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There is a cheap and easy lab test that can give you a lot of information about your risk for scary things like heart attack, stroke, dementia, brain shrinkage, osteoporosis and more. It could save your life. But most doctors won't order it unless you ask them to because they don't know what to do with the results. But you're about to. Let's talk about homocysteine.come to my website: www.healthcouragecollective.comemail me: healthcouragecollective@gmail.com
In this episode, we review the high-yield topic of 5-Alpha Reductase Deficiency from the Reproductive section.Follow Medbullets on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbullets
This study explored the effects of elderberry extract on testosterone levels in rats experiencing testosterone deficiency syndrome (TDS). The researchers focused on how elderberry extract affected key enzymes involved in testosterone production and metabolism. They found that the extract increased total testosterone levels by 113.4% in the low-dose group, 219.3% in the mid-dose group, and 267.1% in the high-dose group compared to the control group. 1 Importantly, the high-dose group's testosterone levels were restored to levels similar to those of young rats. 2 The extract also increased free testosterone (the active form that's not bound to proteins) and improved sperm motility. 3 Furthermore, the researchers found no negative effects on prostate health, liver function, or kidney function, suggesting that elderberry extract could be a safe and effective natural approach for managing testosterone deficiency. #elderberry #testosterone #menshealth #hormones #naturalremedies #supplements #diet #aging #testosteronedeficiency #lowtestosterone #malehormones #andropause #fertility #libido #energy #moodenhancing #sambucus Kim J, An J, Song Y, Jang M, Kong H, Kim S. Effect of Elderberry (Sambucus nigra L.) Extract Intake on Normalizing Testosterone Concentration in Testosterone Deficiency Syndrome Rat Model Through Regulation of 17β-HSD, 5α-Reductase, and CYP19A1 Expression. Nutrients. 2024; 16(23):4169. https://doi.org/10.3390/nu16234169 --- Support this podcast: https://podcasters.spotify.com/pod/show/ralph-turchiano/support
References Nature Communications 2024. volume 15,1541. Campbell, Ian. 1963. The Sun is Burning. https://youtu.be/3L2Tn-YFlKk?si=pFTaj6iG9q4x-LR7 --- Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support
Audio Commentary by Dr. Valentin Fuster, Emeritus Editor in Chief
ACC.24: ARISE-HF Trial
References Dr Guerra-Graduate lipid biochemistry lectures Biochem J. 2022 Sep 30; 479(18): 1917–1940 Front Cell Dev Biol. 2022; 10: 946393. Nat Commun. 2019; 10: 97. Lennon-McCartney 1965. "Ive Just Seen a Face" https://youtu.be/m8LbJfC0SYM?si=gl_URu_yPTn9iZSd McShee, J./Traditional/Pentangle.1969 "Light Flight" https://youtu.be/2tyVezuUtCA?si=THxBJ0reUETkwDLa Mozart, WA. 1785.Piano Concerto No. 21 in C Major, K. 467 https://youtu.be/whTEVQ2OizI?si=YDMhOhlwmpKYqK-t --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support
Natural Treatments for Hair Loss | The ATP Project 422 In this hair-raising episode, Nic and Steve comb through the details of hair loss – from daily shedding stats to the three epic phases of hair drama. Find out why your follicles might be staging a protest against 5α-Reductase, how hormones and menopause can mess with your mane, and why stress is basically the arch-nemesis of luscious locks. But fear not! We've got the lowdown on everything from medical treatments to natural hair-boosting secrets with unbelievable research. Steve is such a fan that he has created his own treatment, tune in to find out more! So, whether you're a hair-itage expert or a follicle rookie, The ATP Project has your locks covered. Tune in, and let's turn those tresses into a glorious crown of victory!
Testo-Launch course - everything you need to know about testosterone optimization
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.14.536458v1?rss=1 Authors: Dutta, D., Kanca, O., Byeon, S. K., Marcogliese, P. C., Zuo, Z., Shridharan, R. V., Park, J. H., Undiagnosed Diseases Network,, Lin, G., Ge, M., Heimer, G., Kohler, J. N., Wheeler, M. T., Kaipparettu, B. A., Pandey, A., Bellen, H. J. Abstract: In most eukaryotic cells fatty acid synthesis occurs in the cytoplasm as well as in mitochondria. However, the relative contribution of mitochondrial fatty acid synthesis (mtFAS) to the cellular lipidome of metazoans is ill-defined. Hence, we studied the function of the fly Mitochondria enoyl CoA reductase (Mecr), the enzyme required for the last step of mtFAS. Loss of mecr causes lethality while neuronal loss leads to progressive neurological defects. We observe an elevated level of ceramides, a defect in Fe-S cluster biogenesis and increased iron levels in mecr mutants. Reducing the levels of either iron or ceramide suppresses the neurodegenerative phenotypes indicating that increased ceramides and iron metabolism are interrelated and play an important role in the pathogenesis. Mutations in human MECR cause pediatric-onset neurodegeneration and patient-derived fibroblasts display similar elevated ceramide levels and impaired iron homeostasis. In summary, this study shows an as-yet-unidentified role of mecr/MECR in ceramide and iron metabolism providing a mechanistic link between mtFAS and neurodegeneration Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
5α-Reductase inhibitors, medications such as finasteride and dutasteride, are commonly used as treatments for male-pattern baldness and benign prostatic hyperplasia, or BPH. In recent years, concerns for an increased risk of cognitive decline and dementia from taking these drugs has surfaced. In a new study published in the journal JAMA Network Open, researchers in Sweden […] The post 364. Male-pattern baldness drugs linked to depression appeared first on Dr. David Geier - Feel and Perform Better Than Ever.
Lexman interviews comedian and actor Mark Normand about his new children's book, Reens: A Reductase Story. They discuss baby reens, reductase, and the difficulties of parenting in the modern era.
Interview with Lars Björnebo, MSc, and Anna Lantz, MD, PhD, authors of Association of 5α-Reductase Inhibitors With Prostate Cancer Mortality. Hosted by Jack West, MD.
Interview with Lars Björnebo, MSc, and Anna Lantz, MD, PhD, authors of Association of 5α-Reductase Inhibitors With Prostate Cancer Mortality. Hosted by Jack West, MD.
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In this episode, we review the high-yield topic of 5-Alpha Reductase Deficiency from the Reproductive section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbulletsIn this episode --- Send in a voice message: https://anchor.fm/medbulletsstep1/message
Cell Metabolism 2020 31472-492 Amino Acids. 2012 Oct;43(4):1803-7 Molecular Cell Volume 81, Issue 18, 16 September 2021, Pages 3677-3690 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support
This podcast covers the regulation of HMG CoA reductase by hormones, cholesterol and statins. This biochemistry content may be useful to premedical and medical students. --- Send in a voice message: https://anchor.fm/a-j-ghalayini/message
In this episode we finish our recap of the book Middlesex by Jeffrey Eugenides. Then we dive into some topics surrounding intersex individuals and human rights.Sources:Middlesex by Jeffrey Eugenideshttps://interactadvocates.org/faq/ https://www.bbc.com/news/world-africa-39780214 https://www.bbc.com/news/magazine-34290981
Rob English is a medical editor who specializes in hair loss disorders. He sits on the editorial board of Dermatology and Therapy, and he's the founder of perfecthairhealth.com – a website dedicated to showcasing evidence-based protocols for hair regrowth, with or without drugs. His fascination with hair loss began in 2007 – right after he was diagnosed with androgenic alopecia. Today, he spends his time managing a small team of researchers and teaching other hair loss sufferers how to avoid his treatment mistakes. By employing an approach that prioritizes education over product purchases and one-on-one support over "one-size-fits-all" solutions, he has helped thousands of men and women improve their hair loss – and on their terms (most often without drugs). You can see his clients' testimonials and find his work at perfecthairhealth.com. Time stamps: 0:10:25 Podcast begins 0:11:30 Robert’s story of hair regrowth 0:21:35 Hormones and how they affect us and our performance 0:32:25 A Preliminary Investigation of the Enzymatic Inhibition of 5α-Reductase and Growth of Prostatic Carcinoma Cell Line LNCap-FGC by Natural Astaxanthin and Saw Palmetto Lipid Extract In Vitro 0:33:25 Everything is always dose dependent 0:36:05 What are the different types of hair loss? 0:48:35 Hair loss and how it relates to what we eat 0:54:32 Besides eating properly, what can we do to improve our hair growth? 1:12:25 Improving blood flow to the scalp and how it affects hair growth 1:17:45 Grey hair.. what causes it? 1:22:25 Robert's current experience with carnivore 1:26:15 Results of hair growth from carnivore 1:35:45 The general consensus is that diet does not help with hair regrowth 1:50:25 Reframing Nutritional Microbiota Studies To Reflect an Inherent Metabolic Flexibility of the Human Gut: a Narrative Review Focusing on High-Fat Diets 1:53:25 Further results of hair growth by simply changing their gut microbiota 2:07:55 What is the most radical thing Robert has done recently? Sponsors: Heart & Soil: www.heartandsoil.co White Oak Pastures: www.Whiteoakpastures.com, use code: CarnivoreMD for 10% off your first order Belcampo: www.belcampo.com use code: CarnivoreMD for 20% off your order Sacred Hunting: www.sacredhunting.com/Paul for $250 off your hunt Joovv: www.joovv.com/paul
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.31.363549v1?rss=1 Authors: L, L., V, V., Srihari, R., CN, P. Abstract: Introduction: Type 2 Diabetes Mellitus (T2DM) is a long-term metabolic disorder that primarily characterized by impaired insulin resistance to become hyperglycemia. People suffering from T2DM have a higher risk of developing various diseases but, on top of that, some diabetic drugs are also suspected of increasing the risk in some cases. Aldose reductase is a key target enzyme to catalyze the reduction of glucose to sorbitol and does not readily diffuse across cell membranes and cause retinopathy and neuropathy. The aldolase reductase inhibitors prevent the conversion of glucose to sorbitol and may have the capacity of preventing and / or treating several diabetic complications. It will be expected to be twofold in the subsequent decade due to intensification in the senile population with the number of people affected, thus adding to the liability on medical providers in poor developed countries using herbal medicine to control the diabetes. In recent investigation, the antidiabetic property of phytochemicals extracted from leafs of Abutilon indicum (L.) is elucidated using animal models. Materials and Methods: In the current study using aldose reductase enzyme assay inhibitor of Rat lens Aldose reductase were treated with A. indicum methanolic leaf extract at different concentrations (6.25, 12.5, 25, 50, 100, and 200microgram/mL). Copper sulphate was used as reference drug and docking studies to predict the screen the best aldose reductase inhibitor. Results and Discussion: The crude extract exhibited cytotoxicity against rat lens aldose reductase (IC50 = 135.8 {+/-} 956;g/L vs ref 13.60 {+/-} 956;g/L) using In Vitro. The docking is performed with 11 compounds shows Ertugliflozin, 9H-Cycloisolongifolene, 8-oxo and 7-hydroxycadalene showed a good binding interaction with aldose reductase. Conclusion: We are concluding that the invitro and in silico analysis helps researchers to utilize these compound for aldose reductase inhibitors and further can be used for clinical applications. Copy rights belong to original authors. Visit the link for more info
Regulation of cholesterol synthesis is very important: cholesterol is a component of cell membranes and a precursor of steroid hormones and bile acids, yet high levels of cholesterol can be toxic to cells and can contribute to heart disease. Cells in our body obtain cholesterol one of two ways – by taking it up from the bloodstream (via low-density lipoprotein or LDL) or by synthesizing it intracellularly. In Part 1 of his iBioSeminar, Dr. Russell DeBose-Boyd provides an overview of cholesterol regulation with a focus on HMG CoA reductase, the rate-limiting enzyme of cholesterol synthesis. He describes how the effects of statins, drugs prescribed to lower LDL in the blood, are blunted due to the disruption of feedback control of HMG CoA reductase. In the presence of sterols, HMG CoA reductase protein stability is decreased. This sterol-accelerated degradation of HMG CoA reductase is dependent on the enzyme’s membrane domain in a process known as ER-associated degradation (ERAD). DeBose-Boyd describes his lab’s contributions to a model of HMG CoA reductase ERAD in which polyubiquitination of the enzyme in response to sterols is mediated by two proteins, Insig-1 and Insig-2, leading to its ERAD by the 26S proteasome.
Regulation of cholesterol synthesis is very important: cholesterol is a component of cell membranes and a precursor of steroid hormones and bile acids, yet high levels of cholesterol can be toxic to cells and can contribute to heart disease. Cells in our body obtain cholesterol one of two ways – by taking it up from the bloodstream (via low-density lipoprotein or LDL) or by synthesizing it intracellularly. In Part 1 of his iBioSeminar, Dr. Russell DeBose-Boyd provides an overview of cholesterol regulation with a focus on HMG CoA reductase, the rate-limiting enzyme of cholesterol synthesis. He describes how the effects of statins, drugs prescribed to lower LDL in the blood, are blunted due to the disruption of feedback control of HMG CoA reductase. In the presence of sterols, HMG CoA reductase protein stability is decreased. This sterol-accelerated degradation of HMG CoA reductase is dependent on the enzyme's membrane domain in a process known as ER-associated degradation (ERAD). DeBose-Boyd describes his lab's contributions to a model of HMG CoA reductase ERAD in which polyubiquitination of the enzyme in response to sterols is mediated by two proteins, Insig-1 and Insig-2, leading to its ERAD by the 26S proteasome.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.15.291609v1?rss=1 Authors: Bosse, G. D., Cadeddu, R., Floris, G., Farero, R., Vigato, E., Lee, J., Zhang, T., Gaikwad, N., Keefe, K., Phillips, P. E. M., Bortolato, M., Peterson, R. T. Abstract: Opioid use disorder (OUD) has become a leading cause of death in the US, yet current therapeutic strategies remain highly inadequate. To identify novel potential treatments for OUD, we screened a targeted selection of over 100 drugs, using a recently developed opioid self-administration assay in zebrafish. This paradigm showed that finasteride, a steroidogenesis inhibitor approved for the treatment of benign prostatic hyperplasia and androgenetic alopecia, reduced self-administration of multiple opioids without affecting locomotion or feeding behavior. These findings were confirmed in rats; furthermore, finasteride did not interfere with the antinociceptive effect of opioids in rat models of neuropathic pain. Steroidomic analyses of the brains of fish treated with finasteride revealed a significant increase in dehydroepiandrosterone sulfate (DHEAS). Treatment with precursors of DHEAS reduced opioid self-administration in zebrafish, in a fashion akin to the effects of finasteride. Our results highlight the importance of steroidogenic pathways as a rich source of therapeutic targets for OUD and point to the potential of finasteride as a new option for this disorder. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.23.217620v1?rss=1 Authors: Han, Y., Zhuang, Q., Sun, B., Lv, W., Wang, S., Xiao, Q., Chi, P., Pang, B., Zhou, Y., Wang, F., Wang, Q., Li, Z., Zhu, L., Li, F., Deng, D., Chiang, Y.-C., Li, Z., Ren, R. Abstract: Steroid hormones are essential in stress response, immune system regulation, and reproduction in mammals. Steroids with 3-oxo-{Delta}4 structure, such as testosterone, androstenedione and progesterone, could be catalyzed by steroid 5-reductases (SRD5As) to generate their corresponding 3-oxo-5 steroids, which are essential for multiple physiological and pathological processes. Abnormal activities of SRD5As will lead to benign prostatic hyperplasia, alopecia, prostatic cancer or infertility due to the poor quality of sperms. However, the detailed reduction mechanisms of SRD5As remain elusive. Here we report the crystal structure of PbSRD5A, which shares 60.6% and 51.5% sequence similarities with human SRD5A1 and -2 respectively, from Proteobacteria bacterium in complex with the cofactor NADPH at 2.0 [A] resolution. PbSRD5A exists as a monomer comprised of seven transmembrane segments (TMs). The TM1-4 enclose a hydrophobic cavity for steroids substrates binding, whereas TM5-7 coordinate with cofactor NADPH through extensive hydrogen bonds network. Homology-based structural models of HsSRD5A1 and -2, together with extensive biochemical characterizations, for the first time unveiled the substrate recognition of SRD5As and provide an important framework for further understanding of the mechanism of NADPH mediated steroids 3-oxo-{Delta}4 reduction. Based on these analyses, the design of therapeutic molecules targeting SRD5As with improved specificity and therapeutic efficacy would be possible. One Sentence SummaryStructural and biochemical characterizations decipher the evolutionarily conserved mechanism in steroid 5-reductases catalyzing NADPH mediated steroids reduction. Copy rights belong to original authors. Visit the link for more info
Dr. Keyan Salari, a urologic oncologist at Massachusetts General Hospital and instructor in surgery, Harvard Medical School discusses his Abstract presentation from the American Urological Association (AUA2020) Annual Meeting titled "5-alpha reductase inhibitors and risk of overall and fatal bladder cancer".
Editor's Summary by Howard Bauchner, MD, Editor in Chief of JAMA, the Journal of the American Medical Association, for the February 18, 2020 issue
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"
HMG-COA reductase regulation via phosphorylation and Dephosphorylation --- Support this podcast: https://anchor.fm/kamesa-anota/support
The 4 Phase Cycle Podcast with Zesty Ginger || Hormone Balance | Women's Health | Mindset
Summary: This episode from Dr. Alex is all about symptoms of testosterone disturbances in women and how it relates to the symptoms that show up. It goes into common patterns we see on functional testing that lead to problems such as male pattern hair loss and facial hair growth. There’s also a discussion of how testosterone relates to issues like poor blood sugar regulation, PCOS, and other systemic issues. Important Links: Follow us on IG: @zesty_ginger Find us on FB: facebook.com/zesty_ginger Zestyginger.com to learn more about the 4 Phase Cycle Approach. Zestyginger.com/cycle to get our FREE Wild Feminine Cycle Guide to get started with everything you need to know about living in sync with your cycles. Zestyginger.com/healthyhormones to join our 3 month Healthy Hormones Group Program. This program includes functional lab work with a complete hormone and neurotransmitter panel, with a personalized protocol created for each participant based on their results.
Methylenetetrahydrofolate Reductase: a gene mutation with almost as many letters as health issues it causes. Artist Jamie Rhodes discusses her history and symptoms of MTHFR, as well as strategies for dealing with it—just short of living in a bubble.
Statins, also known as HMG-CoA reductase inhibitors, are a class of lipid-lowering medications. Should you take them or not? Dr. Greg shares with us the dubious nature of these frequently prescribed drugs so that you can make an informed decision as to whether or not they're right for you. Send your questions to: askdrpatrick@twwclinics.com Find a clinic: https://twwclinics.com/clinics/ Find a lab test: http://www.twwlabs.com/ FACEBOOK: https://www.facebook.com/TheHormoneWh… https://www.facebook.com/TheWellnessWay/
Real Life Pharmacology - Pharmacology Education for Health Care Professionals
5 Alpha-Reductase Inhibitors are most often used in the setting of BPH. I discuss mechanism of action, uses, adverse drug reactions as well as some medications that can exacerbate BPH. Hope you enjoy the episode! All subscribers to the website/podcast will get access to a FREE Top 200 Drug Study Guide where I highlight the 3 most highly testable pearls from each medication (this is a 31 page PDF!) In addition, you'll get a free 100 question pharmacology test. Both resources are free, simply for following the podcast! What are you waiting for? Click Here to Subscribe
This podcast reviews HMG COA reductase inhibiors or "Statins" for hypercholesterolemia. Use, action, and easy to remember tips for side-effects are reviewed.
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 17/19
Thu, 15 May 2014 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/18304/ https://edoc.ub.uni-muenchen.de/18304/1/Kirsch_Julian.pdf Kirsch, Julian dd
Fakultät für Chemie und Pharmazie - Digitale Hochschulschriften der LMU - Teil 04/06
Fri, 11 Feb 2011 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/15465/ https://edoc.ub.uni-muenchen.de/15465/1/Hellfritsch_Juliane.pdf Hellfritsch, Juliane ddc:540, ddc:500, Fakultät f
Fakultät für Biologie - Digitale Hochschulschriften der LMU - Teil 03/06
Tue, 23 Mar 2010 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/12163/ https://edoc.ub.uni-muenchen.de/12163/1/Perisic_Tamara.pdf Perisic, Tamara ddc:57
Professor David Matthews on the history of research into the treatment of diabetes and how patients can manage the condition by modifying their behaviour.
Professor David Matthews on the history of research into the treatment of diabetes and how patients can manage the condition by modifying their behaviour.
Transcript -- Professor David Matthews on the history of research into the treatment of diabetes and how patients can manage the condition by modifying their behaviour.
Transcript -- Professor David Matthews on the history of research into the treatment of diabetes and how patients can manage the condition by modifying their behaviour.
Transcript -- Professor David Mathhews on the history of research into the treatment of diabetes and how patients can manage the condition by modifying their behaviour.
Professor David Mathhews on the history of research into the treatment of diabetes and how patients can manage the condition by modifying their behaviour.
Transcript -- Professor David Mathhews on the history of research into the treatment of diabetes and how patients can manage the condition by modifying their behaviour.
Professor David Mathhews on the history of research into the treatment of diabetes and how patients can manage the condition by modifying their behaviour.
Fakultät für Biologie - Digitale Hochschulschriften der LMU - Teil 02/06
Gene duplication is an opportunity for evolving new functions from the newer gene, but also has a disadvantage due to local gene-rearrangement effects and, if duplications are numerous, through alterations of genome size. Therefore, selection is playing a central role in determining the fate of a duplicate gene. Plants are known to harbor numerous gene families, and are thus an ideal system to test the fate of gene duplicates. This thesis tackles the tropinone-reductase like enzymes (further TRL) and the tau GSTs located upstream from this gene family. TRL enzymes are short-chain dehydrogenases that are involved in a reduction step downstream in the synthesis of tropane alkaloids in Solanaceae, important defense compounds of plants. The function of TRLs in Brassicaceae is not clear, since most of the plants in this family do not produce tropane alkaloids, but some have been associated with the oxidative-stress response. This gene family contains 80% of its members duplicated in tandem in Arabidopsis thaliana. We profited from this fact to isolate 12 TRL (+ pseudogenes) from this species, further six species of Brassicaceae (A. thaliana, A. lyrata, A. cebennensis, Capsella rubella, Boechera divaricarpa and Brassica rapa), and one species from a closely related plant family, Cleome spinosa. We tested the role that selection plays in maintaining large numbers of this gene family. We used phylogenetic methods to analyze non-coding sequence evolution and identified regulatory motifs. We analyzed non-coding sequence evolution. Microarray expression data from A. thaliana and qPCR for A. thaliana and A. lyrata were analyzed to detect divergence in the expression patterns of orthologs and paralogs. TRL genes follow a gene birth and death dynamics. More probable, they originated from non-equal recombination of tandem duplicated genes. Positive selection at the origin of the duplicated genes allowed these to acquire differential expression patterns, leading to the preservation of numerous TRLs. The analysis of coding and non-coding sequences shows them to display correlated evolution, particularly in species recently separated by speciation. We further tested for selection on the tau glutathione-S-transferases (GST) enzymes, adjacent 3' in the genome to TRLs. Tau GSTs are unique to plants and are involved in detoxification. Multiple copies of these enzymes will allow flexibility in substrate specificity, which is important for the detoxification function. We detected positive selection among paralogs of tau GSTs supporting their potential of functional diversity, but we also detected negative selection among paralogs and groups of orthologs, indicating that more often their functions are conserved.
Background: Parkinson's disease is a genetically complex disease with mixed mode of inheritance. Recently, a haplotype across the sepiapterin reductase (SPR) gene, which is located in the PARK3 linkage region, was shown to modulate age of onset of Parkinson's disease in sibships from North America.Objective: To make a thorough assessment of the SPR gene region in sporadic Parkinson's disease.Methods: A linkage study in 122 European sibship families with five microsatellite and 17 single nucleotide polymorphism (SNP) markers in and around the SPR gene region, and an association analysis in 340 sporadic cases of Parkinson's disease and 680 control subjects from Germany with 40 SNPs. Linkage was evaluated by non-parametric linkage scores and genotypic or haplotype association was tested by regression analysis, assuming different risk effect models.Results: Significant LOD scores between 2 and 3 were obtained at the two SPR-flanking markers D2S2110 and D2S1394 and seven SNP markers around the SPR gene. We found the previously reported promoter SNP rs1876487 also significantly associated with age of onset in our sib pair families (p-value 0.02). One strong linkage disequilibrium (LD) block of 45 kb including the entire SPR gene was observed. Within this LD block all 14 inter-correlated SNPs were significantly associated with Parkinson's disease affection status (p-value 0.004).Conclusions: DNA polymorphisms in a highly intercorrelated LD block, which includes the SPR gene, appear to be associated with both sporadic and familial Parkinson's disease. This confirms a previous study showing that SPR potentially modulates the onset of or risk for Parkinson's disease.
The ubiquinol-cytochrome c reductase complex, like the other proton-pumping respiratory complexes of mitochondria, is an assembly of many different subunits. However, only a few of these subunits participate directly in the electron transfer and proton translocation. The roles of the other subunits are largely unknown. We discuss here some intriguing features of two of these subunits.
The Fe/S protein of complex III is encoded by a nuclear gene, synthesized in the cytoplasm as a precursor with a 32 residue amino-terminal extension, and transported to the outer surface of the inner mitochondrial membrane. Our data suggest the following transport pathway. First, the precursor is translocated via translocation contact sites into the matrix. There, cleavage to an intermediate containing an eight residue extension occurs. The intermediate is then redirected across the inner membrane, processed to the mature subunit, and assembled into complex III. We suggest that the folding and membrane-translocation pathway in the endosymbiotic ancestor of mitochondria has been conserved during evolution of eukaryotic cells; transfer of the gene for Fe/S protein to the nucleus has led to addition of the presequence, which routes the precursor back to its “ancestral” assembly pathway.
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