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12 episodes with dutasteride
6 episodes with dutasteride
2 episodes with dutasteride
2 episodes with dutasteride
3 episodes with dutasteride
3 episodes with dutasteride
Dr. Azi and Nurse Lacie are back with an episode that gets to the root of one of the most talked-about topics in beauty: hair loss. From hormonal imbalances to genetic causes and the latest treatment options, they're breaking down the science behind why we lose hair—and what we can do about it. Together, they answer your most asked questions: How do you know if you're really losing hair? What treatments actually work? Can you support your hair growth with the right ingredients? And what's the deal with PRP, Spironolactone, and Dutasteride? Whether you're dealing with shedding, thinning, or patchy spots, this episode of More Than a Pretty Face is packed with the facts (and a few rapid-fire fun moments, too). Timeline of what was discussed: 00:00 Introduction 02:25 Beauty & Blemish 08:05 The Most Common Type of Hair Loss 12:57 Ways to Test If You're Going Through Hair Loss 15:39 What Are Some Treatment Options? 21:23 PRP Treatment & Dutasteride Injections 23:51 Taking Spironolactone for Hair Loss 24:29 The Science Behind Hair Growth Cycles 29:48 New Hair Loss Research & Innovations 31:32 Alopecia Areata: What You Should Know 34:23 Rapid Fire Questions ______________________________________________________________ Submit your questions for the podcast to Dr. Azi on Instagram @morethanaprettyfacepodcast, @skinbydrazi, on YouTube, and TikTok @skinbydrazi. Email morethanaprettyfacepodcast@gmail.com. Shop skincare at https://azimdskincare.com and learn more about the practice at https://www.lajollalaserderm.com/ The content of this podcast is for entertainment, educational, and informational purposes and does not constitute formal medical advice. © Azadeh Shirazi, MD FAAD.
After a long run, my knees hurt upon standing up from my chair. Is this arthritis?My new gynecologist says I don't need progesterone while taking estriol. What say you?I lost 100 pounds after gastric bypass but now I have incapacitating blood sugar spikes after meals.I have a positive ANA but all other tests are negative. Should I be concerned?Should I be concerned about the side effects of minoxidil compounded with dutasteride for hair loss?
Happy New Year, from the HairPod team! This week, we're going through my top 5 HairPod moments of 2024. Tune in for some of the most impactful moments we've had so far on this podcast, and check out the resources section at the bottom for links to all of these episodes in full! What is TrichoView? with Steve Barth Steve Barth, one of the founding fathers of HairClub, joined Kevin on episode 23 to discuss the development of TrichoView, a cutting-edge technology for personalized hair and scalp analysis. This system revolutionized HairClub's approach, combining physiological data with psychological insights to offer individualized treatment plans. It's one of the most important advancements in hair care, and this clip dives into the science behind it. Finasteride vs. Dutasteride with Dr. Angela Phipps In episode 34, Dr. Angela Phipps helped me understand the effectiveness of the hair loss medication finasteride. I share my personal experience as well, because after years on finasteride, I still found I was losing some hair. Dr. Phipps explains why about 10% of patients need a second medication, dutasteride, to fight their male pattern hair loss. Nutrition's Impact on Hair Loss with Eva Proudman Your diet plays a huge role in how much hair you lose and how fast. In episode 24 with Eva Proudman, I learned just how important it can be. In this clip, she shares essential dietary advice for hair health, emphasizing the importance of protein and the foods that nourish your hair. If you've been noticing hair loss after changing your diet or rapid weight loss, check out her episode using the link below. Joey Logano's Hair System Journey NASCAR legend Joey Logano shared his hair loss journey in episode 1, and as a hair system user myself, I was curious to know how far he pushes his system and whether he worries if it will come off while he's driving in a hot stock car. From initial doubts to confidently racing in extreme temperatures, Joey talks about how his hair system stays put even under the hottest conditions. The Science Behind Laser Hair Therapy with Dr. Angela Phipps Laser hair therapy was another highlight from episode 42, where Dr. Phipps explained how low-level light therapy can stimulate hair follicle cells, improving hair health and promoting regrowth. While not a miracle cure, laser therapy can have significant impacts when used consistently, as long as it works for your type of hair loss. Dr. Phipps clarifies why and how it works, as well as who laser therapy isn't a good option for to help listeners develop realistic expectations. Resources Book a Free Consultation today! Episode 23: The Creation of TrichoView with Steve Barth Episode 34: Male and Female Pattern Hair Loss with Dr. Angie Phipps Episode 24: Ask a Trichologist: What is Causing My Hair Loss? With Eva Proudman Episode 1: Alopecia Doesn't Slow Me Down with Joey Logano Episode 42: Laser Hair Therapy Benefits with Dr. Angie Phipps Thanks for listening to HairPod. We hope you enjoyed this episode. If you did, please leave us a rating or review wherever you get your podcasts. If you'd like to connect with us on social media to share your story, check us out on Instagram @HairClub. HairPod is a production of TSE Studios. Our theme music is from SoundStripe.
Summary In this episode of the Future of Dermatology podcast, Dr. Farah Kamangar interviews Dr. Paradi Mirmirani, MD, a leading expert in hair disorders. They discuss the latest advancements in treating hair loss, particularly focusing on frontal fibrosing alopecia and scarring alopecia. Dr. Mirmirani shares her treatment algorithms, emphasizing the importance of removing triggers and using innovative therapies like oral minoxidil and JAK inhibitors. The conversation highlights the evolving landscape of dermatology and the exciting future of hair loss treatments. Dr. Mirmirani's paper that is spoken about in this podcast will be published on November 20th, 2024. Takeaways Dr. Mirmirani is a leading expert in hair disorders. Frontal fibrosing alopecia is increasingly common. Removing environmental triggers can significantly improve patient outcomes. Dutasteride is preferred over finasteride for treating FFA. Oral minoxidil is an effective treatment for hair loss. Dermatoscopy is essential for assessing hair loss conditions. New treatments for alopecia areata are now FDA-approved. Patient education is crucial for effective treatment. The landscape of hair loss treatments is rapidly evolving. Future research will focus on personalized treatment options for hair disorders. Chapters 00:00 - Introduction to Dermatology and Dr. Mirmirani's Expertise 02:09 - Frontal Fibrosing Alopecia: Treatment Approaches 10:24 - Innovative Therapies for Scarring Alopecia 18:46 - Future of Hair Loss Treatments and Research
Real Life Pharmacology - Pharmacology Education for Health Care Professionals
On this episode of the Real Life Pharmacology podcast, we cover 5 more medications in the top 200. Metronidazole is an antibiotic for infection. One of the most common complaints from patients involves reporting of a metallic taste in the mouth. Levetiracetam is an anti-seizure medication. Sedation, dizziness, and other adverse effects of the central nervous system are the most common complications. Colchicine is a gout medication. The most memorable side effect associated with this medication is diarrhea. Olanzapine is an antipsychotic. Olanzapine carries a higher risk for metabolic syndrome compared to other antipsychotics. Dutasteride is a 5 alpha-reductase inhibitor that is indicated for the treatment of BPH. If you are looking for all of our study materials and Amazon books, check them out at Meded101.com/store!
1) Combination therapy with imiquimod and 5 fluorouracil cream for the treatment of AK, a prospective open-label non-randomised uncontrolled pilot trial2) Association between dermatology follow-up and melanoma survival: a population based cohort studty3) Dupilumab therapy for atopic dermatitis is associated with an increased risk of cutaneous T cell lymphoma; a retrospective cohort study4) Lessons from a scoping review: clinical presentations of central centrifugal cicatricial alopecia5) Dutasteride in the treatment of frontal fibrosing alopecia: systematic review and meta-analysis6) Paediatric-onset lymphomatoid papulosis: results of a multi-centre retrospective cohort study on behalf of the EORTC Cutaneous Lymphoma Tumours Group CLTG. 7) PAMI syndrome8) Shorts (ILVEN needs genotyping, Onychopapillomas and BAP1 tumour predisposition syndrome, SKINTED)9) Isla Galpin. Violin Sonata in G minor, 1st and 2nd movement by Eccles
Here it is...Hair loss and what you can do about it, especially if you've got thyroid issues. I brought the heavy-hitter Dr. Alan Bauman on board to unravel the latest and most advanced hair restoration techniques. We left no stone unturned, from the ins and outs of medications like Finasteride and Dutasteride to ground-breaking non-surgical treatments such as PRP and TED. And let me tell you, the insights we discussed are doable, particularly if you've been struggling with hair thinning, breakage, or drastic changes in your hair's texture and volume. Dr. Bauman didn't hold back on the details, explaining everything from how stress and nutrition affect hair loss to the personal touch he brings to each diagnosis and treatment plan. We even tackled the controversial and often misunderstood links between thyroid medications, postpartum changes, and hair health. Before you think about snipping those ends or wearing that cap one more time, listen in – I promise you'll walk away armed with invaluable knowledge to help you reclaim your hair health. Dr. Bauman's medical practice: https://www.baumanmedical.com/ Ask Dr. Bauman a Question: https://www.baumanmedical.com/ask-a-question/ Facebook: https://www.facebook.com/baumanmedical Instagram: https://www.instagram.com/baumanmedical Podcast mentioned: 374: All About Hair Loss: https://open.spotify.com/episode/2oOzBeKtZCSDuwERUaNPqQ Shop ALL of Dr. Amie's Fixxr® Supplements: betterlifedoctor.com LET'S GET YOUR LIFE BACK...Connect with Dr. Amie Hornaman Book a free application call: https://dramiehornaman.com/pages/book-a-call FREE DOWNLOADS… What Are the Optimal Lab Ranges? What Steps Can I Take? Don't know where to start...don't know which labs are useful? And what to do when you get your results? “How To” Guide For Supplements Here's your Fixxr® supplement timeline and guide. Fix Your Thyroid and Adrenals To Fix Your Life Check your symptoms of hypothyroidism and know OPTIMAL thyroid lab values. Learn why you are being told you're “NORMAL” by your doctor. Can Supplements Help with Hypothyroidism? Grab this thorough guide to help you select the most advantageous supplements that will best suit your health circumstances. RATE, REVIEW AND FOLLOW ON APPLE PODCASTS Show your love for Amie and The Thyroid Fixer Podcast! If you're enjoying our journey together, I'd be thrilled if you could take a moment to rate and review the show on Apple Podcasts. Your support helps me reach and help more people just like you, guiding them towards their optimal selves! Just click HERE, scroll all the way down, give us those 5 stars, and share what you enjoy about my episodes in a review. Haven't subscribed yet? Make sure to follow The Thyroid Fixer Podcast to catch all the new episodes that come out every week. Follow HERE and never miss out on a moment of the journey! CONNECT WITH ME ON SOCIAL MEDIA: Join my exclusive Facebook Group, Dr. Amie…The Thyroid Fixer®...Love Your Mirror, for a Community of HOPE and Support in your thyroid journey. https://www.facebook.com/groups/dramie/ Like me on Facebook: Amie Hornaman Nutrition and Functional Medicine Subscribe on Youtube: Dr. Amie Hornaman Follow me on Instagram: @dramiehornaman
Dr. Kyle Gillett enjoys providing holistic individualized care to his patients. His practice includes preventative medicine, aesthetics, sports medicine, hormone optimization, obstetrics and infertility, integrative medicine, and precision medicine including genomics. He believes that each human is a unique creation that requires attention to their body, mind, and soul. He uses shared decision-making and an evidence-based approach. He firmly believes “food is medicine” and “exercise is medicine”. Dr. Gillett describes the “7 pillars of health”: exercise, diet, sleep, stress, social, sunlight, and spirit. These are more powerful than any medication or supplement. He enjoys spending time outdoors on the farm with his wife, two sons, and two wolfhounds. Along with Dr. Gillett, we're examining the complex world of women's hormones today. We'll be focusing on androgens like testosterone, DHEA, and dihydrotestosterone, and their profound impact on female health. Dr. Gillett provides insights on the role of binding globulins, hormone replacement therapy, and the interplay between insulin and androgens. We also discuss the challenges of menopausal weight gain, the benefits of GLP-1 medications for weight loss, and practical strategies anyone can use for maintaining lean body mass. In this episode: How androgens such as testosterone, DHEA, and dihydrotestosterone affect women's well-being. Why sex hormone binding globulin (SHBG) is critical for hormone dynamics and stability. Understanding the impact of thyroid binding globulin and cortisol binding globulin on hormone balance. How hormone replacement therapy (HRT) influences women's bodies, especially regarding androgens. Managing testosterone replacement therapy to avoid virilization symptoms like facial hair and voice changes. The role of DHT blockers in managing androgen-related conditions. How SHBG can be harnessed for overall hormone stability and health benefits. Challenges of menopausal weight gain and how hormonal changes affect body composition. Why integrating proper lifestyle habits is essential alongside GLP-1 medications for effective weight loss. How to maintain lean body mass through hormone therapy and lifestyle changes. How oral contraceptives and other synthetic hormones impact SHBG levels and overall hormone balance. The significance of SHBG levels for individuals on hormone replacement therapy or contraceptives. Exploring different forms of testosterone administration, including subcutaneous and intramuscular injections. How estrogen and progesterone influence testosterone levels through negative feedback inhibition. How poor sleep quality and hormonal changes contribute to menopausal weight gain. The paradoxical effects of hormone replacement therapy on body composition and fat gain. Why high SHBG must be paired with adequate hormone levels to avoid feeling unwell. Discussing the challenges faced when SHBG levels are artificially high due to medication. Sponsors Timeline is offering 10% off your first order of Mitopure. Go to https://www.timeline.com/KARENMARTEL and use code HORMONE to get 10% off your order. Get 15% off your Apollo wearable at https://apolloneuro.com/karen Get 15% off any Quicksilver products like their Advanced Push catch system. https://www.quicksilverscientific.com/karen use coupon code KAREN15 for 15% off. https://gilletthealth.com/ Social handle @kylegillettmd Podcast Gillett Health Interested in joining our NEW Peptide Weight Loss Program? Join today and get the details here. Join our Women's Group Coaching Program OnTrack TODAY! Karen Martel, Certified Hormone Specialist & Transformational Nutrition Coach and weight loss expert. Visit https://karenmartel.com/ Karen's Facebook Karen's Instagram
Dr. Gillett and James O'Hara NP, review an anti-aging protocol. 00:00 Intro01:21 When to take HCG for fertility?03:04 What was your optimized Free T before TRT? 08:00 Does L-Carnitine Raise TMAO10:38 Total testosterone with vericocele 11:48 Do the providers recommend SubQ13:37 Why are we calling Dutasteride anabolic?14:37 Adverse effects of 5 alpha-reductase inhibitors. 16:50 what would a constantly high SHBG mean?18:22 Testosterone and Dutasteride Question 21:07 How high is our endogenous testosterone? 21:42 What does Kyle mean when he refers to a traffic jam? 24:18 Should you be scared of creatine and hair loss?24:49 Are we available in California?25:18 Kyle's favorite canned sardines?25:42 Will creatine help post op surgery?26:18 Why is James on TRT?30:03 Are we concerned with PFS?32:11 Turkesteron/Ecdysteroids and Tongkat/Fadogia35:15 Thoughts on compounded test creams?36:54 Thoughts on Varicoceles 39:52 Does L-Carnatine have an impact on hair? 40:43 Does gorilla minds sigma impact Dutasteride/Finasteride?45:12 Lab work question 47:13 How can I get 12.5” guns 48:14 Should I switch to Dutasteride? 49:33 Proviron For High-quality labs:► https://gilletthealth.com/order-lab-panels/For information on the Gillett Health clinic, lab panels, and health coaching:► https://GillettHealth.comFollow Gillett Health for more content from James and Kyle► https://instagram.com/gilletthealth► https://www.tiktok.com/@gilletthealth► https://twitter.com/gilletthealth► https://www.facebook.com/gilletthealthFollow Kyle Gillett, MD► https://instagram.com/kylegillettmdFollow James O'Hara, NP► https://Instagram.com/jamesoharanpFor 10% off Gorilla Mind products including SIGMA: Use code “GH10”► https://gorillamind.com/For discounts on high-quality supplements►https://www.thorne.com/u/GillettHealth#podcast #hairloss #trtAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
Dr. Gillett and Nurse Practitioner James O'Hara answer a variety of different questions from our viewers. 00:00 Intro00:31 How much Sun exposure is too much?03:11 What's helped patients with PFS the most?05:48 Does Dutasteride affect facial hair 07:49 Does DHEA convert to Estradiol? 08:56 How much tadalafil is too much? 12:20 Does Fadogia affect testicular size?13:49 Why are doctors prescribing Ketamine?16:52 Does Creatine affect Finasteride?18:11 Does activating MTOR help with depression?21:25 Frequency of topical Dutasteride?23:45 Trusting research data 24:33 Do you have to refrigerate Omega-3s?27:17 Does Mesothearpy only have a localized effect?30:02 Does Finasteride affect OCD?31:25 Outro For High-quality labs:► https://gilletthealth.com/order-lab-panels/For information on the Gillett Health clinic, lab panels, and health coaching:► https://GillettHealth.comFollow Gillett Health for more content from James and Kyle► https://instagram.com/gilletthealth► https://www.tiktok.com/@gilletthealth► https://twitter.com/gilletthealth► https://www.facebook.com/gilletthealthFollow Kyle Gillett, MD► https://instagram.com/kylegillettmdFollow James O'Hara, NP► https://Instagram.com/jamesoharanpFor 10% off Gorilla Mind products including SIGMA: Use code “GH10”► https://gorillamind.com/For discounts on high-quality supplements►https://www.thorne.com/u/GillettHealth#podcast #questions #hairloss #supplements #healthAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
Dr. Gillett and Nurse Practitioner James O'Hara answer a wide variety of questions from the comment section and Instagram. 00:00 Intro00:25 How to avoid sensitivity issues with Dutasteride03:28 Is there a safe medication or supplement to loose fat05:25 Does Natesto suppress HPTA?07:45 Cheaper GLP1 09:36 Do we prefer brand name medication?12:57 CAG Repeat question from the UK15:34 Different Forms of DHEA19:32 Does Red Yeast rice compare to statins? 21:09 reason for .5mg of Dutasteride23:08 Topical BPC-15724:38 Sperm count after discontinuing Dutasteride26:54 How to switch from daily Finasteride to Dutasteride 30:39 Sugar Black market32:13 Fish oil and TRT33:54 Carnivore diet and plaque 36:45 GLP1 and Thyroid Cancer 40:17 Finasteride and Marijuana40:40 How much sun exposure is too much? For High-quality labs:► https://gilletthealth.com/order-lab-panels/For information on the Gillett Health clinic, lab panels, and health coaching:► https://GillettHealth.comFollow Gillett Health for more content from James and Kyle► https://instagram.com/gilletthealth► https://www.tiktok.com/@gilletthealth► https://twitter.com/gilletthealth► https://www.facebook.com/gilletthealthFollow Kyle Gillett, MD► https://instagram.com/kylegillettmdFollow James O'Hara, NP► https://Instagram.com/jamesoharanpFor 10% off Gorilla Mind products including SIGMA: Use code “GH10”► https://gorillamind.com/For discounts on high-quality supplements►https://www.thorne.com/u/GillettHealth#podcast #questions #hairloss #supplements #workoutAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
In this episode of Hart2Heart with host Dr. Mike Hart. Dr. Mike Hart sits down with James O'Hara to discuss topics including testosterone replacement therapy (TRT), cardiovascular risk, managing cholesterol, SSRIs, risk factors of birth control, and treatments for hair loss. Guest Bio and Links: James O'Hara is a Nurse Practitioner practicing with Dr. Kyle Gillett in Kansas City. He co-hosts the Gillett Health Podcast and shares health insights on Instagram @jamesoharanp Resources: Adverse Events Associated with Testosterone Administration https://examine.com/ Show Notes: [0:00] Welcome back to the Hart2Heart Podcast with Dr. Mike Hart. Dr. Hart introduces James O'Hara to the listeners [0:55] Adverse Events Associated with Testosterone Administration [2:00] In-depth analysis of TRT and cardiovascular health [8:00] The role of testosterone in managing blood pressure and cholesterol [15:00] Types of fibers to use to help lower your LDL [24:00] Viagra or Cialis… verdict is in [26:30] The versatility of Cialis beyond erectile dysfunction [29:00] SSRIs and sexual health [34:15] Long-term effects of birth control pills [37:30] Benefits of Boron [44:00] Approaches to hair loss treatments and DHT's role [51:30] Latanoprost for eyelash growth --- Dr. Mike Hart is a Cannabis Physician and Lifestyle Strategist. In April 2014, Dr. Hart became the first physician in London, Ontario to open a cannabis clinic. While Dr. Hart continues to treat patients at his clinic, his primary focus has shifted to correcting the medical cannabis educational gap which exists in the medical community. Connect on social with Dr. Mike Hart: Social Links: Instagram: @drmikehart Twitter: @drmikehart Facebook: @drmikehart
Dr. Gillett and Nurse Practitioner James O'Hara Answer your questions about Finasteride and Dutasteride. 00:23 Commencement of AMA (Initial Segment)02:27 Dosage Considerations05:13 Exploring Topical Dutasteride and its Half-life08:50 Front-loading Dutasteride: Is it Necessary?10:27 Contemplating the Switch from Finasteride to Dutasteride (Derek Reel)14:21 Assessing the Comparative Side Effects of Oral Dutasteride15:26 Examining Dutasteride's Potency in Inhibiting Type 218:46 Manipulating Net Androgens for Individuals on TRT21:07 Unraveling the Mystery of Reversing Grey Hair22:55 Understanding the Challenge of Detecting Systemic Absorption in Topical Dutasteride24:40 Strategies for Managing Male Pattern Baldness25:53 Exploring Hair Loss Treatments Minus Sexual Side Effects27:02 Addressing a Cluster of Questions30:52 Gillett Health's Insights into Finasteride's Side Effects31:37 Optimal Dosing Protocols32:30 Navigating Finasteride and Saw Palmetto Interactions32:59 Neurological Side Effects: Is Dutasteride a Safer Option?35:41 Crafting a Recommended Hair Loss Protocol37:29 Establishing Protocols for Prostate Cancer Prevention38:40 Continual Hair Loss Eight Months In: What to Do?39:05 Managing Post-Finasteride Syndrome (PFS)41:50 Alternative Hair Growth Treatments for Women43:06 Updates on Antiandrogen Drugs43:44 Gillett Health's Offerings: How We Can Assist YouFor High-quality labs:► https://gilletthealth.com/order-lab-panels/For information on the Gillett Health clinic, lab panels, and health coaching:► https://GillettHealth.comFollow Gillett Health for more content from James and Kyle► https://instagram.com/gilletthealth► https://www.tiktok.com/@gilletthealth► https://twitter.com/gilletthealth► https://www.facebook.com/gilletthealthFollow Kyle Gillett, MD► https://instagram.com/kylegillettmdFollow James O'Hara, NP► https://Instagram.com/jamesoharanpFor 10% off Gorilla Mind products including SIGMA: Use code “GH10”► https://gorillamind.com/For discounts on high-quality supplements►https://www.thorne.com/u/GillettHealth#podcast #aşk #finasteride #hairloss #hormones #gilletthealthAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
Treatment Options for BPHMen with moderate to severe BPH symptoms, meaning those significantly bothered by their symptoms, should discuss the benefits, risks, and costs of various treatments with their doctors. Here are some common treatment options:Watchful Waiting:For men with mild symptoms or those not too bothered by their symptoms, doctors may suggest waiting and monitoring the condition. Annual check-ups and lifestyle changes, like adjustments in diet and exercise, can be helpful during this period.Medication:Various medications can manage BPH symptoms:Alpha-Blockers:These medicines, such as Alfuzosin and Tamsulosin, are commonly used and can help by relaxing the muscles in the prostate. They can cause side effects like dizziness and ejaculation problems. 5-alpha Reductase Inhibitors:Drugs like Finasteride and Dutasteride can reduce the size of the prostate. However, they may cause sexual side effects, such as lowered sexual desire or erectile problems. Combination Therapy: Combining an alpha-blocker with a 5-alpha reductase inhibitor may be more effective in some cases.Phosphodiesterase-5 Inhibitors:Medicines like Tadalafil can be used to treat BPH symptoms and may also enhance sexual function.Minimally Invasive Procedures:There are non-surgical procedures, like transurethral needle ablation and microwave thermotherapy, that can improve symptoms. They may not be as effective as surgery but are less invasive.Surgery:Surgical procedures are recommended for more severe cases. Different surgical options are available based on the patient's needs and the doctor's recommendations.Making a Decision:Doctors will consider the severity of symptoms, the size of the prostate, and the patient's overall health when suggesting a treatment option. It's crucial to discuss and understand the potential benefits and risks of each choice to make a decision that's best suited to the individual's needs and lifestyle. Hosted on Acast. See acast.com/privacy for more information.
In this episode, my guest is Dr. Michael Eisenberg, MD, a urologist and professor specializing in male sexual function and fertility at Stanford University. Based on his clinical work and research, he is considered a top world expert on male sexual and reproductive health. We discuss testosterone levels and what really impacts them, testosterone therapy, sperm quality and counts, penile and testicular health and function, pelvic floor and prostate and urinary tract health, erectile function and dysfunction and the various causes and treatments for common male sexual, hormonal and reproductive challenges. We also address post-finasteride syndrome and trends in penile length. This episode is rich in actionable information about men's sexual and reproductive health, including key tests and at-home evaluations, and the behavioral, nutritional, exercise and prescription-based tools that can support male sexual and reproductive health. For show notes, including referenced articles and additional resources, please visit hubermanlab.com. Thank you to our sponsors AG1: https://drinkag1.com/huberman ROKA: https://roka.com/huberman Eight Sleep: https://eightsleep.com/huberman LMNT: https://drinklmnt.com/huberman Momentous: https://www.livemomentous.com/huberman Timestamps (00:00:00) Dr. Michael Eisenberg (00:01:49) Sponsors: ROKA & Eight Sleep (00:04:20) Sperm Quality, Geographic & Environmental Factors (00:12:00) Fertility & Sperm Quality; Testosterone, Cell Phones & Heat (00:19:26) Testosterone, Age, Obesity (00:26:49) Tool: Optimize Sperm Quality, Exogenous Testosterone, hCG (00:35:26) Sponsor: AG1 (00:36:57) Tool: Lifestyle Factors & Sperm Quality, Alcohol (00:43:27) Sperm Quality, Recreational & Over-the-Counter Drugs, Cannabis (00:46:56) High-Impact Sports, Traumatic Brain Injury (TBI), Pituitary & Testosterone (00:49:55) Bicycling, Numbness & Sexual Dysfunction; Walking & Testosterone (00:55:39) Exogenous Testosterone Therapy & Cancer (00:58:39) Sponsor: LMNT (00:59:57) Sexual & Urinary Health, Nighttime Urination (01:03:12) Sleep & Semen Quality; Overall Health (01:09:19) Tool: Sperm Analysis & Overall Health; Sperm Banking (01:13:21) Paternal Age & Puberty Trends; Older Fathers & Child Health Risk (01:26:42) Tool: Prostate Health, Urination; Tadalafil (Cialis) (01:33:02) Urinary Tract Infections (UTIs); Erectile Dysfunction Causes (01:38:21) Blood Flow & Erectile Dysfunction, Medication; Cardiovascular Health (01:44:30) Mechanical Erectile Dysfunction Treatments; Peptides; Delayed Ejaculation (01:52:36) Pelvic Floor Health, Urology & Physical Therapy; Split-Stream Urination (01:59:03) Penile Length & Trends; Dihydrotestosterone (DHT), Puberty (02:09:01) Hair Loss, Dutasteride, Finasteride & Sexual Health; Post-Finasteride Syndrome (02:16:11) Clomiphene, Testosterone & Estrogen Signaling (02:19:31) Follicle-Stimulating Hormone (FSH) Therapy; Prolactin, Estrogen (02:24:15) Varicocele; Peyronie's Disease (02:27:26) Testis & Cancer Risk; Insurance, Blood Profiles & Semen Analysis (02:35:03) Zero-Cost Support, Spotify & Apple Reviews, Sponsors, YouTube Feedback, Momentous, Social Media, Neural Network Newsletter Title Card Photo Credit: Mike Blabac Disclaimer
On today's podcast Dr. Gillett and James O'Hara NP, take a deep dive into Finasteride and Dutasteride.Intro (00:00):DHT Receptors (01:58): The discussion centers around the number of DHT receptors in the body.Net Androgens (02:22): Exploring the concept of net androgens in the body.Fin & Dut and Depression (04:36): Investigating whether Finasteride and Dutasteride cause depression.Erectile Dysfunction (09:30): Discussing the potential relationship between these drugs and erectile dysfunction.Decreased Libido (11:53): Exploring the impact on libido due to Finasteride and Dutasteride.Impaired Spermatogenesis (12:51): Discussing the potential adverse effects on sperm production.Effect on the Liver (15:03): Exploring the impact of these drugs on liver function.Adverse Ocular Effects (16:32): Discussing potential negative effects on the eyes.New Type 3 5-alpha Reductase Deficiency (17:48): Discussing a new type of deficiency related to 5-alpha reductase.Renal Effects (19:25): Exploring potential effects on the kidneys.Diabetes (19:31): Discussing the relationship between these drugs and diabetes.Choosing a Specialist (20:34): Discussing whom to consult regarding these medications.Type 1 vs. Type 2 (26:23): Differentiating between Type 1 and Type 2 conditions.Second Attia Pod (27:37): Referring to a previous podcast episode by Peter Attia.Prostate Cancer (31:26): Discussing the relation between these drugs and prostate cancer.Hair Transplant (35:05): Exploring the option of hair transplant.Risks of Inflated Figures (36:29): Discussing potential risks related to inflated figures in research or statistics.Post-Finasteride Syndrome (PFS) (43:24): Discussing the potential syndrome associated with Finasteride.Fin (MK-906) (55:47): Discussing Finasteride and its identification as MK-906.Dut (Gi 1198745) (57:52): Discussing Dutasteride and its identification as Gi 1198745.Anti-aging (01:01:11): Exploring the potential anti-aging aspects related to these drugs.Studies/References ► https://pubmed.ncbi.nlm.nih.gov/37697052/ ► https://pubmed.ncbi.nlm.nih.gov/34925443/► https://fcdgc.rarediseasesnetwork.org/diseases-studied/srd5a3-cdg► https://pubmed.ncbi.nlm.nih.gov/26390988/► https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7308241/For High-quality labs:► https://gilletthealth.com/order-lab-panels/For information on the Gillett Health clinic, lab panels, and health coaching:► https://GillettHealth.comFollow Gillett Health for more content from James and Kyle► https://instagram.com/gilletthealth► https://www.tiktok.com/@gilletthealth► https://twitter.com/gilletthealth► https://www.facebook.com/gilletthealthFollow Kyle Gillett, MD► https://instagram.com/kylegillettmdFollow James O'Hara, NP► https://Instagram.com/jamesoharanpFor 10% off Gorilla Mind products including SIGMA: Use code “GH10”► https://gorillamind.com/For discounts on high-quality supplements►https://www.thorne.com/u/GillettHealth#podcast #finasteride #hairloss #hormones #pfs #dutasterideAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
On today's podcast Dr. Gillett and James O'Hara NP, discuss Pre-Menstrual Dysphoric Disorder. They do a comprehensive "Non-Systematic Review". 00:00 Intro00:29 Differences in treatment for PMDD and sex offenders: explores the contrasting approaches to treating Premenstrual Dysphoric Disorder (PMDD) and sex offenders, highlighting how the two conditions require very similar treatment strategies.02:12 Non-systematic review of the evidence: analysis of research and evidence related to PMDD and sex offender treatment13:21 SSRIs: (SSRIs), a type of antidepressant medication, and their role in the treatment of PMDD or possibly other conditions.17:58 Oral Contraceptives: discusses the use of oral contraceptives as a treatment option for PMDD or related topics.19:24 "Treatments with strong scientific evidence": This segment may list and discuss various treatment options that have a claimed robust scientific basis for their effectiveness in addressing PMDD or other conditions.21:50 Same heading more aggressive treatments: This section might delve into treatment options that are considered more aggressive in addressing PMDD or similar conditions, potentially involving interventions beyond medication.23:52 Treatments with limited but promising evidence: We explore treatment approaches with limited scientific support but "promising" in managing PMDD or related issues.32:20 Closest to the root cause: We discuss treatments that aim to address the underlying causes or mechanisms of PMDD rather than just alleviating symptoms.40:41 Not effective: Treatments or approaches that have been found to be ineffective in managing PMDD or related conditions.44:55 Dutasteride study: A specific study or research involving the use of Dutasteride, a medication often used for enlarged prostate, and its potential effects on PMDD or a related topic.47:38 Low dose of Fluoxetine: The use of a low dose of Fluoxetine, an SSRI, in the context of PMDD or another condition.49:19 Effects of acute estradiol and progesterone/Suicidal: The effects of acute administration of estradiol and progesterone and their potential connection to suicidal tendencies or related issues.1:00:25 Outro:For High-quality labs:► https://gilletthealth.com/order-lab-panels/For information on the Gillett Health clinic, lab panels, and health coaching:► https://GillettHealth.comFollow Gillett Health for more content from James and Kyle► https://instagram.com/gilletthealth► https://www.tiktok.com/@gilletthealth► https://twitter.com/gilletthealth► https://www.facebook.com/gilletthealthFollow Kyle Gillett, MD► https://instagram.com/kylegillettmdFollow James O'Hara, NP► https://Instagram.com/jamesoharanpFor 10% off Gorilla Mind products including SIGMA: Use code “GH10”► https://gorillamind.com/For discounts on high-quality supplements►https://www.thorne.com/u/GillettHealth#podcast #womenshealth #hormones #female #women #gilletthealthAdvertising Inquiries: https://redcircle.com/brandsPrivacy & Opt-Out: https://redcircle.com/privacy
Hair Regrowth after Minoxidil and Dutasteride Tattooing - with Carlos Wambier! - Tapering Dupilumab in Atopic Dermatitis - Needlestick and Sharps Injuries in Derm Surgery - Narrow-Toed Shoes and the Toe-to-Toe Sign - Congenital Hypertrophy of the Hallux Nail Folds - Carlos Wambier Twitter: @WambierMD Check out our video content on VuMedi!: https://www.vumedi.com/channel/dermasphere/ Luke's PDPC course and the Intermountain Derm Society meeting: https://registration.socio.events/e/idspdpc23/promo-codes/ATTENDEE The University of Utah's Dermatology ECHO: https://physicians.utah.edu/echo/dermatology-primarycareConnect with us! - Web: https://dermaspherepodcast.com/ - Twitter: @DermaspherePC - Instagram: dermaspherepodcast - Facebook: https://www.facebook.com/DermaspherePodcast/ - Check out Luke and Michelle's other podcast, SkinCast! https://healthcare.utah.edu/dermatology/skincast/ Luke and Michelle report no significant conflicts of interest… BUT check out our friends at: - Kikoxp.com(a social platform for doctors to share knowledge) - https://www.levelex.com/games/top-derm (A free dermatology game to learn more dermatology!)
Huberman Lab Podcast Notes Key Takeaways Different hairs on your body have different lengths of growth phases (for example, hair on the head will grow for 2-8 years, and hair on the eyebrows will fall out every few months) The rate of hair growth is relatively stable across hair – what differs is the length of the growth phaseMicroneedling procedures, PRP injections, and Minoxidil all center around the general idea of increasing blood flow, increasing oxygen and delivery of nutrients, or increasing inflammation just enough locally to set off a cascade of regrowthCombination treatments that combine a mechanical stimulus (such as microneedling) with chemical stimulus (such as minoxidil) will always be better than either alone But be realistic, it's unlikely to grow a full head of hair again if you are baldPeople are highly individual in response and side effects to hair growth treatments – start with minimum effective dose and be patient with experimentation timeAndrogens (especially DHT) are potent inhibitors of IGF-1 and cyclic AMP which stimulate hair growthRead the full notes @ podcastnotes.orgIn this episode, I explain the biology of hair, hair growth, why hair growth slows and what cause hair to stop growing and/or “fall out.” I discuss the essential role of hair stem cells and other supporting biological factors for healthy hair growth. Then I describe various approaches (mechanical and chemical) to slow hair loss by increasing blood flow to hair stem cells, including minoxidil, tadalafil, PRP, microneedling, Botox and ketoconazole treatments. I also discuss how age-related hormone changes cause hair loss and explain the effectiveness of treatments such as caffeine, saw palmetto, growth hormone, finasteride and dutasteride. For all hair growth options, I describe potential side effects, how soon to expect results and the amount of hair regrowth to expect and I highlight effective combination treatments for hair regrowth even in hair “dead” (bald) zones. For many listeners, thinning, brittle hair, or pattern baldness are a source of anxiety and stress. This episode explains the mechanisms underlying hair regrowth tools and the science behind them so that you can evaluate potential treatments and associated side-effect profiles and select the best one(s) for you. For the full show notes, visit hubermanlab.com. Thank you to our sponsors AG1 (Athletic Greens): https://athleticgreens.com/huberman Helix Sleep: https://eightsleep.com/huberman HVMN: https://hvmn.com/huberman ROKA: https://roka.com/huberman LMNT: https://drinklmnt.com/huberman Supplements from Momentous https://www.livemomentous.com/huberman Timestamps (00:00:00) Hair (00:04:13) Sponsors: Helix Sleep, HVMN, ROKA (00:08:04) Psychological States & Hair (00:13:19) Hair Anatomy & Stem Cells (00:26:05) 3 Phases of Hair Growth (00:35:40) Sponsor: AG1 (Athletic Greens) (00:36:55) Minoxidil & Blood Flow (00:45:37) Increase Blood Flow: Massage, Tadalafil, Platelet-Rich Plasma (PRP), Microneedling (00:56:10) Microneedling, Minoxidil & “Dead Zones” (01:00:13) Sponsor: LMNT (01:01:25) Botox Treatments (01:06:27) Androgens, Hair Growth & Pattern Hair Loss; Scalp vs. Beard Hair (01:15:46) Topical Caffeine & Slowing Hair Loss (01:21:06) IGF-1: Growth Hormone & Sermorelin; Insulin Sensitivity: Myo-Inositol (01:25:52) Iron & Hair Growth (01:27:04) 5-Alpha Reductase & Saw Palmetto; Curcumin (01:33:22) Ketoconazole & Offsetting Hair Loss (01:38:46) Topical & Oral Finasteride (01:51:00) Post- Finasteride Syndrome (01:56:01) Dutasteride (01:58:53) Mechanical & Chemical Stimulation for Hair Growth (02:02:46) Zero-Cost Support, YouTube Feedback, Spotify & Apple Reviews, Sponsors, Momentous, Social Media, Neural Network Newsletter Title Card Photo Credit: Mike Blabac Disclaimer
In this episode, I explain the biology of hair, hair growth, why hair growth slows and what cause hair to stop growing and/or “fall out.” I discuss the essential role of hair stem cells and other supporting biological factors for healthy hair growth. Then I describe various approaches (mechanical and chemical) to slow hair loss by increasing blood flow to hair stem cells, including minoxidil, tadalafil, PRP, microneedling, Botox and ketoconazole treatments. I also discuss how age-related hormone changes cause hair loss and explain the effectiveness of treatments such as caffeine, saw palmetto, growth hormone, finasteride and dutasteride. For all hair growth options, I describe potential side effects, how soon to expect results and the amount of hair regrowth to expect and I highlight effective combination treatments for hair regrowth even in hair “dead” (bald) zones. For many listeners, thinning, brittle hair, or pattern baldness are a source of anxiety and stress. This episode explains the mechanisms underlying hair regrowth tools and the science behind them so that you can evaluate potential treatments and associated side-effect profiles and select the best one(s) for you. For the full show notes, visit hubermanlab.com. Thank you to our sponsors AG1 (Athletic Greens): https://athleticgreens.com/huberman Helix Sleep: https://eightsleep.com/huberman HVMN: https://hvmn.com/huberman ROKA: https://roka.com/huberman LMNT: https://drinklmnt.com/huberman Supplements from Momentous https://www.livemomentous.com/huberman Timestamps (00:00:00) Hair (00:04:13) Sponsors: Helix Sleep, HVMN, ROKA (00:08:04) Psychological States & Hair (00:13:19) Hair Anatomy & Stem Cells (00:26:05) 3 Phases of Hair Growth (00:35:40) Sponsor: AG1 (Athletic Greens) (00:36:55) Minoxidil & Blood Flow (00:45:37) Increase Blood Flow: Massage, Tadalafil, Platelet-Rich Plasma (PRP), Microneedling (00:56:10) Microneedling, Minoxidil & “Dead Zones” (01:00:13) Sponsor: LMNT (01:01:25) Botox Treatments (01:06:27) Androgens, Hair Growth & Pattern Hair Loss; Scalp vs. Beard Hair (01:15:46) Topical Caffeine & Slowing Hair Loss (01:21:06) IGF-1: Growth Hormone & Sermorelin; Insulin Sensitivity: Myo-Inositol (01:25:52) Iron & Hair Growth (01:27:04) 5-Alpha Reductase & Saw Palmetto; Curcumin (01:33:22) Ketoconazole & Offsetting Hair Loss (01:38:46) Topical & Oral Finasteride (01:51:00) Post- Finasteride Syndrome (01:56:01) Dutasteride (01:58:53) Mechanical & Chemical Stimulation for Hair Growth (02:02:46) Zero-Cost Support, YouTube Feedback, Spotify & Apple Reviews, Sponsors, Momentous, Social Media, Neural Network Newsletter Title Card Photo Credit: Mike Blabac Disclaimer
Real Life Pharmacology - Pharmacology Education for Health Care Professionals
Dutasteride (Avodart) is a 5-alpha-reductase inhibitor. I discuss the pharmacology, adverse effects, and drug interactions on this podcast. Dutasteride reduces the size of the prostate over time. It takes a significant amount of time to provide symptom relief (usually at least 3-6 months). Dutasteride is broken down by CYP3A4 to a minor extent which means that strong CYP3A4 inhibitors may increase drug concentrations. When using dutasteride for BPH, remember to review the medication list for drugs that can cause urinary retention such as anticholintiercs and alpha-agonists.
See all the Healthcasts at https://www.biobalancehealth.com/healthcast-blog/ The list of the factors that bind T so you can't use it and those that produce estrogens block free testosterone in both men and women of all ages. The list of lifestyle choices and is much longer than the list of factors you can use to stimulate testosterone. Soy in many foods: It is a fact that foods that are processed have many “fillers” that are invisible to the person eating them. These fillers are often the culprit decreasing naturally produced testosterone levels and available or active T called free T. The biggest problem at the present is the addition of soy to nearly every processed food, even ice cream. Soy is a phytoestrogen. Phyto Estrogens in food (not medical estrogen) act as a female hormone, limiting the effectiveness of testosterone and the production of T. To avoid soy in everything you eat, you must do two things: 1. Eat basic meals cooked by you or a family member from fresh foods that do not include canned or processed foods, and 2. you have to look at the label and only buy products without soy. Currently there are only 2 brands of ice cream that don't add soy. Soy gives men a “Beer Belly” and all other foods with soy will also increase the fat collection in the abdominal area of both sexes. Soy is the primary proteins of vegans and therefore it is consumed in large volume therefore has more of an effect on lowering free T and T levels. Eating out of and microwaving in plastic containers (even drinking water out of plastic) causes our bodies to absorb the plastic chemical's estrogen. This does us no good and is a contaminant and toxin that we store in our body fat. It is the biggest enemy of T. It is everywhere and is considered the leading cause of lowering the average T level of men aged 15-40. It is everywhere so stop cooking in it and drinking from it when you can! Don't eat out of plastic bags, or microwave plastic containers, or plastic bags with food in it. Diabetes should be treated, and blood levels of sugar should be kept in control as low as possible for type 2 diabetes. Omega 6 fatty acids shrink the testes while the Omega 3 FA increase the activity of the testes Dairy has inherent estrogen in it and animal feed often contains soy, and that makes the milk and meat higher in estrogen. Trans Fats—Are in most processed foods. Chips, any snack food that is not dried fruit or nuts Commercial baked goods, such as cakes, cookies, and pies. Microwave popcorn. Frozen pizza. Refrigerated dough, such as biscuits and rolls. Fried foods, including french fries, doughnuts, and fried chicken. Nondairy coffee creamer. Stick margarine. Alcohol is a toxin and slows fat loss, damages the liver, and increases estrogen production in the liver, which inactivates testosterone. Obesity is dangerous to us in so many ways. The mere fact of being obese increases our risk for multiple diseases, but fat also converts testosterone in to estrone and estradiol in both men and women. The fatter a person is the less free testosterone he or she has. Being a Couch Potatoe. being inactive, is deadly for testosterone production and free Testosterone. Inactivity increases fat production and estrogen production. Moderate exercise every day is the answer! Over activity causes an increase in SHBG which binds testosterone. Marathoners and professional athletes run the risk of binding their good total testosterone so that it is not free to bind to Testosterone receptors. Fasting can cause increase in free testosterone by increasing SHBG. Humans were built to eat small amounts often, and eating one meal a day increases SHBG, that inactivates free T. Licorice root (in black licorice), Ashwaghanda and all mint family herbs even basil decrease active Testosterone blood levels. Phytoestrogens are in many women's natural supplements that are touted to decrease hot flashes. They only provide minimal relief, but also increase fat gain and estrone levels that cause inactivity of testosterone. Medications can lower the testosterone levels in both men and women Oral contraceptives increase estrone so much that they inactivate testosterone and suppress FSH and LH that stimulated the production of T from the ovary. Oral menopausal ERT and HRT binds up T and causes decrease of all of the benefits of T from replacement and natural T production however minimal after menopause. Finasteride and Dutasteride given to prevent hair loss or prostate enlargement causes a decrease of DHT to a point where sex drive, erectile function and muscle mass are impaired. Arimidex can cause an increase in testicular production of T, but in a small production of men and women it can inactivate the receptors for DHT and T. As the research about testosterone progress, we will find more and more lifestyle issues that decrease T total and T free levels that can interfere with normal production of T and free T in both men and women. As these are studied researched, we will update you on the issues you can base your lifestyle and medical treatments on.
ANDROGENETIC ALOPECIA STUDIES Sanabria et al (starts at 4:40). Prospective cardiovascular evaluation with 24-h Holter and 24-h ambulatory blood pressure monitoring in men using 5 mg oral minoxidil for androgenetic alopecia. J Am Acad Dermatol. 2022 May 18; Klein E et al (starts at 13:40). Comparing combination low-dose oral minoxidil and topical minoxidil with oral minoxidil alone for the treatment of non-scarring alopecia; a retrospective chart review. J Cosmet Dermatol. 2022 Jun 1. Cao L et al (starts at 21:19). Nailfold capillaroscopy alterations in androgenetic alopecia: A cross-sectional study. Indian J Dermatol Venereol Leprol. 2022 Feb 28;1-7. doi: 10.25259/IJDVL_714_2021. Emmanuel Sánchez-Meza et al (starts at 28:17). Microneedling plus topical dutasteride solution for androgenetic alopecia: a randomized placebo-controlled study. J Eur Acad Dermatol Venereol. 2022 Jun 1. doi: 10.1111/jdv.18285. David Saceda-Corralo et al. Mesotherapy with Dutasteride in the Treatment of Androgenetic Alopecia. Int J Trichology. 2017 Jul-Sep; 9(3): 143–145. Liamsombut S et al (starts at 34:45). Sleep quality in men with androgenetic alopecia. Sleep and Breathing. 2022 Apr 25. ALOPECIA AREATA STUDIES Anna Waśkiel-Burnat et al (starts at 41:33). Patients with alopecia areata are at risk of endothelial dysfunction: results of a case-control study. Clin Exp Dermatol. 2022 Mar 31. Conic et al. Prevalence of cardiac and metabolic diseases among patients with alopecia areata.J Eur Acad Dermatol Venereol . 2021 Feb;35(2):e128-e129. Youssef S et al (starts at 48:28). Tofacitinib Therapy for Alopecia Areata is not Associated with Adverse Events during COVID-19 Infection. J Am Acad Dermatol. 2022 May 9;S0190-9622(22)00795-2. McKenzie P et al (starts at 53:32). Evaluation of the Prevalence and Incidence of Pediatric Alopecia Areata Using Electronic Health Record Data. JAMA Dermatol. 2022 May 1;158(5):547-551.
Thanks for tuning in to the Armor Men's Health Hour Podcast today, where we bring you the latest and greatest in urology care and the best urology humor out there.In this segment, Dr. Mistry and Donna Lee answer a listener's question about the impact medication can have on testosterone levels. This 73 year old man was diagnosed with an enlarged prostate with urethral obstruction and placed on Dutasteride and Tamsulosin to shrink the prostate so a Rezum procedure could be performed. Shortly thereafter, he began having symptoms of low testosterone, and lab work confirmed he had a T level of 400 with no free testosterone. His urologist stopped the Dutasteride and began giving him 100 milligrams of Testosterone Cypionate weekly, which greatly improved his symptoms. But after 9 weeks of hormone therapy, his T level had jumped to over 1500 and he was immediately taken off the T injections. He wonders what caused his T level elevation and whether it would be safe to resume T therapy because it was very helpful. Dr. Mistry explains that medications like Dutasteride and Finasteride, often taken for hair growth, can definitely cause symptoms of ED as well as lowered sperm counts. Younger men or men trying to conceive should be aware of the risk of these side effects. In the case of our listener, it is likely that the sudden surge in his T levels may be a simple lab error, since diagnostic machines often fail and have to be recalibrated. Because hormone therapy was so beneficial in mitigating his symptoms, he should definitely find a urologist who is comfortable with prescribing testosterone for men's health and try again. If you or someone you love is experincing symptoms of ED or low testosterone after taking Dutasteride or Finasteride, please call us today and check out our podcast on what we call "post-Finasteride syndrome."This episode previously aired on 9.11.21. Don't forget to like, subscribe, and share us with a friend! As always, be well!Check our our award winning podcast!https://blog.feedspot.com/sex_therapy_podcasts/https://blog.feedspot.com/mens_health_podcasts/Dr. Mistry is a board-certified urologist and has been treating patients in the Austin and Greater Williamson County area since he started his private practice in 2007.We enjoy hearing from you! Email us at armormenshealth@gmail.com and we'll answer your question in an upcoming episode!Phone: (512) 238-0762Email: Armormenshealth@gmail.comWebsite: Armormenshealth.comOur Locations:Round Rock Office970 Hester's Crossing RoadSuite 101Round Rock, TX 78681South Austin Office6501 South CongressSuite 1-103Austin, TX 78745Lakeline Office12505 Hymeadow DriveSuite 2CAustin, TX 78750Dripping Springs Office170 Benney LaneSuite 202Dripping Springs, TX 78620
Everything you ever need to know about medical hair loss management Delving deep into all aspects of hairloss.I am joined this week by Dr Ben Benham, a specialist in dermatology and hair restoration.Along with his brother, they developed the website Happyhead, to give easy access for patients to Doctors and prescriptions online.Many women are seeking treatment for hair loss, and early treatment can give a better prognosis.Ben gives so much information, he really is a hugely knowledgeable guest!We look at:MinoxidilAldactoneFinasterideDutasterideDermarolleringMicroneedlingPRP & stem cellsWe also discuss the best & worst habits for hair loss, such as smoking, vaping, nutrition, supplements and protein powders.Connect with Dr Ben:Website- www.happyhead.comEmail- Doctor@happyhead.comFacebook- Happy Head | Facebook Instagram- Custom Hair Loss Solution (@hihappyhead) • Instagram photos and videos Twitter- Happy Head (@HiHappyHead) / TwitterYoutube- Happy Head - YouTube Connect with Hair therapy:Facebook- https://www.facebook.com/HairTherapyUKInstagram- https://www.instagram.com/hairtherapyuk/Twitter- https://twitter.com/HairTherapyUKClubhouse- @Hair.TherapyThinking of starting your own podcast? Click on the link below to start
Thanks for tuning in to the Armor Men's Health Hour Podcast today, where we bring you the latest and greatest in urology care and the best urology humor out there.In this segment, Dr. Mistry and Donna Lee answer a listener's question about the impact medication can have on testosterone levels. This 73YO man was diagnosed with an enlarged prostate with urethral obstruction and placed on Dutasteride and Tamsulosin to shrink the prostate so a Rezum procedure could be performed. Shortly thereafter, he began having symptoms of low testosterone, and lab work confirmed he had a T level of 400 with no free testosterone. His urologist stopped the Dutasteride and began giving him 100 milligrams of Testosterone Cypionate weekly, which greatly improved his symptoms. But after 9 weeks of hormone therapy, his T level had jumped to over 1500 and he was immediately taken off the T injections. He wonders what caused his T level elevation and whether it would be safe to resume T therapy because it was very helpful. Dr. Mistry explains that medications like Dutasteride and Finasteride, often taken for hair growth, can definitely cause symptoms of ED as well as lowered sperm counts. Younger men or men trying to conceive should be aware of the risk of these side effects. In the case of our listener, it is likely that the sudden surge in his T levels may be a simple lab error, since diagnostic machines often fail and have to be recalibrated. Because hormone therapy was so beneficial in mitigating his symptoms, he should definitely find a urologist who is comfortable with prescribing testosterone for men's health and try again. If you or someone you love is experincing symptoms of ED or low testosterone after taking Dutasteride or Finasteride, please call us today and check out our podcast on what we call "post-Finasteride syndrome." This episode previously aired on 9.11.21. Don't forget to like, subscribe, and share us with a friend! As always, be well!Check our our award winning podcast!https://blog.feedspot.com/sex_therapy_podcasts/https://blog.feedspot.com/mens_health_podcasts/Dr. Mistry is a board-certified urologist and has been treating patients in the Austin and Greater Williamson County area since he started his private practice in 2007.We enjoy hearing from you! Email us at armormenshealth@gmail.com and we'll answer your question in an upcoming episode!Phone: (512) 238-0762Email: Armormenshealth@gmail.comWebsite: Armormenshealth.comOur Locations:Round Rock Office970 Hester's Crossing RoadSuite 101Round Rock, TX 78681South Austin Office6501 South CongressSuite 1-103Austin, TX 78745Lakeline Office12505 Hymeadow DriveSuite 2CAustin, TX 78750Dripping Springs Office170 Benney LaneSuite 202Dripping Springs, TX 78620
Thanks for tuning in to the Armor Men's Health Hour Podcast today, where we bring you the latest and greatest in urology care and the best urology humor out there.In this segment, Dr. Mistry and Donna Lee answer a listener's question about the impact medication can have on testosterone levels. This 73YO man was diagnosed with an enlarged prostate with urethral obstruction and placed on Dutasteride and Tamsulosin to shrink the prostate so a Rezum procedure could be performed. Shortly thereafter, he began having symptoms of low testosterone, and lab work confirmed he had a T level of 400 with no free testosterone. His urologist stopped the Dutasteride and began giving him 100 milligrams of Testosterone Cypionate weekly, which greatly improved his symptoms. But after 9 weeks of hormone therapy, his T level had jumped to over 1500 and he was immediately taken off the T injections. He wonders what caused his T level elevation and whether it would be safe to resume T therapy because it was very helpful. Dr. Mistry explains that medications like Dutasteride and Finasteride, often taken for hair growth, can definitely cause symptoms of ED as well as lowered sperm counts. Younger men or men trying to conceive should be aware of the risk of these side effects. In the case of our listener, it is likely that the sudden surge in his T levels may be a simple lab error, since diagnostic machines often fail and have to be recalibrated. Because hormone therapy was so beneficial in mitigating his symptoms, he should definitely find a urologist who is comfortable with prescribing testosterone for men's health and try again. If you or someone you love is experincing symptoms of ED or low testosterone after taking Dutasteride or Finasteride, please call us today and check out our podcast on what we call "post-Finasteride syndrome." If you enjoyed this episode, don't forget to like, subscribe, and share us with a friend! As always, be well! Check our our award winning podcast!https://blog.feedspot.com/sex_therapy_podcasts/https://blog.feedspot.com/mens_health_podcasts/Dr. Mistry is a board-certified urologist and has been treating patients in the Austin and Greater Williamson County area since he started his private practice in 2007.We enjoy hearing from you! Email us at armormenshealth@gmail.com and we'll answer your question in an upcoming episode!Phone: (512) 238-0762Email: Armormenshealth@gmail.comWebsite: Armormenshealth.comOur Locations:Round Rock Office970 Hester's Crossing RoadSuite 101Round Rock, TX 78681South Austin Office6501 South CongressSuite 1-103Austin, TX 78745Lakeline Office12505 Hymeadow DriveSuite 2CAustin, TX 78750Dripping Springs Office170 Benney LaneSuite 202Dripping Springs, TX 78620
Dallas hair transplant surgeon Dr. Sam Lam talks about Dutasteride (Avodart) & Topical Dutasteride. If you need a consult with Dr. Lam please contact us by ⠀ ⠀
See all the Healthcasts at https://www.biobalancehealth.com/healthcast-blog/ FINASTERIDE is a name of a medication that is commonly used in both dermatology and urology. It is an oral enzyme inhibitor that is used to decrease hair loss and to treat prostate enlargement. Finasteride is called a 5-alpha reductase inhibitor (5-ARI). It inhibits the enzyme that makes DHT out of free- testosterone. DHT is not a bad hormone, it is only a problem for us if it is too high or too low. DHT is one of the hormones that you need in the right quantity for normal sexuality, normal brain function, normal muscle mass and strength et al, but it is not healthy to have too much which can cause male pattern hair loss, facial hair on women, hair loss at the temples in women, and prostate enlargement and trouble urinating in men. Because men have a high incidence of hair loss, and prostate enlargement as they age, dermatologists, urologists and family docs start these men on Finasteride/Propecia/Proscar, but don't think about the side effects or how the drug works. It is sometimes even started for genetic hair loss, which is not successfully treated with Finasteride. What is the function of 5-alpha reductase inhibitor? 5-alpha reductase is vital to the development of male characteristics such as facial hair, deep voice, muscle growth, prostate enlargement male libido and prevention of ED. What are finasteride and it's brother medication, Dutasteride used to treat? Male Pattern hair loss (Androgenic alopecia) in men and postmenopausal women Benign Prostate enlargement (BPH) High DHT causing acne and facial hair in postmenopausal women (off label and only after spironolactone is found to not be enough in women only) ****Women who are of child-bearing age should not take this drug! What are the names of the two drugs available that are 5-alpha reductase inhibitors? Finasteride® and Dutasteride® These medications decrease the amount of circulating DHT by 70-98%. Therefore, when it is used to decrease hair loss and shrink an enlarged prostate, all of the DHT is decreased which results in blocking all the positive actions of DHT such as libido, energy, muscle maintenance, Penile length, erectile function, and male pattern body hair. These male characteristics are blunted for the sake of a thick head of hair and to shrink the prostate. It takes a much higher testosterone blood level and free testosterone to maintain male characteristics when on these meds. In some men there is no amount of 5-alpha-reductase inhibitors is safe. Side Effects of 5-alph-reductase inhibitors: Loss Sexual Dysfunction (Overall rate of sexual dysfunction 3.7%) Decreased ejaculatory volume-1.5-3.7% Ejaculation Disorders-0.2-0.8% of libido ED/Impotence 5-8% of the users have this Infertility 34% decreased sperm count, and 14.5% reduced sperm volume after 26 weeks of use. Normalization of seminal quality usually returns after discontinuation of finasteride Depression and Suicide Breast tissue dysfunction-0.9-2.5% (men) https://www.accessdata.fda.gov/drugsatfda_docs/label/2010/020180s037lbl.pdf, accessed January 25, 2021 POST FINASTERIDE SYNDROME: SOMETIMES THE SIDE EFFECTS ARE PERMANENT AND CAN ONLY BE TREATED BY TESTOSTERONE REPLACEMENT OVER TIME….THIS IS A LIFE LONG PROCESS OF REGROWING TESTOSTERONE RECEPTOR SITES. New Study Links Finasteride to Long-Term Sexual Dysfunction Finasteride users may experience severe sexual side effects for months or years after they discontinue use of the medication. Kiguradze T, Temps WH, Yarnold PR, Cashy J, Brannigan RE, Nardone B, Micali G, West DP, Belknap SM. Persistent erectile dysfunction in men exposed to the 5α-reductase Inhibitors, finasteride, or dutasteride. PeerJ. 2017 Mar 9;5:e3020. doi: 10.7717/peerj.3020. PMID: 28289563; PMCID: PMC5346286. HOW LONG WILL THIS LAST? ***POST FINASTERIDE SYNDROME CAN LAST 3 MONTHS or PERMANENTLY. Replacing testosterone helps recover the DHT receptors and is the only treatment known. ARE THE SEXUAL SIDE EFFECTS WORTH THICK HAIR? THE SIDE EFFECTS ARE …. -DECREASED OR NO LIBIDO -DECREASED SEMEN VOLUME --LOSS OF AM ERECTIONS --ED -PEYRONIE'S DISEASE (SCAR TISSUE --LOSS OF PLEASURABLE ORGASMS --PENILE SHRINKAGE AND SCROTAL SHRINKAGE AND NUMBNESS OTHER SIDE EFFECTS OF POST FINASTERIDE SYNDROME: -NO OIL FROM SCALP—DRY BRITTLE HAIR -MELASMA APATHY AND CHRONIC FATIGUE -GYNECOMASTIA -OBESITY -MUSCLE SHRINKAGE AND WEAKNESS -DECREASED BODY TEMPERATURE --PREDIABETES AND HIGH TRIGLYCERIDES= IR --INSOMNIA --DEPRESSION --DECREASED PROBLEM SOLVING --EMOTIONAL FLATNESS What to expect after stopping? 6 weeks of hair loss but that is not a good reason to restart. Alternative treatments for hair loss and BPD instead of Propecia, Proscar, Topical finasteride-only if it is not absorbed systemically Topical Minoxidil Oral zinc 30 mg/day Saw Palmetto 500-700 mg day Pumpkin seed extract Stinging nettle 200 mg/day
See all the Healthcast at https://www.biobalancehealth.com/healthcast-blog/ Our practice (BioBalance Health) is a hormone replacement practice that specializes in the replacement of hormones lost as the body ages. We focus our attention primarily on men and women who are in their forties and fifties and older. However, there are some younger men who need our help because their bodies are not making the appropriate and healthy amount of testosterone. We look carefully at these men and see if we can do something to stimulate the natural production of adequate amounts of testosterone without replacement. We do not want to stop their bodies' natural processes; we want to enhance them. This is possible in men under 50 but is generally possible in men who are under 50. That is why we replace instead of stimulate T production in aging men. Currently, there are increasing numbers of men who are experiencing the symptoms of low T at a younger age and the appropriate treatment for them is to stimulate their own production of T, with medication, instead of shutting their own production down and replacing their Testosterone like we do in aging men. If a man gets replacement testosterone then his own testosterone stops being made, leading to questions about the best way forward when treating the loss of Testosterone. Replacement of T in young men can suppress fertility, can scar the testicles and make it impossible for them to restart their testosterone on their own. Some young men can return to their baseline of T production after T replacement and some cannot. This is why we attempt stimulation in young men before ever replacing their T. In the last few months the US federal government has ended the ability of men to receive compounded HCG, a medicine with few side effects which mimics the hormones made from the pituitary LH and FSH, and stimulates the testes to make more testosterone, and when compounded is affordable. This drug has mysteriously been banned by governmental agencies by preventing compounding pharmacies from making it. This leaves young men and the doctors taking care of them from treating them in the most conservative manner. Doctors who take care of these men have lost their most effective tool. The government just banned its use, without public information to explain why. So, for us, it is back to the drawing board. What can we do to appropriately provide the necessary testosterone for these men? First, let's look at the symptoms of low Testosterone: Low libido Ed Poor ejaculation Lack of sexual climax Fatigue Insomnia Loss of muscle mass strength and stamina Loss of ability to think Depression/anxiety Irritability Belly fat and weight gain Hair loss Loss of body hair Joint pain It is important to note that the treatment for low T we are talking about is for young men who still have responsive testicles that make more T when exposed to more LH and FSH prom the pituitary. Older men must have their T replaced because stimulatory medications rarely stimulate the testicles as age makes them resistant to stimulatory drugs. Most men over 50 must have their T replaced, since they do not make enough naturally, and stimulation doesn't work. Because doctors can no longer acquire HCG to help these young men, we must turn to other medicines which can stimulate the production of testosterone. So now we are using alternate drugs Clomid, Arimidex, Anastrazole and Dutasteride instead. These drugs are much more expensive than HCG, and the side effect profile of them is higher, and the effectiveness is lower than HCG was. Interestingly, the FDA has just approved a new HCG drug that is meant for infertility and it is very expensive! By eliminating the competition, the very wealthy will be able to afford it! Not fair! What we know is that we can do some things to encourage the production of testosterone naturally when the body begins to stop making it. But the process is expensive, and we are not allowed to utilize the most efficient and cost -effective drugs. We are not told why, but our patients still need help and we try to find ways to provide that help. The focus of our practice is not on young men in particular, but they do come to us for help, and we will try to find ways to treat them and help them become more healthy and functional, in spite of the efforts of the federal government to prevent our ability to do so. We have to utilize informed consent in order to help them, as they need to know the side effects that are possible if they receive this treatment and they need to know the benefit/cost ratio for living without testosterone or trying to stimulate the body to make an adequate and functional amount.
Vidcast: https://youtu.be/hMEHBR2pb08 Men with greater androgen signaling and abundant circulating androgens have more severe CoVid infections with accompanying lung, heart, and kidney damage. A collaborative Yale, Harvard, and UC-San Francisco study of 454 hospitalized CoVid positive British patients. The free androgen level was significantly associated with viral susceptibility and disease severity in men but not in women. Androgens are known to increase expression of the ACE2 molecule in human tissues, and it is this protein that binds CoVid19 permitting it to enter and infect cells. The researchers suggest that already FDA approved androgen inhibiting drugs such as dutasteride and finasteride may have potential for inhibiting CoVid19 infections. https://www.biorxiv.org/content/10.1101/2020.05.12.091082v2.full.pdf #covid #pandemic #ace2 #androgens #5alphareductaseinhibitor #dutasteride #finasteride
This article will be a continually updated log for my injectable SARMs cycle and review of injectable LGD-4033 (Magnalone). Rather than publish a separate article for each update, I will come back and update this article accordingly with any blood work or new findings. For those that are just here find out where to buy injectable SARMs, these are the only companies I currently use for my own personal research: Swiss Chems – 11% off coupon code “DC11” The Goal Of This Experiment In my log introduction I outlined the goal of this experiment. https://youtu.be/F3L7xhE6tlM My goal of this experiment was to truly evaluate how anabolic injectable SARMs are without any interfering factors. To be more specific, I wanted to find out if injectable LGD-4033 could "replace" a TRT dose of Testosterone entirely in a muscle growth/retention context. If injectable SARMs could replicate the same muscle building potential as traditionally used anabolic steroids with a fraction of the androgenic activity, the potential applications would be endless. LGD-4033 is purported to have a 500:1 anabolic to androgenic ratio. The following graph illustrates the data derived from the preclinical studies which exhibits how much LGD-4033 stimulated muscle growth relative to prostate growth in comparison to Testosterone. LGD-4033 Selectivity For Muscle To Prostate Compared To Testosterone LGD-4033 stacked up against Testosterone very well in the preclinical models with a greater than 500x tissue selectivity of muscle to prostate. As LGD-4033 is so tissue selective, individuals who are extremely prone to the androgenic side effects of Testosterone may be able to utilize LGD-4033 as a way to build supraphysiological amounts of muscle mass, or retain it, with a relative absence of those same side effects. How I Determined Exactly How Anabolic Injectable LGD-4033 Is By Utilizing Exogenous Estradiol Most guys using injectable SARMs are using them alongside a Testosterone base at minimum. To truly evaluate the efficacy of injectable LGD-4033 in an anabolism context, all other androgens would need to be removed from the equation. As I just finished a Nandrolone monotherapy experiment prior to starting LGD-4033, my endogenous androgen production was completely shutdown. Estrogen is what has shown to be neuroprotective and not Testosterone (and potentially cardioprotective as well). Estrogen also supports several other functions in the body that would be inhibited if I were to forgo Estrogen replacement during this experiment. These include but are not limited to muscle growth and fat loss. I needed to isolate LGD-4033 and keep myself shut down to accurately assess how anabolic it is, so adding an exogenous aromatizing compound was not an option. The most common solution to insufficient Estrogen would be a Testosterone base, DHEA, HCG, or an aromatizing anabolic steroid like Dianabol or Trestolone to act as a makeshift "Test base". None of these were viable options as they would add anabolic and androgenic activity to my body and skew my findings. The only option was to utilize exogenous Estradiol at a physiologic dose. This is because exogenous Estradiol would prevent my natural Testosterone production from turning back on (endogenous Testosterone production would also skew my findings), it would activate Estrogen receptors sufficiently to bandaid the issue of insufficient aromatization to fulfill physiologic functions, and it would not elevate androgenic activity in the body at all. In theory, by maintaining a physiologic level of Estrogen in the body I could largely avert the inhibition of anabolic pathways and assess exactly how anabolic LGD-4033 is with no factors interfering. The only potential drawback here is that aromatase is what normally regulates Estrogen production endogenously, and by bypassing this process entirely I could very well be missing out on some downstream anabolic pathways that would otherwise be fulfilled by Testosterone aromatizing into Estrogen. Just one of these being the IGF-1 pathway. The experiment is not perfect, but it is the closest I am going to get to it. Prior to my Nandrolone experiment I was maintaining my physique on 100 mg of Testosterone per week, and I was able to retain the same level of muscle mass and strength during my Nandrolone experiment with no other factors changed. If injectable LGD-4033 proved capable of maintaining my physique with no factors changed in my diet or training, then I would know that it is at least as anabolic as Testosterone and Nandrolone, but with a fraction of the androgenic activity. Oral SARMs Vs. Injectable SARMs Oral SARMs have shown to have a handful of common side effects in a clinical setting, with numerous other side effects cropping up when utilized in a performance enhancing context at higher dosages. The main side effects that are consistently seen both clinically as well as anecdotally with oral SARMs are: Negative Effect On Lipid Profile Natural Testosterone Suppression Liver Toxicity (less common) https://youtu.be/Lhis3HWWKbQ Other less common side effects start to crop up once the dosage used greatly exceeds what has been evaluated on humans clinically. The potential benefits that injectable SARMs have over oral SARMs mainly come down to increased bioavailability and skipping the first pass effect in the body after administration. Bioavailability Many SARMs have undisclosed oral bioavailability and are presumed to be low based on the lack of published data. Obviously this isn't a scientific way to go about determining a SARM's oral bioavailability, but until these pharmaceutical companies start to release more transparent data, researchers will speculate and make assumptions that could be true, or could be way off. Some SARMs have shown to have reasonable levels of oral bioavailability, but we don't have exact figures for the majority of them. The closer a SARM is to 100% the closer it is to complete absorption after oral dosing. With injection, complete bioavailability is guaranteed as we are basically forcing the body to assimilate it into the blood and carry it to target tissues, whereas with oral administration we are giving the body's oral drug metabolism an opportunity to break down the compound however it sees fit. By ensuring complete bioavailability with injection, we may be able to minimize the dosage required to yield a desired effect. In theory, this should result in less side effects and more anabolic activity milligram for milligram. This is the first potential benefit of injectable SARMs over oral SARMs. In some cases, like with SR9009 (not a SARM but is commonly lumped into the "SARMs" category), the body nearly completely breaks it down when it is administered orally, rendering it ineffective. Some oral SARMs are very bioavailable as is and we do have the data to reinforce that. For example, the SARM S23 is 96% orally bioavailable [R]. This means that S23 can be administered orally, as opposed to requiring injections to achieve maximal blood serum concentration levels, which is obviously advantageous when it comes to ease of use and adoption. The First Pass Effect - Drug Metabolism Despite having nearly 100% bioavailability, oral S23 administration may have a completely different effect in the body simply by injecting it. The same could apply for any other SARM too, not just S23. After a drug is swallowed, the digestive system absorbs it and it enters the hepatic portal system. Afterwards, the portal vein carries it into the liver for metabolization, which then essentially regulates how much is filtered out prior to delivery to the circulatory system for delivery to target tissues. Not only can this process greatly reduce how much of a drug actually gets through for utilization, but it can produce a variety of side effects that wouldn't occur with methods of administration that skip the first pass. Methods of administration like transdermal delivery or injection skip the first pass and can avoid the hepatotoxicity often associated with oral drug metabolism, as well as other side effects that can stem from the drug metabolism process itself. More often than not, this is a good thing. However, in the case of anabolic agents, it seems that the first pass can actually be responsbile for the potentiation of certain compounds, rather than the other way around. You can see how this can start to make injectable SARMs vs. oral SARMs murky territory, as we basically need to experiment with it ourselves to see if the increased bioavailability and skipping the first pass improves the anabolic activity relative to the side effect profile of SARMs, or makes it worse. For what it is worth, as of now the results seem promising, with the majority of individuals noting only drastically increased levels of anabolic activity at lower dosages, and less side effects. However, regardless of how promising and exciting this may seem, we need to consider the possibility of negative outcomes and not let the hype around injectable SARMs shroud our judgment. Examples Of How The First Pass Effect Can Greatly Impact Drug Effects The following are two examples of how drastic of a difference just changing the method of administration can have when it comes to a drug's effects on the body. The first shows how injectable and transdermal estradiol was superior to oral estradiol, and the second shows how oral Superdrol was superior to injectable Superdrol (in a tissue selectivity context, not a hepatotoxicity or lipid dysfunction context). Oral Estrogen Vs. Transdermal Or Injectable Estrogen A few of the most notable drawbacks of oral estrogen pills are that they can be somewhat liver toxic, they significantly spike SHBG levels, and they result in the production of clotting factors in the blood that do not develop with forms of administration that skip the first pass. Also, the ratio of Estrone-to-Estradiol is skewed with massive elevations in Estrone with oral Estrogen administration. None of these issues occur with transdermal topical application, or injection. High levels of serum Estrone sulfate (E1S) were found after long-term oral estrogen treatment of commonly prescribed dosages, whereas there was a small increase in E1S levels after transdermal Estradiol (E2) therapy. The mean maximum E1S levels were more than 20-fold higher with oral estradiol (E2) when compared with the 0.05 mg/day transdermal estradiol patch. This is consistent with the 20-fold higher dose of E2 when compared with the transdermal dose [R]. Oral estrogen also has very low bioavailability, thus requiring a much higher dosage to achieve the same effect that could be achieved with a much lower dosage of injectable estrogen. Oral Superdrol Vs. Injectable Superdrol Not only is the side effect profile of oral Superdrol compared to injectable Superdrol substantially different, but even its anabolic to androgenic ratio changes based on the method of administration. When administered orally, Superdrol was more anabolic than methyltestosterone and several times less androgenic than methyltestosterone. Methyltestosterone has an anabolic to androgenic ratio similar to that of testosterone (close to 1:1). When administered via injection, Superdrol was nearly twice as anabolic as testosterone and twice as androgenic as testosterone. The results of subsequent assays to determine Superdrol's anabolic and androgenic activity found that that Superdrol possessed the oral bioavailability of methyltestosterone while being 400% as anabolic and 20% as androgenic, yielding an anabolic to androgenic ratio of 20:1 [R]. In the case of Superdrol, injecting it actually made it less tissue selective, despite oral administration having the obvious drawback of lower bioavailability and hepatotoxicity. My Daily Injectable LGD-4033 And Estradiol Dosage As the goal of this experiment was to determine the lowest effective dose of LGD-4033 that could replicate the same anabolic activity as 100 mg of Testosterone per week and 100 mg of Nandrolone per week, my dose was much lower than what most are utilizing in their own experiments. Once I could determine the lowest effective dosage, I could evaluate the side effect profile of that dosage, how my blood work looks on that dose, how I feel, and then make an informed decision about the overall efficacy profile of injectable LGD-4033 based on all of those factors. As injectable LGD-4033 is more bioavailable, the dosage required to replicate the anabolic activity I was shooting for would likely be much lower than you would expect via oral dosing. I spoke to Tony and Trevor about this experiment and asked for their feedback on what dose they think I should start at. They were the two who brought injectable SARMs to my attention in the first place, and nobody else I know had any experience with them at the time. At 7:02 in the following video Tony and Trevor are referring to me, and that is partially what influenced my decision to go with 3 mg per day as my daily dose. https://youtu.be/F2OcSnQZ99Q?t=422 I also applied 2.5 grams of transdermal Estrogel (delivering 1.5 mg Estradiol) per day for the first couple weeks. I got my blood test results back from my Nandrolone experiment a couple weeks into my LGD-4033 experiment which showed that I was absorbing Estrogel very poorly, which prompted me to switch to oral Estradiol pills. Ideally I would have switched to Estradiol injections, but I did not have any injectable Estradiol on hand, so I was forced to use oral pills if I wanted to maintain an optimal Estradiol level throughout the experiment. Injectable LGD-4033 Half-Life And Dosing Schedule Orally, LGD-4033 displayed a prolonged elimination half-life (24–36 hours), linear pharmacokinetics, and predictable accumulation with multiple dosing [R]. There was a dose-proportional increase in LGD-4033 concentrations on days 1 and 21 because of its long half-life. Serum LGD-4033 concentrations were nearly threefold higher on day 21 than on day 1, reflecting accumulation upon multiple dosing. There is not any human data we can refer to that evaluates the pharmacokinetics of injectable LGD-4033, so any statements made about how often it should be dosed are largely based on speculation and educated guesses. Tony and Trevor believe that injectable LGD-4033 can be dosed every other day and still maintain stable blood serum concentrations. https://youtu.be/1aTQWN3ML3U For the sake of ensuring stability once dose saturation was reached, I maintained a daily dosing schedule from day 1 where I administered 3 mg every 24 hours. Muscle Growth And Strength Levels https://youtu.be/Iq-fm1qJ5To How I assess if something is working or not is by comparing it to my previous baseline metrics I have established on a therapeutic dose of TRT. If I suddenly start getting stronger while using the exact same diet and training regimen with the only factor changed being a drug, I can logically conclude that the drug is stronger milligram for milligram than my baseline on TRT. By now, I know exactly how my body responds to 100 mg of Testosterone per week, as well as 100 mg of Nandrolone per week. After swapping to injectable LGD-4033 with no other factors changed, it was very easy to assess if there were any positive or negative changes in my body composition or strength. Other than feeling a bit deflated, I didn't experience any changes in my strength or size. My weight stayed exactly the same, my strength stayed exactly the same, and my body composition stayed the same, with the exception of being a bit flatter. Perhaps the reason I'm flatter is that LGD-4033 has less "off target" activation than something like Testosterone and Nandrolone, whereby they can increase intramuscular fullness via indirect mechanisms. That is just speculation though. At the end of the day, I haven't lost any contractile tissue, which is the most important thing to note. I believe that a relatively low dose of injectable LGD-4033 is at least as anabolic as 100 mg of Testosterone per week or 100 mg of Nandrolone per week. While this is promising for those on TRT or who use "low" dosages of anabolic steroids, the main drawback we have seen in the past with oral SARMs is that the ceiling where diminishing returns starts to set in is far lower than with anabolic steroids. Whether or not injectable LGD-4033 has that same drawback remains to be seen. Anecdotally, other users have reported that the ceiling of diminishing returns is much higher with injectable LGD-4033, but I cannot confirm or deny this myself as that is beyond the scope of my experiment (at least for now). My only hope for this experiment was that I could retain all my muscle with just a SARM, which I did. I may consider a "blast" phase in the future where I titrate the dose up and evaluate how well it can support supraphysiological muscle growth, but that will be dictated by its androgenicity in practical application. Injectable LGD-4033's androgenicity still needs to be explored more via further experimentation, as I did have a few red flags of androgenic activity that have me a bit hesitant to utilize a higher dose. If injectable LGD-4033 is as tissue selective as the clinical data has shown, there are several doors that open up in a bodybuilding and hair loss prevention context. Side Effects Changes In Libido My sex drive went up substantially after swapping Nandrolone out for LGD-4033. Many were quick to comment on my YouTube video about how exogenous Estradiol (E2) is the reason why my libido spiked. I was already on exogenous Estradiol prior to the injectable LGD-4033 for my Nandrolone-only experiment. I have been on the same dose of transdermal E2 for almost 3 months, the only thing that changed was swapping NPP out for LGD. The libido change was from the swap. No other factors were changed. After I switched from transdermal Estradiol to oral Estradiol, my libido was no different either. The change in libido occurred almost overnight after adding LGD-4033 in. Several other individuals have come forward since that video was published reporting that injectable LGD-4033 increased their libido as well. They were all using a dose at least 5-10x higher than I was, but it is still notable nonetheless. As LGD-4033 is supposed to be so tissue selective and have such a lack of androgenicity I was very surprised that my libido spiked. If anything, I was expecting my libido to drop. With a 500:1 anabolic to androgenic ratio, obviously you wouldn't expect one of the biggest red flags of androgenic activity to spike. Keep in mind, 100 mg of Nandrolone per week is not nothing. Despite Nandrolone being one of the least androgenic steroids ever developed (if not the least of the mainstream anabolic steroids), 100 mg per week has shown to be a high enough dose to cause virilization in women. Within 12 weeks, some women will experience virilization on Nandrolone even using only 100 mg every 2 weeks. When duration of use exceeds a year, significant virilization in women is found even at a dosage of only 50 mg every 2 weeks. My libido doubled after switching from NPP to injectable LGD-4033, which is a red flag and should be noted. My libido isn't as high as it is on 100 mg per week of Testosterone, but it is significantly higher than on Nandrolone. Hair Loss I noticed an increase in shedding using injectable LGD-4033. However, less than 10% of the hairs I shed are miniaturized. This leads me to believe that it is less likely to be androgenic alopecia, and is more likely telogen effluvium caused by the massive hormone fluctuation I put my body through by switching from TRT to a Nandrolone only protocol, and then subsequently switching from Nandrolone to injectable LGD-4033. Further experimentation will be needed before I have a concrete conclusion on the androgenicity of injectable LGD-4033. If it ends up being hair safe, there are several applications I have in mind for this compound. Not only would it be a potent androgen receptor agonist for use in a bodybuilding context, but it could also be utilized during a hair recovery phase. For example, if you have any androgenic alopecia, periodically switching to SARMs with exogenous Estradiol (or an Estrogen precursor) in cycles could be a way to maintain muscle built via supraphysiological steroid use in the past, while reducing the androgen load on the scalp significantly enough to allow for regrowth. Or, if you don't use steroids, it could serve as a means of recovering hair lost via endogenous androgen induced miniaturization by reducing androgenicity below baseline periodically throughout the year. Basically like a makeshift anti-androgen that won't strip the muscle off your body. These are hypothetical examples, but these are just a few of the potential applications I see for SARMs in the future. Changes In Body Hair Growth This one was a metric I should have kept a closer eye on, but I usually manscape every single week so it wasn't something I originally planned on evaluating. A few weeks into my LGD-4033 experiment I noticed that my body hair seemed to be growing a bit faster than usual. Whether this was in my head or not, I'm not positive as I was not even planning on using this as a metric, but I got backlogged on work throughout the holidays and ended up skipping my weekly manscaping sessions. While it may not be fair to say for certain that LGD-4033 increased my rate of body hair growth, I can confidently say that at the absolute least, it did not reduce my body hair growth. This is notable as well because I had no androgens in my body. If I only had Estrogen in my system and no androgens I would notice a drastic reduction in body hair growth and libido, just like transgenders who transition from male to female. The only anabolic compound in my body throughout this entire experiment was injectable LGD-4033, and I didn't notice a reduction in androgenic activity via body hair growth either. When I crushed my DHT levels to 0 with Dutasteride, I noticed a significant reduction in back hair growth. On injectable LGD-4033, I did not notice a reduction in body hair growth at all. However, on Nandrolone I did not experience a significant reduction in body hair growth either, despite it dramatically reducing my libido. While this metric isn't a scientific way to assess androgenic activity, in general, the body can tell you pretty accurately when androgenic activity is high or low when sufficient Estrogen is present to support erections. Increase the androgenic activity in your body and you will likely experience an increase in libido, an increase in scalp hair loss, and an increase in body hair growth (in general). Decrease the androgenic activity in your body and you will likely experience a decrease in libido, a decrease in scalp hair loss, and a decrease in body hair growth (in general). Changes In Blood Pressure My blood pressure on injectable LGD-4033 is identical to what it is normally on TRT. My blood pressure on injectable LGD-4033 and TRT is far better than it is on Nandrolone. For whatever reason, Nandrolone has a unique negative impact on systolic blood pressure, making it difficult to maintain healthy levels. On only 100 mg of NPP per week my systolic blood pressure was consistently 125-128 eating the exact same diet I was on TRT and LGD-4033. So far so good in regards to blood pressure on injectable LGD-4033 though. Changes In Resting Heart Rate My resting heart rate did not increase on injectable LGD-4033 and is no different than what it is on TRT. Potential In Preventing Or Reversing Cardiovascular Issues Caused By Steroid Use Even if injectable LGD-4033 does not end up being as purely anabolic as we hoped, there is another very promising application I see for injectable SARMs that is largely overlooked. That is the potential lack of heart stimulation. Anecdotally, many users have reported far better outcomes using SARMs than anabolic steroids in a cardiovascular health context. One example is a friend of mine, Alek Mitrevski. He used 100 mg of oral S4 (Andarine) with 0.5 mg oral Estradiol per day for over a year straight. During that time he did not experience any cardiac hypertrophy, LVH, or any kind of deleterious effect on his cardiovascular system. At the start of 2019 Alek ran a high dose Deca only cycle with Anadrol intermittently added in. https://youtu.be/qDgk7XLcqqU Within 9 months, he experienced significant thickening and enlargement of his heart. He switched back to SARMs only to try and reverse this damage while maintaining the muscle he built with the Deca + Anadrol blast. Although the reports are obscure and not well documented, I have seen a handful of individuals report the reversal of cardiomyopathy and LVH after switching to SARMs only. SARMs are supposed to be tissue selective, whereas anabolic steroids have shown to significantly impair cardiac health. The potential applications this may have for athletes seeking supraphysiological muscle growth with a minimization of cardiac hypertrophy, LVH, etc. makes injectable SARMs worth further exploration in itself. Athletes seeking to reverse cardiovascular issues as a result of past AAS abuse while maintaining most (or all) of their hard earned muscle mass would also be strong candidates for benefiting from injectable SARMs if the hype around them turns out to be justified. My Blood Test Results I will be updating this section with my blood test results in the near future. Reviews From Other Users I have curated all of the injectable LGD-4033 reviews I could find and included them here for your reference as well. https://youtu.be/rJFmwpPvBfQ https://youtu.be/c1BWS-sP7nM The following comments weren't reviews about injectable LGD-4033 specifically, but they were relevant to include nonetheless: Conclusion Some of the classic signs of androgenic activity are red flags worth keeping an eye on. But other than that, so far so good. I feel good, I am not depressed and have not experienced any negative mental or physical side effects so far despite the near complete absence of Testosterone and DHT in my body. The fact that injectable LGD-4033 has proved capable of maintaining the same amount of muscle and strength that I could maintain on 100 mg of Testosterone per week and 100 mg of Nandrolone per week is a good sign. I was hoping for that outcome, and expecting more than that is wishful thinking. If a relatively low dose of injectable SARMs can replicate the same anabolic activity of traditionally used steroids, then it is absolutely worth further experimentation. I'm going to continue digging into injectable SARMs, and I look forward to seeing more data come from other researchers in the community as well. This is a very promising area of research, and I hope that more individuals start to come forward with their personal findings too. I'll keep you guys updated, but that is where we're at with my injectable SARMs experiment so far. Where To Buy Injectable SARMs I strongly advise that before you buy SARMs from a company online you thoroughly evaluate their track record, their third party test results, and how they are marketing their products in general. These are my current go to companies for injectable SARMs: Disclaimer: The information included in this article is intended for entertainment and informational purposes only. It is not intended nor implied to be a substitute for professional medical advice. Prior to buying anything, check that it is compliant where you live with your current government laws.
RU58841 vs. Finasteride. As of now RU58841 is the most commonly used topical anti-androgen used for hair loss prevention, and Finasteride is the most commonly used 5α-Reductase inhibitor for hair loss prevention. Which is better for hair loss prevention? This is a common question I get asked and a dedicated post is long overdue. https://youtu.be/p39W1nBhxYE Study Comparing RU58841 Vs. Finasteride Head To Head While there are tons of anecdotal reviews comparing Finasteride to RU58841, there is very little scientific data for us to refer to. There is some though that is worth delving into. In this study, Finasteride was stacked up against RU58841 to see which would be more effective for hair loss prevention, and how much each would impact systemic hormone levels [R]. RU58841 was applied either in a 5% solution, a 0.5% solution, or just a vehicle with no RU58841 in it for 6 months to the bald scalp of 10 stump-tailed macaques. The 5% solution was applied to 4 of the 10 bald stump-tailed macaques, the 0.5% solution was applied to 3 of the 10 bald stump-tailed macaques, and the vehicle with no RU58841 was applied to the last 3 of the 10 bald stump-tailed macaques. The common dosing protocol for RU58841 is typically a 5% solution applied to androgenic alopecia affected areas, so this study was right in line with what we would want to see. Oral Finasteride was given in a dose of 1 mg/kg/day for 6 months to 10 bald stump-tailed macaques. An oral placebo was also given to 10 bald stump-tailed macaques. Male stump-tailed macaques weigh on average between 9.7–10.2 kg, so that would equate to a Finasteride dosage of roughly 10 mg orally per day. This dosage greatly exceeds the point of diminishing returns with Finasteride use, so this is also a great way for us to compare the efficacy of a standard dose of RU58841 to a maxed out dose of Finasteride. The stump-tailed macaque has shown to be a suitable biological model for human androgenetic alopecia as it possesses hereditary balding characteristics similar in many respects to that of androgenetic alopecia in humans [R]. Results Skin biopsies for micromorphometric analysis (folliculogram) were taken at 0 and 6 months for Finasteride treated macaques and at 0 and 4 months for RU58841 treated macaques. The amount of anagen follicles (hairs in the active growth phase) and vellus follicles (short, thin, and barely noticeable hairs) enlarged to terminal size were compared to those in pre-treatment stages. Anagen follicles increased an average of 88% with Finasteride. Anagen follicles increased an average of 103% with 5% strength RU58841. The growth of vellus follicles to terminal size (thick, strong, pigmented hairs that have fully matured) was 12% with Finasteride. The growth of vellus follicles to terminal size was 26% with 5% strength RU58841. The 0.5% strength RU58841 solution induced almost no effect. Expectedly, the Finasteride placebo induced no effect. The 5% strength RU58841 solution induced the most hair growth after only 2 months of treatment. RU58841 was given less time to work and still significantly outperformed Finasteride in this study. Although Finasteride significantly reduced DHT levels, DHT remaining and produced by Type I 5α-reductase isoenzyme still contributed to hair follicle miniaturization. Because Testosterone and DHT both bind to the androgen receptor, a locally sufficient dose of an "AR blocker" (topical anti-androgen) appears to suppress Testosterone and DHT induced follicular regression more effectively than 5α-reductase inhibition. Systemic Effects Plasma RU58841 and metabolites (10-20 ng/ml) were detected in 2 of the stump-tailed macaques that were applied the 5% strength RU58841 solution at the 3 month mark of treatment. Only 1 of the stump-tailed macaques had detectable plasma RU58841 and metabolites at at the 6 month mark of treatment. RU58841 had no significant impact on serum DHT or Testosterone levels at any point. Finasteride decreased serum DHT levels by about 70%, and Testosterone levels increased as a result of the 5α-reductase blockade. If Estrogen levels were assessed in the Finasteride treated group, their Estrogen levels would have showed significant elevation as well as a result of increased aromatization. My Concluding Thoughts On This Study This study shows that RU58841 can go systemic when topically applied, although there is no effect on endogenous androgen levels. First of all, I do believe that RU58841 can go systemic, in fact, I think it is an inevitable outcome. However, the degree to which it goes systemic and if the amount that goes systemic will cause anti-androgenic side effects will be based on several factors. These factors include but are not limited to endogenous androgen production, sex hormone metabolism, androgen receptor density and expression, scalp skin porosity, the dosage used, if there are open wounds on the scalp or not, the vehicle used, frequency of administration, and more. Does this ensure side effects? No. However, applying anything to your skin with a low enough molecular weight to be absorbed and not expecting it to go systemic at all is wishful thinking. The molecular weight of RU58841 is 369.34 g/mol [R]. 1 Da (dalton) = 1 g/mol. The molecular weight of a compound must be under 500 Dalton to allow skin absorption (which RU58841 is) [R]. With that being said, RU58841 is well tolerated by the majority of users for a reason. In the study, at the 3 month mark 2 of the stump-tailed macaques had detectable plasma RU58841 and metabolites. By the 6 month mark, only 1 of the stump-tailed macaques had detectable plasma RU58841 and metabolites. If there was a cumulative drug effect we would have seen more animals with detectable metabolites after an additional 3 months of dosing, not less. What most fail to consider is that RU58841 is non-steroidal and acts as a competitive silent antagonist of the androgen receptor. This means that even if RU58841 goes systemic, by creating a blockade of the androgen receptor, RU58841 prevents the negative feedback androgens would normally create via the hypothalamic–pituitary–gonadal axis (HPG axis) in men. By binding to androgen receptors, RU58841 will induce anti-androgen effects without reducing serum androgen levels in the body. Finasteride on the other hand works by directly crushing DHT levels rather than by occupying androgen receptors. The ideal treatment would be a topical non-steroidal anti-androgen or SARM with a high binding affinity, and harmless metabolites void of anti-androgenic activity upon systemic absorption. Achieving Complete Hair Loss Protection By Addressing The Androgen Receptor, Not Just 5α-Reductase When you inhibit 5α-Reductase with Finasteride or Dutasteride, serum Testosterone and Estrogen levels increase will increase. A common mistake is to ignore the fact that scalp Testosterone levels rise dramatically after inhibiting 5α-Reductase. This occurs to an even greater degree with Dutasteride use, and I believe is the reason why some men experience accelerated hair loss after switching from Finasteride to Dutasteride. Typically, most men will see better results with Dutasteride as scalp DHT is almost always going to be more of a problem than scalp Testosterone. However, the consequent spike in scalp Testosterone levels with Dutasteride use is significant, and Testosterone will bind to androgen receptors and induce miniaturization just the same. 5 mg of Finasteride resulted in a 23% increase in scalp Testosterone levels with a concurrent 41% suppression of scalp DHT levels. 0.5 mg Dutasteride resulted in a 99% increase in scalp Testosterone levels with a concurrent 51% suppression of scalp DHT levels. This is why the androgen receptor needs to be addressed, not just nuking 5α-reductase with Dutasteride. Scalp Testosterone will still slowly chip away at your hair, regardless if DHT is there or not. In addition, Finasteride is insufficient to completely eliminate scalp DHT, which also needs to be taken into account and addressed. When you inhibit 5α-reductase, that Testosterone that would have otherwise converted to DHT doesn't just disappear, it remains as the parent hormone, thus raising total Testosterone levels in the body. Dutasteride doesn't just randomly stop working one day, Testosterone and other endogenous androgens are still eating away at your hair, just at a much slower pace than DHT would. The only way to prevent other androgens from binding to androgen receptors and miniaturizing hair follicles is by competing with them for androgen receptor binding. That's where the therapeutic promise of topical anti-androgens, anti-androgens in general, selective androgen receptor modulators, and other similar compounds that bind to androgen receptors can come into play and provide a compounding level of protection when needed, or as a form of monotherapy on their own if sufficient. If you only inhibit 5α-reductase with Finasteride, not only will you have residual amounts of DHT, but you will also have a spike in scalp Testosterone that is totally unaccounted for. Unfortunately, you can't just partially inhibit 5α-reductase and expect complete protection for life unless you have very mild hair loss to begin with. Permanent prevention can only be achieved by addressing the androgen receptor itself. For some individuals, Finasteride monotherapy will be sufficient to stave off hair loss for a couple decades, but that residual DHT and spike in Testosterone will continue to chip away and eventually win in the end. For some with aggressive hair loss, Finasteride monotherapy isn't even sufficient in the short-term. At the end of the day, regardless of how aggressive your hair loss is, prevention is mediated via the androgen receptor. Other treatment options may be implemented that interact with different downstream mechanisms in the cascade of events that lead to hair loss, but they will unlikely prove sufficient to completely mitigate androgenic alopecia on their own, and will be best utilized as an adjunct treatment to achieve a compounding level of protection with other compounds. Which Is Better For Hair Loss Prevention? RU58841 and Finasteride work via different mechanisms of action. They shouldn't be pitted against one another as neither are likely to prove sufficient to completely prevent hair loss on their own. DHT has a much higher binding affinity than RU58841, but Testosterone doesn't. Those with very aggressive hair loss would likely need to use a massive dose of RU58841 to compete with all of their scalp DHT and Testosterone. On the other hand, Finasteride can significantly decrease DHT levels, but causes a subsequent spike in scalp Testosterone that goes completely unaccounted for that will still work in tandem with the residual DHT to miniaturize hair follicles. A more complete level of protection would be achieved by using both Finasteride and RU58841, not one or the other. Finasteride will significantly reduce the amount of scalp DHT, and leave a hormonal environment that RU58841 is more capable of dealing with. RU58841's binding affinity is at least as high as Testosterone, so if most of the DHT is cleared out of the way, RU58841 only has to compete with Testosterone and a much lower amount of DHT. Expecting RU58841 to out-compete all endogenous DHT and Testosterone without any assistance when its binding affinity is several times lower than DHT is a strategy that would likely only work long-term for someone with mild hair loss. The dose and frequency of administration relative to the half-life needs to be kept in mind as well. There's a dose-dependent response with all drugs, including anti-androgens. Just because a 5% RU58841 solution applied once per day proves sufficient for one guy, that doesn't mean that dosage will be sufficient for you too. Hair loss is basically just a giant chess match where the most efficacious treatments will either knock out the opponent (decrease endogenous androgen levels), or occupy a more advantageous position on the chess board (binding to androgen receptors). The more chess pieces you have, the better your chance of winning against the finite number of opponent chess pieces. This is why certain anti-androgens with very poor binding affinity can still be effective in a clinical setting. An anti-androgen dosed very aggressively will eventually overpower Testosterone and DHT just by sheer volume (e.g. Bicalutamide). The same applies for RU58841, assuming it gets absorbed, which will boil down to scalp skin porosity, vehicle, and so on. If you opted for CB-03-01 instead of RU58841, the same concept would apply, it would just need to be dosed even more aggressively until sufficient AR binding is achieved. For those prone to side effects, that strategy may be the better alternative with CB-03-01 rather than RU58841 as it seems that the metabolites of CB-03-01 may be better tolerated at higher dosages than those of RU58841. The binding affinity of CB-03-01 is much lower than RU58841 though and it is very cost prohibitive, so for the time being, that strategy is likely not viable for most. Where To Buy RU58841 Most RU58841 sources do not third party test their products, nor do they have any satisfactory level of quality control whatsoever. I strongly advise that before you buy RU58841 from a company online you thoroughly evaluate their track record, their third party test results, and how they are marketing their products in general. These are the only companies I currently use for my own personal research: (Greater Than 99% Purity: FTIR, HPLC, GC-MS, LC-MS & NMR Tested) Science.bio – 10% off coupon code “DC10” Chemyo – 10% off coupon code “DC10” Anageninc - 5% off coupon code "DC5"
There's a misconception that Finasteride is a reliable source of remedy for hair loss prevention caused by the intake of all anabolic steroids. For anyone who has reviewed the downstream mechanisms of Finasteride in the body, it is clear that this is not true.…
I finally got around to trying CB-03-01. I had heard varying opinions on its therapeutic promise in the community, but at the end of the day I had to do a CB-03-01 review myself to see if this compound is superior to other alternatives we already have at our disposal.…
I've already written about if Finasteride lowers Testosterone levels. I felt an article on Dutasteride was justified as well. If you read the Finasteride article, you already know that Finasteride does not lower Testosterone, which is a common misconception. It actually increases Testosterone levels, as does Dutasteride.…
How Relevant Is DHT To Hair Loss? The first thing I want to make clear in regards to my Dutasteride and Testosterone experiment is that DHT is the worst hormone in your body for your hair. I don’t want anyone to misinterpret my videos and articles exhibiting the androgenicity of Testosterone as disregarding how bad DHT is.…
The potent synthetic androgen Trestolone, also known as 7α-methyl-19-norTestosterone (MENT), does not require 5α-reduction to exert its' maximal androgenic effects. It is an Anabolic Androgenic Steroid (AAS), which has been under development for potential use as a form of hormonal birth control for men and in androgen replacement therapy for low Testosterone levels in men but has never been approved for clinical usage.…
About 50% of men and women are going to experience some form of hair loss by the time they hit 50. That means that either you, or someone you know, is going through this process right now. A lot of the common questions we hear are: why am I losing my hair, is there anything I can do that actually works, and who can you can I talk to to if this is something that’s upsetting me? During this podcast we discuss with Dr.Sam, who is a highly qualified and experienced hair restoration surgeon, the facts and myths surrounding hair loss, and find out what are the very best treatments and techniques available today to manage hair loss. Show-Notes 0.40 - Hair Loss is a chronic medical conditions, and as such it is treatable. 2.20 - The difference between gene-protected and non-gene-protected hair. 4.00 - Dr.Sam explains hair loss patterns, how this is influenced by genetics, and the role of DHT (Dihydrotestosterone) in hair loss. 5.40 - How the miniaturisation process of hair follicles works. 9.11 - When a hair falls out, is the hair follicle actually dead? 13.03 - We discuss the medications for hair loss, Finasteride and Dutasteride. 15.50 - Discussing the potential side effects and worries surrounding Dutasteride and Finasteride. 25.30 - What are the downfalls of breaking tablets for consumption, do we get the full effect? Do they work? 33.29 - Dr.Sam explains some of the different types of hair loss. 39.09 - What are the steps you can take when you are experiencing hair loss? 42.45 - In a nutshell, what treatments are relevant to you personally? 48.44 - Dan explains that knowledge and education when it comes to hair loss is so important. PRP is a bit of a modern buzzword, and if your hair loss doesn't bother you, that's OK too! 51.31 - Hair loss can be viewed like diabetes, it's not a quick fix, and requires ongoing management. 54.50 - There is nothing inherently wrong or shameful about hair loss, it's normal, it's not vanity, and it can contribute to significant confidence issues. 56.30 - We are observing some social changes in mindset when it comes to these types of treatments. 59.20 - There can be many psychological effects attached to hair loss. 1.0.54 - We discuss the observation that many clients are very private about the treatments and don't want anyone to know. 1.02.47 - Hair loss can often become a burden, and a distraction from other things in life, and people often experience hurtful comments from the opposite sex. 1.06.19 - Many clients tell us when they return for a follow up that they have actually forgotten about their hair issues, which is exactly the point. 1.08.05 - Dr.Sam discusses his own hair loss story. 1.11.47 - Hair loss touches many lives, roughly 50% of the population will experience hair loss at some stage in life. 1.13.19 - We need more honesty in the industry, and less people praying on desperate clients. Check out our previous podcast about Stem Cells with Dr.Ali Ghanem.
Testosterone Also Causes Hair Loss – Not Just DHT I see A LOT of misinformation on the Internet in regards to hair loss (male pattern baldness/androgenic alopecia). Especially when it comes to why it occurs on a hormonal level, and the mechanism of action behind what is actually happening to your hair follicles.…
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