OnLine First

Yeah, I got that. But I still want to know and doing it here attracts more attention from others like you, which raises the likelihood of a response. And I ain't looking for no fights. I'm paid as a scientist and so is Dr. Scally., So relax, he and I both know what that entails. The powers that be can move or delete my comments as they see fit, not a big deal.

Any way you can dig up that conversation?
 
I never said it was a big deal:).. YOU, However placed OWNERSHIP on scally with the CONTEXT or your GRAMMAR. Don't play coy.

Yeah, I got that. But I still want to know and doing it here attracts more attention from others like you, which raises the likelihood of a response. And I ain't looking for no fights. I'm paid as a scientist and so is Dr. Scally., So relax, he and I both know what that entails. The powers that be can move or delete my comments as they see fit, not a big deal.
 
Any way you can dig up that conversation?

Come on, I frikkin' remembered it. Least you can do is try to dig it up yourself. ... I'll find it if you can't .

I never said it was a big deal:).. YOU, However placed OWNERSHIP on scally with the CONTEXT or your GRAMMAR. Don't play coy.

Not playing coy, have no idea what you're talking about.
 
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I recall you arguing with HAN not so long ago that this was bullshit. Have you relaxed that position based on this new evidence?

I regret interfering with this thread which I monitor daily. That should've been a PM instead of a public post. I apologize and hope Dr. Scally continues this valuable activity.
 
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It should be noted that AAS dependence is NOT recognized by the ICD or DSM. In fact, this is stated by a very few of which Pope et al. are the main promoters. This article needs to be read with a great deal of skepticism.


Brennan BP, Kanayama G, Hudson JI, Pope JHG. Human Growth Hormone Abuse in Male Weightlifters. The American Journal on Addictions 2011;20(1):9-13. Human Growth Hormone Abuse in Male Weightlifters - Brennan - 2010 - The American Journal on Addictions - Wiley Online Library

In a study of performance-enhancing substance use among 231 experienced young male weightlifters, we found that 27 (12%) reported illicit use of human growth hormone (HGH) or its bioactive derivative, insulin-like growth factor-1. All of these 27 men also reported use of anabolic-androgenic steroids (AAS) and 22 (81%) met criteria for current or past AAS dependence. Fifteen (56%) also reported current or past dependence on opioids, cocaine, and/or ecstasy. These findings suggest that among young male weightlifters, illicit HGH use has become a common form of substance abuse, frequently associated with both AAS dependence and classical substance dependence.
 
It should be noted that AAS dependence is NOT recognized by the ICD or DSM. In fact, this is stated by a very few of which Pope et al. are the main promoters. This article needs to be read with a great deal of skepticism.

If the diagnosis doesn't exist, why not make up your definitions with a modified version of DSM criteria?!
 
This drug has had some serious setbacks for FDA approval. Many of these are found at the company website, Arena Pharmaceuticals - Arena Pharmaceuticals . I do NOT see approval. [Email me for the full-text article.]


Martin CK, Redman LM, Zhang J, et al. Lorcaserin, A 5-HT2C Receptor Agonist, Reduces Body Weight by Decreasing Energy Intake without Influencing Energy Expenditure. J Clin Endocrinol Metab. http://jcem.endojournals.org/cgi/content/abstract/jc.2010-1848v1

Context: Lorcaserin, a selective 5-hydroxytryptamine (5-HT)2C receptor agonist, reduces body weight. It is unclear whether weight loss is due to reduced energy intake (EI) or also to enhanced energy expenditure (EE).

Objective: This study tested the effect of lorcaserin on EI and EE.

Design, Participants, and Intervention: In a double-blind, randomized, placebo-controlled trial, 57 (39 women) overweight and obese (body mass index, 27-45 kg/m(2)) adults were randomized to placebo (n = 28) or 10 mg twice daily lorcaserin (n = 29) for 56 d. Weight maintenance was imposed during d 1-7. Beginning on d 8, participants followed a diet and exercise plan targeting a 600 kcal/d deficit.

Outcomes: At baseline and after 7 and 56 d of treatment, we measured body weight, body composition (dual x-ray absorptiometry), blood pressure, heart rate, EI at lunch and dinner, subjective appetite ratings, and 24-h EE and 24-h-respiratory quotient (RQ), measured by indirect calorimetry in a respiratory chamber.

Results: After 7 d of weight maintenance, EI was significantly (P < 0.01) reduced with lorcaserin but not placebo (mean +/- SEM for lorcaserin, -286 +/- 86 kcal; placebo, -147 +/- 89 kcal). After 56 d, lorcaserin resulted in significantly larger reductions in body weight (lorcaserin, -3.8 +/- 0.4 kg; placebo, -2.2 +/- 0.5 kg; P < 0.01), EI (lorcaserin, -470 +/- 87 kcal; placebo, -205 +/- 91 kcal; P < .05), and appetite ratings than in placebo. Changes in 24-h EE and 24-h RQ did not differ between groups, even after 24-h EE was adjusted for body weight and composition. Compared with placebo, lorcaserin had no effect on systolic or diastolic blood pressure or heart rate after 56 d.

Conclusions: Lorcaserin reduces body weight through reduced EI, not altered EE or RQ.
 
[Email me for the full-text article.]

Vitamin D deficiency is currently considered an important public health problem being associated with musculoskeletal diseases, cardiovascular disease, cancer, and infectious and autoimmune diseases. The vitamin D receptor (VDR), as well as key enzymes for vitamin D metabolism, are widely expressed in human tissues and cells. Previous studies suggest that vitamin D deficiency may contribute to reduced fertility and hypogonadism. These results are of particular interest because both, vitamin D deficiency and hypogonadism are associated with skeletal diseases (e. g., osteoporosis or muscle weakness) as well as extra-skeletal disorders (e. g., cardiovascular disease or obesity). Recently, a study showed in 2,299 men referred for coronary angiography that 25-hydroxyvitamin D [25(OH)D] levels are significantly associated with testosterone levels and that both hormones reveal similar seasonal variations with a peak at the end of summer. Whether there exists a causal link between vitamin D and testosterone status is currently not known. A subgroup analysis of a previously published prospective, randomized vitamin D supplementation trial was performed in overweight subjects. Here, they present results on serum testosterone concentrations in the male participants of this study.


Pilz S, Frisch S, Koertke H, et al. Effect of Vitamin D Supplementation on Testosterone Levels in Men. Horm Metab Res. Effect of Vitamin D Supplementation on Testosteron... [Horm Metab Res. 2010] - PubMed result

The male reproductive tract has been identified as a target tissue for vitamin D, and previous data suggest an association of 25-hydroxyvitamin D [25(OH)D] with testosterone levels in men. We therefore aimed to evaluate whether vitamin D supplementation influences testosterone levels in men. Healthy overweight men undergoing a weight reduction program who participated in a randomized controlled trial were analyzed for testosterone levels. The entire study included 200 nondiabetic subjects, of whom 165 participants (54 men) completed the trial. Participants received either 83 mug (3,332 IU) vitamin D daily for 1 year (n=31) or placebo (n=23). Initial 25(OH)D concentrations were in the deficiency range (<50 nmol/l) and testosterone values were at the lower end of the reference range (9.09-55.28 nmol/l for males aged 20-49 years) in both groups. Mean circulating 25(OH)D concentrations increased significantly by 53.5 nmol/l in the vitamin D group, but remained almost constant in the placebo group. Compared to baseline values, a significant increase in total testosterone levels (from 10.7+/-3.9 nmol/l to 13.4+/-4.7 nmol/l; p<0.001), bioactive testosterone (from 5.21+/-1.87 nmol/l to 6.25+/-2.01 nmol/l; p=0.001), and free testosterone levels (from 0.222+/-0.080 nmol/l to 0.267+/-0.087 nmol/l; p=0.001) were observed in the vitamin D supplemented group. By contrast, there was no significant change in any testosterone measure in the placebo group. Our results suggest that vitamin D supplementation might increase testosterone levels. Further randomized controlled trials are warranted to confirm this hypothesis.


I recall you arguing with HAN not so long ago that this was bullshit. Have you relaxed that position based on this new evidence?

Yeah, I got that. But I still want to know and doing it here attracts more attention from others like you, which raises the likelihood of a response. And I ain't looking for no fights. I'm paid as a scientist and so is Dr. Scally., So relax, he and I both know what that entails. The powers that be can move or delete my comments as they see fit, not a big deal.

Any way you can dig up that conversation?



GirlyMan is spot on for my outspoken criticism of HAN's claim for the effect of Vitamin D on T levels. While I have softened somewhat for my Vitamin D claims, I would NOT get too happy or giddy. [Note: I AM posting the Vitamin D studies so I am NOT afraid of being shown wrong. I do think Vitamin D deficiency is an under appreciated concern. See: https://thinksteroids.com/community/threads/134294407 ] I still disbelieve the HAN claim that the T level ~doubled with Vitamin D. Moreover, as is typical for ALL of HAN's posts/claims they are absent details. I still have alot of skepticism that correction of Vitamin D levels will fix hypogonadal T levels. At most, the evidence points out some limited or minor effect on T levels.

In the study cited, there are a number of MAJOR problems. First, this is admittedly a subset analysis.
A subgroup analysis of a previously published prospective, randomized vitamin D supplementation trial was performed in overweight subjects.
This is tantamount to stating we do not believe the results are actually significant so we are going to couch our conclusions in that light.
Our results suggest that vitamin D supplementation might increase testosterone levels.

In other words, please do NOT cite us as evidence that vitamin D treatment WILL effect T levels, but, instead, they MIGHT (or MIGHT NOT). In research, this is called a hedge against embarrassment for later independent studies. What would have these authors being so careful? [This is why I offer the full-text article.]

Table 1 contains the SUBSET data. In the Table, which uses faulty stat analysis, they fail to include a comparison of end values for the placebo group. In this case for Vitamin D & T values. There is clearly an effect of Vitamin D treatment on Vit. D levels. But, if you look at the T levels, they are not significantly different!!!

P value and statistical significance: The two-tailed P value equals 0.6169. By conventional criteria, this difference is considered to be not statistically significant. Confidence interval: The mean of Group One minus Group Two equals -0.700. 95% confidence interval of this difference: From -3.491 to 2.091. GraphPad QuickCalcs: t test calculator

What caused the T level rise in the Vitamin D treatment group. It MIGHT NOT be Vitamin D at all. Further, the effect, if believed, is small, <100 ng/dL. This, for me, points to a downstream effect on T synthesis. Possibly something along the line of cholesterol utilization.
 
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[This is why I offer the full-text article.]

Table 1 contains the SUBSET data. In the Table, which uses faulty stat analysis, they fail to include a comparison of end values for the placebo group. In this case for Vitamin D & T values. There is clearly an effect of Vitamin D treatment on Vit. D levels. But, if you look at the T levels, they are not significantly different!!!
]

Internet experts ONLY read the abstracts. That's rule number one of being a guru on the forums. In the age of twitter, its mandatory that we learn about science in 140 characters or less whenever possible. :rolleyes:

(yes, sarcasm :D )
 
In the study cited, there are a number of MAJOR problems. First, this is admittedly a subset analysis.
....
P value and statistical significance: The two-tailed P value equals 0.6169. By conventional criteria, this difference is considered to be not statistically significant.
wtf? How does shit like that get by the reviewers? Is "Hormone and Metabolic Research"
a respected, peer-reviewed journal or some sort of SPIE conference where anyone can get published?

All right, now I want to read the full paper to see how they statistically justify their subsampling methodology.

Thanks!
 
[Email me for the full-text article.]

There are both chronic risk factors for the development of heart disease as well as acute risk factors that may trigger an acute coronary event. Chronic risk factors associated with the development of atherosclerosis include dyslipidemia, diabetes, smoking, hypertension, metabolic syndrome, lack of physical exertion, and obesity. Acute risk factors usually involve some form of stress—physical, emotional, or both—that increases the sympathetic nervous system and releases catecholamines. The subsequent increase in heart rate, blood pressure, and ventricular contractility increases oxygen demand and may change the shear stress of blood against an atherosclerotic plaque, contributing to plaque fracture. Stimulation of alpha receptors in the vasculature may actually increase vascular resistance, increasing afterload and constricting coronary vessels (including frank coronary vasospasm), thus increasing oxygen demand at the same time as limiting oxygen supply to the heart. Catecholamine excess can also increase platelet aggregability as well as contribute to arrhythmias.

Situations in which certain stressors can trigger cardiovascular events, thought to occur through these mechanisms, include emotional stress, heavy physical exertion, moderate physical exertion, lack of sleep, overeating, and a host of other stressful situations. Sports fans may demonstrate an increase in cardiac events during emotionally charged soccer games, as demonstrated from analyses during World Cup soccer. Previously, it was observed that total and cardiac mortality rates in Los Angeles County were increased during the 1980 Super Bowl loss; in contrast, there was an overall reduction in total mortality associated with the 1984 Super Bowl win. To what extent age, sex, or race played a role in these deaths is unknown.


This study analyzed data on men, women, those aged <65 years, those aged ?65 years, those of white/Hispanic ethnicity, and those of nonwhite/non-Hispanic ethnicity, considering the effect of both a Super Bowl win and a Super Bowl loss on total as well as cardiac mortality in Los Angeles County. In conclusion, a SBL triggered increased deaths in both men and women and especially in older patients, whereas a SBW reduced death more in those aged ?65 years and in women.


Kloner RA, McDonald SA, Leeka J, Poole WK. Role of Age, Sex, and Race on Cardiac and Total Mortality Associated With Super Bowl Wins and Losses. Clinical Cardiology. Role of Age, Sex, and Race on Cardiac and Total Mortality Associated With Super Bowl Wins and Losses - Kloner - 2011 - Clinical Cardiology - Wiley Online Library

Background - Total and cardiac mortality rates in Los Angeles County, Califorina, increased after the 1980 Super Bowl loss (SBL), but there was an overall reduction in total mortality after the 1984 Super Bowl win (SBW). Hypothesis We hypothesized that age, sex, and race may have played a role in the Super Bowl related differences in death rates.

Methods - We compared mortality rates for SB-related days with non-SB control days assessing differences in demographics. We ran regression models predicting daily death rates per 100,000 including SB variable versus non-SB control days for age, sex, race, and interactions for these covariates.

Results - After the SBL, daily death rates increased for both males and females. People aged ?65 years had a larger absolute increase in all cause mortality during the SBL days compared with those aged <65 years, with significant interaction between age and SBL-variable for all-cause and cardiac-related mortality. Whites and Hispanics had increased death rates on SBL days. There were trends suggesting less death in older patients and females associated with the SBW.

Conclusion - A SBL triggered increased deaths in both men and women and especially in older patients, whereas a SBW reduced death more in those aged ?65 years and in women.
 
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[Email me for the full-text article.]

Vitamin D receptors and metabolizing enzymes have been found in several human brain areas, including the prefrontal cortex, hippocampus, cingulate gyrus, thalamus, hypothalamus, and substantia nigra where autocrine and paracrine activity has been suggested. Vitamin D has been implicated in the regulation of behavior, stimulation of neurotrophin release, and protection of the brain by buffering antioxidant and antiinflammatory defenses. Hypovitaminosis D is prevalent in psychiatric patients and several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, and schizophrenia. In regions that have historically suffered from hypovitaminosis D, an impact on personality dimensions, lower mean levels of sociosexuality, extraversion, and openness have been reported.

This study explored whether the multifunctional 1,25 (OH)2D3 might be associated with basic personality traits finding Vitamin D might influence personality traits, promoting extrovert and open behavior.



Ubbenhorst A, Striebich S, Lang F, Lang UE. Exploring the relationship between vitamin D and basic personality traits. Psychopharmacology (Berl). Exploring the relationship between vitamin D and b... [Psychopharmacology (Berl). 2011] - PubMed result

RATIONALE: Several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia. A recent study confirms neophobic responses in vitamin D receptor mutant mice. We explored whether the plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)(2)D(3)), the active form of vitamin D, are correlated with basic personality traits.

METHODS: A total of 206 healthy unrelated volunteers (108 male, 98 female, age 31 +/- 13 years) completed the German version of the NEO Five-Factor Inventory (NEO-FFI), which allows reliable and valid assessment of personality along the dimensions neuroticism, extraversion, openness to new experiences, agreeableness and conscientiousness.

RESULTS: We found a significant correlation between 1,25(OH)(2)D(3) concentration and the factor extraversion (n = 206, r = 0.202, p = 0.004) and the factor openness (n = 206, r = 0.148, p = 0.034).

CONCLUSION: The possible mechanisms by which 1,25(OH)(2)D(3) acts on the brain might include Ca(2+) signaling, buffering antioxidant, and anti-inflammatory defenses against vascular injury, stimulating neurotrophins and improving metabolic and cardiovascular function. In conclusion, we suggest that 1,25(OH)(2)D(3) might influence personality traits, promoting extrovert and open behavior.
 
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[Email me for the full-text article.]

Compared to the published scientific literature on low sexual desire in women, very little has been written about the parallel experience in men. Hypoactive desire in men has most frequently been considered within the literature on hypogonadism, where reduced sexual interest is a well documented symptom of low androgen levels and testosterone supplementation among hypogonadal men with low desire is an effective treatment. There may be five overlapping categories of etiology for low desire: (i) a pattern of no pathological significance; (ii) a symptom of another, more fundamental psychiatric disorder; (iii) a symptom of relationship alienation; (iv) a symptom of a physical abnormality; and (v) a symptom of hypoactive sexual desire disorder (HSDD). Comparisons have been made between sexual desire in women vs. men and, contrary to earlier theories about gender differences, more recent theorists purport that there are likely more within-gender than between-gender differences; if correct, this has implications for the diagnostic classification of desire disorders.

With the upcoming revision of the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5), due to be published in 2013, a reevaluation of whether or not problems related to low sexual desire in men are expressed in the same manner as in women is needed. The goal of this article is to review the available literature on the prevalence, description of, and associated features of low sexual desire in men. The article will conclude with the presentation of three possible options for how HSDD in men might be considered in DSM-5. Given that a similar review on hypoactive sexual desire in women has already been published, this article will make direct comparisons to the proposed new criteria outlined in this earlier review. It is important to note at the outset, however, that any recommendation for change in the diagnostic criteria for men will be based on relatively little data, compared to women where the evidence for change was stronger because more research has been carried out on women’s sexual desire. Ultimately, the adoption of any significant change in diagnostic criteria should be based on the best available data infused with sound clinical judgment. Moreover, it is highly advisable, if a more radical change is adopted for DSM-5, that the change is based on the positive results of field testing across a variety of independent sites.


Brotto LA. The DSM diagnostic criteria for Hypoactive Sexual Desire Disorder in men. J Sex Med 2010;7(6):2015-30. The DSM diagnostic criteria for Hypoactive Sexual ... [J Sex Med. 2010] - PubMed result

INTRODUCTION: Hypoactive Sexual Desire Disorder (HSDD) is one of two sexual desire disorders in the Diagnostic and Statistical Manual of Mental Disorders (DSM) and is defined by two criteria: A-"persistently or recurrently deficient (or absent) sexual fantasies and desire for sexual activity" and B-"marked distress or interpersonal difficulty." AIM: This paper reviews the prevalence and correlates of low desire in men and qualitative and quantitative research on the experience of sexual desire in men and women.

METHODS: A literature search of Medline, PudMed, and PsychInfo was used to identify any publication on low desire in men.

MAIN OUTCOME MEASURE: The strength of empirical findings was used as a basis for making proposed revisions to the diagnostic criteria for HSDD in men.

RESULTS: The dilemma of whether desire and arousal can be reliably differentiated in men is discussed, and parallels to the literature in women are drawn. Finally, I consider three options for the diagnosis of low desire in men for DSM-5. Option 1 proposes that the DSM-IV-TR name and criteria are preserved for men in DSM-5. Option 2 proposes that the recently proposed criteria for Sexual Interest/Arousal Disorder in women are also adopted for men, which would result in one gender-neutral category. Option 3 proposes that the criteria for Sexual Interest/Arousal Disorder also be applied to men, with a minor modification to one criterion (i.e., that absent or reduced genital and/or nongenital physical changes not be included as a criterion); this diagnosis would then be applied only to men.

CONCLUSIONS: The evidence supporting each of these proposals is presented and critiqued. It is concluded that the proposal for DSM-5 should be made on the basis of field testing of new criteria.
 
[Email me for the full-text article.]

Insomnia is defined by difficulty falling asleep, difficulty staying asleep, nonrestorative sleep, and waking symptoms such as fatigue, impaired concentration, and mood disturbance. The prevalence of insomnia is approximately 5% to 20% in the general adult population and 20% to 30% in primary care medical settings. Insomnia is commonly comorbid with physical and mental disorders and chronic, persisting for a year or longer in 74% of individuals. The health and functional consequences of insomnia include reduced quality of life, increased health care utilization and costs, disability, and risk for psychiatric disorders and cardiovascular disease. Insomnia is especially relevant for older adults, given its high prevalence (estimated at 15%-35%), persistence, and association with falls and hip fractures. Older adults are prescribed hypnotic agents disproportionately frequently and for disproportionately long-term use and are more likely than other populations to experience adverse drug effects.

Pharmacologic and behavioral treatments for chronic insomnia have approximately equivalent efficacy. Each has specific merits and drawbacks. Hypnotic agents approved by the US Food and Drug Administration, including benzodiazepine receptor agonist (BZRA) drugs, are widely available, easy to use, and have rapid and sustained efficacy. However, BZRA safety concerns include dependence and abuse, cognitive impairment, and increased risk of falls and hip fractures, particularly in older adults. Behavioral and psychological techniques include sleep education, restriction of time in bed, stimulus control (strengthening associations between bed and sleep), and addressing anxiety-provoking beliefs about sleep. These treatments, particularly multicomponent cognitive behavioral therapy for insomnia (CBTI), are often preferred by patients and have consistent short-term and long-term efficacy with few apparent adverse effects. However, widespread use of CBTI is limited by the number of specialty-trained clinicians and by the duration, intensity, and initial cost of 6 to 8 individual treatment sessions. Moreover, most efficacy trials of pharmacologic and behavioral treatments have studied patients with primary insomnia and excluded the larger group of patients with substantial medical and psychiatric comorbidities, which includes many older adults.

The present study was conducted to test a behavioral treatment of insomnia that offers potential for widespread use. For a behavioral treatment to be relevant in general medical settings, it must be brief, acceptable to patients, deliverable by nurses or other allied health professionals, and efficacious over a short time interval in patients with typical comorbidities. The specific aim of this study was to test the short-term efficacy and 6-month durability of brief behavioral treatment for insomnia (BBTI) vs an information control (IC) intervention among older adults with insomnia.


Buysse DJ, Germain A, Moul DE, et al. Efficacy of Brief Behavioral Treatment for Chronic Insomnia in Older Adults. Arch Intern Med:archinternmed.2010.535. http://archinte.ama-assn.org/cgi/content/abstract/archinternmed.2010.535v1

Background Chronic insomnia is a common health problem with substantial consequences in older adults. Cognitive behavioral treatments are efficacious but not widely available. The aim of this study was to test the efficacy of brief behavioral treatment for insomnia (BBTI) vs an information control (IC) condition.

Methods A total of 79 older adults (mean age, 71.7 years; 54 women [70%]) with chronic insomnia and common comorbidities were recruited from the community and 1 primary care clinic. Participants were randomly assigned to either BBTI, consisting of individualized behavioral instructions delivered in 2 intervention sessions and 2 telephone calls, or IC, consisting of printed educational material. Both interventions were delivered by a nurse clinician. The primary outcome was categorically defined treatment response at 4 weeks, based on sleep questionnaires and diaries. Secondary outcomes included self-report symptom and health measures, sleep diaries, actigraphy, and polysomnography.

Results Categorically defined response (67% [n = 26] vs 25% [n = 10]; {chi}2 = 13.8) (P < .001) and the proportion of participants without insomnia (55% [n = 21] vs 13% [n = 5]; {chi}2 = 15.5) (P < .001) were significantly higher for BBTI than for IC. The number needed to treat was 2.4 for each outcome. No differential effects were found for subgroups according to hypnotic or antidepressant use, sleep apnea, or recruitment source. The BBTI produced significantly better outcomes in self-reported sleep and health (group x time interaction, F5,73 = 5.99, P < .001), sleep diary (F8,70 = 4.32, P < .001), and actigraphy (F4,74 = 17.72, P < .001), but not polysomnography. Improvements were maintained at 6months.

Conclusion We found that BBTI is a simple, efficacious, and durable intervention for chronic insomnia in older adults that has potential for dissemination across medical settings.

Trial Registration clinicaltrials.gov Identifier: NCT00177203
 
[IMO, this is nowhere near a possible drug for male contraception. The very severe HPTA suppression after stopping is sure to weigh heavily on its use. Also, there is the paradoxical effect with the higher dose!]

Attardi BJ, Engbring J, Gropp D, Hild SA. Development of Dimethandrolone 17{beta}-Undecanoate (DMAU) as an Oral Male Hormonal Contraceptive: Induction of Infertility and Recovery of Fertility in Adult Male Rabbits. J Androl. Development of Dimethandrolone 17{beta}-Undecanoate (DMAU) as an Oral Male Hormonal Contraceptive: Induction of Infertility and Recovery of Fertility in Adult Male Rabbits -- Attardi et al., 10.2164/jandrol.110.011817 -- Journal of Andrology

DMAU (7alpha,11beta-dimethyl-19-nortestosterone 17beta-undecanoate) is a potent orally active androgen with progestational activity which is in development for therapeutic uses in men. We hypothesized that due to its dual activity, DMAU might have potential as a single-agent oral hormonal contraceptive.

To test this possibility, adult male rabbits (5/group) of proven fertility were treated orally with vehicle or DMAU at 1.0, 2.5, 5.0, or 10.0 mg/kg/day for 12 or 13 weeks. Semen and blood samples were collected every other week through week 30. Sperm were decreased (P <0.05) in semen samples from DMAU-treated rabbits at 2.5 and 5.0 mg/kg/day at weeks 12, 14, 16, 18, and 20 compared to week 0 (prior to treatment). The percentage of forward progressive motile sperm in those rabbits which still had measurable sperm was also reduced by DMAU treatment at 2.5 mg/kg/day at weeks 14, 16, 18, and 20 and at 5.0 mg/kg/day at week 18 (P <0.05). At 1.0 mg/kg/day only one rabbit had reduced sperm numbers and motility. A mating trial was performed at week 15. The number of bred males which were fertile was 4 of 4 (vehicle-treated group) and 4 of 5, 0 of 4, and 2 of 5 in the 1.0, 2.5, and 5.0 mg/kg/day DMAU treatment groups. By week 22, sperm numbers and forward progressive motility increased, and they returned to pretreatment levels in all DMAU-treated rabbits by week 30. All bred males were fertile at week 31. Serum levels of testosterone, FSH, and LH were significantly suppressed in DMAU (1.0, 2.5, or 5.0 mg/kg/day)-treated rabbits during the 12-week dosing interval, but were comparable to pretreatment levels after cessation of dosing.

These data indicate that DMAU suppressed the hypothalamic-pituitary-gonadal axis, resulting in severe oligospermia in the majority of rabbits in the 2.5 and 5.0 mg/kg/day dosing groups. Infertility was observed when sperm numbers decreased to about 10% of pretreatment levels. In rabbits dosed with DMAU at 10.0 mg/kg/day, no effect on sperm numbers or motility was observed by week 12. Dosing continued for another week, and the rabbits underwent a gross necropsy on week 13 with removal of testes and epididymides for histology and preparation of testicular cytosol. Serum testosterone, FSH, and LH levels were considerably suppressed in these rabbits as in the lower dose groups. The lack of oligospermia in the 10.0 mg/kg group as well as in the 2 fertile males in the 5.0 mg/kg group may have been due to high intratesticular levels of DMA (7alpha,11beta-dimethyl-19-nortestosterone), the active metabolite of DMAU. Hence, as observed previously for testosterone, DMAU has a biphasic effect on spermatogenesis. Collectively, these data indicate that DMAU has the potential to be an orally active single-agent male hormonal contraceptive at an appropriate dose level and should be tested for contraceptive efficacy in nonhuman primates.
DMAU_.gif
 
Attardi BJ, Marck BT, Matsumoto AM, Koduri S, Hild SA. Long-Term Effects of Dimethandrolone 17{beta}-Undecanoate and 11{beta}-Methyl-19-Nortestosterone 17{beta}-Dodecylcarbonate on Body Composition, Bone Mineral Density, Serum Gonadotropins, and Androgenic/Anabolic Activity in Castrated Male Rats. J Androl 2011;32(2):183-92. Long-Term Effects of Dimethandrolone 17{beta}-Undecanoate (DMAU) and 11{beta}-Methyl-19-Nortestosterone 17{beta}-Dodecylcarbonate (11{beta}-MNTDC) on Body Composition, Bone Mineral Density, Serum Gonadotropins, and Androgenic/Anabolic Activity in Cas

The potent androgens dimethandrolone 17beta-undecanoate (DMAU) and 11beta-methyl-19-nortestosterone 17beta-dodecylcarbonate (11beta-MNTDC) are in development for androgen replacement therapy and hormonal contraception in men. They can be delivered either orally or as long-acting injectables. In the current study, their long-term effects on body composition (percentage lean and fat mass); bone mineral density (BMD); serum gonadotropin levels; and weights of the prostate, seminal vesicles, and levator ani muscle were assessed. Four-week-old male rats were sham-operated (intact) or castrated (Cx) and treated subcutaneously for 16 weeks postsurgery with vehicle (Cx, intact), DMAU, or 11beta-MNTDC every 4 weeks; testosterone enanthate (TE) every 2 weeks; or a testosterone (T) implant. There were significant differences in body weights over time with a general trend of intact = Cx + T = Cx + TE > Cx + 11beta-MNTDC > Cx > Cx + DMAU. At week 18, rats were evaluated by dual-energy x-ray absorptiometry using the whole-body function of the Hologic software. The percentage lean body mass and BMD were lower (P < .05) in Cx rats than intact rats but equivalent in all groups of androgen-treated Cx rats and intact rats (P > .05). The highest percentage body fat was observed in Cx rats. Only DMAU- and 11beta-MNTDC-treated rats had lower percentage body fat compared with Cx rats (P < .05). Prostate, seminal vesicles, and levator ani muscle weights, corrected for final body weight, were decreased (P < .05) in Cx compared with intact rats and increased to varying extents in androgen-treated Cx rats compared with Cx rats (P < .05). The most marked increases were observed in the DMAU-treated rats in which prostate and seminal vesicle weights/kg body weight were 2.4 to 2.7 times those of intact rats, and levator ani muscle weights were increased approximately 1.5-fold. Blood was collected from the tail vein at weeks 4, 8, 12, and 16 for measurement of serum levels of androgens and at necropsy at week 18 for measurement of serum gonadotropins. Serum levels of luteinizing hormone and follicle-stimulating hormone were greatly elevated in Cx rats at week 18 and suppressed to levels comparable to those in intact rats by DMAU, 11beta-MNTDC, and T implants (P > .05). Collectively, our data indicate that androgen replacement with DMAU or 11beta-MNTDC in Cx rats resulted in favorable changes in body composition and maintenance of BMD comparable to those of T.
 
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