their T-cell therapies for transplant patients, their platform can potentially be applied to any virus to create virus-specific T-cells. This versatility allowed AlloVir to pivot and create T-cells against SARS-CoV-2, the virus that causes COVID-19. This new investigational therapy, called ALVR109, is being developed as a stand-alone treatment, though it may also be incorporated into their ALVR106 respiratory virus therapy at some point in the future.

Normally, the body would make virus-specific T-cells on their own and these would clear the virus, commented Dr. Melian. We enable that process in patients who otherwise would be T-cell deficient to restore T-cell immunity by giving ex vivo expanded cells that come from patients who already have demonstrated a potent immune response and have cleared the infection.

The process of creating coronavirus-specific T-cells is the same as creating their other virus-specific T-cell therapies. First, blood is taken from people who have recovered from COVID-19 and the T-cells are isolated. Then, the cells are stimulated with viral antigens in the lab, expanded, and cryopreserved.

We purposely choose a broad range of viral antigens to stimulate the T-cells to ensure the virus cant circumvent the virus-specific T-cell therapy by mutating or developing resistance, Dr. Melian said. Working with a wide spectrum of viral activity is different than other approaches that just focus on one viral antigen.

An open-label Phase 1 trial (called BAT IT) is anticipated to start within the next few months. Initial clinical studies of ALVR109 aim to treat high-risk COVID-19 patients, such as the elderly, to prevent organ damage. Prophylaxis studies, where the T-cells could be given to high-risk or immunocompromised patients who are not currently sick with COVID-19, may be considered later.

Coronavirus-specific T-cells vs. COVID-19 convalescent plasma

You may be wondering if another treatment that uses blood from COVID-19 survivors, called convalescent plasma therapy, is similar to AlloVirs T-cell therapy. In convalescent plasma treatment, antibodies from COVID-19 survivors are isolated from their blood by separating out their plasma (the liquid part of the blood). The plasma is given to COVID-19 patients to help their immune system fight off the infection.

Although convalescent plasma and AlloVirs coronavirus-specific T-cell treatments are both derived from COVID-19 survivors blood, the two treatments are fundamentally different.

Antibodies and T-cells work in different areas of the immune system, explained Dr. Melian. Antibodies can go after viruses in circulating blood but cant necessarily see viruses in infected cells. On the other hand, T-cells are pleotropic and directly attack virally infected cells, turning off the viral factories. T-cells are interesting because it is a live therapy they can home to virally-infected cells and direct the immune system.

Dr. Melian went on to explain that T-cell approach may be more comprehensive because they can support other immune cells that work against viruses, such as B-cells that make viral-specific antibodies. T-cells can also stimulate cytokines including interferon (a group of signaling proteins the immune system uses to respond to viruses), which further activates the bodys antiviral response.

Providing virus-specific antibodies may be beneficial and protective for some viral infections, Dr. Melian added. We dont know how these antibodies affect COVID-19 patients yet, but COVID-19 has a high mortality rate despite standard of care treatment. In this respect, it is important that all viable approaches to treatment be evaluated and I am very pleased to see these therapies have entered clinical testing.

Convalescent plasma and AlloVirs coronavirus-specific T-cell therapies are not mutually exclusive, so they could even be used together.

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Equipping the Immune System to Fight Against COVID-19 - BioSpace

A Deep Dive Into Testosterone Booster Ingredients For Optimal Health – generationiron.com

Posted on January 6, 2022 by Prof Baldwin

Maybe you have used a testosterone booster before, maybe you havent. But if or when you do, knowing what ingredients to look for can be helpful. Each company will have their own formulas and unique take on a testosterone booster but there are some key testosterone booster ingredients that can work to boost your low T levels. As athletes, and in particular strength athletes, having optimal testosterone levels is imperative to good performance. And when it comes to your health, this is imperative.

Having low testosterone levels can be a killer when it comes to daily life as well as training and performance. For those suffering from low T levels, you may experience things like low sex drive, loss of muscle mass, low energy and increased exhaustion, and the unfortunate fat gain. But fear not, for testosterone boosters can greatly help especially when it comes to tackling those low levels as you look to get to peak shape.

Lets take a look at testosterone boosters and check out some key ingredients to look for on the label. Knowing what to look for can give you all you need to tackle those unfortunate low levels.

Testosterone boosters essentially work to give your body that boost in raising your levels so you reach optimal capacity. Since testosterone is a vital sex hormone, it aids in many bodily functions that you cant afford to have lacking. While it is possible to boost testosterone naturally, having a supplement like a testosterone booster can give you that edge you need most so you dont suffer any deficiency.

With a wide range of benefits, testosterone boosters can increase muscle growth and strength, help burn stored fat when mixed with regular exercise, boost your sex drive and overall libido, increase vitality, among others. With the right ingredients packed into a powerful formula, all those testosterone wants and needs can be taken care of no problem.

Check out our list of the Best Testosterone Boosters for more great products!

When it comes to knowing about your testosterone boosters, the right ingredients are crucial. Here are some key and potential ingredients to look for in your testosterone boosting supplement.

A combination of aspartic acid and L-aspartate, this can release hormones in your brain that work for better testosterone production. It also increases levels of follicle-stimulating hormone and luteinizing hormone which stimulate the testes to produce more testosterone (1).

Rich in vitamins and minerals, this ancient herb can increase libido and get your performance back on track by naturally increasing testosterone with powerful compounds (2).

By combing to receptors, this will assist with raising T levels since it is a bioidentical hormone for testosterone. Through increased testosterone, this will work to boost your sex drive as well (3).

This will work for building muscle and encourage fat metabolism as well as widen your blood vessels for better blood and nutrient flow. While it may not help increase T levels directly, it can help with certain symptoms that hinder your health and performance.

Since these convert food to energy, through metabolizing fat, you can provide for more consistent testosterone production with B vitamins. With these changes, it also works to build muscle mass and strength.

By increasing nitric oxide levels, this can increase blood flow and allow the testicles to better produce more testosterone (4).

Containing L-Dopa, which increases the pleasure hormone dopamine, it will allow for better mood thus stimulating testosterone production (5).

Can reduce estrogen and increase testosterone while also promoting muscle mass and is a key ingredient for optimizing testosterone levels (6).

May lower estrogen and cortisol which can negatively impact testosterone production. It is also a good libido enhancer.

It can increase the bioavailability of testosterone and allow for more free testosterone. When taken along with vitamin D, it can increase absorption so you get the most out of this ingredient (7).

Can reduce cortisol and works as a stress reliever, thus allowing for better testosterone production (8).

Can help with managing testosterone levels by adjusting your bodies balance of testosterone and estrogen working to increase testosterone and decrease estrogen (9).

Allows your body to absorb these nutrients better so the ingredients in your supplement hit you more effectively.

As a supplement, testosterone boosters are safe to use. What to look for is the reputation of the company and what is included in the supplement. Hidden ingredients or formulas is just something to avoid with any supplement but especially one that works to aid in your health and vitality. Always read the label and if you have more concerns, talk with your doctor or an expert to see if this is the right approach for you.

As for the effectiveness of the supplement, the right product can increase your levels and you will be back on track both inside and out of the gym. A healthy diet and quality training routine are important and can work in tandem with your booster so you see those gains you want most.

Check out our list of the Best Testosterone Boosters for more great products!

Testosterone boosters are that supplement you need to get those levels elevated and tackle any deficiencies. The right ingredients with a quality formula will get you back on track and doing what you love. Dont let low T levels ruin you sex life, training, performance, and vitality, and work to get those levels where you want them. Knowing the ingredients to look for on the label will better prepare you to find the right testosterone booster so you thrive inside and out of the gym.

Let us know what you think in the comments below.Also, be sure to follow Generation Iron onFacebook, Twitter, andInstagram.

*Images courtesy of Envato

References

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A Deep Dive Into Testosterone Booster Ingredients For Optimal Health - generationiron.com

Low T Not Necessarily Troublesome for the Heart – Physician’s Weekly

Posted on January 6, 2022 by Prof Baldwin

Testosterone levels unlikely to cause age-related increase in CV disease

The latest data on testosterone levels and cardiovascular (CV) risk offer both good news and just-okay news: Men with lower total testosterone concentrations were not at increased risk for myocardial infarction (MI), stroke, heart failure (HF), or major adverse CV events (MACE), although some other testosterone-based markers were linked with higher risks for some CV events.

In a cohort study of participants in the U.K. Biobank, lower total testosterone concentration (quintile 1 versus quintile 5) was not associated with incident MI (fully adjusted hazard ratio 0.89, (95% CI 0.80 to 1.00), according to Bu B. Yeap, PhD, of the University of Western Australia in Crawley, and co-authors. In quintile 1, the median testosterone concentration was 7.75 nmol/L and 223 ng/dL versus 16/73 nmol/L and 482 ng/dL for quintile 5.

The study authors also reported the following in the Annals of Internal Medicine with regard to a lack of association between lower total testostrone concentrations and:

However, Yeap and co-authors reported that [c]alculated free testosterone may be associated with risk for MACE, and that men with lower SHBG [sex hormone-binding globulin] concentrations have higher risk for MI but lower risk for IS and HF. SHBG is the major binding protein for circulating testosterone, yet few studies have assessed whether SHBG concentrations might be associated with incident CVD events, independent of testosterone, they explained.

As for lower total testosterone, the authors suggested that it may be a marker for various sociodemographic, lifestyle, and medical factors that are associated with risk for CVD events, rather than an independent risk factor for these outcomes.

But the study had several limitations, most notably its observational design; thus, causality cannot be determined. Also, serum total testosterone, SHBG, and other covariates were measured only once at baseline, according to the authors, and the U.K. Biobank population has a predominantly Anglo-Celtic ethnic background, so the results may not apply to other racial/ethnic groups. Some previous studies have reported differences among ethnic groups for age-related drops in testosterone levels.

Still, the results in 210,700 men followed for 9 yearsof whom 4.2% had an incident CV eventwere in line with previous data, such as a 2014 study of men in the Cardiovascular Health Study, a 2016 study in men ages 17 to 97 (also by Yeap and colleagues), 2019 research specifically on SHBG levels and incident CV events, and the 2020 MrOS Prospective Study.

The current findings may help some clinicians and their patients sort out the mixed messaging regarding testosterone therapy. In 2015, the FDA supported testosterone therapy, but only for men with documented low endogenous testosterone levels caused by primary or secondary hypogonadism, explained Eliseo Guallar, MD, DrPH, of Johns Hopkins University, and Di Zhao, PhD, of Johns Hopkins University Bloomberg School of Public Health, both in Baltimore in an editorial accompanying the study.

They noted that the agency warned about possible therapy-related CV adverse events and that, a few years later, an Endocrine Society clinical practice guideline recommended against starting testosterone therapy for men with chronic conditions, including uncontrolled HF, MI, or stroke within the past six months.

The results from Yeaps group provide some warning against the use of testosterone therapy for the prevention of CVD in men, Guallar and Zhao wrote, adding that the CV safety profile of the therapy remains uncertain, and careful evaluation of the individual cardiovascular risk profile is needed before initiation of testosterone therapy for any patient.

From the U.K. Biobank, Yeap and co-authors analyzed data from community-dwelling men, age 40 to 69 years (about 95% White; <4% South Asian). The age group was on the younger side, so our ndings cannot be extrapolated to older men, nor can we address whether higher testosterone concentrations might be protective in men aged 70 years or older, they pointed out.

Assay tests were done for testosterone and SHBG, and free testosterone was calculated. Cox proportional hazard regression was done for the outcomes of incident MI, strokes, HF, and MACE. All were adjusted for sociodemographic, lifestyle, and medical factors.

They reported that men with lower calculated free testosterone values had a lower incidence of MACE (HR 0.90, 95% CI 0.84 to 0.97). Also, lower SHBG concentrations were linked with:

Finally, Yeaps group calculated the cumulative five-year incidences of all the CV events in the study for U.K. Biobank male participants with total testosterone, SHBG, cFT (free testosterone calculated using the Vermeulen formula), or FTZ (free testosterone calculated using empirical equation) values at the medians of quintile 1 and quintile 5, and reported that the change in absolute risk attributable to this difference in total testosterone concentrations was small, being 0.14% or less across outcomes. Findings were similar with cFT and FTZ. A slightly larger difference of 0.19% was seen for risk for MI related to the difference in SHBG concentrations.

Whether the results will mean anything to the $15 million-plus global testosterone supplementation market remains to be seen, although theres less doubt about the impact of direct-to-consumer (DTC) marketing of such products.

A 2017 JAMA study of DTC advertising, testosterone testing, and initiation in the U.S. (2009 to 2013) found that the former was associated with substantial overall increases in testosterone testing and initiation, and that DTC adverts was tied to more initiation of testosterone without recent serum testing, contrary to treatment guidelines, according to J. Bradley Layton, PhD, of the University of North Carolina at Chapel Hill, and co-authors. A separate 2017 European Urology Focus study also found similar results, and added that [t]here is a high prevalence of misinformation [on testosterone supplementation] on Internet advertising.

In a 2020 Andrology review, Arcangelo Barbonetti, MD, PhD, of the University of LAquila, in LAquila, Italy, and co-authors advised that in pateints with late-onset hypogonadism (LOH) [c]linicians must consider the unique characteristics of each patient and make the necessary adjustments in the management of LOH in order to provide the safest and most beneficial results of testosterone therapy, and emphasized that the therapy should not be started in case of a severe chronic heart failure myocardial infarction or stroke within the last 6 months, or thrombophilia. In case of decision to treat, hypogonadal men with chronic heart failure should be followed carefully with clinical assessment and T [testosterone] and haematocrit measurements on a regular basis.

Men with lower total testosterone concentrations were not at increased risk for myocardial infarction (MI), stroke, heart failure (HF), or major adverse CV events (MACE).

Calculated free testosterone may be tied to a risk for MACE, while men with lower sex hormone-binding globulin concentrations had higher risk for MI but lower risk for ischemic stroke and HF.

Shalmali Pal, Contributing Writer, BreakingMED

The study was supported by the Western Australian Health Translation Network, the Australian Governments Medical Research Future Fund/Applied Research Translation program, and Lawley Pharmaceuticals, Western Australia/University of Western Australia.

Yeap reported support from, and/or relationships with, Western Australian Health Translation Network, the Australian Governments Medical Research Future Fund, Lawley Pharmaceuticals, and Bayer. Co-authors reported support from, and/or relationships with, Western Australian Health Translation Network, the Australian Governments Medical Research Future Fund, UK Biobank, Lawley Pharmaceuticals, Western Australia, Bayer, Bristol Myers Squibb, American Heart Association, AC Immune, AbbVie, UpToDate, GlaxoSmithKline, NIH, The Swedish Research Council, the Swedish state/Swedish government/county councils, the ALF-agreement, the Torsten Sderberg Foundation, the Novo Nordisk Foundation, the Knut and Alice Wallenberg Foundation, National Institute on Aging, Transition Therapeutics, Metro International Biotechnology, Alivegen, National Institute of Nursing Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, McGraw Hill, Aditum, OPKO, Johnson & Johnson, CSL, Merck Foundation, Galapagos/Gilead, Pfizer, Ipsen, Novartis, Novo Nordisk, and the European Academy of Andrology, as well as patents/patent applications in the field of probiotics and bone health, and the measurement of free testosterone.

Guallar reported serving as an Annals of Internal Medicine associate editor. Zhao reported no relationships relevant to the contents of this paper to disclose.

Cat ID: 358

Topic ID: 74,358,730,358,914,109,187,192,925

Continued here:
Low T Not Necessarily Troublesome for the Heart - Physician's Weekly

Low Testosterone in Women – How to Increase a Woman’s Low T-levels – L.A. Weekly

Posted on July 9, 2021 by Prof Baldwin

There are many things that can cause low levels of testosterone in women, such as menopause, aging, and problems with the ovaries or the pituitary or adrenal glands. So how can you increase levels of testosterone in women?

There are some ways you can boost your level of this hormone naturally. In this article we will discuss how to raise female testosterone production, why women would want to raise their T hormone levels and what steps should be taken and which supplements help with the process.

Women produce much of their testosterone in the Ledydig cells in their ovaries. Several factors including aging and disease can decrease female testosterone production, causing weak bones and many other problems. Hypoactive sexual desire disorder, adrenal insufficiency and weight gain are other symptoms of low testosterone in women.

Thankfully, there are several things women can do to increase testosterone production.

There are two main reasons.

Supplements are an effective and quick solution to both of the above reasons.

There are dozens of T-boosting supplements on the market. Most of them are aimed at men, obviously, as men make up 90% of the market. There is no reason why women cannot use these products. The opposite is true in the weight loss market where most products are aimed at the female marketplace but this doesnt exclude men from using.

Women want to increase their testosterone levels because either they need to or they want to. The need is covered in this article in great detail, this is due to conditions (postmenopausal women, hormone replacement therapy). The other other group is women who want more testosterone if they are keen bodybuilders and want increased muscle mass.

Here are the best T boosters for each group.

TestoPrime is a naturally formulated supplement suitable for anyone over the age of 18 that suffers from testosterone deficiency.

You will have to look past the male centric web copy as the product has a larger male customer base.

TestoPrime is arguably the most effective and efficient product of its ilk. It has lots of clinical data to enforce its claims. At the bottom of the official website there are 18 points of reference to clinical studies.

This is the most suitable, most effective and safest testosterone supplement for men.

Click here to find out more on TestoPrime

Testo Max is part of the Crazy Bulk bodybuilding supplement range. It is a more edgy product that delivers top end of testosterone treatment benefits.

It is classed as a legal steroid but doesnt actually contain any steroidal substance.

If you want to gain muscle mass, strength and lose body fat then Testo Max is the supplement for you.

Click here to find out more on Testo Max

Although testosterone is the male sex hormone levels, women produce a small amount of it in their bodies as well and it plays a surprisingly important role in maintaining female good health.

Women need adequate testosterone levels to sustain bone density, support muscle growth, and maintain healthy brain function.

A few of the other roles the male sex hormone plays in a womans body include:

The things men do to improve testosterone levels and production work equally well for women. Many of the changes that raise female testosterone levels are lifestyle-related and, in addition to boosting hormone production, will help support general good health.

Research shows lifting weights can improve testosterone levels in women and men. This type of resistance training is also good for improving muscle tone and muscle mass and provides the classic beach body so many women crave. It can also help to reduce body fat.

Several studies have explored the way resistance training can influence how much testosterone women produce in their bodies. The results of one of them suggest this type of exercise may increase free testosterone levels by as much as 25 percent.

Lifting weights is not the only type of exercise that can favorably influence testosterone levels and hormone production. Many other athletic pursuits, such as running and sports, can do it too.

A lot of the studies evaluating the way exercise affects hormone production were conducted on men. However, a number of studies were women-only or had participants of both sexes.

The results of one women-only study involving treadmill activity show prolonged aerobic exercise produced short-term elevations in testosterone.

Stress can reduce testosterone in men and women so, where possible, its best to avoid people and situations that cause it.

During periods of stress, your body starts producing extra cortisol (stress hormone). High cortisol can have a lot of undesirable effects on the female body. One of the things it can do is cause irregular periods.

Your body produces cortisol from one of the same precursors it needs to manufacture testosterone. So, when the demand for cortisol increases, your body may not have enough of one of the raw ingredients that are necessary to make testosterone.

If you cannot avoid the things that cause stress, you need to control it. There are many ways you can do this but certain ones may work better for some women than they do for others.

For instance, some women like to de-stress at the gym. Others prefer to take a leisurely stroll. Yoga and mediation are also good for calming the mind. So are music, painting, and other artistic pursuits.

Its also a good idea to get plenty of sleep. Constantly trying to burn the candle at both ends increases cortisol and stress.

If you find it hard to get to sleep, a cup of chamomile tea may help. The herb ashwagandha may be doubly useful because, as well as aiding sleep, it reduces anxiety and stress.

Several nutrients have a role to play in testosterone production including B vitamins, Vitamin D, zinc, and magnesium. Eating foods that provide Omega-3 fatty acids is another good way to boost testosterone.

Some of the best testosterone-boosting foods are:

Vitamin D and zinc are often considered to be two of the most important testosterone boosting nutrients. A lot of the best testosterone boosting supplements contain one of them. Most contain both.

In addition to boosting testosterone levels, getting plenty of Vitamin D and zinc also enhances immune function. Many people take these vitamins in pill form for that reason, often combining them with Vitamin C.

Several herbs and plants provide compounds that can stimulate increased testosterone levels. The best of them are often combined in testosterone-boosting supplements but many of them, such as ashwagandha and ginseng can be purchased in concentrated form in capsules and pills.

Ashwagandha (Withania somnifera) is a popular adaptogen herb thats a mainstay of traditional Indian medicine and has now become a popular herbal supplement all over the world.

The herb appears to boost testosterone production by stimulating the release of extra luteinizing hormone (a fore-runner to testosterone). However, Ashwagandha is possibly more famous for its ability to reduce stress.

In addition to being a key player in many products that boost testosterone, Ashwagandha is often added to beauty products because its ability to support increases in collagen production helps beautify the skin from the inside out.

Most of the best supplements provide Ashwagandha as KSM 66. This is a patented extract that provides Ashwagandha in a consistently potent form.

Traditional Chinese healers hold ginseng in high regard for its versatility as a medicinal herb. The Chinese also believe ginseng is a herb that can extend life.

People living in the west are also becoming increasingly aware of the herbs curative abilities but often have greater interest in its reputation as an aphrodisiac.

People often use ginseng supplements to increase sexual desire. Some of its prowess as a libido booster appears to be due to its ability to boost testosterone but most of the studies that show this were conducted on men.

But can it do the same for women? The results from a study conducted at the University of Edinburgh suggest that it may. However, it appears women who are older may attain the greatest level of benefit.

Green tea provides potent antioxidants that help the body get rid of toxins, encourage fat loss, and may help prevent aging. These antioxidants (green tea catechins) are only present in green tea.

One of the most important catechins in green tea, epigallocatechin gallate (EGCG) also helps to maintain circulating testosterone levels by preventing it from being converted to Dihydrotestosterone (DHT).

Most women are familiar with fenugreek. Its a very popular Indian cooking herb. Some women may also have noticed fenugreek listed as an ingredient in some of their cosmetic products because its sometimes used in facial toners and cleansers and similar products that aim to provide glowing, healthy skin.

However, fenugreek is very versatile and is associated with many health benefits, some of which are probably related to its ability to raise female testosterone levels.

Pomegranate is nutritious, tasty, and very good for your health. The ellagic acid it provides cleans the arteries and helps improve circulation. This removes unnecessary strain from the heart.

Research from 2012 suggests pomegranate extracts are also good for boosting testosterone levels and, like several other natural testosterone boosting ingredients, pomegranate provides antioxidants that can help improve the look of your skin.

Women may not require as much testosterone as men do but they still need it women produce testosterone but not as much as men. It helps keep their bones strong, improves body composition, maintains libido, and supports many other aspects of physical and mental wellbeing.

It is important to be aware to not go overboard as too much testosterone can have just an impact as too little.

Unfortunately, many women struggle with low testosterone levels. Contrary to popular belief, this is not a problem that only affects men.

Fortunately, there are plenty of things women can do to increase their natural testosterone production such as avoiding stress, adopting healthier lifestyles, and placing extra focus on foods that provide testosterone-boosting nutrients. Testosterone replacement therapy is another option (with testosterone injections, pellets or patches) but this can be quite invasive. Testosterone therapy and hormone therapy can be quite costly

Certain herbs also can boost female free testosterone levels. The best ones can be purchased individually or combined in supplements that have been developed to function as natural testosterone boosters.

However, if you are suffering from low hormone levels, the best course of action may be to hit the problem from all sides.

Avoid stress where you can, get more exercise, and eat a healthy well-balanced diet that is rich in nutrients and low in sugar and saturated fats. Then, if you want to maximize the overall benefits, take a suitable testosterone boosting supplement as well. TestoPrime and Testo Max are arguably the best examples of female T-boosters.

In addition to increasing low testosterone in women, this combination of changes should help you feel and look healthier and experience an increased joie de vivre.

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Low Testosterone in Women - How to Increase a Woman's Low T-levels - L.A. Weekly

"Hawkeye" reminds us why Jeremy Renner’s archer is the least Avenger – Salon

Posted on November 26, 2021 by Prof Baldwin

The opening episode of "Hawkeye" meets up with the mostly retired heroic archer operating in the uncharacteristic role of the powerless witness. Clint Barton is off the clock, having brought his kids to see a Broadway show during a holiday trip to New York City. The musical in question, "Rogers," is a ludicrous ode to Captain America highlighted by the 2012 intergalactic invasion that the Avengers thwarted.

In that showstopper tune the Avengers' super-powered members are center stage as the actor playing Steve sings their praises, and Black Widow's double ridiculously high-kicks her way across the stage. But it takes a minute to notice whether Hawkeye is being portrayed, too. He is, but at first he blends into the background.

RELATED: "Black Widow" is a triumph for Marvel fans, yet that's what makes it so infuriating

Lining up all the heroes in the "Avengers" pantheon, Hawkeye is the one most people could probably take or leave. He's also the hero whom dedicated nutballs could persuade themselves they could actually become with enough archery training, protein powder, push-ups, "low T" supplements, yams, and inspirational speeches from Joe Rogan.

An unenhanced marksman who never misses his targets and is an expert in hand-to-hand combat, Clint is a problematic fave. While he's saved the world a few times, he outright murdered a slew of criminals in his guise as the Ronin when half the universe wasn't looking.

Renner hasn't done such a bang-up job of winning widespread endearment either. Infuriating headlines like "Jeremy Renner won't stop calling Black Widow a 'slut'" or "Jeremy Renner says it's 'not my job' to help female costars get equal pay" keep popping up in answer to questions of, "Remind me, why don't we like Jeremy Renner?" The good news there is that thisproves how little time most of us spend thinking about Jeremy Renner.

Actors are not the characters they play. We know this. But some are happy to court the public's association them with the most popular of their fictional personas. Chris Evans, the actor behind the first Captain America, happily parted from Marvel while continuing to embrace the hero's nice guy reputation. It's good for his brand.

Renner approaches the whole hero business with a resounding "meh," which is his prerogative. Along the way he's been dogged by ugly allegations surrounding a custody battle with his ex-wife Sonni Pacheco, which he's either refuted or refused to comment upon, and still doesn't leave the most flattering impression.

Neither have we been trained to expect much from his solo efforts, like his very basic acid-washed jeans rock or his starring role as an organized crime "fixer" in the Paramount+ series "Mayor of Kingstown," a 2003-era brood fest that somehow time-traveled to 2021.

What does all this have to do with "Hawkeye"? Simple it explains why a show named for the least of the world's mightiest superheroes works best as an introduction to the wonderful Hailee Steinfeld and her character Kate Bishop, set up via this series to inherit Hawkeye's mantle.

That makes "Hawkeye" the latest in a trend of properties named for or associated with alpha males being reforged as a female fighter's story.In the same way that Netflix's "Master of the Universe" animated series was not, in fact, about He-Man and "Mad Max: Fury Road" stars Charlize Theron's post-apocalyptic Amazon Furiosa, "Hawkeye" introduces Steinfeld's heroine as a wealthy young woman with a vigilante's soul.

This wasn't Kate's plan, to be clear. Danger comes into her house in the present day, the same way it dropped out of the clouds in 2012 and decimated New York, where she witnesses some of the battle and Hawkeye's derring-do from the blown-out window of her family's luxury midtown apartment. She returns from her university's holiday break having destroyed a landmark while showing off her archery skills and discovers her mother Eleanor (Vera Farmiga) has become romantically involved with a snake-like jerk (Tony Dalton of "Better Call Saul," smartly here).

Kate can sense something's not right about the guy, confirmed when she tails him to a black market auction offering an array of contraband for the 1%. She gets no such hit off Clint, which she wouldn't since she's the latest in a line of women who make Hawkeye a better man.

This directly contradicts what much of the public knows or thinks it knows about Renner, a man who couldn't make it through presenting a Golden Globe without ogling and commenting upon his partner Jennifer Lopez's cleavage. Whether acting as a force lawful good or "taking out the trash" as an antihero, Clint Barton's charisma is increased by his proximity to one or both of the women in his life who could vouch for him, like his wife Laura (played by Linda Cardellini), or have, as best friend Natasha Romanoff (Scarlett Johansson) often did.

Kate continues this trend by informing Clint that he's her hero, something he views as more of a nuisance than a responsibility. Her Christmas wish is for him to help her become the superhero she's trained her whole life to be. His is to wrap up the inconvenient public resurrection of his shameful past in time to get home in time to carve the Christmas roast with his own daughter.

This erector set of a premise is made to charm, as if Marvel is asking both Renner and the public to lighten up a little by placing him in inside a Christmas-themed buddy action romp with the star of "Dickinson," a superb performer.

Want a daily wrap-up of all the news and commentary Salon has to offer? Subscribe to our morning newsletter, Crash Course.

Steinfeld deserves a better introduction than this piece of tinsel which, in its first two episodes, never transcends the rating of fine. Nevertheless, her presence and performance elevate a story into which Hawkeye has glaring downward in disappointment before eventually figuring out how to have fun again.

This scenario makes one wonder if Marvel'snoticed that when Florence Pugh's Yelena Belova received orders to assassinate Hawkeye in the "Black Widow" post-credits sequence, more than a few people were into the idea and may have been rooting for Yelena's success. (Pugh is confirmed to appear in "Hawkeye.")

To be fair, Renner and Hawkeye have their fans, otherwise he would not be toplining this show. His (likely Dockers-wearing, American pick-up driving, dog-loving) constituency still loves him for his excellent performance in "The Hurt Locker" and, remembering how well he and Taylor Sheridan worked together in 2017's "Wind River," are committed to seeing whether "Mayor of Kingstown" goes anywhere.

Next to that gloom "Hawkeye" is a sugar plum hit teasing us with the prospect that Kate can somehow help Clint shed his Grinch persona and help him to turn around what she calls his branding problem. "People want sincerity," she says while championing the cause of wearing one's heart on one's sleeve.

The man called Hawkeye may have to be reminded of that, but the audience already knows that to be true about Renner himself. He trades in an image of being rough, unvarnished and real, a guy who told Men's Health in a recent profile that he'd rather collect and restore decommissioned fire trucks than slap his name on a vanity tequila brand. "So f**k you, Ryan Reynolds or George Clooney or whoever," he tells his interviewer. "I'll come put out the fire on your agave farm."

Good one, as long as you forget Renner's role in the Great Jeremy Renner Vanity App Debacle of 2019. We very well might by the end of the six-episode run of "Hawkeye," which could shape up to be the most forgettable Marvel Cinematic Universe property since "Iron Man 3" and make Renner's Hawkeye fade into the curtains yet again. But he's an Avenger of a bygone era. As long as Renner doesn't dim Steinfeld's light we'll be fine to see him step back to let the next generation shine.

New episodes of "Hawkeye" premiere Wednesdays on Disney+.

Expert Reveals Key Information That Men Need to Know About Testosterone – KMJ Now

Posted on February 14, 2021 by Prof Baldwin

Studies have shown that men over the age of 65 may benefit from taking the hormone testosterone. According toDr. Mirkin.comstudies have shown that testosterone increases bone density, raises hemoglobin levels in men with anemia, and improves sexual function. Reviews were mixed on whether testosterone improved heart health, however.

According to a study published in JAMA, testosterone significantly increased plaque in the arteries that lead to the heart. However, another study found that using testosterone gel for threeyears reduced the rate of heart attacks in men by 25%.

Dr. David B. Samadhi, a board-certified urologist, a Newsmax contributor, the director of Mens Health and Urologic Oncology at St. Francis Hospital in Roselyn, New York, and the author ofThe Ultimate MANual: Dr. Samadhis Guide to Mens Health and Wellness, tells Newsmaxthat the hormone is quite often overused because of its macho man association.

Of course, testosterone is a necessary and potent chemical messenger that indeed directly influences many physiological processes in a mans body, Samadi explains. Testosterone influences mens sex drive, bone mass, fat distribution, and muscle mass and strength, among other things. What man doesnt want to look strong, muscular, and ready for sex at the drop of a hat?

But the expert warns that advertisers understand this and play upon this notion by touting unproven products.

I remember a 2014 Time magazine cover story titled, Manopause that featured aprovocative cover and delved into the clever marketing and tons of money spent into making men believe that more testosterone is their quick fix and best remedy for remaining youthful and virile.

Thats why on any given day of the year, you see or hear commercials hawking a testosterone supplement promising to bring back mens youthful vigor, says Samadi.

As a urologist and prostate cancer surgeon, my advice to men is stay away from any spa, TV ads or any nonmedical person selling supplements for low T, he says. Testing testosterone and getting an accurate measurement can be tricky since levels fluctuate during the day.Only a doctor should be checking a mans testosterone levels. Testosterone levels should be checked before 9:00 a.m. when levels are their highest. Also, two tests are necessary to check for accuracy.

Samadi says that testosterone deficiency may or may not have symptoms.

But I can tell you, men with low T are like a car thats run out of gas they may be depressed, lack energy, motivation, and self-confidence, have reduced muscle mass and increased fat mass, loss of body hair, hot flashes, fewer spontaneous erections or difficulty sustaining erections, and have little interest in sex, he adds.

For any man who does have low testosterone, the benefits of hormone replacement therapy usually outweigh the risk., advises the expert. When men are selected correctly for using this therapy, it can be very helpful. Testosterone therapy for these men can help maintain muscle mass, slow osteoporosis, boost energy and stamina, and bring back their love life. But, I stress, its critical these men must be under surveillance with their doctor. Testosterone levels must be checked regularly as one possible side effect of testosterone therapy is it could stimulate the growth of prostate cancer cells.

Men who think they have low T, should talk to their doctor, get tested, and if therapy is needed, follow-up with their doctor periodically to have testosterone levels checked making sure the therapy is not causing any health problems, says Samadhi.

Excerpt from:
Expert Reveals Key Information That Men Need to Know About Testosterone - KMJ Now

Men Infected With COVID-19 Have 3 Times Higher Risk of ED – KMJ Now

Posted on April 4, 2021 by Prof Baldwin

Doctors at the University of Rome found that 28% of men with an average age of 33 who had COVID-19 said they were experiencing erectile dysfunction.

According to the Daily Mail, only 9 of the 100 men surveyed who did not have COVID-19 reported problems with sexual function. The researchers said that ED likely occurs because of inflammation caused by the virus that narrows the blood vessels leading to the genitals. This obstructs the blood flow and hinders sexual response.

Another reason why men experience ED from COVID-19 is that the virus responsible for the illness binds to ACE2 receptors in the body. That is how it gains entry to our cells.

One of the devious ways the virus gets into the body is by its spike protein binding to a receptor found at quite high concentrations not only in the lungs but also in the reproductive organs,said Dr. Channa Jayasena, a consultant in reproductive endocrinology and andrology at Hammersmith and St. Marys hospitals in London. When COVID-19 binds to these receptors, they can no longer perform in their normal function.

According to the Daily Mail, ACE2 receptors are found abundantly in the testes. Dr. Jayasena suggested that COVID-19 may also lower the testosterone levels in men who become infected. While this can present sexual issues, lower T levels also affects overall general health.

Last November, researchers at the University of Miami Miller School of Medicine said that some men with COVID-19 sufferedfrom impaired spermatogenesis,or the production of sperm, which could result in lower sperm count, according to a study they published in the World Journal of Mens Health.

According to the New York Post, the scientists examined tissue from the autopsies of 6 men who died from the COVID-19 infection and found the virus was still in their testicles. Further research found that men who had COVID-19 and went on to test negative for the virus, still had the pathogen in their testes. According to the National Library of Medicine, Chinese researchers published a study that had similar findings.

So, the patient tested negative and was asymptomatic after having COVID-19 but still showed the presence of the virus inside the testes. The finding is novel, remarkable, and certainly worthy of further exploration,said Dr. Dr. Ranjith Ramasamy, a urologist and one of the authors of the study, according to the Post. Im fairly certain, just like mumps, about 20 to 30% of men are going to have some sort of affected fertility in their future.

Another study published in The Aging Male found that men with lower testosterone levels could be at higher risk of contracting COVID-19 and that the virus itself could cause lower T levels. Mike Kirby, a former professor at the University of Hertfordshire in the U.K., and the editor of The Aging Male, said that doctors should test the testosterone levels of their male patients with COVID-19 and supplement if needed.

Kirby said that low T levels are associated with increased cardiovascular risks, type 2 diabetes, muscular weakness and depression, loss of sexual desire and fertility, according to the Daily Mail.

Dr. Jayasena suggested that the lower sex hormone levels may be temporary.

If you had severe flu, then it might take at least another several weeks for your testes to start working properly,he said, according to the Daily Mail. A mans sperm count can drop to zero during flu and it can take three months to recover fully. So I think its reasonable to suggest a similarly severe illness such as COVID-19 would do at least that.

Original post:
Men Infected With COVID-19 Have 3 Times Higher Risk of ED - KMJ Now

Erectile Dysfunction: A Look at the Most Common Causes – Feed Leader

Posted on October 8, 2020 by Prof Baldwin

Erectile dysfunctions are more common than most men believe, and while they can always leave someone in an embarrassing position at an awkward time, the reasons can be benign as well. Unfortunately, not every case of unexpected ED is harmless or temporary. As we look through the common reasons behind erectile dysfunctions, it will uncover both relatively harmless, as well as a few potentially fatal conditions that can be responsible for impotence in men.

The primary action behind impotence can be identified as a lack of blood supply to the penis, which is universal in nature. The causes that can be responsible for the lack of sufficient blood supply are plenty, but the action is always the same, irrespective of the reason. This is directly related to conditions of the heart and the arteries, as it is the heart that pumps blood through arteries and sends them to the extremities via veins and blood vessels.

As a result, any heart condition or vascular condition that can constrict or slow down the flow of blood could at times be responsible for impotence. Common cardiac and arterial health issues that have been proven to cause erectile dysfunction are as follows:

As we age, we lose muscle mass and sexual potency, but the rate of loss is not equal or even similar in all men. Aside from genetics, there are also additional factors that contribute to lowered testosterone in men as young as 30. To know whether or not lowered testosterone levels are responsible for your ED, check the low T symptoms identified by Manual. If you can relate to the symptoms, then rest assured that low T is not just one of the most common causes of impotence, but it is also very treatable with appropriate steps and meds.

Consult with experts to know what sildenafil can do for you and how it should be administered to help you overcome your ED, alongside all the other associated symptoms. Testosterone is the prime male hormone, and in order for a mans body and mind to function in the way that it should, there needs to be a sufficient natural production of it. In case that cannot be achieved, external testosterone therapy might be essential for preventing impotence, hair fall, depression and several other similar symptoms.

Diabetes is a direct and acute cause for erectile dysfunction and that applies to men with both Type I and Type II diabetes. However, men suffering from Type II diabetes experience ED far more often than men with Type I diabetes. Potentially, the damage can be permanent for men with diabetes if they do not act in time to control the disease itself.

Unlike most of the other causes mentioned so far, diabetic men who did not or could not treat their condition from an early stage are likely to experience permanent nerve and blood vessel damage, leading to perpetual impotence. On the other hand, if their blood sugar is kept under control from an early stage with changes in lifestyle and medication, it is possible for men with diabetes to lead a healthy and sexually satisfying life. If you are experiencing frequent episodes of ED, it is probably a good idea to get checked for diabetes. The urgency of the situation will gain more severity in case the patient also has one or more diabetic parent/parents.

Depression is often defined as a purely psychological cause for erectile dysfunction, but it is medically incorrect to use the classification universally. Temporary depression from a genuine cause such as the death of a close family member is mostly psychological in nature. In most cases, men get over temporary and acute depression on their own, or perhaps just by talking about the cause with someone close, or even a professional. However, the same cannot be said about clinical depression, where the brain becomes incapable of producing sufficient levels of dopamine and serotonin.

Unfortunately for those suffering from clinical depression, antidepressants are often found to be directly responsible for causing impotence in men. Since this is a unique scenario where both the disease and the cure can individually and simultaneously cause erectile dysfunctions, its a very tricky situation to deal with. If clinical depression is indeed affecting you and you have been prescribed antidepressants for managing the chemical imbalance, countering the entire scenario would require a combined effort from you, your psychiatrist and your partner. The idea should be to find alternatives to SSRIs and use break periods to help lessen the pharmaceutical and psychophysical causes of impotence as best as possible.

There are two different types of stress, although they often fuel each other, making it difficult to separate one from the other. Physical stress is a result of strenuous physical activities and mental stress is a result of worry, mental trauma, anxiety, depression and the like. As mentioned, one can often be a reason for bringing about the other, but they need not always be mutually inclusive either. Both physical and mental stress is directly linked to erectile dysfunctions though.

If the body is worked to a point of extreme tiredness, it simply may not have enough physical and/or mental energy to power and hold an erection. On the other hand, mental stress creates a distraction for the brain in a negative manner, which keeps it from acting in the way that it should in presence of sexual stimuli. ED caused by physical stress can be easily recovered from with a proper diet and restful sleep, unless it has been going on for a significant while at a stretch.

When the body is being stressed continuously without the sufficient rest and nutrition it needs, that will lead to mental stress accumulation as well. When left unaddressed for a long enough period, the impotence from such cases can take a long time to heal, if at all possible. Mental stress has the same effect and it can disrupt sleep, which is absolutely crucial for the body to recover and be productive during sexual activities. In fact, both physical and mental stress can lead to low testosterone levels, which would then require professional help, as mentioned previously.

Only a doctor with the necessary expertise (endocrinologist or urologist) and experience can help patients uncover the real reason/reasons behind their ED episodes. Even if you believe that you are aware of the cause and it isnt anything to worry about too much, get yourself checked. On the other hand, if it happens only in very rare circumstances, chances are that you have nothing to worry about. Keep an eye on the frequency though, and consult a doctor immediately if the ED episodes seem to be increasing in their occurrence. Not only is that necessary to maintain healthy conjugal relationships, but medical investigations may also reveal one of the more serious causes that we already discussed.

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Erectile Dysfunction: A Look at the Most Common Causes - Feed Leader

Low T Therapy Market Size, Trends, Production, Demand and Profit Is Statistical Analyzed in 2021 Report: AbbVie, Endo International, Eli Lilly …

Posted on January 25, 2021 by Prof Baldwin

Low T Therapy Market Report recently published by Worldwide Market Reports company focuses mostly on required solutions to the users. The study includes analysis, forecast, and revenue from 2021 to 2026. The advancement rate is evaluated dependent on insightful examination that gives credible information on the worldwide market. Imperatives and advancement points are merged together after a significant comprehension of the improvement of this market.

There is Continuous growth in the Low T Therapy Market in the last five years and also continued for the forecasted period. Low T Therapy industry report analyses the outline of the global market with respect to major regions and segmented by types and applications. This report covers top manufacturers, product scope, market overview, market opportunities, market risk, market driving force, technological advancement, distributors, traders, dealers, research findings.

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The top players covered in Low T Therapy Market are: AbbVie, Endo International, Eli Lilly, Pfizer, Actavis (Allergan), Bayer, Novartis, Teva, Mylan, Upsher-Smith, Ferring Pharmaceuticals, Kyowa Kirin, Acerus Pharmaceuticals

The point-to-point elucidation of the markets assembling system, the usage of advancement, conclusions of the world market players, dealers and suppliers order, and the explicit business data and their improvement plans would help our customers for future courses of action and movement planned to make due in the Low T Therapy market.

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Points Covered of this Low T Therapy Market report are:

The international Low T Therapy market has been characterized by several primary factors, with each factor tends to play a crucial role in the boom of the market. The growth in the products has doubled with the smoother availability of the customer base that has been helping the company flourishing globally. On the other hand, the presence of a dynamic supply chain has helped the company to grow exponentially.

The analysis and forecast of the global market of Low T Therapy have no longer been, specifically, analyzed that are not only on a global foundation but additionally on a neighborhood foundation. When a better look taken at the areas, the market has concentrated, and the file interior the important makes a strong point of Europe, Middle East & Africa, Asia Pacific, Latin America, and North America. These areas have studied regarding the hooked-up traits and the diverse possibilities in addition to the outlook that allows inside the benefitting of the market ultimately.

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The Low T Therapy market report has been prepared after thorough market research being conducted. It has been prepared as per Porters Five Force Model. In terms of timeline, the market takes the period between 2021-2026 into account for assessment. Apart from this, a comprehensive SWOT analysis has been provided for swift business decision making.

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Low T Therapy Market Size, Trends, Production, Demand and Profit Is Statistical Analyzed in 2021 Report: AbbVie, Endo International, Eli Lilly ...

Indianapolis Low T Center & Men’s Clinic | Sleep Apnea …

Posted on September 28, 2020 by Prof Baldwin

Indianapolis is the capital city of the state of Indiana and the world-famous Indianapolis 500 car race. This thriving metropolitan area boasts more than 2 million residents and covers 368 square miles of territory. Along with car racing and a booming economy, for men in the area, the Indianapolis Low T Center is an innovative mens health clinic that offers testosterone replacement therapy (TRT) for those with hypogonadism and other hormonal imbalance issues. We work with men to find practical and effective solutions for symptoms related to low T levels and other health symptoms that might be tied to low testosterone levels. This mens clinics offers testing and treatment for allergies, diabetes, cholesterol issues and is a one-stop shop for mens annual physicals.

Men with low testosterone levels often experience a range of symptoms that include fatigue and lethargy, reduced physical desire and a limited ability to achieve an erection, redistribution of body fat and loss of muscle mass. Some men may notice diminished cognitive abilities as a result of low T levels. At the Indianapolis Low T Center, we diagnose and treat issues associated with low testosterone to help you feel your best.

If you frequently awaken during the night choking or gasping for breath, you may be suffering from a condition called sleep apnea. Loud snoring, headaches, fatigue and sleepiness during the day are often attributable to this medical condition, which may affect more than 22 million Americans. Indianapolis Low T Center offers health assessment services and testing for sleep apnea, which may include home sleep monitoring systems to determine the presence and severity of this condition. Our medical staff will work with you to design a treatment plan for your needs and your lifestyle.

Low T Sleep Center Details

If you need help with issues related to your health including having an annual physical, or with the management of certain conditions, including low T levels and sleep apnea, Low T Center of Indianapolis offers comprehensive help and treatment options for you. Schedule your health assessment online today with our team of men's healthcare providers. We are here to serve your needs now and in the future.

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Indianapolis Low T Center & Men's Clinic | Sleep Apnea ...

Whats Causing My Low Testosterone?

Posted on September 28, 2020 by Prof Baldwin

Low testosterone prevalence

Low testosterone (low T) affects 4 to 5 million men in the US.

Testosterone is an important hormone in the human body. But it starts to decrease each year after age 30. In some men this can be substantial. Between 19 and 39 percent of older men may have low levels of testosterone.

Older men with low T have increasingly sought testosterone replacement therapy (TRT) in recent years. TRT addresses symptoms such as low libido, poor muscle mass, and low energy.

Its not just older men that are affected by low T. Young men, even babies and children, can also have this problem.

Low levels of testosterone that are atypical of normal aging are due to other primary or secondary causes of hypogonadism. Hypogonadism in males happens when the testicles dont produce enough testosterone. Hypogonadism can start during fetal development, during puberty, or during adulthood.

If hypogonadism begins during fetal development, the primary result is impaired growth of external sex organs. Depending on when hypogonadism starts and the level of testosterone present during fetal development, a male child can develop:

Normal growth can be jeopardized if hypogonadism occurs during puberty. Problems occur with:

Later in life, insufficient testosterone can lead to other problems. Symptoms include:

Fatigue and mental fogginess are some commonly reported mental and emotional symptoms in men with low T.

9 Warning signs of low testosterone

The two basic types of hypogonadism are primary and secondary hypogonadism.

Underactive testes cause primary hypogonadism. Thats because they dont manufacture sufficient levels of testosterone for optimal growth and health. This underactivity can be caused by an inherited trait. It can also be acquired by accident or illness.

Inherited conditions include:

Types of testicle damage that can lead to primary hypogonadism include:

Secondary hypogonadism is caused by damage to the pituitary gland or hypothalamus. These parts of the brain control hormone production by the testes.

Inherited or disease conditions in this category include:

Acquired circumstances that can lead to secondary hypogonadism include:

You may be affected by primary, secondary, or a mixed hypogonadism. Mixed hypogonadism is more common with increased age. People undergoing glucocorticoid therapy can develop the condition. It also can affect people with sickle-cell disease, thalassemia, or alcoholism.

Learn more: 5 Natural testosterone boosters

If youre experiencing symptoms of low T, lifestyle changes may help to ease your symptoms.

A good first step is increasing activity levels and maintaining a healthy diet in order to reduce body fat. It can also be helpful to avoid glucocorticoid medications such as prednisone as well as opioid pain medications.

Diet right: 8 Testosterone boosting foods

If lifestyle changes dont work for you, you may need to begin testosterone replacement therapy (TRT) for treatment of low T. TRT can be very important for helping teenage males with hypogonadism experience normal masculine development. Sufficient testosterone levels help maintain health and well-being in adult males.

TRT has side effects, however, including:

A carefully formulated TRT treatment plan should avoid many of these undesirable side effects. Talk with your doctor to evaluate your options.

Options for increasing your testosterone

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Whats Causing My Low Testosterone?

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