Podcasts about leydig

DISCLAMER >>>>>>    The Ditch Lab Coat podcast serves solely for general informational purposes and does not serve as a substitute for professional medical services such as medicine or nursing. It does not establish a doctor/patient relationship, and the use of information from the podcast or linked materials is at the user's own risk. The content does not aim to replace professional medical advice, diagnosis, or treatment, and users should promptly seek guidance from healthcare professionals for any medical conditions.   >>>>>> The expressed opinions belong solely to the hosts and guests, and they do not necessarily reflect the views or opinions of the Hospitals, Clinics, Universities, or any other organization associated with the host or guests.       Disclosures: Ditch The Lab Coat podcast is produced by (Podkind.co) and is independent of Dr. Bonta's teaching and research roles at McMaster University, Temerty Faculty of Medicine and Queens University. Welcome to another episode of "Ditch the Lab Coat," the podcast where we delve into science-based skepticism and medical insights. I'm your host, Dr. Mark Bonta, and today's episode is an eye-opener for anyone curious about men's health, specifically testosterone. I'm joined by Dr. Adam Millar, a leading expert who will help us navigate the complexities and common misconceptions surrounding this vital hormone.We'll discuss the optimal timing and conditions for measuring testosterone levels, the overprescription concerns, and the often overlooked role of the pituitary gland in testosterone production. We'll also touch on hypogonadism and its impact on testosterone and sperm production. Our conversation will differentiate between evidence-based medical advice and the often misleading claims from social media influencers.Dr. Millar will share insights from high-quality studies, including the pivotal Traverse trial, and highlight the importance of informed decision-making when it comes to testosterone therapy. We'll explore natural ways to boost testosterone and the potential risks of unwarranted treatments.Whether you're considering testosterone therapy or just want to understand more about what drives these discussions, this episode is packed with valuable information. So, sit back and get ready to ditch the lab coat for some straightforward, evidence-based talk on testosterone. Don't forget to check out our blog at ditchthelabcoat.com for more resources and share this episode to spread the knowledge!05:11 - Growing interest and increasing prescriptions for testosterone worldwide.08:31 - Non-uniform hypogonadism diagnosis complicates treatment decisions.12:30 - Symptoms alone are not reliable indicators of low testosterone.15:23 - Testosterone production occurs in Leydig cells, stimulated by LH.17:26 - Semen analysis helps assess sperm production and fertility.21:40 - Testosterone boosts energy and strength but can impair fertility.24:39 - Potential harms of testosterone include reproductive and cardiovascular issues.28:17 - Discussion on testosterone's necessity; symptoms are often nonspecific.31:53 - Is testosterone's effect truly objective or just placebo?35:08 - Exploring the role of testosterone in men's health and aging.39:35 - Testosterone gel is not linked to increased heart issues.41:41 - Randomized studies suggest testosterone may not cause harm.47:19 - Valuable conversation emphasizing informed health guidance.50:19 - Empowering the audience to research and make informed decisions.51:33 - Closing discussion on testosterone; visit ditchthelabcoat.com.

Dr. Geo Espinosa is a renowned Naturopathic and Functional Medicine doctor specializing in urology and men's health. He has over two decades of experience and has provided care to thousands of men, addressing various urological and male health issues, from sexual dysfunction and low testosterone to different prostate conditions, including cancer. Leveraging natural therapeutics and integrative medicine based on rigorous clinical and scientific research, he and his team strive to offer the most up-to-date information and treatments. As a faculty member at the NYU Langone Department of Urology, Dr. Espinosa collaborates with some of the world's leading urologists. Dr. Geo is the Chief Medical Officer (CMO) and formulator at the male-focused nutraceutical company XY Wellness, LLC and its sister company Mr. Happy. He is the co-founder and producer of the popular male health website, DrGeo.com, and the popular urological and male-focused podcast, The Dr. Geo Podcast. As an avid researcher and writer, Dr. Geo has authored numerous scientific papers and books, including co-editing the Integrative Sexual Health book, and author of the best-selling prostate cancer book: Thrive, Don't Only Survive. Together Dr. Geo and I address some of the most commonly asked questions regarding men's health, from testosterone levels to prostate cancer prevention and the impact and potentially negative effects of testosterone replacement therapy on fertility and sperm production. Dr. Geo highlights ways to boost testosterone naturally, including nutraceuticals and lifestyle choices, and underscores the importance of recent findings from research addressing high levels of testosterone replacement therapy. He offers baseline screening advice for practitioners who are not specialized in men's health, insights into the key differences between prostatitis and benign prostatic hyperplasia (BPH), and shares his approach to treating nocturia, or excessive nighttime urination. This conversation is filled with clinical pearls and insights into the world of prostate health.   I'm your host, Evelyne Lambrecht, thank you for designing a well world with us.   Episode Resources: Dr. Geo Espinosa - https://drgeo.com/   Designs for Health - https://www.designsforhealth.com/   Clinical Study: Geranylgeraniol Supplementation May Benefit Males With Low Testosterone - https://americanrivernutrition.com/geranylgeraniol-supplementation-may-benefit-males-with-low-testosterone-clinical-study/   Nutrition Blog: The Biochemistry of Ashwagandha - https://www.casi.org/biochemistry-of-ashwagandha Science Update: New review demonstrates the role of ashwagandha in male infertility - https://www.casi.org/node/746   Nutrition Blog: Zinc - One of the Major Influencers of Male Fertility - https://www.casi.org/node/1109   Lifestyle Vlog: Magnesium for Men's Health - https://www.casi.org/patient-blog/magnesium-for-men-s-health   Research Blog: Boron – Not Boring at All - https://www.casi.org/node/790   Research Blog: Natural Ways to Boost Testosterone - https://www.casi.org/natural-ways-to-boost-testosterone Visit the Designs for Health Research and Education Library which houses medical journals, protocols, webinars, and our blog. https://www.designsforhealth.com/research-and-education/education   Chapters: 00:00 Intro. 02:06 Dr. Geo explains how the field of men's health chose him and has continued to fascinate him. 05:36 An overview of the role of testosterone, how and where in the body it's made, and common process interruption points. 08:47 Nutrients that Leydig cells need in order to effectively produce testosterone.  10:26 Lab markers and hormones, in addition to total testosterone, that Dr. Geo looks for in a new patient. 14:12 Dr. Geo's recommendations for clomiphene, a drug that is used to stimulate the production of testosterone. 15:58 Considerations and cautions for testosterone hormone replacement therapy and levels for SHGB and DHT. 21:41 Testosterone metabolism measurements and the utilization of DIM and chrysin to address high estrogen levels. 22:58 The impact and potentially negative effects of testosterone replacement therapy on fertility and sperm production. 29:11 Findings from research addressing high levels of testosterone replacement therapy.  30:16 Ways to boost testosterone naturally include tonkadale, ashwagandha, and fenugreek.  31:37 Lifestyle changes that can increase testosterone levels including improved sleep and exercise.  35:32 Controversy around PSA (prostate-specific antigen) testing for prostate health and prostate cancer screening.  38:58 Unraveling the numbers behind PSA density, 4k scores, and IsoPSA testing when screening for prostate cancer.  42:41 Baseline screening advice for practitioners who are not specialized in men's health.  44:49 Dr. Geo's advice for prostate cancer prevention through healthy lifestyle choices and formulated nutraceuticals. 52:39 Insights and key differences of prostatitis and benign prostatic hyperplasia (BPH).  56:07 Dr. Geo's approach to treating nocturia, or excessive nighttime urination.  1:00:44 Nutraceutical recommendations for prostatitis and benign prostatic hyperplasia.  1:03:15 Dr. Geo's changed opinion of medicines in the field of urology, his favorite personal supplements, and his favorite health practices.

Organes reproducteurs masculins, les testicules sont contenus dans une poche tissulaire appelée scrotum. Celle-ci pend au niveau de l'entrejambe. L'un des premiers gestes médicaux chez un nouveau-né garçon consiste d'ailleurs à vérifier la présence des deux glandes dans le scrotum. Cette localisation inhabituelle par rapport aux autres organes internes s'explique d'un point de vue reproductif. Étudions en détail les mécanismes de la fertilité et l'influence de la position des testicules sur la reproduction humaine.Anatomie et fonction des testiculesLes testicules sont suspendus dans le scrotum, une structure située à l'extérieur du corps. Ils comportent différents compartiments.Les tubules séminifères sont les canaux où se déroule la production des spermatozoïdes.Les cellules de Leydig se situent entre ces canaux et produisent l'hormone mâle sexuelle, la testostérone.L'épididyme forme un conduit enroulé dans lequel les spermatozoïdes mûrissent et sont stockés avant l'éjaculation.Les testicules servent donc à la fois à produire des millions de spermatozoïdes quotidiennement, et à produire la testostérone qui régule la libido, le développement des caractères sexuels masculins ainsi que la masse musculaire.Pourquoi une localisation externe ?La production de spermatozoïdes de qualité nécessite une température légèrement plus basse que celle de la température corporelle normale, autour de 35°C au lieu des 37°C mesurés dans les organes internes. Si la température est trop élevée, la spermatogénèse est inhibée et les spermatozoïdes produits ne sont plus efficaces. C'est d'ailleurs ce principe qui est utilisé dans la contraception avec des slips chauffants : ces dispositifs augmentent localement la température des testicules pour contrer la fertilité masculine.Les testicules étant situés à l'extérieur du corps, il est plus facile pour l'organisme d'y maintenir une température un peu plus basse. Le scrotum possède en outre ses propres mécanismes de régulation pour contrer une éventuelle chaleur néfaste à la spermatogénèse.Les muscles du scrotum et leur influence sur la températureLe scrotum contient deux muscles essentiels pour réguler sa température. Le muscle crémaster soulève ou abaisse les testicules dans le scrotum en fonction des besoins. S'il fait chaud, il se relâche pour les éloigner du corps et les refroidir. S'il fait froid, il se contracte afin de rapprocher les testicules du corps pour les réchauffer.Le muscle dartos, lui, peut aussi se contracter ou se détendre en réaction à la température. Il va alors réduire ou augmenter la surface exposée des testicules, permettant un refroidissement ou un réchauffement plus efficace. Hébergé par Acast. Visitez acast.com/privacy pour plus d'informations.

In this episode of the Crackin' Backs Podcast, we delve into the evolving challenges of sports psychology with our distinguished guest, Dr. Scott Leydig, a licensed clinical psychologist specializing in sports psychology. With a rich background as a former competitive athlete and holding a master's and doctorate in Clinical Psychology from Nova Southeastern University, Dr. Leydig offers a unique blend of professional expertise and personal insight into the psychological dynamics of sports .Episode Overview:Navigating the Mental Landscape Post-Pandemic: The episode kicks off with an exploration of the global pandemic's impact on the sports world. Dr. Leydig discusses strategies for athletes and coaches to navigate the psychological aftermath, addressing the increased anxiety, isolation, and uncertainty that have become prevalent.Tough vs. Soft Coaching Tactics: Dr. Leydig weighs in on the debate surrounding coaching styles, examining how both tough and soft tactics affect an athlete's mental health and performance. The discussion pivots towards more effective approaches that coaches can employ to inspire peak performance without compromising athletes' psychological well-being.The Drive for Extreme Challenges: Dr. Leydig delves into the psychological factors motivating athletes to pursue grueling events like the Spartan Death Race and the Barkley Marathons. He offers insights into how athletes prepare for and recover from such intense competitions and what everyday athletes can learn about mental toughness and resilience from these extreme sports.Managing Performance Anxiety: With performance anxiety on the rise, Dr. Leydig shares practical advice on how athletes can manage this pressure and harness it to enhance their performance, providing listeners with actionable strategies to improve their mental game.Confronting Body Image Issues: The conversation then shifts to the pervasive issue of body image among athletes, exacerbated by the rise of social media. Dr. Leydig discusses how he addresses these concerns with athletes and the critical role of positive body image in mental health and performance.The Psychological Impact of AI: The episode concludes with a look at the increasing use of AI. Addressing the potential dangers of what is real and what is not and how to navigate this increasingly complicated issue.Listeners can expect a comprehensive journey through the critical aspects of sports psychology, offering insights and strategies to foster mental resilience in the face of modern sporting challenges. Join us on the Crackin' Backs Podcast for an enlightening discussion with Dr. Scott Leydig, where we uncover the psychological tools needed for athletic excellence in today's complex world.We are two sports chiropractors, seeking knowledge from some of the best resources in the world of health. From our perspective, health is more than just “Crackin Backs” but a deep dive into physical, mental, and nutritional well-being philosophies. Join us as we talk to some of the greatest minds and discover some of the most incredible gems you can use to maintain a higher level of health. Crackin Backs Podcast

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.21.550040v1?rss=1 Authors: Reyes-Serratos, E., Santos, J. R. L., Puttagunta, L., Lewis, S., Watanabe, M., Gonshor, A., Buck, R., Befus, A. D., Marcet-Palacios, M. Abstract: Calcium binding protein, spermatid associated 1 (CABS1) is a protein most widely studied in spermatogenesis. However, mRNA for CABS1 has been found in numerous tissues, albeit with little information about the protein. Previously, we identified CABS1 mRNA and protein in human salivary glands and provided evidence that in humans CABS1 contains a heptapeptide near its carboxyl terminus that has anti-inflammatory activities. Moreover, levels of an immunoreactive form of CABS1 were elevated in psychological stress. To more fully characterize human CABS1 we developed additional polyclonal and monoclonal antibodies to different sections of the protein and used these antibodies to characterize CABS1 in an overexpression cell lysate, human salivary glands, saliva, serum and testes using western blot, immunohistochemistry and bioinformatics approaches exploiting the Gene Expression Omnibus (GEO) database. CABS1 appears to have multiple molecular weight forms, consistent with its recognition as a structurally disordered protein, a protein with structural plasticity. Interestingly, in human testes, its cellular distribution differs from that in rodents and pigs, and includes Leydig cells, primary spermatogonia, Sertoli cells and developing spermatocytes and spermatids, Geodata suggests that CABS1 is much more widely distributed than previously recognized, including in the urogenital, gastrointestinal and respiratory tracts, as well as in the nervous system, immune system and other tissues. Much remains to be learned about this intriguing protein. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Testosterone And Enokitake Mushroom Show 1135 MAY 2023 This study showed that the ingestion of adenosine-containing mushrooms and vegetables may effectively increase testicular testosterone production. We conclude that mushrooms with a relatively high adenosine content, such as enokitake, may be useful against aging and fatigue. #enokitake #testosterone #leydig Iguchi, K., Nagashima, K., Mochizuki, J., Yamamoto, H., Unno, K., & Miyoshi, N. (2023). Enokitake Mushroom and Its Active Component, Adenosine, Which Restores Testosterone Production in Impaired and Fatigued Mouse Models. Nutrients, 15(9), 2142. https://doi.org/10.3390/nu15092142 Adenosine, enokitake mushroom, enoki, testosterone, male menopause, mushrooms, Leydig cells, polyphenols, Flammulina velutipes. Golden needle, winter mushroom, fatigue, anti aging, --- Support this podcast: https://podcasters.spotify.com/pod/show/ralph-turchiano/support

Testosterone And Enokitake Mushroom Show 1135 MAY 2023 This study showed that the ingestion of adenosine-containing mushrooms and vegetables may effectively increase testicular testosterone production. We conclude that mushrooms with a relatively high adenosine content, such as enokitake, may be useful against aging and fatigue. #enokitake #testosterone #leydig Iguchi, K., Nagashima, K., Mochizuki, J., Yamamoto, H., Unno, K., & Miyoshi, N. (2023). Enokitake Mushroom and Its Active Component, Adenosine, Which Restores Testosterone Production in Impaired and Fatigued Mouse Models. Nutrients, 15(9), 2142. https://doi.org/10.3390/nu15092142 Adenosine, enokitake mushroom, enoki, testosterone, male menopause, mushrooms, Leydig cells, polyphenols, Flammulina velutipes. Golden needle, winter mushroom, fatigue, anti aging, --- Support this podcast: https://podcasters.spotify.com/pod/show/ralph-turchiano/support

Naomi Wolf. 'The Greatest Crime Against Humanity In History': 11 Revelations From Pfizer's Vaccine Documents. 'The Greatest Crime Against Humanity In History': 11 Revelations From Pfizer's Vaccine Documents. #1: Pfizer knew their gene-based injections had negative efficacy as early as November 2020 #2: Shortly after the release of the COVID injections, Pfizer moved to hire 2,400 full-time employees to process the paperwork of the injured #3: Pfizer and the FDA withheld information that the shots cause heart damage in youth for four months while an aggressive propaganda campaign drove many thousands to get injected #4: Rather than staying in the injection site, Pfizer knew the shot's dangerous lipid nanoparticles quickly distribute throughout the body to the brain, liver, and adrenals, and accumulate in the ovaries #5: Pfizer documents acknowledge more than 42,000 adverse events, including 1,200 deaths, in just the first three months, including strokes, hemorrhages, blood clots, lung clots, leg clots, neurological disorders, dementia, guillain-barré, bell's palsy, myalgia, and more #6: Prior to it being legal, more than 1,000 children were injected, and Pfizer's documents indicate a high rate of serious injury #7:Available records of study participants who conceived children show 80% lost their babies #8: Pfizer knew there was a danger to fertility. Lipid Nanoparticles damage the placenta during pregnancy, causing early deliveries #9: Pfizer docs show that lipid nanoparticles also enter breast milk, stunting, injuring, and sometimes killing babies #10: Pfizer docs show 3 to 1 of AEs sustained by women, 16% ‘reproductive disorders.' ‘What kind of monsters look at 16% reproductive disorders and keep going?' Results: ‘13% to 20% drop in live births' #11 Pfizer documents reveal that LNPs “degrade baby boys in utero” by traversing “the testes of fetal baby boys” and damaging “the Sertoli cells and the Leydig cells, which are basically the factories of masculinity”   Speech given March 5-8, 2023 The modern pharmaceutical industry has in many ways proved itself a great benefit to mankind, making health- and life-saving drugs and vaccines widely available. But its reputation has come under attack in the wake of America's opioid epidemic and the COVID pandemic. This fourth and final CCA of the 2022-23 academic year will consider the rise of Big Pharma, its role in the declining state of American health, and ideas for reform. What's in the Pfizer Documents? Naomi Wolf CEO, The Daily Clout Mar 6, 2023   Watch this presentation on Rumble- https://rumble.com/v2hpryu-naomi-wolf-whats-in-the-pfizer-documents.html   Grateful acknowledgment- Tweet from @KanekoaTheGreat KanekoaTheGreat @KanekoaTheGreat https://lifesitenews.com/news/the-greatest-crime-against-humanity-in-history-naomi-wolfs-11-revelations-from-pfizer-vaccine-documents/   Book Mentioned- War Room/DailyClout Pfizer Documents Analysis Volunteers' Reports eBook: Find Out What Pfizer, FDA Tried to Conceal Kindle Edition by Pfizer Documents Investigation Team  The Pfizer Reports book contains 50 reports written by the highly-credentialed War Room/DailyClout Pfizer Documents Analysis Project volunteers between March and December 2022. The reports are based on information in the primary source Pfizer documents released under court order by the U.S. Food and Drug Administration, as well as on other key medical studies and literature that relate to Pfizer's experimental gene therapy mRNA COVID vaccine. These important documents have been ignored by the mainstream media; however, to date, no one has challenged the accuracy of what they report. Now, for the first time, the 2022 Pfizer Reports are available in book format. Order the book at- https://www.amazon.com/DailyClout-Documents-Analysis-Volunteers-Reports-ebook/dp/B0BSK6LV5D/ref=sr_1_1?crid=5X81GVOH6JSH&keywords=pfizer+documents&qid=1674412497&sprefix=pfizer+documents%2Caps%2C98&sr=8-1 Free e-Document at https://campaigns.dailyclout.io/campaign/brand/cc3b3e5a-6536-4738-8ed6-5ee368c67240   Recent books by Dr. Naomi Wolf.- The Bodies of Others: The New Authoritarians, COVID-19 and The War Against the Human. by Naomi Wolf . May 31, 2022   The Bodies of Others is about how we came to the harrowing civilizational crossroads at which we find ourselves - engaged in a war against vast impersonal forces with limitless power over our lives and which threaten the freedoms we have always taken for granted.  In her most provocative book yet, Dr. Naomi Wolf shows how these forces -- from Big Tech and Big Pharma to the CCP and our oligarchical elites -- seized upon two years of COVID-19 panic in sinister new ways, to not only undermine our Republic but to fundamentally reorient human relations.  Their target is humanity itself. Their end goal is to ensure that our pre-March 2020 world is gone forever. Irretrievable. To be replaced with a world in which all human endeavor-all human joy, all human fellowship, all human advancement, all human culture, all human song, all human drama, all worship, all surprise, all flirtation, all celebration-is behind a digital paywall. A world in which we will all have to ask technology's permission to be human.  But we, the people of the world, did not vote to abandon our old systems and destroy our old ways so absolutely they could never be recovered. And Wolf shows how, against overwhelming odds, we still might win.

Dr. Ranjith Ramasamy explains the known effects of the COVID-19 virus and the pandemic on testosterone levels, vasculogenic erectile dysfunction, male fertility, and sexual practice patterns. Additionally, Dr. Ramaswamy uses evidence-based medicine to debunk myths about the adverse effects of the COVID-19 vaccine on men's health. --- EARN CME Reflect on how this Podcast applies to your day-to-day and earn AMA PRA Category 1 CMEs: https://earnc.me/7hBgDv --- SHOW NOTES In this episode of BackTable Urology, Dr. Aditya Bagrodia and Dr. Ranjith Ramasamy discuss the effects of the COVID-19 pandemic and COVID vaccines on various men's health topics, including testosterone levels, erectile dysfunction, and male fertility. First, Dr. Ramasamy discusses the effects of COVID-19 on hypogonadism. He notes that in the initial stages of the pandemic, many providers attributed low testosterone levels as result of a sedentary and less active lifestyle because of the lockdown. However, it was later discovered that the SARS-CoV-2 virus binds to the ACE2 receptor, an important receptor present on the surface of testosterone-producing Leydig cells. Thus, temporary testosterone deficiency is a direct impact of COVID-19 infection. Dr. Ramasamy advises his recovered patients to naturally increase their testosterone levels by eating, exercising, and sleeping well. COVID-19 is also linked to higher rates of erectile dysfunction. Dr. Ramasamy explains that the cause of ED may not be psychogenic, as the SARS-CoV-2 virus affects endothelial cells lining blood vessels. Studies have also shown that the virus can be present in penile tissue seven to 9 months post-infection. As a result, Dr. Ramasamy urges urologists to differentiate between psychogenic and vasculogenic erectile dysfunction. Next, the doctors discuss the impact of COVID-19 on fertility. Research has shown that a COVID-19 infection may decrease sperm count in semen three to six months post-infection. Most patients have normal sperm counts after 6 months. Although birth rates have declined due to the uncertainty during the pandemic, Dr. Ramasamy notes that more male patients have requested fertility consultations with him as a proactive family planning measure. Finally, Dr. Ramasamy uses evidence-based medicine to debunk myths about the mRNA COVID-19 vaccination on male sexual and gonadal function. He cites his most recently published article, “Sperm Parameters Before and After COVID-19 mRNA Vaccination” (JAMA) and emphasizes that there is no link between the vaccine and declining sperm count.

Saw palmetto boosts testosterone synthesis Kyung Hee University (South Korea), June 30 2021.   The June 2021 issue of the Journal of Medicinal Food reported the finding of a beneficial effect for saw palmetto against symptoms of andropause in rats.  "Andropause, the male equivalent of menopause, is the set of symptoms caused by the age-related deficiency in male hormones that begins to occur in men in their late 40s to early 50s," Jeong Moon Yun and colleagues explained. "The symptoms of andropause include physical, psychological, and sexual problems, such as fatigue, increased body fat, decreased muscle strength and sexual function, depression, and memory loss." Dr Yun and associates evaluated the effects of an extract of saw palmetto in Leydig cells (in which testosterone biosynthesis occurs) subjected to oxidative stress and in aged rats. In Leydig cells, the administration of testosterone lowered 5 alpha-reductase (which converts testosterone to dihydrotestosterone) and increased total testosterone.  In rats, one of three doses of saw palmetto extract was administered for four weeks. A control group of animals received no treatment. At the end of the treatment period, saw palmetto supplemented rats had significantly less fat tissue weight gain and total weight gain compared to the controls, without a gain in other tissue weight. Serum triglycerides, total cholesterol and the LDL to VLDL cholesterol ratio were also lower in the supplemented groups. Serum total and free testosterone and sperm counts were higher, and sex hormone binding globulin (SHBG) and 5 alpha-reductase levels were lower in all supplemented groups in comparison with the controls. In tests of muscle endurance, rats that received saw palmetto had longer swimming times compared to the control group.  "We suggest that supplementation of saw palmetto may relieve the symptoms of andropause syndrome, including decreased spermatogenesis and muscle endurance and metabolic syndrome by increasing testosterone biosynthesis and bioavailability," the authors concluded.         Diet rich in omega 3 fatty acids may help reduce headaches Trial provides 'grounds for optimism' for many people with persistent headaches and those who care for them University of North Carolina, July 1, 2021 Eating a diet rich in omega 3 (n-3) fatty acids reduces the frequency of headaches compared with a diet with normal intake of omega 3 and omega 6 (n-6) fatty acids, finds a study published by The BMJ today. Modern industrialised diets tend to be low in omega 3 fatty acids and high in omega 6 fatty acids. These fatty acids are precursors to oxylipins - molecules involved in regulating pain and inflammation. Oxylipins derived from omega 3 fatty acids are associated with pain-reducing effects, while oxylipins derived from omega 6 fatty acids worsen pain and can provoke migraine. But previous studies evaluating omega 3 fatty acid supplements for migraine have been inconclusive. So a team of US researchers wanted to find out whether diets rich in omega 3 fatty acids would increase levels of the pain-reducing 17-hydroxydocosahexaenoic acid (17-HDHA) and reduce the frequency and severity of headaches. Their results are based on 182 patients at the University of North Carolina, USA (88% female; average age 38 years) with migraine headaches on 5-20 days per month who were randomly assigned to one of three diets for 16 weeks.  The control diet included typical levels of omega 3 and omega 6 fatty acids. Both interventional diets raised omega 3 fatty acid intake. One kept omega 6 acid intake the same as the control diet, and the other concurrently lowered omega 6 acid intake. During the trial, participants received regular dietary counseling and access to online support information. They also completed the headache impact test (HIT-6) - a questionnaire assessing headache impact on quality of life. Headache frequency was assessed daily with an electronic diary. Over the 16 weeks, both interventional diets increased 17-HDHA levels compared with the control diet, and while HIT-6 scores improved in both interventional groups, they were not statistically significantly different from the control group.  However, headache frequency was statistically significantly decreased in both intervention groups.  The high omega 3 diet was associated with a reduction of 1.3 headache hours per day and two headache days per month. The high omega 3 plus low omega 6 diet group saw a reduction of 1.7 headache hours per day and four headache days per month, suggesting additional benefit from lowering dietary omega-6 fatty acid.  Participants in the intervention groups also reported shorter and less severe headaches compared with those in the control group. This was a high quality, well designed trial, but the researchers do point to some limitations, such as the difficulty for patients to stick to a strict diet and the fact that most participants were relatively young women so results may not apply to children, older adults, men, or other populations.  "While the diets did not significantly improve quality of life, they produced large, robust reductions in frequency and severity of headaches relative to the control diet," they write.  "This study provides a biologically plausible demonstration that pain can be treated through targeted dietary alterations in humans. Collective findings suggest causal mechanisms linking n-3 and n-6 fatty acids to [pain regulation], and open the door to new approaches for managing chronic pain in humans," they conclude. These results support recommending a high omega 3 diet to patients in clinical practice, says Rebecca Burch at the Brigham and Women's Hospital, in a linked editorial. She acknowledges that interpretation of this study's findings is complex, but points out that trials of recently approved drugs for migraine prevention reported reductions of around 2-2.5 headache days per month compared with placebo, suggesting that a dietary intervention can be comparable or better.  What's more, many people with migraine are highly motivated and interested in dietary changes, she adds. These findings "take us one step closer to a goal long sought by headache patients and those who care for them: a migraine diet backed up by robust clinical trial results."     The Southern diet - fried foods and sugary drinks - may raise risk of sudden cardiac death University of Alabama, June 30, 2021  Regularly eating a Southern-style diet may increase the risk of sudden cardiac death, while routinely consuming a Mediterranean diet may reduce that risk, according to new research published today in the Journal of the American Heart Association, an open access journal of the American Heart Association. The Southern diet is characterized by added fats, fried foods, eggs, organ meats (such as liver or giblets), processed meats (such as deli meat, bacon and hotdogs) and sugar-sweetened beverages. The Mediterranean diet is high in fruits, vegetables, fish, whole grains and legumes and low in meat and dairy. "While this study was observational in nature, the results suggest that diet may be a modifiable risk factor for sudden cardiac death, and, therefore, diet is a risk factor that we have some control over," said James M. Shikany, Dr.P.H., F.A.H.A., the study's lead author and professor of medicine and associate director for research in the Division of Preventive Medicine at the University of Alabama at Birmingham. "Improving one's diet - by eating a diet abundant in fruits, vegetables, whole grains and fish such as the Mediterranean diet and low in fried foods, organ meats and processed meats, characteristics of the Southern-style dietary pattern, may decrease one's risk for sudden cardiac death," he said. The study examined data from more than 21,000 people ages 45 and older enrolled in an ongoing national research project called REasons for Geographic and Racial Differences in Stroke (REGARDS), which is examining geographic and racial differences in stroke. Participants were recruited between 2003 and 2007. Of the participants in this analysis, 56% were women; 33% were Black adults; and 56% lived in the southeastern U.S., which is noteworthy as a region recognized as the Stroke Belt because of its higher stroke death rate. The Stroke Belt states included in this study were North Carolina, South Carolina, Georgia, Tennessee, Alabama, Mississippi, Arkansas and Louisiana. This study is the latest research to investigate the association between cardiovascular disease and diet - which foods have a positive vs. negative impact on cardiovascular disease risk. It may be the only study to-date to examine the association between dietary patterns with the risk of sudden cardiac death, which is the abrupt loss of heart function that leads to death within an hour of symptom onset. Sudden cardiac death is a common cause of death and accounted for 1 in every 7.5 deaths in the United States in 2016, or nearly 367,000 deaths, according to 2019 American Heart Association statistics. Researchers included participants with and without a history of coronary heart disease at the beginning of the study and assessed diets through a food frequency questionnaire completed at the beginning of the study. Participants were asked how often and in what quantities they had consumed 110 different food items in the previous year. Researchers calculated a Mediterranean diet score based on specific food groups considered beneficial or detrimental to health. They also derived five dietary patterns. Along with the Southern-style eating pattern, the analysis included a "sweets" dietary pattern, which features foods with added sugars, such as desserts, chocolate, candy and sweetened breakfast foods; a "convenience" eating pattern which relied on easy-to-make foods like mixed dishes, pasta dishes, or items likely to be ordered as take-out such as pizza, Mexican food and Chinese food; a "plant-based" dietary pattern was classified as being high in vegetables, fruits, fruit juices, cereal, bean, fish, poultry and yogurt; and an "alcohol and salad" dietary pattern, which was highly reliant on beer, wine, liquor along with green leafy vegetables, tomatoes and salad dressing. Shikany noted that the patterns are not mutually exclusive. "All participants had some level of adherence to each pattern, but usually adhered more to some patterns and less to others," he explained. "For example, it would not be unusual for an individual who adheres highly to the Southern pattern to also adhere to the plant-based pattern, but to a much lower degree." After an average of nearly 10 years of follow-up every six months to check for cardiovascular disease events, more than 400 sudden cardiac deaths had occurred among the 21,000 study participants. The study found: Overall, participants who ate a Southern-style diet most regularly had a 46% higher risk of sudden cardiac death than people who had the least adherence to this dietary pattern. Also, participants who most closely followed the traditional Mediterranean diet had a 26% lower risk of sudden cardiac death than those with the least adherence to this eating style. The American Heart Association's Diet and Lifestyle recommendations emphasize eating vegetables, fruits, whole grains, lean protein, fish, beans, legumes, nuts and non-tropical vegetable cooking oils such as olive and canola oil. Limiting saturated fats, sodium, added sugar and processed meat are also recommended. Sugary drinks are the number one source of added sugar in the U.S. diet, according to the Centers for Disease Control and Prevention, and the American Heart Association supports sugary drink taxes to drive down consumption of these products. "These findings support the notion that a healthier diet would prevent fatal cardiovascular disease and should encourage all of us to adopt a healthier diet as part of our lifestyles," said Stephen Juraschek, M.D., Ph.D., a member of the American Heart Association's Nutrition Committee of the Lifestyle and Cardiometabolic Health Council. "To the extent that they can, people should evaluate the number of servings of fruit and vegetables they consume each day and try to increase the number to at least 5-6 servings per day, as recommended by the American Heart Association. Optimal would be 8-9 servings per day. "This study also raises important points about health equity, food security and social determinants of health," he continued. "The authors describe the "Southern Diet" based on the U.S. geography associated with this dietary pattern, yet it would be a mistake for us to assume that this is a diet of choice. I think American society needs to look more broadly at why this type of diet is more common in the South and clusters among some racial, ethnic or socioeconomic groups to devise interventions that can improve diet quality. The gap in healthy eating between people with means and those without continues to grow in the U.S., and there is an incredible need to understand the complex societal factors that have led and continue to perpetuate these disparities." This current research expands on earlier studies on participants from the same national stroke project, REGARDS. In a 2018 analysis, Shikany and colleagues reported that adults ages 45 and older with heart disease who had an affinity for the Southern diet had a higher risk of death from any cause, while greater adherence to the Mediterranean diet was associated with a lower risk of death from any cause. And in a 2015 study, the Southern diet was linked to a greater risk of coronary heart disease in the same population. The large population sample and regional diversity, including a significant number of Black participants, are considered strengths of the REGARDS research project. However, potential limitations of this study include that that dietary intake was based on one-time, self-reported questionnaires, thus, it relied on the participants' memory. Self-reported diet can include inaccuracies leading to bias that could reduce the strength of the associations observed. One usual association that remains unexplained is that among individuals with a history of heart disease, those who most adhered to the sweets dietary pattern had a 51% lower risk of sudden cardiac death than participants who followed that pattern the least. Researchers note that they found "no viable explanation for the inverse association of the sweets dietary pattern with risk of sudden cardiac death in those with a history of coronary heart disease."     5-minute workout lowers blood pressure as much as exercise, drugs 'Strength training for breathing muscles' holds promise for host of health benefits University of Colorado, July 2, 2021 Working out just five minutes daily via a practice described as "strength training for your breathing muscles" lowers blood pressure and improves some measures of vascular health as well as, or even more than, aerobic exercise or medication, new CU Boulder research shows. The study, published June 29 in the Journal of the American Heart Association, provides the strongest evidence yet that the ultra-time-efficient maneuver known as High-Resistance Inspiratory Muscle Strength Training (IMST) could play a key role in helping aging adults fend off cardiovascular disease - the nation's leading killer.  In the United States alone, 65% of adults over age 50 have above-normal blood pressure - putting them at greater risk of heart attack or stroke. Yet fewer than 40% meet recommended aerobic exercise guidelines. "There are a lot of lifestyle strategies that we know can help people maintain cardiovascular health as they age. But the reality is, they take a lot of time and effort and can be expensive and hard for some people to access," said lead author Daniel Craighead, an assistant research professor in the Department of Integrative Physiology. "IMST can be done in five minutes in your own home while you watch TV." Developed in the 1980s as a way to help critically ill respiratory disease patients strengthen their diaphragm and other inspiratory (breathing) muscles, IMST involves inhaling vigorously through a hand-held device which provides resistance. Imagine sucking hard through a tube that sucks back.  Initially, when prescribing it for breathing disorders, doctors recommended a 30-minute-per-day regimen at low resistance. But in recent years, Craighead and colleagues have been testing whether a more time-efficient protocol--30 inhalations per day at high resistance, six days per week--could also reap cardiovascular, cognitive and sports performance improvements. For the new study, they recruited 36 otherwise healthy adults ages 50 to 79 with above normal systolic blood pressure (120 millimeters of mercury or higher). Half did High-Resistance IMST for six weeks and half did a placebo protocol in which the resistance was much lower.  After six weeks, the IMST group saw their systolic blood pressure (the top number) dip nine points on average, a reduction which generally exceeds that achieved by walking 30 minutes a day five days a week. That decline is also equal to the effects of some blood pressure-lowering drug regimens.  Even six weeks after they quit doing IMST, the IMST group maintained most of that improvement. "We found that not only is it more time-efficient than traditional exercise programs, the benefits may be longer lasting," Craighead said. The treatment group also saw a 45% improvement in vascular endothelial function, or the ability for arteries to expand upon stimulation, and a significant increase in levels of nitric oxide, a molecule key for dilating arteries and preventing plaque buildup. Nitric oxide levels naturally decline with age.  Markers of inflammation and oxidative stress, which can also boost heart attack risk, were significantly lower after people did IMST. And, remarkably, those in the IMST group completed 95% of the sessions. "We have identified a novel form of therapy that lowers blood pressure without giving people pharmacological compounds and with much higher adherence than aerobic exercise," said senior author Doug Seals, a Distinguished Professor of Integrative Physiology. "That's noteworthy." The practice may be particularly helpful for postmenopausal women. In previous research, Seals' lab showed that postmenopausal women who are not taking supplemental estrogen don't reap as much benefit from aerobic exercise programs as men do when it comes to vascular endothelial function. IMST, the new study showed, improved it just as much in these women as in men.  "If aerobic exercise won't improve this key measure of cardiovascular health for postmenopausal women, they need another lifestyle intervention that will," said Craighead. "This could be it." Preliminary results suggest MST also improved some measures of brain function and physical fitness. And previous studies from other researchers have shown it can be useful for improving sports performance. "If you're running a marathon, your respiratory muscles get tired and begin to steal blood from your skeletal muscles," said Craighead, who uses IMST in his own marathon training. "The idea is that if you build up endurance of those respiratory muscles, that won't happen and your legs won't get as fatigued." Seals said they're uncertain exactly how a maneuver to strengthen breathing muscles ends up lowering blood pressure, but they suspect it prompts the cells lining blood vessels to produce more nitric oxide, enabling them to relax. The National Institutes of Health recently awarded Seals $4 million to launch a larger follow-up study of about 100 people, comparing a 12-week IMST protocol head-to-head with an aerobic exercise program. Meanwhile, the research group is developing a smartphone app to enable people to do the protocol at home using already commercially available devices. Those considering IMST should consult with their doctor first. But thus far, IMST has proven remarkably safe, they said. "It's easy to do, it doesn't take long, and we think it has a lot of potential to help a lot of people," said Craighead.   Research suggests atheroprotective role for chrysin Fu Jen Catholic University (Taiwan), July 1, 2021 According to news reporting originating from New Taipei, Taiwan, research stated, “Atherosclerosis and its related clinical complications are the leading cause of death. MicroRNA (miR)-92a in the inflammatory endothelial dysfunction leads to atherosclerosis.” Our news editors obtained a quote from the research from Fu Jen Catholic University, “Kruppel-like factor 2 (KLF2) is required for vascular integrity and endothelial function maintenance. Flavonoids possess many biological properties. This study investigated the vascular protective effects of chrysin in balloon-injured carotid arteries. Exosomes were extracted from human coronary artery endothelial cell (HCAEC) culture media. Herb flavonoids and chrysin (found in mint, passionflower, honey and propolis) were the treatments in these atheroprotective models. Western blotting and real-time PCRs were performed. In situ hybridization, immunohistochemistry, and immunofluorescence analyses were employed. MiR-92a increased after balloon injury and was present in HCAEC culture media. Chrysin was treated, and significantly attenuated the miR-92a levels after balloon injury, and similar results were obtained in HCAEC cultures in vitro. Balloon injury-induced miR-92a expression, and attenuated KLF2 expression. Chrysin increased the KLF2 but reduced exosomal miR-92a secretion. The addition of chrysin and antagomir-92a, neointimal formation was reduced by 44.8 and 49.0% compared with balloon injury after 14 days, respectively. Chrysin upregulated KLF2 expression in atheroprotection and attenuated endothelial cell-derived miR-92a-containing exosomes.” According to the news editors, the research concluded: “The suppressive effect of miR-92a suggests that chrysin plays an atheroprotective role.” This research has been peer-reviewed.     False-positive mammogram results linked to spike in anxiety prescriptions Penn State University, July 2, 2021 Women who experience a false-positive mammogram result are more likely to begin medication for anxiety or depression than women who received an immediate negative result, according to a study led by Penn State researcher Joel Segel. The finding highlights the importance of swift and accurate follow-up testing to rule out a breast cancer diagnosis. The study found that patients who receive a false-positive mammogram result are also prescribed anxiety or depression medication at a rate 10 to 20 percent higher than patients who receive an immediate negative result. These prescriptions are new and not continuations of previously prescribed medicines. A false-positive result is one where a suspicious finding on the screening mammogram leads to additional testing that does not end up leading to a breast cancer diagnosis. Additionally, within that group of patients who required more than one test to resolve the false-positive there was a 20 to 30 percent increase in those beginning to take anxiety or depression medications. The increase was particularly noticeable among women with commercial insurance who required multiple tests to rule out a breast cancer diagnosis. "The results suggest that efforts to quickly resolve initially positive findings including same-day follow-up tests may help reduce anxiety and even prevent initiation of anxiety or depression medication," said Segel, assistant professor of health policy and administration at Penn State. This study demonstrates that some women who experience a false-positive mammogram may need additional follow-up care to effectively handle the increased anxiety that may accompany the experience, Segel said. More importantly, from a practitioner standpoint, the study identifies sub-populations who may be most at risk of increased anxiety following a false-positive mammogram, Segel said. Specifically, women whose false-positive result requires more than one follow-up test to resolve, women with commercial insurance who undergo a biopsy, women who wait longer than one week to receive a negative result, and women who are under age 50 may all be at higher risk of experiencing clinically significant anxiety or depression. "Regular breast cancer screening is critical to early detection," Segel said. "Patients should continue to work with their providers to ensure they are receiving guideline-appropriate screening and should follow up with their providers if they experience either anxiety or depression following screening or any type of care." Researchers studied commercial- and Medicaid-claims databases to identify women ages 40 to 64 who underwent screening mammography with no prior claims for anxiety or depression medications. The findings recently appeared in Medical Care.     Thymoquinone in Black Seed oil increases the expression of neuroprotective proteins while decreasing expression of pro-inflammatory cytokines Florida A&M University, June 29, 2021    According to news originating from Tallahassee, Florida, research stated, "Neuroinflammation and microglial activation are pathological markers of a number of central nervous system (CNS) diseases. Chronic activation of microglia induces the release of excessive amounts of reactive oxygen species (ROS) and pro-inflammatory cytokines." Our news journalists obtained a quote from the research from Florida A&M University, "Additionally, chronic microglial activation has been implicated in several neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Thymoquinone (TQ) has been identified as one of the major active components of the natural product Nigella sativa seed oil. TQ has been shown to exhibit anti-inflammatory, anti-oxidative, and neuroprotective effects. In this study, lipopolysaccharide (LPS) and interferon gamma (IFN gamma) activated BV-2 microglial cells were treated with TQ (12.5 mu M for 24 h). We performed quantitative proteomic analysis using Orbitrap/Q-Exactive Proteomic LC-MS/MS (Liquid chromatography-mass spectrometry) to globally assess changes in protein expression between the treatment groups. Furthermore, we evaluated the ability of TQ to suppress the inflammatory response using ELISArray ™ for Inflammatory Cytokines. We also assessed TQ's effect on the gene expression of NFKB signaling targets by profiling 84 key genes via real-time reverse transcription (RT2) PCR array. Our results indicated that TQ treatment of LPS/IFN gamma-activated microglial cells significantly increased the expression of 4 antioxidant, neuroprotective proteins: glutaredoxin-3 (21 fold; p< 0.001), biliverdin reductase A (15 fold; p< 0.0001), 3-mercaptopyruvate sulfurtransferase (11 fold; p< 0.01), and mitochondria] Ion protease (> 8 fold; p< 0.001) compared to the untreated, activated cells. Furthermore, TQ treatment significantly (P < 0.0001) reduced the expression of inflammatory cytokines, IL-2 = 38%, IL-4 = 19%, IL-6 = 83%, IL-10 = 237%, and IL-17a = 29%, in the activated microglia compared to the untreated, activated which expression levels were significantly elevated compared to the control microglia: IL-2 = 127%, IL-4 = 151%, IL-6 = 670%, IL-10 = 133%, IL-17a = 127%. Upon assessing the gene expression of NFKB signaling targets, this study also demonstrated that TQ treatment of activated microglia resulted in > 7 fold down-regulation of several NFKB signaling targets genes, including interleukin 6 (IL6), complement factor B (CFB), chemokine (C-C motif) ligand 3 (CXCL3), chemokine (C-C) motif ligand 5 (CCL5) compared to the untreated, activated microglia. This modulation in gene expression counteracts the > 10-fold upregulation of these same genes observed in the activated microglia compared to the controls. Our results show that TQ treatment of LPS/IFN gamma-activated BV-2 microglial cells induce a significant increase in expression of neuroprotective proteins, a significant decrease in expression inflammatory cytokines, and a decrease in the expression of signaling target genes of the NF kappa B pathway. Our findings are the first to show that TQ treatment increased the expression of these neuroprotective proteins (biliverdin reductase-A, 3-mercaptopyruvate sulfurtransferase, glutaredoxin-3, and mitochondrial Ion protease) in the activated BV-2 microglial cells. Additionally, our results indicate that TQ treatment decreased the activation of the NF kappa B signaling pathway, which plays a key role in neuroinflammation." According to the news editors, the research concluded: "Our results demonstrate that TQ treatment reduces the inflammatory response and modulates the expression of specific proteins and genes and hence potentially reduce neuroinflammation and neurodegeneration driven by microglial activation."

In today's episode, we tackle the 'male' reproductive system. The penultimate episode from our series introducing human anatomy systems.  Terms covered in this podcast include; The testes vs testis. Sertoli, Leydig and spermatagonia cells. The rete testis, epididymis and the ductus or vas deferens. Seminal vesicles, prostate, and finally the erectile tissues of the corpus cavernosum and spongiosum.   

Episode 43: Testicular Cancer. Testicular cancer screening and diagnosis (basics), chlorthalidone vs hydrochlorothiazide, and jokes.Today is March 8, 2021. For many years, we have heard about the superiority of chlorthalidone over hydrochlorothiazide to control hypertension, but in clinical practice, hydrochlorothiazide is prescribed more often as the initial therapy for most patients with hypertension as compared to chlorthalidone. As a matter of fact, the Microsoft Word automatic corrector detects hydrochlorothiazide as a correct word, but flags chlorthalidone as misspelled. Also, we know how to abbreviate hydrochlorothiazide (HCTZ), but did you know that chlorthalidone has an abbreviation as CTD?We have been neglecting chlorthalidone regardless its apparent effectivity.  In January 2006, the American Heart Association published on its journal Hypertension, a comparison between chlorthalidone and hydrochlorothiazide to control hyperension[1]. A randomized, single-blinded, 8-week active treatment, crossover study compared 12.5mg/day chlorthalidone (force-titrated to 25 mg/day at week 4) and HCTZ 25mg/day (force-titrated to 50mg/day at week 4) in untreated hypertensive patients. 24-hour BP monitoring was assessed at baseline and week 8 plus standard office BP readings every 2 weeks. 30 patients completed the active treatment period.  At week 8 there was a greater reduction in baseline systolic blood pressure with chlorthalidone 25mg vs HCTZ 50mg. The effectiveness of chlorthalidone was evidenced by ambulatory blood pressure measurement (ABPM) although this difference was not apparent with office BP measurements. It was a short duration study with a small sample size.More recently, in January 2021, the Journal of Hypertension, which is the official journal of the International Society of Hypertension and the European Society of Hypertension[2], published on PDF a more comprehensive review of these long-time rivals. According to the short version of this article, there is no difference in the short-term net clinical benefit between CTD and HCTZ, BUT long-term available data suggests that CTD is better at reducing major adverse cardiovascular events (MACE) over HCTZ. Stay tuned for the final version of this study.Way to go chlorthalidone!______________________________This is Rio Bravo qWeek, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California. Our program is affiliated with UCLA, and it’s sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home.  Page BreakQuestion of the Month: Polyarthralgiaby Claudia Carranza  A 49-year-old female comes to clinic reporting bilateral wrist and ankle pain for 1 month. The pain is worse with movement and responds well to ibuprofen. She denies joint swelling, warmth, or morning stiffness. She reports feeling more fatigued than usual this past month. You note on her chart that she was diagnosed with COVID-19 approximately 6 weeks ago for which she did not need to be hospitalized.  She denies history of diabetes, thyroid disease, lupus, rheumatoid arthritis, trauma, or anemia. She denies fecal, urinary, or vaginal bleeding, no headaches, chest pain, SOB or dizziness. Exam is remarkable for a “tired look” and tenderness to palpation at bilateral wrist and ankles. No signs of inflammation on joints is noted. What do you think is the etiology of this patient’s symptoms and what workup would you order (if any)? Let’s repeat the question: What do you think is the etiology of the symptoms in a 49-year-old female who complains of symmetrical POLYARTHRALGIA and fatigue for 1 month, and what workup would you order (if any)? Clue: Listen carefully to the history of the patient. Send us your answer to rbresidency@clinicasierravista.org before March 22, 2021. The winner will receive a prize.“I am not my body. My body is nothing without me.” Tom Stoppard____________________________Testicular Cancer Testicular cancer is the most common solid tumor among males 15 to 34 years of age, with an estimated 8,850 new cases and 410 deaths in the past years. The good news is that with effective treatment, the overall five-year survival rate is 97%[3]. Risk factors. Cryptorchidism: The relative risk of developing testicular cancer ranges from 2.9 to 6.3; the risk is increased in both testes, although the risk is much higher in the ipsilateral testis (6.3 vs. 1.7). Among these patients, the risk of cancer increases when orchiopexy is delayed until after puberty or never performed compared with early orchiopexy. Even after early orchiopexy, the risk of testicular cancer remains elevated compared with the general population.  Personal or family history of testicular cancer: Patients with a personal history of testicular cancer have a 12-times greater risk of developing a contralateral testicular cancer than the general population. However, the greatest risk is in the first five years after diagnosis. Patients with a father or brother with testicular cancer have a 3.8- and 8.6-times greater risk, respectively. Infertility: Men with infertility have an increased risk of testicular cancer, with a standardized incidence ratio of 1.6 to 2.8, although the underlying mechanism is unclear. HIV: Human immunodeficiency virus infection/AIDS increases the risk of seminoma, but this is negated with highly active antiretroviral treatment.  Inconclusive risk: Associations between testicular cancer and marijuana use, inguinal hernia, diet, maternal smoking, and body size are inconclusive.  Not a risk factor: Testicular microlithiasis, vasectomy, and scrotal trauma are not risk factors for testicular cancer. Screening for testicular cancer. The U.S. Preventive Services Task Force, National Cancer Institute, and American Academy of Family Physicians recommend against screening for testicular cancer (by a clinician or through self-examination) in asymptomatic adolescents and adults because of its low incidence and high survival rate. The American Cancer Society states that a testicular examination should be part of a routine cancer-related checkup but does not include a recommendation on regular testicular self-examinations for all men.Assessment of suspected testicular cancer patient.History and physical exam are the foundation for the diagnosis. Men with symptoms should receive a complete history and physical examination. Scrotal ultrasonography is the preferred initial imaging study. Testicular cancer may present as a painless scrotal mass, an incidental radiologic finding, posttraumatic symptom, or scrotal pain. Less commonly, presenting symptoms may indicate metastatic disease.  Symptoms of testicular cancer include scrotal symptoms such as acute pain in the testis or scrotum, scrotum or abdomen discomfort or aches, painless mass of the testis, scrotal heaviness and swelling. Symptoms related to metastasis are non-specific and depend on the location of metastasis, including dyspepsia, abdominal pain or discomfort, gynecomastia, headaches, low back pain, neck mass, chest pain, cough, dyspnea, and hemoptysis.Testicular changes may be detected by the patient or by a sex partner. Epididymitis is an important part of the differential diagnosis of a scrotal mass.The normal testis is 3.5 to 5 cm in length, smooth, homogenous, movable, and detached from the epididymis. Hard, firm, or fixed areas within or adjacent to the testes are abnormal and warrant further evaluation. Physical examination should also include evaluation of the inguinal and supra-clavicular lymph nodes, the abdomen, and the chest for gynecomastia (related to tumor secretion of beta human chorionic gonadotropin). If a solid intratesticular mass is discovered, orchiectomy is both diagnostic and therapeutic. Imaging.Scrotal ultrasonography is the preferred initial imaging study for evaluating a testicular mass.Ultrasonography has a sensitivity of 92% to 98% and specificity of 95% to 99.8%. A solid intratesticular mass on ultrasonography warrants rapid referral for radical inguinal orchiectomy because this procedure provides pathologic diagnosis and is the cornerstone of treatment.Staging. Staging through chest radiography, chemistry panel, liver function tests, and tumor markers guides treatment. Active surveillance, chemotherapy, retroperitoneal lymph node dissection, and radiation therapy are treatment options following orchiectomy. For patients desiring future fertility, sperm banking should be discussed early in the course of treatment. Treatment. Radical inguinal orchiectomy, including removal of the spermatic cord to the internal inguinal ring, is the primary treatment for any malignant tumor found on surgical exploration of a testicular mass. Testis-sparing surgery is generally not recommended but may be performed for a small tumor in one testis or for small bilateral tumors. Orchiectomy may be delayed if life-threatening metastases require more urgent attention. The risk of testicular cancer recurrence is greatest within two to three years of primary treatment, and surveillance is continued for up to five years.Classification of Testicular Tumors: Germ cell tumors (95% of all testicular cancers)Derived from germ cell neoplasia in situSeminomaNonseminoma (nonseminomatous germ cell tumors)Embryonal carcinomaYolk sac tumor (postpubertal)Trophoblastic tumors (e.g., choriocarcinoma, placental site trophoblastic tumor)Teratoma (postpubertal) with or without malignant transformationMixed and unclassified germ cell tumorsNot derived from germ cell neoplasia in situSpermatocytic tumorTeratoma (prepubertal)Yolk sac tumor (prepubertal)Sex cord–stromal tumors (< 5% of all testicular cancers)Leydig cell tumorSertoli cell tumorGranulosa cell tumorMixed and unclassified sex cord–stromal tumorsMixed germ cell and stromal tumors (proportion of all testicular cancers not well defined) GonadoblastomaMiscellaneous tumors (proportion of all testicular cancers not well defined) Ovarian epithelial-type tumors Hemangioma Hematolymphoid tumors Tumors of the collecting duct and rete testis (adenocarcinoma)Differential diagnosis of testicular cancer.Tip 1: Testicular torsion is one of the most important differential diagnosis of testicular cancer. Testicular torsion is an emergency, and the presentation is quite different than cancer as it presents with acute, sudden, severe, unilateral testicular pain. Patients are very apprehensive to the exam. The scrotum may appear discolored and swollen; and the affected testicle is typically horizontal and at a higher position than expected in the scrotum. The treatment is surgical. In isolated areas, where surgery cannot be performed in a 2-hour period, a manual testicular detorsion can be attempted with appropriate analgesia and/or sedation. Try to rotate the affected testicle twice, 360 degrees, from medial to lateral. A “drop” of the testicle in the scrotum is felt with relief of pain. One-third of patients need detorsion to the opposite direction, from lateral to medial instead. Tip 2: Epididymitis presents as a pain for about 1-2 weeks. Tenderness is located behind the testicle and patient may complain of dysuria as well. Perform a urine test or urethral swab for gonorrhea and chlamydia. In patients younger than 35, consider empiric treatment while you wait for the results with ceftriaxone PLUS doxycycline or azithromycin. In patients older than 35, consider gram negative coverage with levofloxacin or trimethoprim-sulfamethoxazole. Tip 3: Consider other causes of infection in testis or scrotum, including viruses such as mumps (in unvaccinated populations) and even tuberculosis. If you are curious, read my article about it in PubMed titled “A Case of Testicular Granulomatous Inflammation Mistaken for Malignancy: Tuberculosis Identified Post Orchiectomy”[4].  Tip 4: Epidydimal cyst, spermatocele, and hydrocele are asymptomatic or minimally symptomatic, they are not located in the testis, but you can palpate a distinctive mass posterior or higher than the testis. You can try transillumination of these masses, and they should be translucent. Confirm with testicular ultrasound if in doubt. Tip 5: A testicular hematoma can happen after blunt trauma, but don’t be fooled by the history of traumas as up to 10% of testicular cancers may be discovered after trauma. Perform ultrasound and tumor markers to establish a diagnosis. Tip 6: A scrotal hernia may cause concerns in a patient. Clinically, the inguinal canal appears full and the mass in the scrotum is reported to improve with rest. If the mass is exquisitely tender and not reducible, emergent evaluation by surgery is warranted to rule out hernia strangulation, especially if scrotal pain is accompanied by abdominal distension, abdominal pain, nausea, and vomiting.        ____________________________For your Sanity: Jokesby Anonymous Medical AssistantsHow does a deaf gynecologist communicate? They read lips!How do you get a squirrel to like you? Act like a nut.Why did the math book look so sad? It had a lot of problems.Why can’t a nose be 12 inches long? Because then it’d be a foot.What’s brown and sticky? A stick.Why did the rope go to the doctor? Because it had a knot on the stomach.Why did the mattress go to the doctor? Because it had Spring fever. Now we conclude our episode number 43 “Testicular cancer”, marking our podcasts one year anniversary!. Dr. RAVA covered the recommendations given by USPSTF and the American Cancer Society regarding screening for testicular cancer. Screening in asymptomatic adults is mostly not recommended but it can be a part of a cancer-related checkup. As part of our introduction today, we mentioned effective chlorthalidone is in preventing major adverse cardiovascular events. Our question of the month is still on, and we look forward to reading your answers. The question is: What is the etiology of polyarthralgia in a 49-year-old woman with pain on wrists and ankles for 1 month, and what work up would you order (if any)? The listener who sends the best answer will win a prize! Remember, even without trying, every night you go to bed being a little wiser.Thanks for listening to Rio Bravo qWeek. If you have any feedback about this podcast, contact us by email RBresidency@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. This podcast was created with educational purposes only. Visit your primary care physician for additional medical advice. This week we thank Hector Arreaza, Valerie Civelli, Sapna Patel, Manjinder Samra, Dr. RAVA, and voluntarily-unidentified medical assistants. Audio edition: Suraj Amrutia. See you next week! _____________________References:Roush, George C.a; Messerli, Franz H. Chlorthalidone versus hydrochlorothiazide, Journal of Hypertension: January 19, 2021 - Volume Publish Ahead of Print - Issue - doi: 10.1097/HJH.0000000000002771. https://journals.lww.com/jhypertension/Abstract/9000/Chlorthalidone_versus_hydrochlorothiazide__major.96738.aspx Ernst, Michael E., Barry L. Carter, Chris J. Goerdt et al., American Heart Association, Hypertension, Volume 47, Issue 3, 1 March 2006, Pages 352-358, https://doi.org/10.1161/01.HYP.0000203309.07140.d3 Baird DC, Meyers GJ, Hu JS. Testicular Cancer: Diagnosis and Treatment. Am Fam Physician. 2018 Feb 15;97(4):261-268. PMID: 29671528. https://www.aafp.org/afp/2018/0215/p261.html Civelli VF, Heidari A, Valdez MC, Narang VK, Johnson RH. A Case of Testicular Granulomatous Inflammation Mistaken for Malignancy: Tuberculosis Identified Post Orchiectomy. J Investig Med High Impact Case Rep. 2020 Jan-Dec;8:2324709620938947. doi: 10.1177/2324709620938947. PMID: 32618206; PMCID: PMC7493239. https://pubmed.ncbi.nlm.nih.gov/32618206/

An interesting category of Ovarian Cysts, the sex cord stromal. --- Send in a voice message: https://anchor.fm/dr-mcdaniel/message

Probablemente hayas escuchado, y con razón, que no puedes desarrollar músculo sin testosterona. Ya se que esto no es algo que se haya descubierto antes de ayer, ¿verdad? ¿Pero sabías que podrías maximizar tu liberación de testosterona tomando decisiones específicas en el gimnasio? Al preparar cualquier entrenamiento, algunas estrategias son mejores que otras para aumentar naturalmente los niveles de testosterona, y así el crecimiento muscular. ¿Qué es la testosterona? La testosterona es una hormona anabólica androgénica asociada con el aumento de la masa muscular, las ganancias de fuerza y ​​el deseo sexual. Al contrario de lo que algunos podrían pensar, los músculos no liberan testosterona. La testosterona se libera de células específicas, llamadas células de Leydig, ubicadas en los testículos. Regiones específicas de tu cerebro, el hipotálamo y la glándula pituitaria anterior, inician la liberación de testosterona de sus testículos a través de una serie de mensajes hormonales. Tipos de testosterona La testosterona se encuentra típicamente en dos formas en el cuerpo: libre y unida. La testosterona libre es la forma más activa, por lo que puede entrar directamente en una célula objetivo (como la del músculo). Así es como la testosterona puede hacer acciones anabólicas o incluso anti catabólicas. Optimiza tu programa de entrenamiento Echemos un vistazo a una serie de variables de entrenamiento que se han estudiado por su relación con la liberación de testosterona. 1. Intensidad La intensidad se define mejor como el porcentaje de tu repetición máxima (1RM). Si tu máxima de press de banca es de 100 kilos (número redondo), y para hacer 12 repeticiones tienes que bajar a 80 kilos. A 12 repes (12RM) trabajas a tu 80% de tu 1RM. Para optimizar tu respuesta de testosterona, debes trabajar a una intensidad relativamente alta. Cuando todos los demás factores se mantienen iguales, las sesiones con la mayor intensidad general darán como resultado la mayor respuesta de testosterona. En general, la investigación ha demostrado que series de 3-10 repeticiones, tienen una mayor respuesta de tu testosterona. 2. Volumen El volumen es igual a la cantidad total de trabajo realizado, o multiplicar las repeticiones de cada serie por las series por ejercicio por los ejercicios que haces. El volumen es una variable algo difícil de manipular con la esperanza de optimizar la respuesta de testosterona, en parte porque parece haber un punto en el que un mayor volumen no significa una mayor liberación de testosterona. Para alcanzar este umbral, debes estar seguro de que estás haciendo una cantidad relativamente alta de volumen por cada sesión de entrenamiento. Esto da para hablar mucho sobre qué es mucho volumen de entrenamiento. Pero a nivel general y como punto de partida para ir probando haz de entre 10 a 20 series por grupo muscular a la semana. 3. Elección del ejercicio La selección del ejercicio es la variable más importante que se puede manipular cuando se trata de optimizar la testosterona. Sin lugar a dudas, cuanto mayor sea la masa muscular involucrada en un movimiento, mayor será la respuesta de testosterona. Además, la cantidad de testosterona liberada está en relación directa con la cantidad de masa muscular utilizada. Esto significa que una sentadilla siempre tendrá una mayor liberación de testosterona que un press de banca. Los ejercicios multiarticulares, los ejercicios compuestos, los ejercicios básicos de toda la vida liberan más testosterona que los ejercicios de aislamiento. Y debido a que requieren más actividad estabilizadora, los pesos libres son una mejor opción que los ejercicios en máquina. En caso de duda, elige un ejercicio que necesite una gran cantidad de masa muscular. 4. Orden de ejercicio Las investigaciones publicadas han demostrado aumentos significativamente mayores en la respuesta de testosterona cuando se incluyen ejercicios multiarticulares en la misma sesión con ejercicios de aislamiento para grupos musculares más pequeños. Estos mismos aumentos de testosterona se asociaron con un aumento significativamente mayor en la fuerza para el grupo de músculos más pequeños. Así que tendría sentido poner los ejercicios compuestos de pesos altos primero en tu sesión de entrenamiento. Esto asegurará una intensidad y volumen buenos para los ejercicios compuestos que son más duros y demandantes de energía. Y cuando las fuerzas bajan, completa el entrenamiento con ejercicios de aislamiento. No sé si te sonará a nuevo, pero esto ya lo leía en las revistas de culturismo de hace más de 20 años. Nada nuevo bajo el sol. Un saludo y felices agujetas.

In today's episode we discuss: —Epidemiology: Outcomes of COVID-19 in living donor liver transplant (LDLT) recipients are studied by hepatologists and leading liver transplant surgeons from the Institute of Liver Transplantation & Regenerative Medicine in Gurugram, India through a case series of 12 living donor liver transplant patients who tested positive for SARS-CoV-2 via RT-PCR. Most were symptomatic (n=11, 91.7%) with evidence of pneumonia on radiologic imaging (n=9, 75%) and with median duration of detectable virus of 12 days. While the majority (n=10, 83.3%) were on tacrolimus-based immunosuppression, all but one patient (n=11, 91.7%) survived with only supportive care. Because the patient who died had multiple other risk factors for severe COVID-19 (quadruple immunosuppression, hypertension, metabolic syndrome, diabetes), these authors suggest that liver transplant patients as a whole are not at particularly increased risk for mortality from COVID-19. · Hematological manifestations of SARS-CoV-2 in children are explored in a review of 15 articles meeting study criteria and found children with SARS-CoV-2 were less likely to be lymphopenic compared to adults, with the most common abnormalities being leukopenia in older children and lymphocytosis in infants/neonates. Thrombotic complications and platelets and erythrocytes abnormalities were relatively uncommon and more likely in children with multisystem inflammatory syndrome. Authors suggest these findings, which contrast hematologic changes observed in adults, may be a result of pediatric patients' immature ACE-2 expression and immune systems. —Understanding the Pathology: Mechanisms by Which SARS-CoV-2 May Impact Male Fertility are discussed in a letter to the editor based on Dutta and Sengupta's article "SARS-CoV-2 and male infertility: possible multifaceted pathology." They propose viral binding to angiotensin-converting enzyme 2 receptors on spermatogonia, Leydig cells, and Sertoli cells may cause overactivation and negatively impact spermatogenesis. Additionally, they urge further studies on SARS-CoV-2's ability to disrupt sperm formation and function because SARS-CoV-2 seems to disproportionately impact males in some studies. —R&D: Diagnosis & Treatments: REGN-COV2 antibodies prevent and treat SARS-CoV-2 infection in certain species based on virologists from Regeneron Pharmaceuticals results from an in vivo study of their proprietary therapeutic cocktail REGN-COV2's (human antibodies REGN10933, REGN10987) ability to reduce viral load via SARS-CoV-2 spike protein binding in resus macaques and golden hamsters. They found a 50 mg/kg dose significantly reduced SARS-CoV-2 gRNA (p

Your first spiritual centers or chakras are your gonads and the cells of Leydig, which control your human sexual characteristics. To evolve to higher consciousness, we must first find balance at this most primal level. For thousands of years, this has been one of the most off-balance centers of our being! Doctor of human sexuality, sex and relationship expert, and podcast pioneer Emily Morse, from the popular SiriusXM radio show Sex with Emily, will deliver sex, dating, and relationship advice that will impact your life and spiritual growth on today's show.

Bradley R. Cairns, PhD, discusses his lab's work creating a transcriptional cell atlas of the developing human testis during puberty, revealing dramatic developmental changes in both germ and somatic niche cell lineages. Series: "Stem Cell Channel" [Show ID: 35452]

Bradley R. Cairns, PhD, discusses his lab's work creating a transcriptional cell atlas of the developing human testis during puberty, revealing dramatic developmental changes in both germ and somatic niche cell lineages. Series: "Stem Cell Channel" [Show ID: 35452]

Bradley R. Cairns, PhD, discusses his lab's work creating a transcriptional cell atlas of the developing human testis during puberty, revealing dramatic developmental changes in both germ and somatic niche cell lineages. Series: "Stem Cell Channel" [Show ID: 35452]

Bradley R. Cairns, PhD, discusses his lab's work creating a transcriptional cell atlas of the developing human testis during puberty, revealing dramatic developmental changes in both germ and somatic niche cell lineages. Series: "Stem Cell Channel" [Show ID: 35452]

Bradley R. Cairns, PhD, discusses his lab's work creating a transcriptional cell atlas of the developing human testis during puberty, revealing dramatic developmental changes in both germ and somatic niche cell lineages. Series: "Stem Cell Channel" [Show ID: 35452]

Bradley R. Cairns, PhD, discusses his lab's work creating a transcriptional cell atlas of the developing human testis during puberty, revealing dramatic developmental changes in both germ and somatic niche cell lineages. Series: "Stem Cell Channel" [Show ID: 35452]

Bradley R. Cairns, PhD, discusses his lab's work creating a transcriptional cell atlas of the developing human testis during puberty, revealing dramatic developmental changes in both germ and somatic niche cell lineages. Series: "Stem Cell Channel" [Show ID: 35452]

Bradley R. Cairns, PhD, discusses his lab's work creating a transcriptional cell atlas of the developing human testis during puberty, revealing dramatic developmental changes in both germ and somatic niche cell lineages. Series: "Stem Cell Channel" [Show ID: 35452]

What is red light therapy and how does it help to heal your body? In this episode, I interview the co-founder of Red Light Rising, Bryan Gohl, who talks about the benefits of red light therapy and why you should be interested in it. Visit https://www.bodyshotperformance.com/podcasts-blog for the complete show notes of every podcast episode. Topics Discussed in this Episode: Bryan’s wellness journey and how he got into red light therapy What is biohacking What are some examples of biohacking What is red light therapy What are the benefits of red light therapy Red Light Rising and their product offerings Using red light therapy on the genitals Why red light therapy is good for the eyes When is a good time to use the red light therapy Key Takeaways: Biohacking is basically altering your external or your internal environment to improve your health. It’s very closely linked to what we often refer to as ancestral lifestyle practices. Red light therapy is the intersection of science and technology that actually mimics nature. It’s mimicking some of the healthiest types of light that come from the sun. Red and infrared lights cause an increase in energy production on a cellular level. When the cells of the body are stimulated by red and infrared lights, there is also an increase in anti-inflammatory enzymes that get released into the blood. As science moves on and studies what’s happening in terms of red light therapy, they have been able to narrow it down to very specific wavelengths that are represented by numbers. And LED is important because they can be programmed by computers to be exactly on target with those numbers. Infrared light penetrates the body up to a depth of about 5 cm. Red light has been shown to increase energy production in the Leydig cells in the testicles, which are the cells that produce sperm. Action Steps: Give red light therapy a try. Bryan said: “What’s really exciting is that science is really starting to kind of inform us that light is so important. Light can be very, very harmful but it’s also vitally important for optimising our health.” “If you’re spending any amount of time in front of this light, you’re taking a bit of time out of your day to give yourself this therapy, you may as well get the most bang for your buck… You may as well get a boost of energy as well, because healing is very energy-intensive. ” Thanks for listening! If you’re interested in finding out what your health IQ is, take the Health IQ test to find out, and get a free 39-page report built around our six signals, which are sleep, mental health, energy, body composition, digestion, and fitness. If you’ve enjoyed what you’ve heard on this episode and it’s added value to you, share the episode with someone you think could benefit from it. And don’t forget to leave a rating or a review and subscribe on Apple Podcasts. Links to things we discuss in the show: Red Light Rising - Use the discount code BODYSHOTRED and get 5% off your purchase. The Bulletproof Diet: Lose Up to a Pound a Day, Reclaim Energy and Focus, Upgrade Your Life by Dave Asprey More from Bryan Gohl and Red Light Rising: Bryan’s Twitter (@bryangohl) Bryan’s Instagram (@bryan.gohl) Red Light Rising's Website Red Light Rising’s Instagram (@redlightrising) More from Leanne Spencer: Bodyshot Performance Bodyshot Performance Limited Facebook page Remove the Guesswork BOOK by Leanne SpencerRise and Shine BOOK by Leanne Spencer   Leanne’s Email

https://construyetufisico.com/fisiologia-ejercicio/aumentarla-testosterona/ Aumenta la testosterona de forma natural con 3 suplementos que funcionan, 3 hierbas científicamente probadas y 3 suplementos famosos que los estudios dicen que no funcionan. Cómo aumentar la Testosterona de forma natural La testosterona es esencial para la salud de los hombres (y de las mujeres). Que esto no es solo para los tíos petados. Las tías cañón también la necesitan Si le preguntas a la mayoría de los tíos ¿para qué sirve la testosterona? Es probable que digan que aumenta el músculo magro y aumenta la libido. Esta no es una mala respuesta, pero los beneficios de la testosterona van mucho más allá de esto. La testosterona baja tiene un impacto negativo en casi todos los sistemas principales del cuerpo masculino, incluida la resistencia a la insulina, obesidad, vidas más cortas, y enfermedades cardiovasculares. Por otro lado, mantener una erección (esta es la jodida), pérdida de cabello, fatiga, problemas con la memoria, pérdida de masa muscular y dificultad para ganar músculo, disminución de la densidad ósea, aumento de la grasa corporal y dificultad para perderla. Aparte tener un nivel más bajo de testosterona se ha relacionado con mayor riesgo de depresión, problemas cognitivos, trastornos metabólicos, diabetes y osteoporosis. Ahí es na. Lo que pasa es que esto no es algo que se vea de un día para otro. Esto es un proceso constante de meses y hasta años. Y no le prestas atención a los síntomas hasta que son muy evidentes. Algo como perder las ganas de guerra o ya la disfunción eréctil. Estudio1, Estudio2, Estudio3, Estudio4 Los niveles de testosterona, de manera natural, van bajando conforme nos hacemos viejos. Esto es así, asúmelo. Generalmente en 1-2% por año después de los 40 años. El rango normal para los niveles de testosterona varía mucho. En hombres adultos sanos, es entre 315 y 1,000 ng/dL. La mayoría de los hombres que tienen alguno (o varios) de los síntomas de niveles bajos de testosterona piensan que algún suplemento es la solución a sus problemas. No es tan fácil. Solo el 10% de los hombres adultos se encuentran a dos desviaciones estándar de la norma, lo que significa que solo uno de cada 10 puede ver los beneficios de la testosterona suplementaria, y esta tasa solo sube al 20% después de los 60 años. Y porque ahí los niveles ya son muy bajos. ¿Cómo produce la testosterona nuestro organismo? La producción de testosterona comienza en el cerebro. El hipotálamo es el “jefe” que dirige la movida que te voy a contar. Se secreta la hormona liberadora de gonadotropina (GnRH) en el hipotálamo. Esto estimula la liberación tanto de la hormona luteinizante (LH) como de la hormona estimulante del folículo (FSH) desde la hipófisis anterior (esto está en el cerebro). La LH actúa sobre las células de Leydig. Y estas son las que producen la testosterona en los testículos. Lo que lleva a los efectos fisiológicos que benefician la masa muscular magra, la libido, la sensibilidad mejorada a la insulina, etc. La testosterona se secreta en forma de pulsos para evitar inundar el torrente sanguíneo y regular a la baja los receptores de testosterona. Es por eso que tu cuerpo utiliza ciclos de retroalimentación negativa para controlar los niveles de testosterona en el cuerpo. la testosterona alta inhibe la GnRH del hipotálamo y a la LH / FSH de la hipófisis anterior a través del eje hipotálamo-hipófisis-gonadal (HPG) para controlar los niveles óptimos de testosterona. Y después de todo este tostón de teoría voy con lo que de verdad te importa. ¿Cómo cojones aumento los niveles de testosterona de manera natural? Primero saber por qué está baja la testosterona. ¿Qué hace bajar los niveles de testosterona? La barriga cervecera baja tus niveles de testosterona Si tiene una adiposidad abdominal significativa, necesitas perder grasita. La grasa de la barriga aumenta la actividad de una enzima llamada aromatasa, que convierte tu preciada testosterona en estrógeno. Esta es una de las principales causas de baja Testosterona para la mayoría de los hombres. Un 80% de los niveles de estradiol en la sangre se origina en el proceso de aromatización, que suprime el eje HPG, desregulando a la vez la producción natural de testosterona. La inflamación crónica reduce tu testosterona La grasa abdominal alta también está muy asociada con la inflamación crónica La inflamación altera la función mitocondrial saludable, importantísima para la producción normal de testosterona. Hiperinsulinemia Si tienes sobrepeso y tienes una grasa abdominal importante, no solo aumentarás la actividad de la aromatasa y la inflamación sistémica. Esto no solo afecta la producción de testosterona, sino también a los niveles altos de azúcar en la sangre y niveles de insulina. En la mayoría de los casos, esto normalmente es por los carbohidratos simples, procesados y azúcar. Los niveles altos de insulina cambiarán la salida de testosterona hacia la androstenediona, una forma mucho más débil de testosterona, que ocupa los receptores que ocuparía la testosterona normal. Dormir poco, testosterona baja Dormir es una de las mejores formas para aumentar la Testosterona baja. Y lo mejor de todo es que es completamente gratis. La persona promedio duerme aproximadamente seis horas y media por noche, y casi el 30% de la población duerme menos de seis cada noche. Este es un problema importante si tiene problemas con masa muscular, estado de ánimo, libido o salud general. Incluso en hombres jóvenes sanos, la falta de sueño es un factor importante para mantener altos los niveles de testosterona. El Diario de la Asociación Médica Americana encontró recientemente que los hombres saludables (con una edad promedio de 24 años) que dormían solo cinco horas por noche durante una semana experimentan una disminución del 10-15% en la testosterona. Y eso en tíos de 24. Imagínate los que estamos cerca de los 40. Mucho estrés, poca testosterona La hormona del estrés cortisól se deriva de los mismos bloques hormonales que la testosterona. Así que esto es fácil, o lo uno o lo otro. Te dejo un estudio donde se ve que los niveles bajos de testosterona es un síntoma común del sobreentrenamiento. Se producen efectos similares si trabajas largas horas, tienes demasiada presión laboral o no duermes lo suficiente. El estrés también empeora el azúcar en la sangre y el control de la insulina, lo que hace que tengas más grasa abdominal, inflamación crónica, hiperinsulinemia… Tres suplementos para aumentar la testosterona Vitamina D para aumentar la testosterona La vitamina D es esencial para la supervivencia humana. Regula más de 1,000 funciones corporales y está asociada con muchos beneficios para la salud, que incluyen un aumento de la inmunidad, huesos más fuertes y agudeza mental. Y también se relaciona con los niveles de testosterona. Se ha demostrado que los hombres con niveles de vitamina D suficientes, tienen niveles de testosterona significativamente más altos que los hombres con déficit de vitamina D. En un estudio, los hombres que se suplementaron con una dosis diaria de vitamina D durante un año tuvieron niveles de testosterona 25% más altos en comparación con el grupo con placebo. El sol proporciona una fuente importante de vitamina D, pero ya no pasamos suficiente tiempo al aire libre. Así que hay una deficiencia general a nivel mundial de vitamina D. Según el British Medical Journal, la deficiencia de vitamina D es la deficiencia nutricional más común en todo el mundo, tanto en niños como en adultos. El Zinc y la testosterona El zinc es un metal que nuestros cuerpos necesita en cantidades mínimas para asegurar un desarrollo y un crecimiento adecuados. Está en alimentos como la carne, los huevos, las legumbres y los mariscos. Y se pierde a través del sudor, por lo que es un mineral muy importante para los que hacemos ejercicio. En un estudio, unos atletas de élite que tomaron 3 mg de zinc por kg de peso corporal tuvieron niveles de testosterona significativamente más altos en comparación con el placebo. Algo parecido se encontró en hombres sedentarios que hacían ejercicio en una bicicleta estática. Sin embargo, el aumento en los niveles de testosterona solo pasa si hay un deficiente en zinc. Si ya estás tomando suficiente zinc a través de la dieta, tomar más zinc no va a aumentar más los niveles de testosterona. El magnesio y la testosterona El magnesio es otro mineral que se ha demostrado que tiene una relación directa con los niveles de testosterona en los hombres. En un estudio, a unos que practicaban artes marciales se les dio 10 mg de magnesio por kg de peso corporal. Después de cuatro semanas de suplementación diaria, tenían niveles de testosterona significativamente más altos. También es verdad que el mismo efecto se observó en el grupo de control sedentario, pero no fue tan pronunciado. Al igual que con la vitamina D, las deficiencias de magnesio son bastante comunes en el mundo occidental. Un estudio estimó que el 48% de la población de los EE. UU. Tenía niveles de magnesio por debajo del nivel óptimo. Pero como el con el zinc, el magnesio solo aumenta los niveles de testosterona si tienes deficiencia de magnesio (o de zinc). Tres hierbas para subir niveles de testosterona Hierba para potenciar la testosterona: Ashwagandha Ashwagandha es una hierba utilizada en Ayurveda, una rama de la antigua medicina herbal india. Tradicionalmente se ha utilizado para mejorar aspectos de la salud masculina. En sánscrito, ashwagandha se traduce como “olor a caballo”, lo que implica que tomando la hierba tendrás la fuerza y ??la virilidad de un semental. Pero aparte de las magufadas y de las creencias tradicionales, se ha demostrado en una investigación clínica en humanos que la ashwagandha tiene una mejora de la testosterona. Ashwagandha es una hierba adaptógena. ¿Lo cualo? Adaptógena significa que es eficaz para reducir los efectos físicos y químicos del estrés. Los estudios han demostrado que la suplementación con ashwagandha reduce bastante los niveles de cortisól. Te dejo un estudio con sujetos aleatorios, doble ciego, probado contra placebo. Este es de los buenos ¿he? Pues este estudio dice que la ashwagandha es segura y tiene eficacia reduciendo el estrés y la ansiedad. El cortisól es la hormona que el cuerpo libera en respuesta al estrés. Se deriva de la misma materia prima que la testosterona y tiene una relación inversa. menos cortisól = más testosterona. La suplementación con Ashwagandha también ha demostrado ser un estimulante eficaz de la testosterona en hombres infértiles. En otro estudio, hombres no entrenados empezaron un programa de entrenamiento de resistencia y, tomando Ashwagandha, vieron aumentos significativamente mayores en el tamaño muscular, los niveles de testosterona y recuperación muscular comparada con placebo. Ashwagandha es una súper hierba y uno de los únicos refuerzos de testosterona a base de hierbas comprobados. Aparte de por Ashwagandha también la puedes encontrar por el nombre de Withania somnifera. Hierba para potenciar la testosterona: Tongkat Ali Tongkat Ali es una hierba de Malasia que tradicionalmente se ha recetado como afrodisíaco. En un estudio, los sujetos que se suplementaron con 200 mg de Tongkat Ali diariamente durante un mes aumentaron los niveles de testosterona en un 46%. Tampoco nos flipemos. Para empezar hay que tener en cuenta que los sujetos en este estudio tenían niveles muy bajos de testosterona. En otro estudio, los sujetos con estrés crónico que recibieron una dosis diaria de Tongkat Ali durante un mes y tuvieron un aumento del 37% en los niveles de testosterona. Este estudio esta muy bien. Se hizo a 32 hombres y 31 mujeres. Y se encontraron mejoras significativas. El perfil hormonal del estrés (cortisól y testosterona) mejoró significativamente, con una reducción del cortisól (?16%) y un aumento de la testosterona (+ 37%). Aunque estos estudios dicen que la suplementación con Tongkat Ali tiene una influencia positiva en la testosterona, es importante tener en cuenta que los sujetos estaban estresados o tenían niveles muy bajos de testosterona, eso para empezar. Vamos que si tú estás sano y no estás estresado, lo normal es que esto no te haga nada. Lo que te digo es que te ayudará a que tengas niveles normales si están bajos. Pero nada más. Hierba para potenciar la testosterona: Mucuna Pruriens Mucuna Pruriens es un haba que se ha usado tradicionalmente para tratar la enfermedad de Parkinson. Hoy en día, es un ingrediente popular en muchos suplementos de testosterona. Dos estudios han demostrado que la suplementación con Mucuna Pruriens tiene un impacto significativo en los niveles de testosterona en hombres infértiles. El primero dice que la mucuna pruriens mejora la acción del eje hipotálamo-hipófisis-gonadal (HPG) que te conté al principio. Y el otro dice que mejora la calidad del semen, como consecuencia de un aumento de testosterona entre otras cosas. Aún queda por ver si este efecto continúa en hombres sanos. Que es lo que me interesa a mi. Y creo que a ti también. Yo no las he probado (aún), porque según que plantas es difícil que entren en Nueva Zelanda. Pero estoy detrás de ellas. En cuanto la pruebe te cuento. También te digo que después de revisar docenas de potenciadores de testosterona, parece surgir un patrón. Los ingredientes más populares son los que no tienen ninguna investigación que apoye su efectividad. Los siguientes tres suplemento se encuentran entre los que se ven con más frecuencia en los aumentadores de testosterona. Y no funcionan. Tres suplementos que no funcionan para mejorar la testosterona Suplementos demostrados que no aumentan la testosterona: Tribulus Terrestris Tribulus es quizás el ingrediente más popular en los suplementos de testosterona. Varios estudios han demostrado que la suplementación con Tribulus no tiene impacto en los niveles de testosterona, fuerza muscular o composición corporal. Nada más que añadir. Suplementos demostrados que no aumentan la testosterona: Ácido D-aspartámico Este es otro de los que siempre ves como ingrediente de los potenciadores de testosterona. Un primer estudio que observó el efecto del ácido D-aspartámico en la testosterona, reveló que la suplementación subió los niveles de testosterona en un 42% en tan solo 12 días de uso. Otro estudio demostró que la suplementación de ácido D-aspartámico durante 28 días no tuvo impacto en los niveles de testosterona. Después de eso, un tercer estudio reveló que las dosis altas de ácido D-aspartámico, en realidad, disminuían los niveles de testosterona. Entonces ¿en qué quedamos? Pues que no siempre hay que ir con lo que dice la investigación inicial. Lo más importante es mirar el contexto antes de saltar a cualquier conclusión, incluido el período de tiempo del estudio, el diseño del ensayo, el número de sujetos… Y si le preguntas a mi mujer te dirá también: quién lo ha hecho, que revista lo ha publicado, quienes son los revisores… Suplementos demostrados que no aumentan la testosterona: Maca Andina Este está siempre entre los ingredientes mágicos de los potenciadores de la testosterona. Te dejo un estudio de estos buenos, de doble ciego, contra placebo. Hombres entre 21 y 56 años fueron tratados con diferentes dosis de maca andina 1,5 o 3g por día). Miraron durante 12 semanas niveles de hormona luteinizante, hormona folicular, prolactina, 17-alfa hidroxiprogesterona, testosterona y 17-beta estradiol. En conclusión, que no mejora en nada la maca andina. Hay otro donde vieron que, si bien mejora el deseo sexual. No había ninguna mejora a nivel hormonal. ¿Por qué venden cosas que sabemos que no funcionan? Si la evidencia científica no ha encontrado beneficio significativo entre tribulus, maca y ácido aspartámico en los niveles de testosterona, ¿por qué las compañías continúan metiéndolos a sus productos? Se debe a que estos tres ingredientes son estimulantes de la libido. Vamos que aumentan el deseo sexual sin tener ningún efecto sobre la hormona testosterona. Una concentración mayor de la hormona testosterona se traduce en un impulso sexual mayor. Pero al revés no tiene porque ser así. El aumento del deseo sexual no siempre resulta del aumento de testosterona De hecho, estos tres suplementos si que los he probado personalmente. Y te voy a dar una sorpresa. No me hicieron nada de nada. Tu sistema endocrino es muy complejo Si quieres aumentar los niveles de testosterona, ten en cuenta que tu sistema endocrino es demasiado complejo para ser manipulado con una simple pastillita o unos polvos. Lo que tienes que hacer es empezar por el principio, el de este post, y hacer cambios en tu estilo de vida. Lo que se reduce a esto: El exceso de grasa corporal produce una enzima que convierte la testosterona en estrógeno. Asegúrate de comer los macro y (y sobre todo) micronutrientes esenciales. Hazte más fuerte. Dormir de siete a nueve horas cada noche. Nueve mejor que siete. Gestiona tu estrés. Un desequilibrio en estas cinco áreas es lo que te lleva a tener bajos los niveles de testosterona. Y como no cambies todo eso, ya puedes tomar todos los suplementos que quieras, que no habrá manera de que esto suba. Yo soy de los que piensa que los suplementos solo deben usarse para lo que están hechos: para complementar (suplementar) una buena dieta y un buen estilo de vida. No te dejes engañar por el marketing. Si algo parece demasiado bueno para ser verdad, lo más probable es que no lo sea. Yo sé que perder grasa cuesta, comer bien cuesta, dormir lo que necesitas cuesta, entrenar duro cuesta, cambiar el trabajo o tu entorno porque es muy estresante cuesta. Pero si piensas que todo eso lo puedes solucionar con un bote de pastillas por 20 pavos es que no tienes muchas luces. Y yo todo esto lo he montado para tener un ejercito de tíos petados y tías cañón para dominar el mundo. Y no quiero tontos entre mis filas. Un saludo y felices agujetas.

https://construyetufisico.com/fisiologia-ejercicio/aumentarla-testosterona/ Aumenta la testosterona de forma natural con 3 suplementos que funcionan, 3 hierbas científicamente probadas y 3 suplementos famosos que los estudios dicen que no funcionan. Cómo aumentar la Testosterona de forma natural La testosterona es esencial para la salud de los hombres (y de las mujeres). Que esto no es solo para los tíos petados. Las tías cañón también la necesitan Si le preguntas a la mayoría de los tíos ¿para qué sirve la testosterona? Es probable que digan que aumenta el músculo magro y aumenta la libido. Esta no es una mala respuesta, pero los beneficios de la testosterona van mucho más allá de esto. La testosterona baja tiene un impacto negativo en casi todos los sistemas principales del cuerpo masculino, incluida la resistencia a la insulina, obesidad, vidas más cortas, y enfermedades cardiovasculares. Por otro lado, mantener una erección (esta es la jodida), pérdida de cabello, fatiga, problemas con la memoria, pérdida de masa muscular y dificultad para ganar músculo, disminución de la densidad ósea, aumento de la grasa corporal y dificultad para perderla. Aparte tener un nivel más bajo de testosterona se ha relacionado con mayor riesgo de depresión, problemas cognitivos, trastornos metabólicos, diabetes y osteoporosis. Ahí es na. Lo que pasa es que esto no es algo que se vea de un día para otro. Esto es un proceso constante de meses y hasta años. Y no le prestas atención a los síntomas hasta que son muy evidentes. Algo como perder las ganas de guerra o ya la disfunción eréctil. Estudio1, Estudio2, Estudio3, Estudio4 Los niveles de testosterona, de manera natural, van bajando conforme nos hacemos viejos. Esto es así, asúmelo. Generalmente en 1-2% por año después de los 40 años. El rango normal para los niveles de testosterona varía mucho. En hombres adultos sanos, es entre 315 y 1,000 ng/dL. La mayoría de los hombres que tienen alguno (o varios) de los síntomas de niveles bajos de testosterona piensan que algún suplemento es la solución a sus problemas. No es tan fácil. Solo el 10% de los hombres adultos se encuentran a dos desviaciones estándar de la norma, lo que significa que solo uno de cada 10 puede ver los beneficios de la testosterona suplementaria, y esta tasa solo sube al 20% después de los 60 años. Y porque ahí los niveles ya son muy bajos. ¿Cómo produce la testosterona nuestro organismo? La producción de testosterona comienza en el cerebro. El hipotálamo es el “jefe” que dirige la movida que te voy a contar. Se secreta la hormona liberadora de gonadotropina (GnRH) en el hipotálamo. Esto estimula la liberación tanto de la hormona luteinizante (LH) como de la hormona estimulante del folículo (FSH) desde la hipófisis anterior (esto está en el cerebro). La LH actúa sobre las células de Leydig. Y estas son las que producen la testosterona en los testículos. Lo que lleva a los efectos fisiológicos que benefician la masa muscular magra, la libido, la sensibilidad mejorada a la insulina, etc. La testosterona se secreta en forma de pulsos para evitar inundar el torrente sanguíneo y regular a la baja los receptores de testosterona. Es por eso que tu cuerpo utiliza ciclos de retroalimentación negativa para controlar los niveles de testosterona en el cuerpo. la testosterona alta inhibe la GnRH del hipotálamo y a la LH / FSH de la hipófisis anterior a través del eje hipotálamo-hipófisis-gonadal (HPG) para controlar los niveles óptimos de testosterona. Y después de todo este tostón de teoría voy con lo que de verdad te importa. ¿Cómo cojones aumento los niveles de testosterona de manera natural? Primero saber por qué está baja la testosterona. ¿Qué hace bajar los niveles de testosterona? La barriga cervecera baja tus niveles de testosterona Si tiene una adiposidad abdominal significativa, necesitas perder grasita. La grasa de la barriga aumenta la actividad de una enzima llamada aromatasa, que convierte tu preciada testosterona en estrógeno. Esta es una de las principales causas de baja Testosterona para la mayoría de los hombres. Un 80% de los niveles de estradiol en la sangre se origina en el proceso de aromatización, que suprime el eje HPG, desregulando a la vez la producción natural de testosterona. La inflamación crónica reduce tu testosterona La grasa abdominal alta también está muy asociada con la inflamación crónica La inflamación altera la función mitocondrial saludable, importantísima para la producción normal de testosterona. Hiperinsulinemia Si tienes sobrepeso y tienes una grasa abdominal importante, no solo aumentarás la actividad de la aromatasa y la inflamación sistémica. Esto no solo afecta la producción de testosterona, sino también a los niveles altos de azúcar en la sangre y niveles de insulina. En la mayoría de los casos, esto normalmente es por los carbohidratos simples, procesados y azúcar. Los niveles altos de insulina cambiarán la salida de testosterona hacia la androstenediona, una forma mucho más débil de testosterona, que ocupa los receptores que ocuparía la testosterona normal. Dormir poco, testosterona baja Dormir es una de las mejores formas para aumentar la Testosterona baja. Y lo mejor de todo es que es completamente gratis. La persona promedio duerme aproximadamente seis horas y media por noche, y casi el 30% de la población duerme menos de seis cada noche. Este es un problema importante si tiene problemas con masa muscular, estado de ánimo, libido o salud general. Incluso en hombres jóvenes sanos, la falta de sueño es un factor importante para mantener altos los niveles de testosterona. El Diario de la Asociación Médica Americana encontró recientemente que los hombres saludables (con una edad promedio de 24 años) que dormían solo cinco horas por noche durante una semana experimentan una disminución del 10-15% en la testosterona. Y eso en tíos de 24. Imagínate los que estamos cerca de los 40. Mucho estrés, poca testosterona La hormona del estrés cortisól se deriva de los mismos bloques hormonales que la testosterona. Así que esto es fácil, o lo uno o lo otro. Te dejo un estudio donde se ve que los niveles bajos de testosterona es un síntoma común del sobreentrenamiento. Se producen efectos similares si trabajas largas horas, tienes demasiada presión laboral o no duermes lo suficiente. El estrés también empeora el azúcar en la sangre y el control de la insulina, lo que hace que tengas más grasa abdominal, inflamación crónica, hiperinsulinemia… Tres suplementos para aumentar la testosterona Vitamina D para aumentar la testosterona La vitamina D es esencial para la supervivencia humana. Regula más de 1,000 funciones corporales y está asociada con muchos beneficios para la salud, que incluyen un aumento de la inmunidad, huesos más fuertes y agudeza mental. Y también se relaciona con los niveles de testosterona. Se ha demostrado que los hombres con niveles de vitamina D suficientes, tienen niveles de testosterona significativamente más altos que los hombres con déficit de vitamina D. En un estudio, los hombres que se suplementaron con una dosis diaria de vitamina D durante un año tuvieron niveles de testosterona 25% más altos en comparación con el grupo con placebo. El sol proporciona una fuente importante de vitamina D, pero ya no pasamos suficiente tiempo al aire libre. Así que hay una deficiencia general a nivel mundial de vitamina D. Según el British Medical Journal, la deficiencia de vitamina D es la deficiencia nutricional más común en todo el mundo, tanto en niños como en adultos. El Zinc y la testosterona El zinc es un metal que nuestros cuerpos necesita en cantidades mínimas para asegurar un desarrollo y un crecimiento adecuados. Está en alimentos como la carne, los huevos, las legumbres y los mariscos. Y se pierde a través del sudor, por lo que es un mineral muy importante para los que hacemos ejercicio. En un estudio, unos atletas de élite que tomaron 3 mg de zinc por kg de peso corporal tuvieron niveles de testosterona significativamente más altos en comparación con el placebo. Algo parecido se encontró en hombres sedentarios que hacían ejercicio en una bicicleta estática. Sin embargo, el aumento en los niveles de testosterona solo pasa si hay un deficiente en zinc. Si ya estás tomando suficiente zinc a través de la dieta, tomar más zinc no va a aumentar más los niveles de testosterona. El magnesio y la testosterona El magnesio es otro mineral que se ha demostrado que tiene una relación directa con los niveles de testosterona en los hombres. En un estudio, a unos que practicaban artes marciales se les dio 10 mg de magnesio por kg de peso corporal. Después de cuatro semanas de suplementación diaria, tenían niveles de testosterona significativamente más altos. También es verdad que el mismo efecto se observó en el grupo de control sedentario, pero no fue tan pronunciado. Al igual que con la vitamina D, las deficiencias de magnesio son bastante comunes en el mundo occidental. Un estudio estimó que el 48% de la población de los EE. UU. Tenía niveles de magnesio por debajo del nivel óptimo. Pero como el con el zinc, el magnesio solo aumenta los niveles de testosterona si tienes deficiencia de magnesio (o de zinc). Tres hierbas para subir niveles de testosterona Hierba para potenciar la testosterona: Ashwagandha Ashwagandha es una hierba utilizada en Ayurveda, una rama de la antigua medicina herbal india. Tradicionalmente se ha utilizado para mejorar aspectos de la salud masculina. En sánscrito, ashwagandha se traduce como “olor a caballo”, lo que implica que tomando la hierba tendrás la fuerza y ??la virilidad de un semental. Pero aparte de las magufadas y de las creencias tradicionales, se ha demostrado en una investigación clínica en humanos que la ashwagandha tiene una mejora de la testosterona. Ashwagandha es una hierba adaptógena. ¿Lo cualo? Adaptógena significa que es eficaz para reducir los efectos físicos y químicos del estrés. Los estudios han demostrado que la suplementación con ashwagandha reduce bastante los niveles de cortisól. Te dejo un estudio con sujetos aleatorios, doble ciego, probado contra placebo. Este es de los buenos ¿he? Pues este estudio dice que la ashwagandha es segura y tiene eficacia reduciendo el estrés y la ansiedad. El cortisól es la hormona que el cuerpo libera en respuesta al estrés. Se deriva de la misma materia prima que la testosterona y tiene una relación inversa. menos cortisól = más testosterona. La suplementación con Ashwagandha también ha demostrado ser un estimulante eficaz de la testosterona en hombres infértiles. En otro estudio, hombres no entrenados empezaron un programa de entrenamiento de resistencia y, tomando Ashwagandha, vieron aumentos significativamente mayores en el tamaño muscular, los niveles de testosterona y recuperación muscular comparada con placebo. Ashwagandha es una súper hierba y uno de los únicos refuerzos de testosterona a base de hierbas comprobados. Aparte de por Ashwagandha también la puedes encontrar por el nombre de Withania somnifera. Hierba para potenciar la testosterona: Tongkat Ali Tongkat Ali es una hierba de Malasia que tradicionalmente se ha recetado como afrodisíaco. En un estudio, los sujetos que se suplementaron con 200 mg de Tongkat Ali diariamente durante un mes aumentaron los niveles de testosterona en un 46%. Tampoco nos flipemos. Para empezar hay que tener en cuenta que los sujetos en este estudio tenían niveles muy bajos de testosterona. En otro estudio, los sujetos con estrés crónico que recibieron una dosis diaria de Tongkat Ali durante un mes y tuvieron un aumento del 37% en los niveles de testosterona. Este estudio esta muy bien. Se hizo a 32 hombres y 31 mujeres. Y se encontraron mejoras significativas. El perfil hormonal del estrés (cortisól y testosterona) mejoró significativamente, con una reducción del cortisól (?16%) y un aumento de la testosterona (+ 37%). Aunque estos estudios dicen que la suplementación con Tongkat Ali tiene una influencia positiva en la testosterona, es importante tener en cuenta que los sujetos estaban estresados o tenían niveles muy bajos de testosterona, eso para empezar. Vamos que si tú estás sano y no estás estresado, lo normal es que esto no te haga nada. Lo que te digo es que te ayudará a que tengas niveles normales si están bajos. Pero nada más. Hierba para potenciar la testosterona: Mucuna Pruriens Mucuna Pruriens es un haba que se ha usado tradicionalmente para tratar la enfermedad de Parkinson. Hoy en día, es un ingrediente popular en muchos suplementos de testosterona. Dos estudios han demostrado que la suplementación con Mucuna Pruriens tiene un impacto significativo en los niveles de testosterona en hombres infértiles. El primero dice que la mucuna pruriens mejora la acción del eje hipotálamo-hipófisis-gonadal (HPG) que te conté al principio. Y el otro dice que mejora la calidad del semen, como consecuencia de un aumento de testosterona entre otras cosas. Aún queda por ver si este efecto continúa en hombres sanos. Que es lo que me interesa a mi. Y creo que a ti también. Yo no las he probado (aún), porque según que plantas es difícil que entren en Nueva Zelanda. Pero estoy detrás de ellas. En cuanto la pruebe te cuento. También te digo que después de revisar docenas de potenciadores de testosterona, parece surgir un patrón. Los ingredientes más populares son los que no tienen ninguna investigación que apoye su efectividad. Los siguientes tres suplemento se encuentran entre los que se ven con más frecuencia en los aumentadores de testosterona. Y no funcionan. Tres suplementos que no funcionan para mejorar la testosterona Suplementos demostrados que no aumentan la testosterona: Tribulus Terrestris Tribulus es quizás el ingrediente más popular en los suplementos de testosterona. Varios estudios han demostrado que la suplementación con Tribulus no tiene impacto en los niveles de testosterona, fuerza muscular o composición corporal. Nada más que añadir. Suplementos demostrados que no aumentan la testosterona: Ácido D-aspartámico Este es otro de los que siempre ves como ingrediente de los potenciadores de testosterona. Un primer estudio que observó el efecto del ácido D-aspartámico en la testosterona, reveló que la suplementación subió los niveles de testosterona en un 42% en tan solo 12 días de uso. Otro estudio demostró que la suplementación de ácido D-aspartámico durante 28 días no tuvo impacto en los niveles de testosterona. Después de eso, un tercer estudio reveló que las dosis altas de ácido D-aspartámico, en realidad, disminuían los niveles de testosterona. Entonces ¿en qué quedamos? Pues que no siempre hay que ir con lo que dice la investigación inicial. Lo más importante es mirar el contexto antes de saltar a cualquier conclusión, incluido el período de tiempo del estudio, el diseño del ensayo, el número de sujetos… Y si le preguntas a mi mujer te dirá también: quién lo ha hecho, que revista lo ha publicado, quienes son los revisores… Suplementos demostrados que no aumentan la testosterona: Maca Andina Este está siempre entre los ingredientes mágicos de los potenciadores de la testosterona. Te dejo un estudio de estos buenos, de doble ciego, contra placebo. Hombres entre 21 y 56 años fueron tratados con diferentes dosis de maca andina 1,5 o 3g por día). Miraron durante 12 semanas niveles de hormona luteinizante, hormona folicular, prolactina, 17-alfa hidroxiprogesterona, testosterona y 17-beta estradiol. En conclusión, que no mejora en nada la maca andina. Hay otro donde vieron que, si bien mejora el deseo sexual. No había ninguna mejora a nivel hormonal. ¿Por qué venden cosas que sabemos que no funcionan? Si la evidencia científica no ha encontrado beneficio significativo entre tribulus, maca y ácido aspartámico en los niveles de testosterona, ¿por qué las compañías continúan metiéndolos a sus productos? Se debe a que estos tres ingredientes son estimulantes de la libido. Vamos que aumentan el deseo sexual sin tener ningún efecto sobre la hormona testosterona. Una concentración mayor de la hormona testosterona se traduce en un impulso sexual mayor. Pero al revés no tiene porque ser así. El aumento del deseo sexual no siempre resulta del aumento de testosterona De hecho, estos tres suplementos si que los he probado personalmente. Y te voy a dar una sorpresa. No me hicieron nada de nada. Tu sistema endocrino es muy complejo Si quieres aumentar los niveles de testosterona, ten en cuenta que tu sistema endocrino es demasiado complejo para ser manipulado con una simple pastillita o unos polvos. Lo que tienes que hacer es empezar por el principio, el de este post, y hacer cambios en tu estilo de vida. Lo que se reduce a esto: El exceso de grasa corporal produce una enzima que convierte la testosterona en estrógeno. Asegúrate de comer los macro y (y sobre todo) micronutrientes esenciales. Hazte más fuerte. Dormir de siete a nueve horas cada noche. Nueve mejor que siete. Gestiona tu estrés. Un desequilibrio en estas cinco áreas es lo que te lleva a tener bajos los niveles de testosterona. Y como no cambies todo eso, ya puedes tomar todos los suplementos que quieras, que no habrá manera de que esto suba. Yo soy de los que piensa que los suplementos solo deben usarse para lo que están hechos: para complementar (suplementar) una buena dieta y un buen estilo de vida. No te dejes engañar por el marketing. Si algo parece demasiado bueno para ser verdad, lo más probable es que no lo sea. Yo sé que perder grasa cuesta, comer bien cuesta, dormir lo que necesitas cuesta, entrenar duro cuesta, cambiar el trabajo o tu entorno porque es muy estresante cuesta. Pero si piensas que todo eso lo puedes solucionar con un bote de pastillas por 20 pavos es que no tienes muchas luces. Y yo todo esto lo he montado para tener un ejercito de tíos petados y tías cañón para dominar el mundo. Y no quiero tontos entre mis filas. Un saludo y felices agujetas.

1 John 2:18-23 (KJV) 18 Little children, it is the last time: and as ye have heard that antichrist shall come, even now are there many antichrists; whereby we know that it is the last time. 19 They went out from us, but they were not of us; for if they had been of us, they would no doubt have continued with us: but they went out, that they might be made manifest that they were not all of us. 20 But ye have an unction from the Holy One, and ye know all things. 21 I have not written unto you because ye know not the truth, but because ye know it, and that no lie is of the truth. 22 Who is a liar but he that denieth that Jesus is the Christ? He is antichrist, that denieth the Father and the Son. 23 Whosoever denieth the Son, the same hath not the Father: (but) he that acknowledgeth the Son hath the Father also.    

Sat, 1 Jan 2011 12:00:00 +0100 https://epub.ub.uni-muenchen.de/16880/1/10_1159_000330556.pdf Schneider, Marlon R. ddc:610, Medizin

Background: Sertoli-Leyclig cell tumours of the ovary account for only 0.2% of malignant ovarian tumours. Two-thirds of all patients become apparent due to the tumour's hormone production. Methods: A 41-year-old patient (gravida 4, para 4) presented with dyspnoea, enlarged abdominal girth and melaena. Diagnostic imaging was suspicious for an ovarian cancer. The standard tumour marker for ovarian cancer (CA 125) was elevated to 984 U/mL. Results: Surgical exploration of the abdomen revealed a mouldering tumour of both adnexes extending to the level of the navel. Frozen sections showed an undifferentiated carcinoma of unknown origin. Radical surgery was performed. The final histological report described a malignant sex-cord stroma tumour, a Sertoli-Leydig cell tumour, emanating from both ovaries. Analysis of preoperative blood serum showed elevated levels of CYFRA 21-1 (10.4 ng/mL), neuron-specific enolase (36.2 ng/mL), oestradiol (485 pg/mL) and CA-125 (984 U/mL). Adjuvant chemotherapy and regional hyperthermia were performed due to the malignant potential and incomplete resection of the tumour. Conclusions: Undifferentiated Sertoli-Leyclig cell tumours show a poor clinical course. As only two-thirds of patients with this rare disease present with elevated hormone levels, new markers deserve further investigation to offer more specific, individualised tumour monitoring.

In dieser Arbeit wurde das GABAerge System in Leydig-Zellen detailliert analysiert. Mehrere GABAA und GABAC Rezeptor Untereinheiten sowie das GABA synthetisierende Enzym GAD 67 und der vesikuläre GABA Transporter VIAAT konnten mit RT – PCR, Western Blot und Immunfluoreszenz-Experimenten in TM3, Leydig-Tumorzellen, und primären adulten Leydig-Zellen nachgewiesen werden. Es gelang molekulare Signaltransduktionswege von GABA aufzudecken: Gen Array, Western Blot und semiquantitative RT – PCR Experimente zeigten, dass GABA und der GABAA Rezeptor Agonist Isoguvacin den Transkriptionsfaktor egr-1 in TM3 und adulten Leydig-Zellen induzieren. Western Blot Experimente lassen schließen, dass GABA vermittelt über GABAA Rezeptoren die MAP – Kinasen ERK 1/2 in TM3 Zellen phosphoryliert und somit in den enzymatisch aktiven Zustand überführt. In primären adulten Leydig-Zellen konnte weiterhin gezeigt werden, dass GABA die Testosteron Produktion steigert. Elektrophysiologische Untersuchungen der TM3 und der primären adulten Leydig-Zellen zeigten schließlich, dass das initiale GABA Signal nicht über einen für GABAA Rezeptor typischen Cl--Strom vermittelt wird. Die RT – PCR Analyse von postnatalen Mäusehoden ergab ebenfalls, dass GAD 67, VIAAT und mehreren GABAA und GABAC Rezeptor Untereinheiten in dieser Entwicklungsphase des Hodens anwesend sind und lieferten ferner Hinweise dafür, dass sich insbesondere die Expression der Rezeptor Untereinheiten in der postnatalen Periode im Hoden ändert. Darüber hinaus konnte nachgewiesen werden, dass proliferierende interstitielle Zellen im postnatalen Rattenhoden immunopositiv für egr-1 sind. Somit ist eine physiologische Funktion von egr-1 in dieser Phase der Leydig-Zellentwicklung plausibel.

In the present study, the testes of 32 bovine embryos with different crown-rump length (2.5- 90 cm CRL) and of 15 sexually mature bulls (Deutsches Fleckvieh) were investigated using light- and electron microscope as well as glycohistochemical and immunohistochemical methods. The gestation period was divided into 3 stages; early, mid, and late gestation. Developmental changes in the testicular morphogenesis were therefore analyzed in details during these phases. Generally, embryonic development of bovine testis involves the same mechanism described in other mammals. At the first stage of this study (2.5 cm CRL/43 dpc), the anlage of the testes protruded to the coelomic cavity as paired bean-shaped structures on either side of the dorsal mesentery medial to the mesonephros. It consists of primitive testicular cords, interstitium, and rete testis blastema. Proceeding with fetal age, these basic testicular structures are further differentiated. The tunica albuginea is separated into two layers: an outer fibrous layer (tunica fibrosa) with some mesenchymal cells, numerous fibroblast, and much fibrous content and an inner cellular layer with several blood vessels (tunica vasculosa). The testicular cords are surrounded by a marked basal lamina and peritubular cells and lined by two types of cells: a large number of dark polygonal cells with irregular nuclei, pre-Sertoli cells and small number of large light round cells with relatively round nuclei, the prespermatogonia. The average number of the germ cells per cross section of cord increases, particularly form 3.5 to 14 cm CRL, resulting in a germ cell maximum at the end of this stage (14 cm CRL). Although most of the germ cells are located toward the periphery of the cord, some are also found in the center. Pre-Sertoli cells form a complete layer at the periphery of the cords. Generally, these cells are irregular in shape and numerous but considerably smaller than the germ cells. Unlike prespermatogonia, mitotic figures are seen in pre-Sertoli cells during the whole embryonic life. As a consequence of the expansion in the interstitium, the seminiferous cords are progressively separated from each other. The testicular interstitium is rapidly differentiated and is composed of several islets or clusters of polygonal Leydig cells, peritubular flattened cells surrounding the testicular cords, connective tissue cells, and numerous blood vessels. In the present study, fetal Leydig cells were first recognized at 3.5 cm CRL. Thereafter, the average number of these cells is rapidly increased to attain their maximum with the end of the first gestation period (14 cm CRL). This generation of Leydig cells however dedifferentiates progressively with developmental age. A continuous system of basal lamina joins the testicular cords with rete strands from 10 cm CRL and onwards. This system establishes the first connection between these two testicular components via ill-developed uncanalized straight tubules (tubuli recti). Rete testis channels are lined by simple layer of cuboidal epithelium with round nuclei occupying most of the cytoplasm and enclosed by well-defined basal lamina. The adult bovine testis is enclosed by a connective tissue capsule, tunica albuginea, composed predominantly of collagen fibers and few elastic fibers. Most of the testicular parenchyma is made up of the convoluted seminiferous tubules (tubuli seminiferi contorti), two-ended convoluted loops, with both ends opening into the rete testis via specialized terminal segments. The seminiferous tubules of sexually mature bulls are enclosed by a distinct lamina propria and are lined by two cell populations, non-proliferating Sertoli cells and highly proliferating spermatogenic cells. The bovine lamina propria consists of basal lamina, collagen and elastic fibers, and 3-5 layers of partially overlapping myofibroblasts. Additionally, fibrocytes, collagen fibrils, and fibroblasts-like cells form the outermost border of the tubulus. Sertoli cells are easily identifiable elements of the seminiferous epithelium. Adult Sertoli cells are large irregularly shaped cells with their broad bases resting on the basal lamina while the remaining cytoplasmic processes extend upward to the tubular lumen. They are characterized by round or oval euchromatin-rich nuclei situating in the basal portion near the basal lamina of the seminiferous tubules. Adult bovine germ cells are present in four morphologically different groups, i.e., spermatogonia, spermatocytes, spermatids, and spermatozoa. The seminiferous cycle stages are identified using changes in the germ cell nuclei as well as location and shape of spermatids. According to this method, eight stages are defined in the seminiferous epithelium of bovine. The interstitial or intertubular tissue of adult bovine testis consists of Leydig cells, macrophages, scattered lymphocytes and plasma cells, and contains numerous blood and lymph vessels. Not all Leydig cells have contact to blood or lymph capillaries. The excurrent duct system of the adult bovine testis consists of terminal segment of the convoluted seminiferous tubules, straight tubules, and rete testis. The terminal segment can be further subdivided into a proximal (transitional) region, middle portion, and distal part (terminal plug). The proximal region is lined by typical Sertoli cells while the last two parts are lined by modified Sertoli cells. The tubulus rectus of adult bovine testis is composed of three morphologically different regions: a proximal cup-shaped region, a middle narrow stalk, and a distal festooned portion. The rete testis is a complicated centrally positioned meshwork of intercommunicating channels that lies within the mediastinum testis parallel to the long axis of epididymis. The simple cuboidal epithelium of straight tubules and rete testis is shown to contain some lymphocytes and macrophages. The cellular distribution of glycoconjugates within the fetal and adult bovine testis was investigated using thirteen (ConA, PSA, LCA, PNA, GSA-I, ECA, DBA, SBA, HPA, VVA, WGA, UEA-I, LTA) different fluorescein isothiocyanate (FITC) conjugated lectins. In fetal testes, detection of sugar moieties by lectins was carried out on Bouin õ s-fixed paraffin-embedded sections while in adult it was performed on both Bouin õ s-fixed paraffin-embedded and acetone-fixed frozen sections. Only five lectins (PSA, PNA, GSA-I, DBA, WGA) showed a positive reaction in the embryonic testes. PNA, GSA-I, DBA, and WGA were detected in the germ cells whereas PSA, DBA and WGA labeled the fetal Leydig cells. None of the lectins used was observed in the pre-Sertoli cells. Further on, some lectins were seen in tunica albuginea (PSA, PNA, GSA-I, WGA), basal lamina of testicular cords (PSA, WGA), interstitial blood vessels (PSA, GSA-I, WGA), mediastinum testis (PSA, PNA, WGA) and rete testis epithelium (PNA). In adult animals, spermatogonia and spermatocytes were positively stained with PSA, LCA, DBA, SBA, and VVA. All the lectins investigated except that of the fucose-binding lectin (UEA-I and LTA) were definitely detected in the acrosome of round and elongated spermatids. These results indicate a role for carbohydrates in spermiogenesis. Apical Sertoli cells processes and Leydig cells were weakly stained with PSA and LCA as well. DBA binding sites were also seen in the Leydig cells. Immunohistochemical studies were performed using the Avidin-Biotin-Peroxidase Complex (ABC) method for localization of fibroblast growth factor-1 (FGF-1), fibroblast growth factor-2 (FGF-2), S-100, laminin, alpha-smooth muscle actin (á -SMA), vascular endothelial growth factor (VEGF), connexin 43 (Cx43), CD4, CD8, CD68, angiotensin-converting enzyme (ACE), and galactosyltransferase (GalTase) in the bovine testis. The expression of FGF-1 and FGF-2 was further investigated in the adult bovine testis using in situ hybridization and PCR. Immunohistochemically, FGF-1 was seen in the Sertoli cells, Leydig cells, endothelium of the blood vessels, and epithelium of straight tubules and rete testis of fetal and adult testis. It was additionally detected in spermatogonia and spermatids of sexual mature animals. FGF-2 exhibited a striking positive reaction in fetal (from 6 to 30 cm CRL) and adult Leydig cells. Moreover, it showed marked reaction in the endothelium of blood vessels and in the epithelium of tubulus rectus and rete testis. FGF-2 was also localized in some spermatogonia, and myofibroblasts. By means of in situ hybridization, FGF-1 and FGF-2 mRNA were found in Leydig and Sertoli cells as well as in the modified Sertoli cells of the terminal segment. FGF-1 transcripts were additionally recognized in the straight tubules and rete testis epithelium. Distinct S100 immunostaining was observed in the Sertoli cells, endothelium of blood vessels and in the rete testis epithelium of fetal and adult testis. Laminin was localized to the basal lamina of seminiferous tubules, blood vessels, myofibroblasts, and rete testis. Although á -SMA was detected in smooth muscle cells of the blood vessels, no immunoreactivity was seen in the peritubular cells during the whole gestation period. The myofibroblasts surrounding the seminiferous tubules and rete testis showed intense positive reaction for á -SMA in the adult testis. VEGF was detected in the acrosomes of the elongating spermatids. Connexin 43 was localized to gap junctions between Leydig cells in the fetal and adult life as well as to the seminiferous epithelium apical to spermatogonia and basal to spermatocytes, a position correlating with Sertoli-Sertoli cell junctions. The detection of cells positive for CD4, CD8, CD68 within the adult testis interstitium clearly indicate the presence of lymphocytes and macrophages within this testicular compartment. GalTase showed striking positive reaction in the Golgi complex of Sertoli cells, Leydig cells, and some spermatocytes as well as at the cell membrane of elongating spermatids and in the simple cuboidal epithelium of rete testis. ACE positive reaction was found in the prespermatogonia (only at 6-10 cm CRL) and in fetal and adult testicular blood vessels. The functional significance of these immunocytochemically-demonstrated proteins is discussed.

gamma-Aminobutyric acid (GABA) is an emerging signalling molecule in endocrine organs, since it is produced by endocrine cells and acts via GABA(A) receptors in a paracrine/autocrine fashion. Testicular Leydig cells are producers and targets for GABA. These cells express GABA(A) receptor subunits and in the murine Leydig cell line TM3 pharmacological activation leads to increased proliferation. The signalling pathway of GABA in these cells is not known in this study. We therefore attempted to elucidate details of GABA(A) signalling in TM3 and adult mouse Leydig cells using several experimental approaches. TM3 cells not only express GABA(A) receptor subunits, but also bind the GABA agonist {[}H-3] muscimol with a binding affinity in the range reported for other endocrine cells (K-d = 2.740 +/- 0.721 nM). However, they exhibit a low B-max value of 28.08 fmol/mg protein. Typical GABA(A) receptor-associated events, including Cl- currents, changes in resting membrane potential, intracellular Ca2+ or cAMP, were not measurable with the methods employed in TM3 cells, or, as studied in part, in primary mouse Leydig cells. GABA or GABA(A) agonist isoguvacine treatment resulted in increased or decreased levels of several mRNAs, including transcription factors (c-fos, hsf-1, egr-1) and cell cycle-associated genes (Cdk2, cyclin D1). In an attempt to verify the cDNA array results and because egr-1 was recently implied in Leydig cell development, we further studied this factor. RT-PCR and Western blotting confirmed a time-dependent regulation of egr-1 in TM3. In the postnatal testis egr-1 was seen in cytoplasmic and nuclear locations of developing Leydig cells, which bear GABA(A) receptors and correspond well to TM3 cells. Thus, GABA acts via an untypical novel signalling pathway in TM3 cells. Further details of this pathway remain to be elucidated. Copyright (c) 2005 S. Karger AG, Basel

The influence of estrogen-like substances on the gonadal development in frogs (Rana temporaria and Xenopus laevis). Ultrastructural and immunohistochemical investiga-tions on the gonads of frogs (Rana temporaria). The aim of the present thesis was the investigation and assessment of the estrogen pollu-tion of a river in South-Germany above and below a sewage plant outlet and its possible effects on the gonadal development in amphibians. In an exposure experiment with differ-ent sewage dilutions the effect on the indigenous gras frog (Rana temporaria) were com-pared with the effects on the African claw frog (Xenopus laevis). Because of the lack of relevant data in current literature it was necessary to first collect some basic data on light microscopy, ultrastructure and immunohistochemistry with reference to frogs. Furthermore the sexual differentiation of two populations of different origin were compared histologically. Characterisation of the gonads The ovaries of Xenopus laevis displayed a garland-like structure in contrast to the compact ovaries of Rana temporaria. The ovaries of both frog species were surrounded by an epi-thelium and filled with germ cells which enclosed an ovarian cavity. The oogonies were mainly found in the peripheral parts of the organ. The oocytes were characterised by a big and irregularly shaped cell nucleolus with peripherally located nucleoli. They were sur-rounded by a thin one-layered follicular epithelium. Electron microscopical examination of the ovaries of Rana temporaria showed elongated tubular mitochondria in the cytoplasm which were found exclusively in oocytes. Some of the mitochondria from subadult frogs contained yolk crystals. Additionally an accumulation of electron-tight Granule was found just below the plasma membrane, which could be a preliminary stage of the cortical granule. The testis of the frogs were enveloped by an epithelium and a tunica albuginea which al-ready showed a tubular structure. The testis from Rana temporaria and the Xenopus laevis differed in their developmental stages. The testis of juvenile Rana temporaria contained only germ cells whereas the testis of some Xenopus laevis already contained spermato-cytes and spermatozoa. The spermatocysts, characteristic of frog testis, could be seen in conjunction with the appearance of spermatocytes only. By using light microscopy two different types of germ cells in both frog species could be distinguished which probably were primary and secondary germ cells. By electron microscopical investigation of the testis of Rana temporaria the somatic cells could, on the basis of location and morphology, be differentiated in two types. The somatic cells of the first type were located inside the Tubuli seminiferi and have probably the same function as the Sertoli cells of mammals. The cells of the second type, the Leydig cells or interstitial cells, were located outside the Tubuli and were characterized by granular vesicle in the cytoplasm. With view to the sexual differentiation of Rana temporaria a comparative histological inves-tigation of the gonads of juvenile and subadult frogs of a native midland population and a high alpine population was performed. The midland population proved to be a sexually semi-differentiated species since apart from clearly male or female animals it also com-prises intersex individuals in different stages of the transformation process. The genotypi-cally male animals developed female gonads in the first place which secondly converted into testis during a hermaphrodite stage. The transformation process from female into male gonads was, on the basis of morphological criteria, classified into three stages. The highal-pin population on the other hand proved to be a sexually differentiated race. By using the Avidin-Biotin-Complex-Technique five different antibodies were tested on the gonadal tissue of juvenile and subadult Rana temporaria. The test for Laminin, a non-collagen glycoprotein, which is part of the basal membrane in mammals, resulted in a posi-tive reaction. It seems therefore that similar to Laminin in mammals a glycoprotein plays an important part in the basal membrane of frogs. α-Actin, a fibrous protein of the smooth muscles, which was detected in the Theca externa of the layer of follicle cells in different species, could be established in the blood vessel wall only and not in the layer of follicle cells. Furthermore the occurrence of a Zona pellucida by using antibodies against the por-cine glycoprotein ZP3 was investigated. The ovum including the surrounding layer of follicle cells showed a negative reaction which however did not implicitly exclude the occurrence of a glycoprotein layer with a different antigenicity. Until now the existence of a glycoprotein layer in anurans, in connection with microscopical anatomy of ovaries in Rana temporaria or other species of frogs has not been mentioned in references. The examination of the go-nadal tissue as to the occurrence of ACE (Angiotensin Converting Enzymes) turned out negative as well. Example of application With the exception of a temporarily higher concentration of alkylphenol in the beginning of the exposure, the chemical analyses revealed a relatively low degree of pollution with alcyl-phenols and steroids. The results were comparable to other results of German rivers and stayed well below other European comparative data. According to the results of this study the current level of pollution of the experimental water with estrogens does not endanger the amphibian population. The examination did not reveal any influence of the sewage on the embryonal and larval development. Furthermore, the histological investigation of the gonads in exposed and unexposed frogs with reference to the gonadal sexual differentia-tion as well as the sex ratios did not reveal significant changes. There was no correlation as to the frequency of the occurrence of intersex in the groups of exposed and unexposed frogs, neither of Xenopus laevis nor of Rana temporaria. Only the transformation process from ovaries to testis of the sexually semi-differentiated species of Rana temporaria was slowed down in the group of exposed animals in contrast to unexposed animals. The rea-son for this phenomenon could be the inhibitive influence of the low-level but more continu-ous estrogen pollution in sewage than in river water. Conversely, a link between the accel-eration of the transformation process within the group of unexposed animals and the tem-porarily higher alkylphenol level in the beginning of the exposure cannot completely be ruled out. According to references alkylphenol can cause an increase of testosterone. The semiquantitative RT-PCR detecting Vitellogenin-mRNA carried out by the Institute of Freshwater Ecology and Inland Fisheries in Berlin showed a minor increase in females of Xenopus laevis which were exposed to sewage in the ration of a 2:1 dilution in contrast to the unexposed animals. Taking into account the synergistic effects of estrogens, the in-crease could be attributed to the higher estrogen pollution of the sewage. The histopa-thological analysis for the detection of toxical effects of the sewage as well as other poten-tial influential factors provided no hints as to a possibly toxical influence of the sewage.

The major neurotransmitter of the central nervous system, gamma-aminobutyric acid (GABA), exerts its actions through GABA(A), GABA(B) and GABA(C) receptors. GABA and GABA receptors are, however, also present in several non-neural tissues, including the endocrine organs pituitary, pancreas and testis. In the case of the rat testis, GABA appears to be linked to the regulation of steroid synthesis by Leydig cells via GABA(A) receptors, but neither testicular sources of GABA, nor the precise nature of testicular GABA receptors are fully known. We examined these points in rat, mouse, hamster and human testicular samples. RT-PCR followed by sequencing showed that the GABA-synthesizing enzymes glutamate decarboxylase (GAD) 65 and/or GAD67, as well as the vesicular GABA transporter vesicular inhibitory amino acid transporter (VIAAT/VGAT) are expressed. Testicular GAD in the rat was shown to be functionally active by using a GAD assay, and Western blot analysis confirmed the presence of GAD65 and GAD67. Interstitial cells, most of which are Leydig cells according to their location and morphological characteristics, showed positive immunoreaction for GAD and VIAAT/VGAT proteins. In addition, several GABA(A) receptor subunits (alpha1-3, beta1-3, gamma1-3), as well as GABAB receptor subunits R1 and R2, were detected by RT-PCR. Western blot analysis confirmed the results for GABA(A) receptor subunits beta2/3 in the rat, and immunohistochemistry identified interstitial Leydig cells to possess immunoreactive GABA(A) receptor subunits beta2/3 and alpha1. The presence of GABA(A) receptor subunit alpha1 mRNA in interstitial cells of the rat testis was further shown after laser microdissection followed by RT-PCR analysis. In summary, these results describe molecular details of the components of an intratesticular GABAergic system expressed in the endocrine compartment of rodent and human testes. While the physiological significance of this peripheral neuroendocrine system conserved throughout species remains to be elucidated, its mere presence in humans suggests the possibility that clinically used drugs might be able to interfere with testicular function. Copyright (C) 2003 S. Karger AG, Basel.

We have previously described a 30 kDa basic fibroblast growth factor (bFGF)-like protein in rodent testicular homogenates and have shown that pachytene spermatocytes are the sites of predominant immunoreactivity for this bFGF-like protein (Mayerhofer, A., Russell, L.D., Grothe, C., Rudolf, M. and Gratzl, M. (1991) Endocrinology 129, 921–924). We have now addressed the question whether this 30 kDa bFGF-like protein is a large bFGF form and whether it is produced by pachytene spermatocytes. We detected bFGF mRNA in homogenates of isolated mouse spermatocytes (which consisted mainly of pachytene spermatocytes) using S1 nuclease protection assays. As shown by Western blot analyses, the bFGF mRNA in mouse spermatocytes is translated into bFGF of an approximate molecular weight of 30 kDa. Neither bFGF mRNA, nor bFGF itself, was observed in isolated mouse Leydig cells. These results indicate that the immunoreactive bFGF-like protein observed previously in germ cells of the murine testis is identical to bFGF. Thus, germ cells of the testis produce bFGF, which may exert regulatory function in the process of spermatogenesis.

The neural cell adhesion molecule (NCAM) polypeptides are expressed by numerous tissues during embryonic development, where they are involved in cell-cell interactions. In the adult, NCAM expression is confined to a few cell types, including neurons and peptide-hormone-producing cells. Here we demonstrate that the Leydig cells of the adult rat, mouse, and hamster testes express NCAM as well. Western blotting showed that an NCAM of approximately 120 kDa was present in the adult testes of all three species investigated. This form was also found in freshly isolated mouse Leydig cells and in Leydig cells after 2 days in culture. After 4 days in culture, mouse Leydig cells expressed additional NCAM isoforms of approximately 140 and 180 kDa, indicating changes in alternative splicing of NCAM primary transcripts. Also, NCAM mRNA of all isoforms, as detected by S1-nuclease protection assays, increased with time in culture. The expression of the cell adhesion molecule NCAM by adult Leydig cells may explain the aggregation of Leydig cells in clusters in rodent testes, which could be a prerequisite for functional coordination of groups of Leydig cells. Furthermore, the presence of this neural and endocrine marker may indicate a closer relationship between Leydig cells and neural and peptide-hormone-producing cells than is considered to exist at the present time.

To determine the origin of estrogens in infant blood, we measured estrone (E1) and estradiol (E2) in the gonads of 50 girls and 64 boys who died suddenly between birth and 2 yr of age as well as in the adrenals of 18 of these infant girls and 16 of the boys. In the adrenals, E1 [median, 2.8 ng/g (10.4 pmol/g); range, 1.1-4.8 ng/g (4.1- 17.8 pmol/g)] and E2 [median, 3.0 ng/g (10.9 pmol/g); range, 1.2-5.3 ng/g (4.4-19.5 pmol/g)] were found in similar concentrations and were independent of age and sex. In the gonads, E2 was the major estrogen, but the concentrations differed markedly between the sexes; E2 exceeded E1 almost 10-fold in the ovaries and 2-fold in the testes. On the average, the gonads of the infant girls had 5 times more E2 and 2 times more E1 than those of the boys. As in plasma, E2 concentrations were highest in the ovaries of 1- to 6-month-old girls [median, 10.5 ng/g (38.5 pmol/g); range, 1.1-55.1 ng/g (4.0-202.0 pmol/g)] and in testes of 1- to 3-month-old boys [median, 1.8 ng/g (6.6 pmol/g); range, 0.6- 6.4 ng/g (2.3-23.5 pmol/g)]. Ovarian E2 concentrations declined to less than 3.0 ng/g (11.0 pmol/g) by the end of the first year of life, and testicular E2 declined to less than 1.0 ng/g (3.7 pmol/g) after only 6 months of age. Gonadal estrogen concentrations paralleled changes in gonadal morphology. Ovarian weights varied in a pattern of rise and fall similar to that of ovarian E2 concentrations; the biggest ovaries contained multiple macroscopic cysts. Testicular E2 closely correlated with Leydig cell development and testicular testosterone concentrations. We infer, therefore, that the surge of plasma E2 in infant girls originates from ovarian follicles and that of boys from testicular Leydig cells, and that these both occur as a result of the postnatal surge in gonadotropin secretion. The basal plasma E1 and E2 pool, however, is derived from the adrenals and remains at a comparatively constant level in both sexes