Podcasts about g6pd

In today's episode, we're going to talk about a substance that has been around for centuries but is currently gaining some attention in the health and wellness community: methylene blue. You might have heard of it as a chemical used in labs or even in aquariums as a disinfectant or anti-fungal, but what is it actually? We'll break it all down, talk about its potential benefits, and explore the side effects. We'll also get into why some people respond to methylene blue and others don't. So, let's jump right in! What is Methylene Blue? So, first things first, what exactly is methylene blue? Well, it's a synthetic dye that was first created back in the late 1800s. It was first synthesized in 1876 by a German chemist named Heinrich Caro. It was initially used as a dye for fabrics, but it didn't take long for scientists to realize that it had some remarkable medicinal properties. One of the first medical uses of methylene blue was as a treatment for malaria. In fact, it was the first synthetic drug used to treat the disease. Malaria, caused by a parasite spread by mosquitoes, was a major health crisis, particularly in tropical regions. Methylene blue was used as an antimalarial treatment because of its ability to interfere with the parasite's life cycle. In addition to treating malaria, methylene blue was also used as a diagnostic tool. It was used in medical imaging and as a staining agent in laboratories. Its bright blue color made it easy to see in different biological samples, which helped researchers track the progress of diseases and study cellular structures. Later, in the 20th century, methylene blue found other uses in medicine, such as in the treatment of methemoglobinemia, a condition where the blood can't effectively carry oxygen. It was found to be effective in treating this condition by helping to restore the blood's ability to carry oxygen. How Does Methylene Blue Work? Methylene blue boosts mitochondrial function by enhancing cytochrome c oxidase, a key enzyme involved in energy production. This helps cells produce more ATP, increasing overall energy and vitality. Additionally, it affects nitric oxide (NO) levels in the body, influencing blood vessel dilation and oxygen delivery. Let's talk a little science here.  Because methylene blue can inhibit nitric oxide synthase (NOS), particularly endothelial NOS (eNOS), it may reduce nitric oxide production and cause vasoconstriction (narrowing of blood vessels). While this may help manage conditions like sepsis or shock, it can also limit nitric oxide's vasodilatory benefits. The compound also supports nitric oxide recycling by enhancing mitochondrial function, indirectly benefiting blood flow and oxygen delivery. The Potential Benefits of Methylene Blue So, what are the potential benefits of methylene blue? Well, let's break them down. Cognitive Function: One of the most exciting areas of research is methylene blue's potential to improve cognitive function. Some studies suggest that it can enhance memory, focus, and even slow down the progression of neurodegenerative diseases like Alzheimer's. Its ability to improve mitochondrial function means your brain cells could be getting more energy, which could lead to better cognitive performance. Anti-Aging: As we mentioned earlier, its antioxidant properties can help protect cells from oxidative stress, which plays a big role in the aging process. By mitigating this stress, methylene blue may have anti-aging effects on both the brain and the body. Mental Clarity and Mood: Some users report improvements in mood and mental clarity after using methylene blue. This could be linked to its effects on mitochondrial health and energy production, but there's still much more research to be done. Cellular Health and Longevity: Beyond just improving cognitive function, methylene blue is also being studied for its broader impact on overall cellular health. The idea is that by improving mitochondrial function and reducing oxidative stress, it could help to slow down the aging of all types of cells in your body, potentially promoting longevity. So, yeah, sounds pretty cool, right? But, like anything, it's not all sunshine and rainbows. Let's talk about some potential side effects and who may not respond well to methylene blue. The Side Effects of Methylene Blue and Why Some Don't Respond to Methylene Blue As promising as methylene blue sounds, there are some side effects that come with it. For one, high doses of methylene blue can be toxic, so it's important to be cautious with its use. Some people may experience symptoms like nausea, dizziness, or headaches. Additionally, it can cause skin discoloration—yep, your skin might turn a bit blue, though it's temporary. Now, one of the more interesting things about methylene blue is that not everyone responds to it the same way. Some people see significant benefits, while others might not feel much of anything. There are a few reasons for this. First, individual genetics can play a big role. People have different levels of mitochondrial efficiency and varying abilities to process certain compounds, which means that some might not experience the same boost in energy or mental clarity that others do. Secondly, the dosage matters. Methylene blue has a pretty narrow therapeutic window, meaning too little might not have much effect, and too much can lead to toxicity. Finding the right dose is key, and that's where a healthcare provider or a practitioner familiar with it comes in handy. Lastly, if someone has certain conditions, like serotonin syndrome or G6PD deficiency, they should avoid methylene blue, as it can exacerbate those conditions. For example, methylene blue can increase serotonin levels, which could lead to serotonin syndrome in some individuals, a potentially life-threatening condition. What About Methylene Blue Dosing High doses of methylene blue can affect several systems in the body and potentially lead to significant side effects or toxicity. Here's an overview of the areas where high doses can have an impact: 1. Kidneys Renal toxicity: High doses of methylene blue may cause oxidative stress in kidney cells, leading to kidney damage or acute kidney injury (AKI), especially in individuals with pre-existing kidney issues. Hemolysis risk: Methylene blue, particularly at higher doses, can cause hemolysis (destruction of red blood cells), leading to the release of hemoglobin, which can overwhelm the kidneys and cause kidney damage. 2. Central Nervous System Confusion and agitation: Large doses of methylene blue can cause neurotoxicity, leading to symptoms like confusion, agitation, and even delirium. Headaches: A common side effect at higher doses, possibly due to its effects on blood flow and serotonin levels. Seizures: There is a risk of seizures at high doses, especially if the person is already predisposed to neurological issues or is combining methylene blue with other medications that affect the central nervous system. 3. Cardiovascular System Hypertension (High Blood Pressure): Methylene blue can potentially increase blood pressure due to its ability to inhibit nitric oxide production, leading to vasoconstriction (narrowing of blood vessels). This is more pronounced at higher doses. Arrhythmias: High doses may also lead to heart arrhythmias (irregular heartbeats) due to its influence on vascular tone and nitric oxide pathways. 4. Serotonin Levels Serotonin Syndrome: High doses of methylene blue can elevate serotonin levels in the brain. This could potentially lead to serotonin syndrome, a life-threatening condition characterized by symptoms such as agitation, high body temperature, rapid heart rate, and muscle rigidity. This is especially a concern if methylene blue is combined with other serotonergic drugs, like SSRIs, SNRIs, or MAO inhibitors. 5. Gastrointestinal System Nausea and vomiting: High doses of methylene blue can irritate the stomach and cause gastrointestinal discomfort, including nausea, vomiting, and abdominal pain. Diarrhea: Some people may also experience diarrhea as a side effect of higher doses. 6. Skin and Mucous Membranes Discoloration: Methylene blue is known to stain skin and mucous membranes. High doses can cause blue discoloration of the skin, tongue, and urine, though this is not harmful and is usually temporary. 7. Liver Liver toxicity: There is some evidence that high doses of methylene blue might place extra strain on the liver, as it is metabolized by the liver. In extreme cases, this could lead to hepatotoxicity (liver damage), though this is rare and more likely with prolonged use. Where Can I Buy Methylene Blue? Alright, so when you're buying methylene blue, it's super important to get it from a trusted source. Why? Because if you're getting a product that's low quality, it could have impurities or the wrong concentration, and that totally messes with the health benefits. Methylene blue is used in everything from research to nootropics, and its effectiveness really depends on how pure and potent it is.  That's why you want to go with a reputable retailer—like MitoZen, which Chase Hughes actually mentioned on Joe Rogan's podcast. They've got strict standards for quality, so you can trust you're getting the real deal, the right dosage, and none of those unwanted side effects from shady products. Thanks for listening to The Peptide Podcast. If you found this episode helpful, be sure to subscribe and leave a review. And as always, have a happy, healthy week.

Send us a textIn this episode, Ben and Daphna welcome Dr. Sheri Nemerofsky, MD, FAAP, Medical Director of Newborn Services at Children's Hospital at Montefiore, to discuss quality improvement (QI) initiatives for full-term newborns. Dr. Nemerofsky highlights the often-overlooked opportunities in newborn nurseries, sharing insights from her projects on improving hepatitis B vaccination timing, RSV immunization, and safe sleep education. She also explores universal G6PD screening as an equity-focused initiative and emphasizes the importance of interdisciplinary teamwork in QI efforts. This engaging conversation underscores the potential to optimize care for full-term newborns through innovative QI strategies.As always, feel free to send us questions, comments, or suggestions to our email: nicupodcast@gmail.com. You can also contact the show through Instagram or Twitter, @nicupodcast. Or contact Ben and Daphna directly via their Twitter profiles: @drnicu and @doctordaphnamd. The papers discussed in today's episode are listed and timestamped on the webpage linked below. Enjoy!

Dr. Mindy answers questions about no show socks, estrogen replacement, G6PD deficiency, cold symptoms, Flu & COVID shots, Bursitis, constant cough for a kiddo, kids sleeping habits, allergies, the Dr. Mindy Experiment, more kids sleeping habits, Zepbound, optical migraines, numbness in your right cheek and potential thyroid issues.See omnystudio.com/listener for privacy information.

In this episode, we review the high-yield topic of ⁠⁠⁠⁠G6PD Deficiency⁠⁠⁠⁠⁠⁠⁠⁠⁠ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠from the Heme section. Follow ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medbullets⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets Linkedin: https://www.linkedin.com/company/medbullets

In this next episode, it might leave you feeling red in the face. We will dive into the world of glucose-6-phosphate dehydrogenase (G6PD) deficiency. A condition that can lead to hemolytic anemia, a condition where the red blood cells break down prematurely. We'll discuss the genetic condition and its causes, the signs and symptoms your patient might present with, the diagnosis and treatments such as avoiding triggers, regular blood tests and possibly blood transfusions. Join Dr. Niket Sonpal on this often overlooked condition. September 16, 2024

Malaria is not really something we worry about. Yet around 40% of the world's population lives in areas where malaria occurs. An estimated 200 million people contract the disease every year. Around 600,000 die, three quarters of whom are children under the age of five. One person who is trying to change this is Dr Benedikt Ley. He is a public health expert specialising in diagnostics, malaria and G6PD deficiency and found Munich too cold. That's why he has been living in Darwin for ten years. - Über Malaria machen wir uns nicht unbedingt alltäglich Gedanken. Dabei lebt rund 40% der Weltbevölkerung in Gebieten, in denen Malaria vorkommt. Schätzungsweise 200 Millionen Menschen erkranken jährlich daran. Rund 600.000 sterben, drei Viertel davon sind Kinder unter fünf Jahren. Einer, der versucht, das zu ändern, ist Dr. Benedikt Ley. Er ist Experte für öffentliche Gesundheit mit den Schwerpunkten Diagnostik, Malaria und G6PD-Mangel und fand München zu kalt. Darum lebt er seit zehn Jahren in Darwin.

Do you know what a G6PD deficiency is? Listen to the conversation to find out.

In the next part of this heme consult series, we discuss several congenital causes of hemolytic anemias. These diseases are relatively rare, but in patients presenting with concerns for hemolysis on history and on labs, but with a negative DAT, it is important to have these in your differential diagnosis! We take you through how to think about these disorders, their diagnosis, and management. If you have not done so already, be sure to check out Episode 091 where we discuss our initial approach to the diagnosis of hemolytic anemias. We also discuss the most common inherited cause of hemolytic anemia, G6PD deficiency, in that episode!Content: - When should we suspect inherited causes of hemolytic anemia?- What are important examples of membranopathies that can cause hemolytic anemia?- What are important enzyme deficiencies that can cause hemolytic anemia? ** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodesLove what you hear? Tell a friend and leave a review on our podcast streaming platforms!Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

It's time for another heme consult series, this time focusing on hemolytic anemias. In this multi-part series, we will go through our approach to thinking about concerns for hemolytic anemias. This is super high yield for anyone who cares for patients, especially those in hematology/oncology. It's not uncommon to get a consult on the heme consult service for assistance with diagnosis and management of suspected hemolytic anemias! Content: - What is "hemolytic anemia"?- When should we suspect hemolytic anemias?- What is the workup for acquired hemolytic anemias? - What is G6PD deficiency? When should we suspect this? ** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodesLove what you hear? Tell a friend and leave a review on our podcast streaming platforms!Twitter: @TheFellowOnCallInstagram: @TheFellowOnCallListen in on: Apple Podcast, Spotify, and Google Podcast

Ever curious about what results people in the "real world" are achieving with red light therapy? Well this past week on BioLight's Instagram page, we had a feed post to elicit some responses and, oh boy, did it ever. So much that I felt compelled to highlight some of the comments left by people to showcase the variety of ways people are successfully utilizing red light therapy to benefit their health and wellness. From vision to numerous skin health benefits to excelling in exercise/lifting to improving children's sleep and more!The proverbial meat and potatoes of this episode is introducing and learning about methylene blue's reduced version, leucomethylene blue. This is what your body intrinsicly processes methylene blue into that is ingested, but there are some major advantages to taking leucomethylene blue. It's almost instantly bioavailable (as your body does not have to break it down, as it does with MB), the antioxidant effect is nearly immediate (for the same reason) and it has even less toxins than MB (since reducing the MB to leucoMB further removes any metals, toxins. etc; but keep in mind that pharmaceutical grade MB is already very pure. This is only to say the leucoMB is inherently more pure because of it being further reduced and, thus further purified).The above advantages have led to the following personal anecdotal responses since I started using leucomethylene blue: a more rapid cognitive/focus boost and enhanced exercise performance (I have found leucoMB to function essentially as a pre-workout, but without all the junk and jitters. Just clean energy!).After being introduced to leucoMB, I then cover a couple of studies that demonstrate its massive efficacy, particularly as it relates to neurodegeneration in Alzheimer's Disease. We already know that most of the methylene blue ingested ends up in the brain — which is no different for leucoMB — but it appears that leucoMB may have a more pronounced effect. I have no doubt that as time goes on, we'll more more and more about the advantages of methylene blue and leucomethylene blue.Lastly, I announce the release of BioLight's newest supplement: BioBlue Leuco. At the time of this solosode release, this product will be released within the next 24 hours, so stay tuned for more updates! I hope you enjoy the information in today's solosode. Please share this episode with family, friends and colleagues if you find the content especially interesting and/or impactful.As always, light up your health! - Key points:   Introduction and BioLight Supplement: 00:00:01 - 00:01:51 The podcast opens with a tantalizing preview of a methylene blue derivative in the Red Light Report. Dr. Mike Belkowski takes the stage to introduce an intriguing new product: a BioLight supplement designed to promote health and wellness. He encourages listeners to consider the potential benefits of this supplement, setting the stage for an engaging episode. Testimonials on Red Light Therapy: 00:02:15 - 00:06:03  The narrative shifts to user testimonials, showcasing the diverse and positive experiences with red light therapy. Highlights include users reporting improved vision, enhanced skin without makeup, and anti-aging benefits. Dr. Mike underlines the therapy's multifaceted impact on skin, collagen production, and exercise recovery, fostering an atmosphere of excitement and possibility. Diverse Benefits of Red Light Therapy: 00:07:06 - 00:13:38 The episode delves deeper into the myriad benefits of red light therapy, spotlighting user testimonials on improved sleep, reduced anxiety, and overall health enhancement. Noteworthy is a user's preference for red light therapy over Botox for collagen production, emphasizing a natural approach using light instead of neurotoxins. Dr. Mike reflects on the versatility of red light therapy beyond skin health, discussing its impact on mitochondrial function, sleep, thyroid, and exercise performance. Introduction to Lucho Methylene Blue: 00:18:50 - 00:49:32 The narrative seamlessly transitions to the introduction of Lucho Methylene Blue, a compound with promising benefits. Dr. Mike covers the compound's advantages and its synergy with red light therapy, providing listeners with a comprehensive understanding of its potential applications. The discussion delves into the compound's reduced form, cyclic and regenerative antioxidant properties, and the vital role of antioxidants in maintaining cellular redox balance. Impact on Alzheimer's and Neurodegeneration: 00:49:58 - 00:57:13 The focus shifts towards Lucho Methylene Blue's potential impact on Alzheimer's and neurodegeneration. Dr. Mike introduces the significance of Tau pathology in Alzheimer's and sheds light on the neurofilament light chain (NFL) as a crucial factor in neurodegenerative diseases. The correlation between NFL levels, Alzheimer's severity, and the positive results of a phase three trial with Lucho Methylene Blue are explored. BioBlue Lucho Release and Closing: 01:07:49:00 - 01:14:53:28  The episode concludes with the exciting revelation of BioBlue Lucho, a product set to hit the market. Details on pricing, benefits, and considerations for those finding traditional methylene blue intense are shared. Dr. Mike expresses gratitude for listeners' support, encourages reviews, teases future episodes, and invites suggestions. The offer of an exclusive discount code, Lucho15, adds a final touch to the closing remarks. - Articles Referenced in Episode: The Potential of Leucomethylene Blue in Methemoglobinemia Treatment: A New Hope for Patients with G6PD? Leucomethylene blue on PubChem Concentration-Dependent Activity of Hydromethylthionine on Cognitive Decline and Brain Atrophy in Mild to Moderate Alzheimer's Disease TauRx's hydromethylthionine mesylate (HMTM) demonstrates significant reduction in neurodegeneration in Alzheimer's Disease (AD) - BioBlue Leuco release coming tomorrow! - Kindle version of Red Light Therapy Treatment Protocols eBook, 4th Edition - To learn more about red light therapy and shop for the highest-quality red light therapy products, visit https://www.biolight.shop - Dr. Mike's #1 recommendations: Grounding products: Earthing.com EMF-mitigating products: Somavedic Blue light-blocking glasses: Ra Optics - Stay up-to-date on social media: Dr. Mike Belkowski: Instagram LinkedIn   BioLight: Instagram YouTube Facebook

Welcome to this weeks whistlestop tour of haemolytic anaemias! Dr Tom Bond picks Dr Aritri Mandal's brains to understand how the varying types of haemolytic anaemias are classified. In this episode we talk about the pathophysiology of various haemolytic anaemias and touch on initial investigations. Listen in to hear about everything from TTP to G6PD!

You spent wayyyyy too much time learning G6PD in med school. Don't remember that? Yeah, we don't either. But it's okay- time to cover a much more important hematology subject: hemophilia. How to manage bleeding, what to look out for, and how to easily nail it on the boards. Want to experience the greatest in board studying? Check out our interactive question bank podcast- the FIRST of its kind here: emrapidbombs.supercast.com. Cite this podcast as: Briggs, Blake; Husain, Iltifat. 188. Hemophilia: if paper cuts could kill. August 28th, 2023. Accessed [date].

- Theo thống kê của Bộ Y tế, hàng năm có đến 41.000 trẻ tại Việt Nam bị dị tật bẩm sinh như Down, Patau hay Edwards... Song song đó, các bệnh lặn đơn gen như rối loạn chuyển hóa đường galactose; phenylketon niệu; thiếu hụt men G6PD; tan máu bẩm sinh Thalassemia cũng khá phổ biến ở trẻ. Các bệnh lý di truyền nói trên là rất nguy hiểm, gây nhiều nỗi đau về tinh thần và gánh nặng kinh tế cho các gia đình có con mắc phải. Vì vậy, việc sàng lọc, chẩn đoán, điều trị, phòng bệnh di truyền, đặc biệt trong hỗ trợ sinh sản ngày càng quan trọng và cần được quan tâm. Với những tiến bộ vượt bậc trong nghiên cứu, phát triển và ứng dụng khoa học công nghệ, lĩnh vực chẩn đoán di truyền và hỗ trợ sinh sản đang mang đến cơ hội sinh con khỏe mạnh cho hàng vạn cặp vợ chống vô sinh, hiếm muộn tại Việt Nam. Sự kết hợp này đang được thực hiện ra sao và mang lại những lợi ích gì cho hàng chục triệu người dân mang gen các bệnh lý di truyền, góp phần nâng cao chất lượng dân số Việt Nam? Để tìm hiểu về những tiến bộ trong chẩn đoán di truyền và hỗ trợ sinh sản, trong chương trình Đối thoại, chúng tôi sẽ trao đổi để cùng vị khách mời trò chuyện về nội dung này. --- Support this podcast: https://podcasters.spotify.com/pod/show/vov1sukien/support

G6PD stands for glucose-6 phosphate dehydrogenase. In this episode of The Common Sense MD, Dr. Rogers talks about the G6PD blood test, G6PD deficiency, and how it relates to Methylene Blue and High Dose IV Vitamin C. Hope this helps some of you! What did you think of this episode of the podcast? Let us know by leaving a review! Connect with Performance Medicine! Sign up for our weekly newsletter: https://performancemedicine.net/doctors-note-sign-up/ Facebook: @PMedicine Instagram: @PerformancemedicineTN YouTube: Performance Medicine

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.28.530418v1?rss=1 Authors: Zodda, E., Tura-Ceide, O., Mills, N. L., Tarrago-Celada, J., Carini, M., Thomson, T. M., Cascante, M. Abstract: Compelling evidence has accumulated for the role of oxidative stress on the endothelial cell (EC) dysfunction underlying acute coronary syndromes. However, understanding the metabolic determinants of EC dysfunction has been hampered by the scarcity of appropriate cell models. Here, we have generated and phenotypically characterized EC derived from thrombectomy specimens in patients with acute myocardial infarction (AMI). We have found that AMI-derived endothelial cells (AMIECs), but not control EC from health coronary arteries, display impaired growth, migration and tubulogenesis. These phenotypic abnormalities were accompanied with metabolic abnormalities including augmentation of reactive oxygen species (ROS) and glutathione intracellular content, along with diminished glucose consumption coupled to increased lactate production. In AMIECs, the protein levels of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase type 3, PFKFB3, were downregulated, while those of PFKFB4 were upregulated, suggesting a shunting of glycolysis towards the pentose phosphate pathway (PPP) in the pathological ECs. PPP overactivation was further supported by upregulation of G6PD in AMIECs, the key enzyme in the oxidative branch of the PPP, which supplies the bulk of NADPH reducing equivalents necessary for the reduction/turnover and lipid synthesis.. Further, the glutaminolytic enzyme glutaminase (GLS) was upregulated in AMIECs, providing a mechanistic explanation for the observed increase in glutathione content. Finally, AMIECs had higher mitochondrial membrane potential than control ECs, which, together with high ROS levels, suggest a highly coupled mitochondrial activity in patient ECs. We suggest that high proton coupling underlies the abnormally high production of ROS, balanced by PPP-driven glutathione turnover, as a primary, cell-autonomous abnormality driving EC dysfunction in AMI. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In today's episode we are speaking with Becky Rhew. Becky has been a practicing attorney for the last 20 years. Becky has a genetic condition called G6PD Deficiency. G6PD deficiency is an inherited condition. It is when the body doesn't have enough of an enzyme called G6PD (glucose-6-phosphate dehydrogenase). This enzyme helps red blood cells work properly. A lack of this enzyme can cause hemolytic anemia. This is when the red blood cells break down faster than they are made. This caused a variety of digestive issues for her. Becky talks about her journey in discovering her diagnosis of G6PD and her path to healing. Follow us @pelvicorerehab and share any questions you have on Pelvic Health or share your experience overcoming Pelvic Health related issues.

$5 Q-BANK: https://www.patreon.com/highyieldfamilymedicine Intro 0:30, Sickle cell anemia 1:34, Thalassemia 9:03, Hereditary spherocytosis 15:36, G6PD deficiency 17:38, Pyruvate kinase deficiency 19:27, Microangiopathic hemolytic anemia 20:08, Autoimmune hemolytic anemia 24:56, Paroxysmal nocturnal hemoglobinuria 26:59, Blood transfusion reactions 28:31, Drug-induced hemolysis 30:05, Malaria 30:42, Babesiosis 31:47, Iron deficiency anemia 32:34, Megaloblastic anemia 35:34, Lead poisoning 37:59, Porphyria 39:07, Sideroblastic anemia 40:01, Aplastic anemia 41:23, Polycythemia 45:24, Methemoglobinemia 46:34, Carbon monoxide poisoning 47:56, Hemophagocytic lymphohistiocytosis 48:48, Practice questions 49:34

Updated clinical practice guidelines for management of hyperbilirubinemia – including revised phototherapy thresholds – were published in August, the first major change since 2004. Joanna Parga-Belinkie, MD, attending neonatologist, Division of Neonatology, Children's Hospital of Philadelphia, provides a review for the nursery and primary care clinic, including a new name for “breastfeeding jaundice”; determining risk for isoimmune hemolytic disease; the importance of G6PD in bilirubin results; the limits of visual assessment of jaundice; using transcutaneous bilirubin meters in primary care; answers to parent questions such as, “Will sunlight help jaundiced babies?”; management of “rebound bili”; tools to help measure phototherapy thresholds by age as you adjust to the new guidelines; and more. Published December 2022. This podcast is for general informational and educational purposes only and is not to be considered as medical advice for any particular patient. Clinicians must rely on their own informed clinical judgment in making recommendations to their patients. ©2022 by Children's Hospital of Philadelphia, all rights reserved.

Common genetic problems including Cystic Fibrosis, lysosomal storage disease, Wilson Disease, G6PD deficiency, Klinefelter Syndrome, Turner Syndrome, Fragile X Syndrome, Down Syndrome, and Prader-Willi Syndrome.

For our 33rd podcast episode, I review the recommendations for screening and managing hyperbilirubinemia. The American Academy of Pediatrics recommends universal screening of bilirubin levels in newborns, so I review how that can be done, when it should occur, and when it should be repeated. We discuss which infants are more at risk for elevated bilirubin levels and how those risk factors contribute to guidelines for the treatment plan. I discuss the nomograms commonly used and recommended by the American Academy of Pediatrics that guide the care of identifying infants at risk as well as when they should be treated. I review phototherapy, the primary treatment plan for hyperbilirubinemia, including how it effectively lowers bilirubin levels as well as the clinical considerations that should be applied during treatment. Whether you are a neonatal clinician or a parent, this review on how to effectively screen for and manage hyperbilirubinemia will be beneficial. Hyperbilirubinemia is incredibly common in neonates. Clinicians who care for infants whether they are a term newborn in the nursery or an infant in the NICU, will manage infants with elevated bilirubin levels. And parents of either term, healthy infants, or those critically ill in the NICU, it is essential that you understand the risks of hyperbilirubinemia and the screening and management process for it. Tune in now to learn more!Our NICU Roadmap: A Comprehensive NICU Journal: https://empoweringnicuparents.com/nicujournal/NeoTech NeoShades Free Sample: neotechneoshades.comNICU Mama Hats: https://empoweringnicuparents.com/hats/NICU Milestone Cards: https://empoweringnicuparents.com/nicuproducts/Bilirubin Document: https://empoweringnicuparents.com/bili/Empowering NICU Parents Show Notes: https://empoweringnicuparents.com/episode33Empowering NICU Parents Instagram: https://www.instagram.com/empoweringnicuparents/Empowering NICU Parents FB Group: https://www.facebook.com/groups/empoweringnicuparentsPinterest Page: https://pin.it/36MJjmH

It is likely that you have heard the terms jaundiced and/or bilirubin. And although it is very common for infants to develop elevated bilirubin levels otherwise known as hyperbilirubinemia, do you actually know or understand why? As a NICU provider, I think it is essential that parents know the condition their infant is facing, but it is also important to understand the why behind its occurrence. If you do not understand the why, the treatment plan will also not make very much sense to you. I believe parents should be actively involved and partners in their baby's care. But, it is nearly impossible to be actively engaged in the decision-making process if you do not understand the why behind the condition.  For our 32nd podcast episode, I break down how our bodies process bilirubin, how we eliminate it, what causes the skin color to become jaundiced, why we as neonatal clinicians monitor bilirubin levels so closely, and I also review some of the common conditions that increase your infant's risk of developing hyperbilirubinemia. Some of the pathophysiology of hyperbilirubinemia can be confusing, but I review it in a way that will make sense to you so you can learn why elevated bilirubin levels occur, and even more importantly, understand your baby's treatment plan. The review will also be very beneficial for novice NICU clinicians or those that need a refresher on the pathophysiology of hyperbilirubinemia in term and preterm infants. So let's get to it!Our NICU Roadmap: A Comprehensive NICU Journal: https://empoweringnicuparents.com/nicujournal/NeoTech NeoShades Free Sample: neotechneoshades.comNICU Mama Hats: https://empoweringnicuparents.com/hats/Empowering NICU Parents Show Notes: https://empoweringnicuparents.com/episode31Empowering NICU Parents Instagram: https://www.instagram.com/empoweringnicuparents/Empowering NICU Parents FB Group: https://www.facebook.com/groups/empoweringnicuparentsPinterest Page: https://pin.it/36MJjmH

Higher CoQ10 levels linked with improved physical capacity, reduced cardiovascular risk among older individuals Universidad Pablo de Olavide (Spain) March 23 2022.  A study published on January 29, 2022 in Antioxidantsfound lower levels of blood factors related to cardiovascular disease and greater physical capacity and among participants with higher plasma levels of coenzyme Q10 (CoQ10), a factor in the production of energy within the mitochondria of the cells. Higher CoQ10 levels were significantly associated with lower total and non-HDL cholesterol among women (who comprised the majority of participants), indicating lower cardiovascular disease risk. Higher CoQ10 levels were correlated with less sitting time and, among women, were moderately or strongly correlated with better physical activity test scores. “In general, it is clear that higher activity and performance is associated with higher levels of CoQ10 in plasma,” authors Rocío de la Bella-Garzó and colleagues wrote.  CoQ10 levels were higher among participants whose physical assessments indicated low or no frailty risk. When participants were evaluated according to whether their plasma CoQ10 concentrations were below or above average, higher levels were associated with better physical test scores in general, which reached significance in a measurement of balance while moving. “Combination of CoQ10 with physical activity could be an important therapy for avoiding sarcopenia and maintaining higher capacity during aging,” de la Bella-Garzó and associates concluded.      Study: Zinc deficiency linked to immune system response, particularly in older adults Oregon State University, March 23, 2022   Zinc, an important mineral in human health, appears to affect how the immune system responds to stimulation, especially inflammation, new research from Oregon State University shows. Zinc deficiency could play a role in chronic diseases such as cardiovascular disease, cancer and diabetes that involve inflammation. Such diseases often show up in older adults, who are more at risk for zinc deficiency. When you take away zinc, the cells that control inflammation appear to activate and respond differently; this causes the cells to promote more inflammation. In the study, researchers set out to better understand the relationship between zinc deficiency and inflammation. They conducted experiments that indicated zinc deficiency induced an increase in inflammatory response in cells. The researchers were able to show, for the first time, that reducing zinc caused improper immune cell activation and dysregulation of a cytokine IL-6, a protein that affects inflammation in the cell, Ho said. Researchers also compared zinc levels in living mice, young and old. The older mice had low zinc levels that corresponded with increased chronic inflammation and decreased IL-6 methylation, which is an epigenetic mechanism that cells use to control gene expression. Decreased IL-6 methylation also was found in human immune cells from elderly people, Ho said. Together, the studies suggest a potential link between zinc deficiency and increased inflammation that can occur with age. Zinc deficiency is probably a bigger problem than most people realize," she said. "Preventing that deficiency is important."       Lipid and glucose levels at age 35 associated with Alzheimer's disease Boston University School of Medicine, March 23, 2022   Living your best life at 35, ignoring cholesterol and glucose levels, may impact your chances of getting Alzheimer's disease (AD) later in life. According to researchers from Boston University School of Medicine (BUSM), lower HDL (high-density cholesterol) and high triglyceride levels measured in blood as early as age 35 are associated with a higher incidence of AD several decades later in life. They also found that high blood glucose measured between ages 51-60 is associated with risk of AD in the future. "While our findings confirm other studies that linked cholesterol and glucose levelsmeasured in blood with future risk of Alzheimer's disease, we have shown for the first time that these associations extend much earlier in life than previously thought," explains senior author Lindsay A. Farrer, Ph.D., chief of biomedical genetics at BUSM. The researchers found that lower HDL (the good cholesterol) is predictive of AD in early (35-50 years) and middle (51-60 years) adulthood and that high glucose in the blood (a precursor of diabetes) during mid-adulthood is also predictive of AD "These findings show for the first time that cardiovascular risk factors, including HDL which has not been consistently reported as a strong risk factor for AD, contribute to future risk of AD starting as early as age 35," says first and corresponding author Xiaoling Zhang, MD, Ph.D., assistant professor of medicine at BUSM.   Exercise holds even more heart health benefits for people with stress-related conditions Massachusetts General Hospital, March 24, 2022 Regular physical activity had nearly doubled the cardiovascular benefit in individuals with depression or anxiety, compared with individuals without these diagnoses, according to a study presented at the American College of Cardiology's 71st Annual Scientific Session. The research findings add to mounting evidence that exercise improves cardiovascular health by helping to activate parts of the brain that counteract stress. Overall, the study found that people who achieved the recommended amount of physical activity per week were 17% less likely to suffer a major adverse cardiovascular event than those who exercised less. These benefits were significantly greater in those with anxiety or depression, who had a 22% risk reduction vs. a 10% risk reduction in those without either condition. For the study, researchers analyzed health records of more than 50,000 patients in the Massachusetts General Brigham Biobank database. Just over 4,000 of the patients had suffered a major adverse cardiovascular event, which included experiencing a heart attack, having chest pain caused by a blocked artery or undergoing a procedure to open a blocked artery in the heart.     Vitamin B3 to stay younger? A global increase in antioxidant defenses of the body may delay aging and its diseases   Centro Nacional de Investigaciones Oncológicas (Spain), March 15, 2022   The gradual accumulation of cell damage plays a very important role in the origin of ageing. There are many sources of cellular damage, however, which ones are really responsible for ageing and which ones are inconsequential for ageing is a question that still lacks an answer. A group of scientists from the Spanish National Cancer Research Centre have tried to increase the global antioxidant capacity of the cells, rather than just one or a few antioxidant enzymes. To achieve this global improvement in the total antioxidant capacity, researches have focused on increasing the levels of NADPH, a relatively simple molecule that is of key importance in antioxidant reactions and that, however, had not been studied to date in relation to ageing. The results, published today in the journal Nature Communications, indicate that an increase in G6PD and, therefore, in NADPH, increases the natural antioxidant defences of the organism, protecting it from oxidative damage, reducing ageing-related processes, such as insulin resistance, and increasing longevity. "As anticipated, the cells in these transgenic animals are more resistant to highly toxic artificial oxidative treatments, thus proving that an increase in G6PD really improves antioxidant defences," explains Sandrina Nóbrega-Pereira, first author of the study. Furthermore, when researchers analysed long-lived transgenic animals, they noted that their levels of oxidative damage were lower than in non-transgenic animals of the same age.  The greatest surprise for the team was when they measured the ageing process in the transgenic mice: the animals with a high G6PD expression and, therefore, high levels of NADPH, delayed their ageing, metabolised sugar better and presented better movement coordination as they aged. In addition, transgenic females lived 14% longer than non-transgenic mice, while no significant effect on the longevity of males was observed.       Artificial sweeteners may not be safe sugar alternatives: study French National Institute for Health and Medical Research (Inserm) and Sorbonne Paris University, March 24, 2022   Artificial sweeteners reduce added sugar content and corresponding calories while maintaining sweetness. A study publishing March 24th in PLOS Medicine suggests that some artificial sweeteners are associated with increased cancer risk. Many food products and beverages containing artificial sweeteners are consumed by millions of people daily. However, the safety of these additives has been a subject of debate. The researchers found that enrollees consuming larger quantities of artificial sweeteners, particularly aspartame and acesulfame-K, had higher risk of overall cancer compared to non-consumers (hazard ratio 1.13, 95% confidence interval 1.03 to 1.25). Higher risks were observed for breast cancer and obesity-related cancers. Results from the NutriNet-Santé cohort (n=102,865) suggest that artificial sweeteners found in many food and beverage brands worldwide may be associated with increased cancer risk, in line with several experimental in vivo / in vitro studies. These findings provide novel information for the re-evaluation of these food additives by health agencies."

In this episode, we review the high-yield topic of G6PD Deficiency from the Heme section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets

An interview with Dr. Loretta Nastoupil from MD Anderson Cancer Center, author on “Management of Immune-Related Adverse Events in Patients Treated With Immune Checkpoint Inhibitor Therapy: ASCO Guideline Update.” She discusses the identification, evaluation, and management of hematologic toxicities in patients receiving ICPis, including hemolytic anemia among others in Part 10 of this 13-part series. For more information visit www.asco.org/supportive-care-guidelines   TRANSCRIPT [MUSIC PLAYING] SPEAKER: The purpose of this podcast is to educate and to inform. This is not a substitute for professional medical care and is not intended for use in the diagnosis or treatment of individual conditions. Guests on this podcast express their own opinions, experience, and conclusions. The mention of any product, service, organization, activity, or therapy should not be construed as an ASCO endorsement. BRITTANY HARVEY: Hello, and welcome to the ASCO Guidelines podcast series brought to you by the ASCO Podcast Network, a collection of nine programs covering a range of educational and scientific content and offering enriching insight into the world of cancer care. You can find all the shows, including this one, at ASCO.org/podcasts. My name is Brittany Harvey. And today, we're continuing our series on the management of immune-related adverse events. I am joined by Dr. Loretta Nastoupil from the University of Texas M.D. Anderson Cancer Center in Houston, Texas, author on Management of Immune-Related Adverse Events in Patients Treated With Immune Checkpoint Inhibitor Therapy, ASCO Guideline Update, and Management of Immune-Related Adverse Events in Patients Treated With Chimeric Antigen Receptor T-Cell Therapy ASCO Guideline. And today, we're focusing on hematologic toxicities in patients treated with immune-checkpoint inhibitor therapy. Thank you for being here, Dr. Nastoupil. LORETTA NASTOUPIL: Thanks, Brittany. I'm happy to be here. BRITTANY HARVEY: Great. Then first I'd like to note that ASCO takes great care in the development of its guidelines and ensuring that the ASCO conflict of interest policy is followed for each guideline. The full conflict of interest information for this guideline panel is available online with the publication of the guidelines in the Journal of Clinical Oncology. Dr. Nastoupil, do you have any relevant disclosures that are related to these guidelines? LORETTA NASTOUPIL: Yes, Brittany. So I have received honorarium for participation in advisory boards from the following companies, including BMS/Celgene, Genentech, Janssen, Novartis, Merck, MorphoSys TG Therapeutics, and Takeda. And I've also received research funding support from BMS/Celgene, Gilead Kite, Genentech, Janssen, Novartis and Takeda. BRITTANY HARVEY: I thank you for those disclosures. Then let's get into what we're here today to talk about. So what are the immune-related hematologic toxicities addressed in this guideline? LORETTA NASTOUPIL: So it's important to recognize that hematologic toxicities that are immune-related as a result of immune therapy are infrequent occurrences. So it's important to recognize when they do occur and some of the unique workups given that they are so infrequent. So probably one of the most common is hemolytic anemia. It's important to recognize that these are cancer patients. And they may have multiple reasons for the development of acute or new onset anemia, but recognizing if they're on either checkpoint inhibitors or immune therapies, it's important to recognize that it might be spurred on as a result of immune-mediated anemia. We advise in terms of history and workup to consider whether or not they've been exposed to new drugs, whether or not they've had a recent insect or snakebite exposure. The recommended workup includes a CBC with also a peripheral blood smear to look for evidence of hemolysis or macroketosis. In addition, other hemolytic anemia workup includes evaluation for LDH, haptoglobin, reticulocyte count, bilirubin, and free hemoglobin. Other potential diagnoses on the differential include DIC, so a panel, including coags, PT, INR, and PTT, exploring autoimmune serologies, PNH screening, evaluation for infection such as viral or bacterial causes of hemolysis, and also consideration for bone marrow failure syndrome, including evaluation for potentially reversible causes, such as B12, folate, copper, parvovirus, iron, thyroid, infection, et cetera. G6PD level is helpful in the evaluation, as well as exploration as I mentioned of potentially new drugs that might be linked, including ribavirin, rifampin, dapsone, interferon, some of the antibiotics, such as cephalosporins, penicillins, NSAIDs, ciprofloxacin, for instance, et cetera. So as part of the workup, if we have excluded alternative causes and we think that the immune-checkpoint inhibitor might be the underlying cause of the autoimmune hemolytic anemia, then generally we will continue unless they have grade 2 or higher toxicity, which is generally a hemoglobin less than 10. In which case, we would recommend to hold the immune-checkpoint inhibitor, again, with significant anemia. So those with grade 2 or higher, you might consider initiating corticosteroids, including 1.5 to 1 milligram per kilogram per day until improvement. For grade 3 or higher-- so this is more severe anemia So hemoglobin is less than 8. Generally, we're recommending permanent discontinuation of the checkpoint inhibitor and potentially higher doses, including up to 2 milligrams per kilogram per day of prednisone or corticosteroid equivalent to speed up the recovery. In regards to transfusion requirements or consideration, we are suggesting you evaluate or consider your local or regional guidelines. We generally do not transfuse for a target hemoglobin greater than seven to eight. And we also recommend supplementation with folic acid. BRITTANY HARVEY: Great. And then beyond those recommendations for hemolytic anemia, what are the key recommendations for identification, evaluation, and management of acquired thrombotic thrombocytopenia purpura? LORETTA NASTOUPIL: Sure. So fortunately, TTP is quite rare, but, again, something that is worth exploring. Some of the challenges are in the clinical syndrome. And that it can mimic some of the other toxicities that are covered in other sections, particularly the neurotoxicity section. But essentially, for patients who have pretty dramatic change in platelet count, again, they may have additional clinical sequelae such as neurologic toxicity or adverse events. It's important to recognize that TTP might be an underlying cause, again, for patients who are on immune-checkpoint inhibitors. This is where a hematology consult early in the clinical course would be particularly of importance to recognize it and potentially to minimize offending agents. Drug exposure is always important, because many of these patients might have other drugs, in addition to their immune-checkpoint inhibitors, such as chemotherapy, sirolimus, tacrolimus, antibiotics et cetera. And so exploring offending agents is important. An ADAMTS13 level, an inhibitor titer, would be important to send if you're considering TTP, in addition to evaluating the peripheral smear, and the hemolytic anemia workup, as I just mentioned, including LDH, haptoglobin and reticulocyte count. Exploring infectious etiology, including CMV titers or serology, would be particularly helpful, an additional clinical evaluation, such as brain imaging with CT or MRI, echocardiogram, and EKG would be of help. For all grades of TTP, again, even with a clinical suspicion for the diagnosis, in addition to hematology consult, we recommend stabilizing the patient. That might require care in an acute care setting, making sure that they have adequate organ function and that this is stabilized. For grade 1 or higher, we recommend holding the immune-checkpoint inhibitor. And you might consider, again, initiation of corticosteroids with 0.5 to 1 milligram per kilogram per day of prednisone or an equivalent. For grade 3 or higher, we would, again, in addition to holding the checkpoint inhibitor and in conjunction with your hematology colleagues, you might initiate a therapeutic plasma exchange. Again, in accordance with existing guidelines, you may consider higher doses of steroids, including methylprednisolone 1 gram IV daily for three days. You could consider some additional supportive agents, such as rituximab or pembrolizumab if the ADAMTS13 level is less than 10 or less than 10% of normal and an inhibitor or elevated ADAMTS13 IgG has been detected. BRITTANY HARVEY: I appreciate you going through the details for TTP. So then, additionally, this guideline addresses aplastic anemia. So what are the key recommendations for identification, evaluation, and management of aplastic anemia? LORETTA NASTOUPIL: Yeah. So fortunately, again, these are quite rare situations. So with aplastic anemia, similar to what we've discussed in terms of workup of anemia, globally, it's important to explore potentially causes of, again, bone marrow failure syndrome. And aplastic anemia is one of those such causes. Exploration of a bone marrow biopsy in conjunction, again, with your hematology consult would be critically important, and exploring potentially reversible causes, again, such as deficiencies and important nutrients, viral etiologies, in addition to parvovirus, CMV, HHV-6 is important to consider and rule out. But I think the end of the day, a bone marrow biopsy and aspirate is going to be the most helpful assessment to ensure that aplastic anemia has been considered and worked up. In regards to management of aplastic anemia, we're going to hold the immune-checkpoint inhibitor. You may need to provide additional support such as growth factors. And close follow-up, I think is the most critical aspect of this. Sometimes we initiate patients on corticosteroids. We hold the checkpoint inhibitor. And then we may monitor them less frequently. Oftentimes, these patients with high malignancies are going to need to be followed very closely, sometimes weekly or multiple times a week. So in regards to management of aplastic anemia that might be immune mediated as a result of immune-checkpoint inhibitors and in conjunction with your hematology and colleagues, consideration of management might include administration of horse ATG and cyclosporine, but again transfusion support, growth factor support, even consideration for HLA typing and evaluation first. Stem cell transplantation might be appropriate, particularly for a young patient with minimal comorbidities. For grade 3 or higher, in addition to these considerations, we're going to hold the checkpoint inhibitor and monitor weekly for improvement. If no response, you might consider repeating immune suppression with Rabbit ATG plus cyclosporine or cyclophosphamide. And for refractory patients, consider eltrombopag plus best supportive care. BRITTANY HARVEY: Great. Thank you. Those are important notes on the management of aplastic anemia. So then, additionally, what are the key recommendations for the identification, evaluation, and management of lymphopenia? LORETTA NASTOUPIL: Yeah. I think one of the challenges with lymphopenia, it's common for patients who've had cancer-directed therapy, particularly things like chemotherapy. And so understanding whether or not this is a new onset after exposure to checkpoint inhibitors is one of the critical aspects, in addition to considering alternative causes. But for patients in which we do think the lymphopenia is a result of the immune-checkpoint inhibitor, we're not generally advising discontinuation or holding of the immune-checkpoint inhibitor, but it is important to consider best supportive measures, including whether or not patients might benefit from monitoring for reactivation of certain viral etiologies, including CMV and HHV-6, for instance, in addition to potential consideration for prophylactic strategies, such as PJP prophylaxis. Also, zoster reactivation might be something that these patients might indeed be at risk for. So as opposed to holding your checkpoint inhibitor and initiating things like corticosteroids, if we have excluded alternative causes and think lymphopenia is a result of the immune-checkpoint inhibitor or as immune mediated, ensuring that they are receiving best supportive care to mitigate some of their toxicity that may result as the result of the lymphopenia. BRITTANY HARVEY: Understood. And it's important to note for clinicians that management is different from a lot of the management of the other hematologic toxicities. So then the last hematologic toxicity that was addressed in this guideline was acquired hemophilia A. So what are those key recommendations? LORETTA NASTOUPIL: Acquired hemophilia A, again, fortunately is very rare and uncommon, but this is one situation where engagement of a hematologist, who is an expert in management of hemophilia, will be critical. So that would potentially be step one. In terms of laboratory assessment, that would be helpful, in addition to your CBC, where you're assessing things like platelet count, coagulation workup, including fibrinogen, PT, PTT, INR, that would be informative. Patients with acquired hemophilia A will likely have a prolonged activated PTT with a normal PT. So that might be one of the clues. Imaging would be helpful to ensure the patients don't have any signs of spontaneous bleeding or hematoma basis, such as MRI, CT, or ultrasound, if particularly they have any localizing symptoms. Medication review to look for alternative causes would always be helpful. And determination of the Bethesda unit level of inhibitor would be critical. In regards to management, we would hold the checkpoint inhibitor, initiate corticosteroids, transfusion support as indicated, and you want to treat the underlying acquired hemophilia with conjunction of a hematologist. For grade 2 or higher, this may require factor replacement. And the choice is usually based on the Bethesda unit of the titer. Administration of prednisone, in addition to rituximab 375 milligrams per meter squared weekly for four weeks or cyclophosphamide dosed at 1 to 2 milligrams per kilogram per day may be patient specific. And, again, that decision should be made in conjunction with your hematology consult. Prednisone, rituximab, and cyclophosphamide should be given for a minimum of five weeks. And factors should be prescribed to increase the level, particularly during bleeding episodes. And, again, the choice of the factor is based on the presence or absence of an inhibitor. For grade 3 or higher, we advise to permanently discontinue the immune-checkpoint inhibitor. These patients generally will be admitted for stabilization. They do require factor replacement. Bypassing agents may also be required, including factor VII. Caution should be taken in elderly patients and those with coronary artery disease. Corticosteroids, rituximab, and cyclophosphamide should also be considered, transfusion support, if they're having active bleeding. And if worsening or no improvement, you could consider adding cyclosporine or immune suppression to try and stabilize these patients. Again, acquired hemophilia A requires special clinical and laboratory expertise. This would require consult and potentially even transfer to a specialized center, and consultation with a hemophilia center should be initiated as soon as this is considered or confirmed. BRITTANY HARVEY: That's a great summary of these recommendations. The expert panel and you clearly put in a lot of work into these recommendations. So then in your view, how will these recommendations for the management of hematologic toxicities impact both clinicians and patients? LORETTA NASTOUPIL: I think the most important thing are disseminating this information. I think ASCO plays a critical role in helping clinicians first recognize some of the toxicities that are different from what we have traditionally seen with chemotherapy and may have different management strategies. So guidelines, such as this, are critically helpful. Podcasts, such as this, are incredibly helpful to get the information out, recognizing that all of us authors are more than willing to provide additional guidance and are willing to be contacted in this situation where someone's facing one of these unique and rare toxicities and would like some additional guidance in terms of further management. Hematologic toxicities are sometimes hard to distinguish or maybe potentially hard to recognize, given many of these patients may have been on prior chemotherapy agents, and anemia or thrombocytopenia may not be unusual, but recognizing if it's new or more severe than what has been seen previously and that, at least, consideration of an immune-mediated hematologic toxicity, be considered, because the management might be unique. And so I hope that we've outlined today some of the hematologic toxicities that are rare that may be seen with immune therapy and some of the strategies to work up alternative diagnoses and management if it is indeed immune-mediated toxicity. BRITTANY HARVEY: Definitely. And I really appreciate you going through these rare but very important toxicities. So thank you for your work on these guidelines and for taking the time to speak with me today, Dr. Nastoupil. LORETTA NASTOUPIL: Thanks, Brittany. BRITTANY HARVEY: And thank you to all of our listeners for tuning in to the ASCO Guidelines podcast series. Stay tuned for additional episodes on the management of immune-related adverse events. To read the full guideline, go to www.ASCO.org/supportive care guidlines. You can also find many of our guidelines and interactive resources in the free ASCO Guidelines app available in iTunes or the Google Play store. If you have enjoyed what you've heard today, please rate and review the podcast, and be sure to subscribe so you never miss an episode. [MUSIC PLAYING]

Eating more plants is the best thing we can do for our health. But it's not as basic as getting all the nutrition we need from fruits and veggies. There is no one-size-fits-all plant-based diet. My guests Ellie Busby (Vojo Health) and Bradley Jafir (Vegan Powah) join me in this episode to discuss the complex factors of nutrition and living a plant-based lifestyle according to our own individual genetic needs. About my guests: Ellie Busby of Vojo Health: Ellie went plant-based in 2011 after living in a Buddhist monastery. For the first few years everything was great. But 5 years in, her health started falling apart. Ellie was doing everything “right”. But it wasn't working. She was fatigued, had brain fog, and her hair was falling out. She was suffering from joint pain, running injuries and struggling more than ever with weight fluctuations. She realised she had a choice – give up, or make it work. Well, she's too stubborn to give up. So she went back to university to research precision nutrition. What she discovered was mind-blowing. Ellie researched how genetics affect our health, and analysed her own and her family's genes. Her genes explained everything – from weight and health struggles to diabetes and dementia in her family. Vojo was founded by Ellie Busby, a published scientist and nutritionist (MSc) in the UK registered with the British Association of Nutrition and Lifestyle Medicine (BANT, CMA approved). She's been plant-based for 10 years, founded a vegan restaurant in 2014, and founded Vojo as a solo female founder in 2020. Bradley Jafir of Vegan Powah: Vegan Powah is a supplement that provides vegans with nutrients that are hard to find or absent on a vegan diet. They have been carefully selected by biomedical scientists and nutritionists with the intention of enhancing the health effects of a vegan diet and preventing nutritional deficiencies in vegans with a range of different genetics. My own Vojo Health DNA analysis revealed that I carry the G6PD deficiency, which is form of anemia. G6PD deficiency is a common genetic condition caused by defects in an enzyme called glucose-6- phosphate dehydrogenase, or G6PD. The G6PD enzyme helps protect red blood cells from damage. In people with G6PD deficiency, red blood cells are destroyed upon exposure to certain environmental triggers, which can lead to episodes of anemia. This test includes two common variants linked to G6PD deficiency. I have both of the genetic variants tested that are associated with an increased genetic risk of anaemia caused by G6PD deficiency. About 400 million people have the condition globally. Most of the time, those who are affected have no symptoms. Following a specific trigger, symptoms such as yellowish skin, dark urine, shortness of breath, and feeling tired may develop. Red blood cell breakdown may be triggered by infections, certain medication, stress, or foods such as fava beans. (Ohhh, I love fava beans.) Well, I learned that due to this genetic G6PD deficiency, as well as other genetic factors, my Vojo plant-based diet type is best matched with the South American type. Hey, I'm not South American. I'm genetically Scottish-Irish and Italian, with some Nordic ancestors like Ingvar "The Tall King of Sweden" Eyesteinsson, so you'd think my dietary type might be good with a Nordic type diet. And my Italian genetics might seem best to match with a Mediterranean diet as an ideal plant-based diet as well (mm, pizza al pomodoro!). You'd think oatmeal and soda bread and berries and almond biscotti is just perfect for me. Yet, the South American Vojo diet is rich with beans and leafy greens, which supports my B12 and iron levels best. --- Support this podcast: https://anchor.fm/plantfull/support

  Dr. Joel Rosen: All right. Hello everyone and welcome back to another edition of the less stress life where we teach exhausted and burnt-out adults the truth about adrenal fatigue so that they can get their health back quickly. I'm joined here with my co-host, Becky roux, who is a moderator and administrator, and … Fatigue and G6PD Deficiency Explained with Dr. Bob Miller Read More » The post Fatigue and G6PD Deficiency Explained with Dr. Bob Miller appeared first on The Truth About Adrenal Fatigue.

In this episode, we review the high-yield topic of G6PD Deficiency from the Hematology section. --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

Maxine, G6PD mom, joins the rad dads to discuss being a G6PD mom and how she handles it, and the staple food of her culture.  She talks about being an entrepreneur and single mom and the challenges she has overcome. Stick around to the end of the episode as we review Rabbit Hole!   Follow us on Rad Dads Instagram Subscribe on: Apple Spotify Pandora Stitcher Google Like our Facebook Follow our Blog Follow us on Twitter Visit us at IncreDads.com Email Questions or comments to: theraddadsshow@gmail.com The Rad Dads Show is available on Apple Podcasts, Google Podcast, Podbean, Spotify &  wherever else you listen to podcasts

Greater magnesium intake linked with lower risk of liver cancer Mt Sinai Hospital, March 22 2021.    A study of AARP members revealed a protective effect for increased intake of magnesium against the risk of developing liver cancer. The findings were published in the March 2021 issue of The American Journal of Clinical Nutrition.  For the current study, researchers at Vanderbilt University Medical Center in Nashvilleexamined data from 536,359 participants in the National Institutes of Health-American Association of Retired Persons (NIH-AARP) Diet and Health Study cohort, which is which is one of the largest and longest prospective cohorts that collected data concerning diet and cancer outcomes in the United States. Food frequency questionnaire responses provided by the participants during 1995 to 1996 were analyzed for total magnesium and total calcium intake from supplements and food. The subjects were followed up to December 31, 2011, during which 1,067 cases of primary liver cancer were diagnosed.  Among those whose total magnesium intake was among the top 25% of participants, there was a 35% lower adjusted risk of developing liver cancer in comparison with participants whose intake was among the lowest 25%. Heavy users of alcohol who had a high magnesium intake experienced an even greater protective effect.  As potential mechanisms for magnesium against liver cancer, authors Shalija C. Shah, MD, and colleagues observed that the mineral is a cofactor for enzymes involved in DNA replication and repair, gene expression, cell proliferation and differentiation, and other factors.  “Based on a prospective cohort analysis, we demonstrated that magnesium intake is associated with a lower risk of primary liver cancer, which was more pronounced among moderate and heavy alcohol users,” they concluded. “These findings add clinical value to the current expansive body of translational literature defining the mechanisms through which this essential micronutrient mediates inflammatory and antineoplastic pathways, particularly within the liver.”     Green leafy vegetables essential for muscle strength Eating just one cup of leafy green vegetables every day could boost muscle function, according to new research. Edith Cowan University (Australia), March 24, 2021   Eating just one cup of leafy green vegetables every day could boost muscle function, according to new Edith Cowan University (ECU) research. The study, published today in the Journal of Nutrition, found that people who consumed a nitrate-rich diet, predominantly from vegetables, had significantly better muscle function of their lower limb. Poor muscle function is linked to greater risk of falls and fractures and is considered a key indicator of general health and wellbeing. Researchers examined data from 3,759 Australians taking part in Melbourne's Baker Heart and Diabetes Institute AusDiab study over a 12-year period. They found those with the highest regular nitrate consumption had 11 per cent stronger lower limb strength than those with the lowest nitrate intake. Up to 4 per cent faster walking speeds were also recorded. Lead researcher Dr Marc Sim from ECU's Institute for Nutrition Research said the findings reveal important evidence for the role diet plays in overall health.  "Our study has shown that diets high in nitrate-rich vegetables may bolster your muscle strength independently of any physical activity," he said. "Nevertheless, to optimise muscle function we propose that a balanced diet rich in green leafy vegetables in combination with regular exercise, including weight training, is ideal." Muscle function is vital for maintaining good overall health, especially bone strength later in life. "With around one in three Australians aged over 65 suffering a fall each year, it's important to find ways of preventing these events and their potentially serious consequences," said Dr Sim. Go for green While leafy greens may be some of our least favourite vegetables, they could be the most important, according to Dr Sim. The research found nitrate-rich vegetables, such as lettuce, spinach, kale and even beetroot, provided the greatest health benefits. "Less than one in ten Australians eat the recommended five to six serves of vegetables per day," Dr Sim said. "We should be eating a variety of vegetables every day, with at least one of those serves being leafy greens to gain a range of positive health benefits for the musculoskeletal and cardiovascular system."  "It's also better to eat nitrate-rich vegetables as part of a healthy diet rather than taking supplements. Green leafy vegetables provide a whole range of essential vitamins and minerals critical for health." Building knowledge The study, a collaboration with Deakin University's Institute of Physical Activity and Nutrition and the Baker Heart and Diabetes Institute, builds on Dr Sim's previous research into nitrate and muscle function in older women.  It also adds to growing evidence linking vegetables with cardiovascular health, including a recent ECU study into cruciferous vegetables and blood vessel health. Dr Sim said the next step of his research will be exploring strategies to increase leafy green vegetable consumption in the general population.  "We are currently recruiting for the MODEL Study, which examines how knowledge of disease can be used to prompt people in making long-term improvements to their diet and exercise," said Dr Sim.     Preservative used in hundreds of popular foods may harm the immune system New science suggests the FDA should test all food chemicals for safety Environmental Working Group, March 25, 2021   A food preservative used to prolong the shelf life of Pop-Tarts, Rice Krispies Treats, Cheez-Its and almost 1,250 other popular processed foods may harm the immune system, according to a new peer-reviewed study by Environmental Working Group. For the study, published this week in the International Journal of Environmental Research and Public Health, EWG researchers used data from the Environmental Protection Agency's Toxicity Forecaster, or ToxCast, to assess the health hazards of the most common chemicals added to food, as well as the "forever chemicals" known as PFAS, which can migrate to food from packaging.  EWG's analysis of ToxCast data showed that the preservative tert-butylhydroquinone, or TBHQ, has been found to harm the immune system both in both animal tests and in non-animal tests known as high-throughput in vitro toxicology testing. This finding is of particular concern during the coronavirus pandemic. "The pandemic has focused public and scientific attention on environmental factors that can impact the immune system," said Olga Naidenko, Ph.D., EWG vice president for science investigations and lead author of the new study. "Before the pandemic, chemicals that may harm the immune system's defense against infection or cancer did not receive sufficient attention from public health agencies. To protect public health, this must change." TBHQ TBHQ is a preservative that is pervasive in processed foods. It has been used in foods for many decades and serves no function besides increasing a product's shelf life. Using new non-animal test results from ToxCast, EWG found that TBHQ affected immune cell proteins at doses similar to those that cause harm in traditional studies. Earlier studies have found that TBHQ might influence how well flu vaccines work and may be linked to a rise in food allergies.  PFAS Using ToxCast, EWG analyzed all publicly available studies that show how PFAS migrate to food from packaging materials or processing equipment. This is the first known compilation of available research on PFAS migration from packaging to food. In 2017, nationwide tests showed that many fast-food chains used food wrappers, bags and boxes coated with highly fluorinated chemicals. Human epidemiological studies show that PFAS suppresses immune function and decreases vaccine efficacy. Recently published research has also found a link between high levels of PFAS in the blood and the severity of Covid-19.  Surprisingly, for most PFAS, the ToxCast results did not match previous animal and human test data. This illustrates the limitations of this new chemical testing method. More research is needed to understand how PFAS harm the immune system. Food Chemicals Regulation The Food and Drug Administration's approach to the regulation of food additives does not consider the latest science on the health harms of additives that may be legally added to processed foods manufactured in the U.S. Last year, EWG published Food Additives State of the Science, which highlighted additives known to increase the risk of cancer, harm the nervous system and disrupt the body's hormonal balance.  Chemicals linked to health harms can be legally added to packaged foods because the FDA frequently allows food manufacturers to determine which chemicals are safe. Additives like TBHQ were approved by the FDA decades ago, and the agency does not consider new science to reassess the safety of food chemicals.  "Food manufacturers have no incentive to change their formulas," said Scott Faber, senior vice president for government affairs at EWG. "Too often, the FDA allows the food and chemical industry to determine which ingredients are safe for consumption. Our research shows how important it is that the FDA take a second look at these ingredients and test all food chemicals for safety." Less Toxic Food Preservatives Processed foods can be made without these potentially harmful ingredients, so shoppers should read labels carefully. TBHQ is often, though not always, listed on the ingredient label. It will be listed if it has been added to the product during manufacturing. But it can also be used in food packaging, particularly plastic packaging, in which case it may migrate to food.  EWG's Food Scores database helps consumers find products made with healthier alternatives, and our Healthy Living app allows shoppers to scan products while in stores to choose a better option.  EWG recommends that immunotoxicity testing be prioritized for chemicals in food and food contact materials in order to protect public health from their potential harm to the immune system.  EWG also calls on the FDA to close the regulatory loophole that allows potentially unsafe food additives to remain on the market. The FDA should also promptly review additives like TBHQ to reflect new science.     Transcendental Meditation effective in reducing PTSD, sleep problems, depression symptoms Maharishi International University, March 19, 2021   Veterans with PTSD who practiced the Transcendental Meditation technique showed significant reductions in PTSD symptom severity, according to a new study published today in Journal of Traumatic Stress. Fifty percent of the meditating veterans no longer met criteria for PTSD after three months compared to only 10 percent of controls. The randomized controlled study also showed significant reductions in veterans' symptoms of depression and anxiety, and sleep difficulties.  "Transcendental Meditation is a non-trauma-focused, easy-to-learn technique that was found in this study to improve PTSD symptoms, likely through the experience of physical rest," said Mayer Bellehsen, Ph.D., director of the Unified Behavioral Health Center for Military Veterans and their Families, Northwell Health, and study principal investigator. "In contrast to commonly administered therapies for PTSD that are trauma-focused and based on a patient's recall of past traumatic experiences, this intervention does not require extensive review of traumatic history, which some individuals find difficult to engage in. This intervention may therefore be more tolerable for some individuals struggling with PTSD." The randomized controlled trial, conducted at Northwell Health in Bay Shore, New York, assigned 40 veterans with documented PTSD to either the Transcendental Meditation (TM) group or treatment as usual control group. The TM treatment provided 16 sessions over 12 weeks, with twice-a-day daily home practice. PTSD symptom severity was assessed with the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5), and patient self-report with the PTSD Checklist for DSM -5 (PCL-5).  The results showed large effect sizes, indicating a strong TM treatment impact in reducing trauma symptoms for both PTSD measures. Other factors associated with trauma, such as depression and anxiety symptoms and sleep problems, also showed a strong impact of TM treatment. "This trial corroborates the findings of a large clinical trial published in The Lancet Psychiatry," said Sanford Nidich, Ed.D., Director of the Center for Social-Emotional Health at Maharishi International University Research Institute, and study co-investigator. "The current study further supports the effectiveness of Transcendental Meditation as a first-line treatment for PTSD in veterans. The availability of an additional evidence-based therapy will benefit veterans, both by offering them a greater range of options and by serving as an alternative treatment strategy for those who don't want to engage in trauma-focused treatment or who aren't responding to a previous PTSD intervention."  The authors point out in their research paper that TM may positively affect trauma symptom severity through the reduction of hyperarousal symptoms. Previous research has shown that TM practice decreases physiological responses to stressful stimuli. In addition, recent research indicates that TM may improve resilience and positive coping strategies, providing further benefit to both veterans and active military personnel.     Study: Eating White Bread & Bagels Can Be Worse Than Smoking – 49% Increase In Lung Cancer University of Texas, March 17, 2021 An alarming study has found eating foods high on the glycemic index (GI), such as bagels, white bread, and rice, increase the risk of developing lung cancer by 49 percent — particularly for non-smokers. In fact, when researchers studied the diets of 4,320 people, they were shocked to find non-smokers with diets high on the GI had nearly double the risk to develop the disease than those whose eating habits remained on the low end of the GI. Foods with high GI raise blood glucose and insulin, in turn causing increased insulin growth factors (IGFs), which are associated with greater risk for developing lung cancer. University of Texas MD Anderson Cancer Center conducted the study of 1,905 people who had cancer diagnoses and 2,415 healthy people, which was published this month in the journal Cancer, Epidemiology, Biomarkers & Prevention, RTreported. “The results from this study suggest that, besides maintaining healthy lifestyles, such as avoiding tobacco, limiting alcohol consumption, and being physically active, reducing the consumption of foods and beverages with high glycemic index may serve as a means to lower the risk of lung cancer,” explained Dr. Xifeng Wu, study senior author. Lung cancer is the number one cause of cancer deaths in the United States. More the 150,000 people will die from lung cancer in 2016 alone, according to the American Cancer Society. What’s more, a second study revealed Americans consume more than half their calories via “ultra-processed” foods, which directly contribute to health problems like obesity and heart disease. “Ultra-processed foods are products that contain several manufactured ingredients that are not generally used when cooking from scratch, including natural and artificial flavors or colors, artificial sweeteners, preservatives, and other additives,”CBS News explained. Obvious examples of ultra-processed foods include soft drinks; chicken and fish nuggets, as well as other reconstituted meat products; packaged snacks, both sweet and savory; packaged baked goods; and instant noodle products. Lead author of the study, Professor Carlos Augusto Monteiro at the University of São Paulo School of Public Health, Dept. of Nutrition, explained such highly-processed foods are designed to imitate natural foods, but often “disguise undesirable qualities of the final product.” Where a diet of fresh foods and minimally-processed products — like cheeses and simple breads — are healthiest, Monteiro told CBS News, ultra-processed products “are manufactured and marketed to replace those foods, drinks, dishes, and meals.” Such ‘foods’ are generally high in sugars, saturated fat, and sodium and contribute to a wide range of health issues, including diabetes, obesity, heart disease, and many more. Both studies ultimately suggest the need to cut out highly-processed products and return to a natural diet rich in fruits, vegetables, and whole grains. In other words, food — not products.   Move your body for five minutes every hour to counteract lockdown inactivity Kings College London, March 23, 2021 A study which looked at activity levels before and during the COVID-19 pandemic has found lockdown restrictions significantly reduced light activity associated with socialising and work. The study, published recently in BMJ Neurology and led by King's College London, examined how activity levels changed in study participants with muscular dystrophy and other inheritable myopathies. The sample included people with a range of physical abilities, from highly independent to assisted mobility, including 41 wheelchair users, who are often underrepresented in research. However, the authors say the findings are likely to be relevant to adults of various abilities and backgrounds because many people have lost their usual daily routine during lockdown. The study is unique because it used accelerometers to measure physical activity before and during lockdown as part of an ongoing longitudinal physical activity study from 2019 to 2020. The accelerometers measured activity intensity, frequency and time in vigorous, moderate, light and inactive categories. Researchers found there was a significant reduction in daily activity intensity during lockdown. Before lockdown, participants did a mean of 84.5 minutes per day of light activity and had a relatively low frequency of hourly movement. During lockdown, light activity reduced by a mean of 25 minutes per day and frequency of hourly movement reduced by a median of 11%. Moderate and vigorous activity did not change significantly during lockdown, but this might be explained by low baseline levels in this group.  In lockdown, the reduction in light activity time and frequency of movement was explained by restrictions on going to work, leisure pursuits and socialising. This light activity within daily routine is not exercise-focused so it can be difficult for individuals to detect these subtle light activity losses. However, light activity and regular movement throughout the day are associated with improved health outcomes for everyone, regardless of health conditions. Sarah Roberts-Lewis, the study lead and a Neurological Physiotherapist at King's College London, said; "Even people who don't do much exercise have been impacted by lockdown inactivity. During COVID-19 lockdown, our study detected an extra hour per day of inactivity in disabled and independent adults with neuromuscular diseases. Moving less is detrimental to health. Reduced activity can be especially harmful for those with neuromuscular conditions, disabilities or advanced age."  "The reduction in light activity measured in this study is likely to be similar for anybody whose daily routine has been restricted by lockdown. Based on our findings, we suggest people move their bodies for 5 minutes each hour during the day. Additionally, spend 30 minutes each day doing some extra light activity, like yoga or chair exercises. The World Health Organisation activity guidelines state 'every move counts'; they provide suggestions about light activites suitable for all abilities. Simple changes can help with reconditioning during and after lockdown."     Lifestyle program improves fertility for women with obesity, infertility University of Sherbrooke (Quebec) March 19, 2021 A lifestyle intervention targeting women with obesity and infertility is more effective in increasing the pregnancy rate compared with fertility treatments, according to a study presented virtually at ENDO 2021, the Endocrine Society's annual meeting. The lifestyle intervention, called the Fit-For-Fertility (FFF) program, is a cost-effective alternative to the usual standard of care for women with obesity seeking fertility treatments, according to lead researcher Matea Belan, Ph.D., of the University of Sherbrooke and the Research Center of the Centre Hospitalier Universitaire de Sherbrooke (RC-CHUS) in Quebec, Canada. "Our study shows that the FFF program can significantly improve the pregnancy rate, especially the spontaneous pregnancy rate when no fertility treatments are required, as well as the live-birth rate," she said. Obesity is a known risk factor for infertility in women of childbearing age. Lifestyle changes and a moderate weight loss of 5%-10% of a woman's initial weight have been shown to improve the odds of a pregnancy in women with obesity and infertility, Belan noted. "Lifestyle changes are recommended as the first-line treatment for these women," said study author Jean-Patrice Baillargeon, M.D., M.Sc., professor of the University of Sherbrooke and clinician investigator of the RC-CHUS. The new study tested Fit-For-Fertility, a multidisciplinary lifestyle intervention that includes a nutritionist and a kinesiologist, or human movement specialist. The researchers recruited 130 women receiving treatment at a fertility clinic, and randomly divided them into two groups. The first group had access to the Fit-For-Fertility program alone for the first six months of their participation, and in combination with fertility treatments if no pregnancy occurred after six months. The program included individual sessions with a nutritionist and a kinesiologist every six weeks. Women in the FFF group were also asked to follow at least once each one of the 12 group sessions, which included a 45-minute workshop on topics regarding nutrition, lifestyle changes and lifestyle habits, followed by a 45-minute session of initiation to different types of physical activity, including walking, circuit training, step workout and others. In the second group, the control group, women had access to the fertility treatments from the outset but did not take part in the FFF program. Data was collected for 18 months, or until the end of a pregnancy for women who became pregnant during those 18 months of participation. Of the 108 women who completed at least six months of the study, or became pregnant during the first six months, the FFF program generated a difference of 14.2 percentage points in the live-birth rate (51% for the FFF group and 36.8% for the control group). The spontaneous pregnancy rate (pregnancy without any fertility treatments) was 33.3% in the treatment group, compared with 12.3% in the control group. The researchers estimate the cost per additional newborn resulting from the FFF program at $12,633 (in 2019 Canadian dollars), somewhat similar to the willingness-to-pay for a newborn resulting from in vitro fertilization, which can cost up to $15,000. "We hope this research will give women with obesity and infertility affordable access to a tailored lifestyle intervention adapted to their condition and their specific needs in order to improve their chances of having a pregnancy and building a family," Belan said.     Vitamin B3 to stay younger? A global increase in antioxidant defenses of the body may delay aging and its diseases   Centro Nacional de Investigaciones Oncológicas (Spain), March 15, 2021   The gradual accumulation of cell damage plays a very important role in the origin of ageing. There are many sources of cellular damage, however, which ones are really responsible for ageing and which ones are inconsequential for ageing is a question that still lacks an answer. The Oxidative Hypothesis of Ageing -- also known as the Free Radicals Hypothesis -- was put forward in 1956 by Denham Harman. Since then, the large majority of attempts to prove that oxidative damage is relevant for ageing have failed, including multiple clinical trials in humans with antioxidant compounds. For this reason, although the accumulation of oxidative damage with ageing is undisputed, most scientists believe that it is a minor, almost irrelevant, cause of ageing. However, this may change in light of the recently published observations. A group of scientists from the Spanish National Cancer Research Centre (CNIO) headed by Manuel Serrano, in collaboration with a group from the University of Valencia, directed by José Viña, and researchers at IMDEA Food from Madrid, have tried to increase the global antioxidant capacity of the cells, rather than just one or a few antioxidant enzymes. To achieve this global improvement in the total antioxidant capacity, researches have focused on increasing the levels of NADPH, a relatively simple molecule that is of key importance in antioxidant reactions and that, however, had not been studied to date in relation to ageing. The researchers used a genetic approach to increase NADPH levels. In particular, they generated transgenic mice with an increased expression throughout their bodies of one of the most important enzymes for the production of NADPH, namely, glucose-6-phosphate dehydrogenase (or G6PD). The results, published today in the journal Nature Communications, indicate that an increase in G6PD and, therefore, in NADPH, increases the natural antioxidant defences of the organism, protecting it from oxidative damage, reducing ageing-related processes, such as insulin resistance, and increasing longevity. Antioxidants That Delay Ageing "As anticipated, the cells in these transgenic animals are more resistant to highly toxic artificial oxidative treatments, thus proving that an increase in G6PD really improves antioxidant defences," explains Sandrina Nóbrega-Pereira, first author of the study and currently a researcher at the Institute of Molecular Medicine of the University of Lisbon. Furthermore, when researchers analysed long-lived transgenic animals, they noted that their levels of oxidative damage were lower than in non-transgenic animals of the same age. They also studied the propensity of these animals to develop cancer and found no difference, suggesting that enhancing G6PD activity does not have an important effect on the development of cancer. The greatest surprise for the team was when they measured the ageing process in the transgenic mice: the animals with a high G6PD expression and, therefore, high levels of NADPH, delayed their ageing, metabolised sugar better and presented better movement coordination as they aged. In addition, transgenic females lived 14% longer than non-transgenic mice, while no significant effect on the longevity of males was observed. "This increased longevity, although modest, is striking taking into account that until now attempts to increase longevity by manipulating individual antioxidant enzymes had failed," said Pablo Fernández-Marcos, co-first author of the study and researcher at IMDEA Food. Overall Increase in the Antioxidant Capacity of Cells Perhaps the key is that the researchers involved in this paper enhanced all antioxidant enzymes in a comprehensive manner. "Compared to the traditional approach of administering antioxidants that react directly with oxygen, we have stimulated all the cell's natural antioxidant mechanisms by raising G6PD levels, and its by-product, NADPH," emphasizes Mari Carmen Gómez-Cabrera, co-author of the paper and researcher at the University of Valencia. Based on these results, the authors of the study point to the use of pharmacological agents or nutritional supplements that increase NADPH levels as potential tools for delaying the ageing process in humans and age-related diseases, such as diabetes, among others. More specifically, vitamin B3 and its derivatives are responsible for the synthesis of NADPH precursors and are suitable candidates for future studies.

Vajra Allan, Program Manager in PATH's Diagnostics program, shares more about the G6PD Community of Practice and project.Find out more about the Community of Practice here: https://www.path.org/programs/diagnostics/gorcop/ --- Episode Cover Photo: PATH/Patrick McKernIntro music: Pamgaea by Kevin MacLeodLink: https://incompetech.filmmusic.io/song/4193-pamgaeaLicense: https://filmmusic.io/standard-license

In COVID-19 clinical update #52, Daniel Griffin reviews differences in attack rates between children and adults, J&J vaccine phase III data, G6PD deficiency and vaccines, NIH halts convalescent plasma trial, dexamethasone in hospitalized patients, data on tocilizumab, and long COVID in children. Hosts: Daniel Griffin and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode SARS-CoV-2 attack rates in children and adults (Clin Inf Dis) Documents for J&J COVID-19 vaccine review (FDA) Convalescent plasma and clinical outcomes (JAMA) NIH halts convalescent plasma trial (NIH) Dexamethasone in hospitalized COVID-19 patients (NEJM) Tocilizumab in hospitalized COVID-19 patients (NEJM) Update on long COVID prevalence (UK ONS) Letters read on TWiV 727 Timestamps by Jolene. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

In COVID-19 clinical update #52, Daniel Griffin reviews differences in attack rates between children and adults, J&J vaccine phase III data, G6PD deficiency and vaccines, NIH halts convalescent plasma trial, dexamethasone in hospitalized patients, data on tocilizumab, and long COVID in children. Hosts: Daniel Griffin and Vincent Racaniello Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode SARS-CoV-2 attack rates in children and adults (Clin Inf Dis) Documents for J&J COVID-19 vaccine review (FDA) Convalescent plasma and clinical outcomes (JAMA) NIH halts convalescent plasma trial (NIH) Dexamethasone in hospitalized COVID-19 patients (NEJM) Tocilizumab in hospitalized COVID-19 patients (NEJM) Update on long COVID prevalence (UK ONS) Letters read on TWiV 727 Timestamps by Jolene. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv

This episode covers G6PD deficiency.Written notes can be found at https://zerotofinals.com/paediatrics/haematology/g6pddeficiency/ or in the haematology section of the Zero to Finals paediatrics book.The audio in the episode was expertly edited by Harry Watchman.

G6PD deficiency is a genetic disorder where the body doesn’t have enough G6PD (aka glucose-6-phosphate dehydrogenase) which usually functions to protect the red blood cells from normal oxidative stress. Without enough protective G6PD, the red cells haemolyse, mostly in response to certain triggers like viral illness and certain foods and medications. There is no cure for G6PD but most people with the condition can live normal lives as long as they avoid triggers, although they can often be quite unwell when they first present with symptoms of G6PD deficiency. You don’t want to miss: A case Differentials for haemolysis Explaining the condition to families An overview of the pathophysiology Aetiology Presentation Treatment Prognosis  Links and resources: Follow us on Instagram: https://www.instagram.com/yourekiddingright.pod/ and  Facebook: https://www.facebook.com/yourekiddingrightpod-107273607638323/ Our email is yourekiddingrightpod@gmail.com Make sure you hit SUBSCRIBE/FOLLOW so you don’t miss out on any pearls of wisdom and RATE if you can to help other people find us! (This isn’t individual medical advice, please use your own clinical judgement and local guidelines when caring for your patients)

En este Episodio: Pedro David Santiago "El Cribador" te habla sobre: Parte I Profecía, Historia, Presente y Futuro Parte II Remedios efectivos naturales contra el Coronavirus según Universidad de Ulm. Médicos españoles hacen estudio independiente que contradice la versión oficialista sobre pruebas contra el SARS Coronavirus 2. Semejanzas con el HIV. Datos del propio CDC delatan su falta de evidencia del virus y su daño a tejido humano en la praxis. Datos de Euromomo: COVID, Letalidad, Etnias y el G6PD. Falsedad de la vacuna del Polio y la confesión de su creador: Jonas Salk. Declaración del Dr. Bernard Greenberg HR10541 de 1978 desmiente la baja de incidencias del Polio y como se manipuló las estadísticas por el National Public Health Service para dar apariencias de efectividad de las vacunas. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/radio-acromtica/message Support this podcast: https://anchor.fm/radio-acromtica/support

a continuación intentaremos dar una revisión sistemática por los temas mayormente  preguntados en los exámenes de residencias médicas en Colombia y que frecuentemente son motivo de consulta en atención primaria.  Todas las decisiones médicas y recomendaciones aquí expresadas deben de ser comparadas con la información académica oficial y jamás deben de ser tomados como un absoluto, los actos médicos derivados de estos audios son responsabilidad de aquellos que ejercen. Usted puede ir a nuestro sitio web y dejar una donación para que juntos continuemos con esta actividad. a anemia palúdica grave se debe a mecanismos mediados por TNF-alfa que implican tanto una mayor destrucción como una disminución de la producción de eritrocitos, incluida la lisis celular a medida que los parásitos se replican y salen de los eritrocitos, la eliminación esplénica y la lisis autoinmunitaria de los eritrocitos marcados inmunológicamente, la incorporación deficiente de hierro en nuevas moléculas de hemo y supresión de la médula ósea durante una infección grave que conduce a una disminución de la producción. [1] [3]  La fiebre de aguas negras es una anemia grave con hemoglobinuria e insuficiencia renal en el contexto de "hemólisis intravascular masiva" en el contexto de infecciones repetidas por P. falciparum tratadas con quinina crónica; es poco común y se cree que está asociado con la deficiencia de G6PD. [15]cia Buck E, Finnigan NA. Malaria. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK551711/     Este podcast se distribuye bajo los términos de Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/ ), que permite su uso, duplicación, adaptación, distribución y reproducción en cualquier medio o formato, siempre que otorgue el crédito apropiado al autor o autores originales y la fuente, se proporciona un enlace a la licencia Creative Commons, y se indican los cambios realizados

Metilen mavisi, ilaçların indüklediği semptomatik methemoglobinemi (göğüs ağrısı, nefes darlığı veya konfüzyon gibi hipoksi bulguları) veya MetHb düzeyleri>%20 olan asemptomatik hastalarda ilk seçenek tedavidir. Methemoglobinemi Özet Methemoglobinemi, kanda aşırı methemoglobin bulunması durumudur.Methemoglobinemi, ferröz (Fe++) hem iyonlarının ferrik (Fe+++) duruma oksitlendiği ve hemoglobinin O2 bağlayamamasına yol açan bir durumdur.Normal düzeyi %20, veya anemi veya iskemik kalp hastalığı gibi risk faktörleri varlığında MetHb >%10 ise. Uygun yanıt alınamadıysa 30-60 dakikada metilen mavisi tekrarlanır.Metilen mavisine alternatif : - Askorbik asit (metilen mavisi kontrendikeyse, ör. G6PD eksikliği)             - Exchange transfüzyon             - Hiperbarik oksijen Destek tedavisi ve monitorizasyon Metilen Mavisi ile sonuç alınamama nedenleri Metilen mavisi ile MetHb düzeyleri düşmüyorsa aşağıdaki durumlar göz önünde buludurulmalıdır : Oksidan ajana devam eden masif maruziyetSulfohemoglobinemi (ör. dapson, sulfonamidler)G6PD eksikliğiMethemoglobin redüktaz eksikliğiHemoglobin anormallikleriAşırı metilen mavisi verilmesi (yüksek dozlarda paradoksal etki) Metilen Mavisi Sınıf Heterosiklik aromatik molekül Etki mekanizması Hemoglobin üzerine iki zıt etki Düşük konsantrasyonda : metilen mavisi -> NADPH bağımlı olarak lökometilen mavisine indirgenme (methemoglobin redüktaz etkisiyle) -> methemoglobini indirger -> hemoglobinYüksek konsantrasyonda : metilen mavisi -> indirgenmiş hemogobindeki ferröz demiri ferrik demire çevirir -> methemoglobin oluşur. Guanilat siklazı inhibe ederek (Guanilat siklaz, NO ve diğer mediatörler tarafından stimule edilir) C-GMP ve vasküler düz kas hücre gevşemesini azaltır. MAO inhibisyonu Farmasötik %1MaviOda sıcaklığında muhafaza edilir. Doz Methemoglobinemi: 1-2 mg/kg IV 5 dakika içerisinde; takiben salin flaş, MetHb düzeyleri düşmüyorsa 30-60 dakikada bir tekrarlanır.MetHb yüksekliği günlerce sürüyorsa (ör. dapson toksisitesi) her 6-8 saatte bir doz tekrarlanır. Vazopleji 1.5-2 mg/kg IV 30-60 dakikada. Uygulama 1-2 mg/kg (%1’lik solüsyondan 0.1-0.2 ml/kg) yavaşça IV 5 dakika içerisinde; takiben salin flaş, MetHb düzeyleri düşmüyorsa 30-60 dakikada bir tekrarlanır.Genellikle ilk doz sonrası bir miktar klinik iyileşme görülür; eğer görülmüyor veya çok az ise, 30-60 dakika sonra doz tekrarlanabilir.Dapson ile zehirlenme gibi, methemoglobin oluşumunun günlerce devam edebileceği nadir durumlarda, birkaç gün süresince her 6-8 saatte bir doz tekrarı gerekebilir.Tüm tedaviler süresince MetHb düzeyleri istikrarlı bir düşüş kaydedilene kadar saatlik olarak ölçülmeli.

Deze video is mede mogelijk gemaakt door de G10: kik hier: http://www.g10vandeeconomie.nl Het nieuwe ‘onbekende’ virus dat de hele wereld in z’n greep houdt is niets meer, maar ook niets minder dan een regelrechte verzwakte mutatie van SARS1 uit 2003. Dr. Peter Borger (moleculaire genetica en biochemie, oprichter van The Independent Research Initiative on Information & Origins) licht in een gesprek met Stefan Noordhoek (ondernemer, interviewde eerder Dr. Wolfgang Wodarg) onder andere zijn publicatie in april in het American Journal of Biomedical Science & Research met deze conclusie toe. Wat waren de consequenties geweest als we deze conclusie eerder hadden onderkend? Hadden we al een medicijn kunnen hebben of een vaccin? Hadden we anders kunnen reageren? Hadden we kunnen weten dat het virus zoveel milder blijkt te zijn dan de wereld oorspronkelijk vreesde en nu blijkt? Wat was de rol van de wetenschap dat er na 2008 geen verder onderzoek meer naar SARS werd gedaan? Wat is überhaupt de stand van de medische wetenschap anno 2020? Hoe staat het met falsificatie, peer-review en ’the Replication Crisis'? Wat moet onze regering nu doen, en wat kunnen we in de toekomst doen? 00:02:56 - Coronavirussen, SARS en MERS 00:08:34 - SARS-CoV-2 is SARS1 00:14:16 - Corona PCR tests zeer onspecifiek 00:18:20 - na 2008 geen onderzoek meer? 00:21:33 - kansen vroegere onderkenning 00:36:09 - virussen muteren altijd naar ongevaarlijker varianten 00:39:00 - Hydroxychloroquine, werking, favisme (G6PD deficiëntie) 00:43:00 - vaccin is onwaarschijnlijk (en indien niet goed getest zeer gevaarlijk) 00:51:03 - 70% vd Medical Science is niet reproduceerbaar (en de ‘Replication Crisis') 01:00:41 - wat nu te doen, wat in de toekomst te doen? Met speciale dank aan Guido Versteeg voor het leggen van het contact met Dr. Peter Borger en het mede voorbereiden van het interview.

De inmiddels wereldberoemde Dr. Wolfgang Wodarg - die vanuit meerdere relevante invalshoeken al decennia lang ervaring heeft met virussen, epidemieen en de gevolgen daarvan - geeft zijn visie op de Corona ‘Crisis’. Een kwaadaardige crisis die volledig drijft op misinformatie en paniek. Enerzijds een ‘Corona-test' die oude en al lang onder mensen circulerende corona-virussen detecteert. En die in steeds grotere aantallen uitgevoerd dus in steeds grotere aantallen positieve tests - alarmerende ‘cases’ genoemd - resulteert. Een griepgolf die in de medische wereld en de media alleen nog maar uit ‘Corona’ bestaat en waar alle andere respiratoire virussen die ook meedoen opeens uit beeld verdwenen. Een wereldwijd totaal aantal griepslachtoffers dat volledig in lijn is met andere jaren. Anderzijds een 'ziekte' COVID-19 die geen specifieke symptomen heeft maar voornamelijk van paniek aan elkaar hangt. Paniek die op diverse plekken in de wereld ziekenhuizen en zorgverleners in problemen heeft gebracht, niet vanwege ‘de ziekte zelf’, maar vanwege andere uiteenlopende omstandigheden, waaronder bevolkingsopbouw, gezondheid, kwaliteit en capaciteit vs zorg en de vaak dodelijke (IC/beademing) behandeling. Wodarg is geruststellend voor iedereen die zich zorgen maakt over ‘het virus’. Dat gevaar is niet groter dan in elk andere griepseizoen, constateert hij (inmiddels ook op basis van tientalle internationale wetenschappers die de werkelijke cijfers uit de hele wereld analyseren). Wodarg’s boodschap is verontrustend als je je afvraagt hoe de hele wereld zich op basis van een zo duidelijk feitenvrije ‘paniek’ gek laat maken. Zich laat (ver)leiden tot het inperken van de meest fundamentele vrijheden. En zich denkt te moeten voorbereiden op een ’nieuw normaal’. Waarin ongelofelijk gevaarlijke en uiterst onwenselijke zaken als ‘massale vaccinatie’, ’contact tracing’ en andere ’surveillance’ opeens als aantrekkelijke oplossing worden gezien. Wodarg waarschuwt voor een nieuwe golf van slim veroorzaakte paniek en duizenden onnodige doden als de ‘COVID-19’ (Hydroxy) Chloroquine behandelingen die nu in honderden trials door de WHO worden voorbereid en straks in Afrika worden uitgevoerd. 10-20% vd mannelijke bevolking uit voormalige Malaria-gebieden heeft de aandoening ‘favisme’ (Glucose-6-phosphaat-dehydrogenase deficiëntie (G6PD) ook wel bonenziekte genoemd). Voor deze grote groep mensen is de behandeling met (Hydroxy) Chloroquine vaak dodelijk. Dr. Wolfgang Wodarg roept iedereen dringend op om zich te richten tot de eigen volksvertegenwoordigers. En een appèl te doen aan hun verantwoordelijkheidsgevoel. Zich te informeren. En te zorgen dat de wereldwijde waanzin over de gelogen crisis en de ontzettend gevaarlijke ‘oplossingen’ per direct gekeerd worden.

Sterling Hill joins the show to provide her incredible wealth of knowledge about genetics and how different genes play a huge role in Covid-19 recovery and vulnerability. Find out what you should be doing to boost immunity based on your genes! On today’s podcast, you will learn: What is a genetic G6PD deficiency and how Vitamin C, Hydroxycholoroquine can make you sick if you have this genetic expression. The genetics playing a role in severity and fatalities of COVID-19 infections. The app that can show if you have a genetic vulnerability to COVID19 - could this be why “healthy” young people are dying? Top supplements that strengthen your immune system in preparation for COVID-19 and ones to avoid if you have certain genes. Sterling Hill's Bio: Sterling Hill founded MTHFRSupport.com over 10 years ago after falling very ill and allopathic medicine failed her. Since then she started building genetic apps that show where people may have the need for extra nutraceutical support, she has processed over 70,000 genetic reports. Sterling has devoted her life to research how environmental toxins impact DNA. She was recently awarded congratulations and commendation from Louisiana Senate for defending the Constitutional rights for citizens to make their own fully informed medical decisions and her valorous defense of the health of America's children. Sterling has been involved in a U.S. Congressional Hearing regarding the dangers of glyphosate. She is now studying the environmental impact of 5g and COVID-19 and has built the first genetic app of it's kind regarding COVID-19. Sterling has also built a database for the autism community that is over 33,000 lines long and growing and has also lectured at Autism One and has taught CME's to MD's. You can learn more about Sterling and her Covid-19 genetic app at Are toxic metals causing your fatigue and health issues? Find out by taking Wendy’s Heavy Metals Quiz at

Question: What should people with glucose-6-phosphate dehydrogenase deficiency be doing not just about glutathione, but about folate, vitamin K, fatty acids, and neurotransmitters?   G6PD, glucose-6-phosphate dehydrogenase deficiency, is an inborn error of metabolism. It's the most common one in the world. About 8% globally have some impairment in this enzyme. The reason that it's important is because glucose-6-phosphate dehydrogenase is the enzyme that allows you to make NADPH, which is a specific derivative of niacin that's involved in antioxidant defense, detoxification, synthesis of neurotransmitters, and synthesis of nucleotides, which are needed for cell division because they're parts of DNA.   Someone with G6PD deficiency is vulnerable to hemolysis, or the destruction of red blood cells, because of glutathione deficiency. Glutathione reductase uses energy and NADPH, the thing that you can't make, to recycle glutathione. But it also uses riboflavin. So, one of the adaptations that someone with this impairment has to try to protect themselves is for the glutathione reductase enzyme to hog all the riboflavin so that it says, "I don't have enough of the raw material I need to make this happen, so I'm just going to make myself get way better at using what I do have." That's an adaptation to compensate for not being able to make NADPH is just to get way better at using NADPH to recycle glutathione.   Supplementing glutathione is not necessarily a bad idea. You just have to be aware that at a certain point you just can't solve every one of the dozens of problems that are happening. I think that you should measure your glutathione status. Probably the best test available, not because it's the best we could have available but because there's nothing better right now, is LabCorp's test for glutathione. If that looks low, then I would supplement with glutathione to try to bring that up to normal.    For the folate recycling, you have to consider this basically as if you had a really bad MTHFR polymorphism because G6PD is needed to make the NADPH that MTHFR uses, again, with the help of riboflavin to make the methyl group on methylfolate. You can take some methylfolate, but as I've made the point in my MTHFR protocol at chrismasterjohnphd.com/methylation, you have to take 18,000 times the RDA to compensate for the 18,000 times a day that you add a methyl group to the folate molecule using that enzyme. It's not safe to take anywhere near that much folate.   What I would do is just very strictly follow the MTHFR protocol that I have at chrismasterjohnphd.com/methylation, and that involves doubling your choline intake because you don't need NADPH to use choline to support methylation. Just as if MTHFR didn't work because of genetics and not enzyme, what you would do is you double your choline utilization for methylation because you're not good at using folate.    On recycling vitamin K, it probably just means that you need a high amount of vitamin K in your diet. I think it's probably similar as if you had a bad VKOR polymorphism. VKOR is the enzyme that recycles vitamin K using NADPH that you got from this pathway that's not working right when you have G6PD deficiency.   In terms of all this stuff that you are not good at synthesizing, like cholesterol, fatty acids, nucleotides, and neurotransmitters, I think the only thing that you can do for that is to try to eat a lot of these things preformed. That means eating a diet rich in relatively lean animal foods because they have a lot of preformed stuff, like cholesterol, in them and mainly in the flesh, not the fat. With plants, you want to eat mostly fibrous vegetables because they are highly cellular and rich in nutrients that you can’t make.   You don't want to go extremely low-fat, but if you eat a diet fairly rich in animal foods, you're going to get a lot of the specific fatty acids that you can't make. A high-fat diet is mostly giving you just a bunch of fat that you could have made yourself.   This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/03/08/ask-anything-nutrition-feb-23-2019   If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

My goal with this Podcast is to provide a space where we can share information, our stories, trials, and triumphs regarding G6PD. I invite you to come and be a part of a much needed forum!

Patients with G6PD deficiency who are taking probenecid are at increased risk for hemolytic anemia. In a patient taking probenecid, they need to have adequate kidney function for the drug to work. GI upset is likely the most common adverse effect of probenecid. It can be given with food. Probenecid can raise the concentrations of many common antibiotics like penicillins and cephalosporins. Remember that there are many medications that can oppose the beneficial effects of probenecid. Thiazides, niacin, and some immunosuppressants can raise uric acid.

Dr. James DiNicolantonio, is a Doctor of Pharmacy and a cardiovascular research scientist. A well-respected and internationally known scientist and an expert on health and nutrition, he has contributed extensively to health policy and has testified in front of the Canadian Senate regarding the harms of added sugars. He serves as the associate editor of the British Medical Journal’s Open Heart, a journal published in partnership with the British Cardiovascular Society, and is on the editorial advisory boards of several other medical journals. Dr. DiNicolantonio is the author or coauthor of over 250 publications in the medical literature. He also is the author of three bestselling health books, The Salt Fix, Superfuel and The Longevity Solution. You can follow him on Instagram and Twitter @drjamesdinic and on Facebook at Dr. James DiNicolantonio. You can visit his website at drjamesdinic.com.   Time stamps:   10:25 Electrolytes. How much salt did we have evolutionary ?  13:05 How much salt do humans need? 16:00 Can we go too high on salt consumption? 21:20 Magnesium. 24:45 Insulin Resistance and sodium  27:45 Kidney function. Bumps in BUN and Creatinine. 29:00 How to measure for magnesium deficiency. 31:00 Vitamin C 39:15 Ideal vitamin C intake for humans. 59:45 Concerns of higher vitamin C intake. 1:02::25 Vitamin C and people with G6PD deficiency. 1:07::05 Cadmium and kidneys. 1:11:27 Chlorella and pollutant binding. 1:13:15 Fiber and dioxins. 1:16:35 James' diet. Is it cheaper to eat plant foods? 1:19:35 Molecular xenohormesis. 1:24:30 Are plants beneficial ? 1:32:30 The fear of glucose spikes. 1:34:35 Resistant starch. 1:39:14 Where to find James and the most radical thing he's done recently. Ancestral Supplements https://ancestralsupplements.com/   Code SALADINOMD on the shopify site to receive 10% off.   Use the code CARNIVOREMD at www.whiteoakpastures.com all month for 10% off your order!   JOOVV: www.joovv.com/paul INSIDER: carnivoremd.com   My contact information:   Book: www.thecarnivorecodebook.com   PATREON: https://www.patreon.com/paulsaladinomd   SOCIAL MEDIA  Instagram: @carnivoremd Website: carnivoremd.com Twitter:@carnivoremd  Facebook: Paul Saladino MD email: drpaul@carnivoremd.com

Question: What are the best ways to optimize glutathione status for someone who has a G6PD deficiency?   Riboflavin was shown to be of benefit for normalizing oxidative stress in people who have glucose 6-phosphate dehydrogenase deficiency.   So for people who don't know what this is G6PD is, glucose 6-phosphate dehydrogenase is an enzyme that you use to take energy from glucose specifically, you can't take it from anything else, and you use it to recycle glutathione which is a master antioxidant of the cell.    You also need this to support the recycling of vitamin K and folate and you need this for synthesis of neurotransmitters among other things.   But the big problem with G6PD deficiency is that you can have a lot of things go sideways when you can’t use this pathway. Red blood cells become more vulnerable to hemolysis and that is a result of oxidative stress from poor glutathione recycling in the red blood cell.    One of the adaptive responses to having G6PD deficiency is the glutathione reductase enzyme -- which is the enzyme that uses riboflavin and niacin to recycle glutathione with the energy taken from G6PD.    That enzyme -- glutathione reductase -- it develops a voracious appetite for riboflavin that makes all the riboflavin that won't go anywhere else, get sucked up into that enzyme. So basically you become very dependent on riboflavin support of glutathione reductase because you have lost G6PD, the enzyme that's involved in passing the energy on to riboflavin in glutathione reductase.   There's probably no harm to starting at 400 milligrams of riboflavin a day, but if you feel like you want to be more cautious about it, I'd start at 5 or 10 milligrams a day, test the effect on glutathione status.   You know in this case I think you want to look at erythrocyte glutathione status, I don't usually recommend that test, but it might be a more relevant test specifically for this condition.    What I would usually recommend for glutathione status would be plasma levels of glutathione. I also think LabCorp does whole blood glutathione.  This Q&A can also be found as part of a much longer episode, here: https://chrismasterjohnphd.com/podcast/2019/02/24/ask-anything-nutrition-feb-17-2019/   If you would like to be part of the next live Ask Me Anything About Nutrition, sign up for the CMJ Masterpass, which includes access to these live Zoom sessions, premium features on all my content, and hundreds of dollars of exclusive discounts. You can sign up with a 10% lifetime discount here: https://chrismasterjohnphd.com/q&a

La treizième édition de Santé, Science et Développement se focalise sur un nouveau test de diagnostic rapide des déficiences en G6PD, évalué par des chercheurs mauritaniens et français. Les patients déficients en G6PD s'exposent à des complications lorsqu'ils se font prescrire de la primaquine, le médicament recommandé par l'OMS pour le traitement du paludisme à P. vivax. Le nouveau test permet aux cliniciens de déterminer en quelques minutes si un patient est apte à prendre de la primaquine. Cet épisode s'intéresse également à la vie après Ebola, en allant à la rencontre des personnes guéries de la maladie et en explorant leurs difficultés quotidiennes, entre stigmatisation et séquelles. Santé, Science et Développement, un magazine présenté par Sylvie Akoussan.

In the November 2019 episode of the JAAPA Podcast, our co-hosts Kris Maday, PA-C and Adrian Banning, PA-C discuss CME articles on G6PD deficiency and viral hepatitis A, B, and C. Then, Kris breaks down the "loop technique" for abscess drainage and Adrian discusses the importance of protein intake and strength exercises in older adults. Plus, our co-hosts consider a world tour.      Follow us on social media: JAAPA on Twitter and Instagram: @JAAPAonline Co-Host Adrian Banning, PA-C on Twitter: @theArtofEBM Co-Host Kris Maday, PA-C on Twitter: @PA_Maday Associate Editor Harrison Reed, PA-C on Twitter and Instagram: @HarrisonReedPA

La treizième édition de Santé, Science et Développement se focalise sur un nouveau test de diagnostic rapide des déficiences en G6PD, évalué par des chercheurs mauritaniens et français. Les patients déficients en G6PD s'exposent à des complications lorsqu'ils se font prescrire de la primaquine, le médicament recommandé par l'OMS pour le traitement du paludisme à P. vivax. Le nouveau test permet aux cliniciens de déterminer en quelques minutes si un patient est apte à prendre de la primaquine. Cet épisode s'intéresse également à la vie après Ebola, en allant à la rencontre des personnes guéries de la maladie et en explorant leurs difficultés quotidiennes, entre stigmatisation et séquelles. Santé, Science et Développement, un magazine présenté par Sylvie Akoussan.

Enter #K012trepreneur  - 何卓烽 Desmond Ho Amofia菲菲嘅創辦人 GMPC護膚品廠及印刷廠嘅董事 香港人撐香港品牌聯席主席 香港蠶豆症兒童基金會永譽顧問 Facebook: @Desmond Ho Instagram: @desmondho1 有不少朋友都向我推介訪問Desmond這位真男人，機緣巧合下我倆在西貢食飯，發覺大家價值觀、家庭背境、生意理念、甚至消費習慣也很相似，加上Amofia菲菲這個有機品牌也能幫助我患上G6PD的弟弟，我們便一拍即合。 Desmond自少到外國讀書，跟隨當地的文化13、14歲便出來打工。不太讀書的Desmond有年犯下大錯，鎖自己在房間4天，覺得自己不能再這樣毫無意義的過活，便走到校務處轉讀Triple Major，即使學校最初不批准，他也堅持說服學校教育部，若讀不好才踢他離開。 Desmond 後來順理成章畢業，在當地一間公司由一名公司助理，半年內便升職成為了公司經理，再成為州份經理。原來多得自己在當時還是公司助理身分時，已經向總公司提議工一些改善的意見，更會自己做一些副本給他們，所以大老闆一早已經有留意他。 Desmond享受著外國工作的好處，例如公司的信用卡可以支付所有日常生活開支等，但有一天家人打電話給他，說爸爸準備退休，打算賣了公司，但Desmond深知生意難做，公司是家人的心血，賣了便很可惜，便決定回香港幫忙。 由於Desmond與父親關係不太親密，回來也沒什麼工作給他做，結果一個月後收到一張$8000的支票，但當時2012年大學生畢業已經超於$12000。一下子由在美國的$80000月入跌了10倍，Desmond便開始接觸客戶，打電話關心他們，慢慢接觸了更多不同口，最後便把公司的廠房重新建設，以幾年時間拿到了GMP認證，簽下很多國際性客戶。 後來Desmond生下女兒Fia，可是女兒遇上濕疹問題，而更諷刺的是Fia竟然對自己家族生產的所有產品敏感，而市面上對乳化劑產品監管亦不足夠。眼見女兒深受濕疹的折磨，Desmond決定自家研發能夠舒緩濕疹的產品幫助女兒，結果經過很多次不同的嘗試，終於成功研發出能夠幫助女兒的產品。 起初Desmond都是以幫助自己的女兒為主，但後來很多朋友的兒女也受濕疹影響，便慢慢產生了製作Amofia這個品牌的念頭。 後來這個品牌幫助越來越多受濕疹影響的小朋友，Desmond和太太亦開始研究能夠幫助不同患病的小朋友的產品，甚至能夠讓家長自訂產品給小朋友，為求幫助更多人。 Quick Tips: 年輕人應投放更多資源去感受Life Experience，不應受盡社會而限制感受生命的活動。假如在香港可能很難買車，但一到外國可能就變得很容易，與其做一些在香港很難達到的事情，倒不如在很容易簡單的得到的外國好好感受。
 #K012trepreneur #AskKongtrepreneuerShow #Kongtrepreneur  

Dr James Watson from MORU in Bangkok, Thailand, tells us about his research in the biology of relapse in vivax malaria, as well as the development of statistical models to better understand the pharmacology of antimalarial drugs. Primaquine is a drug used to eliminate vivax malaria from the liver and prevent relapses. However, it causes anaemia in patients with G6PD deficiency. A new, slightly longer regimen with increasing doses of primaquine could allow to safely treat all patients with vivax malaria.

In this episode I cover haemolytic anaemia.If you want to follow along with written notes on haemolytic anaemia go to zerotofinals.com/haemolyticanaemia/ or the haematology section in the Zero to Finals medicine book.This episode covers the definitions, types, tests and causes and treatments of haemolytic anaemia. The audio in the episode was expertly edited by Harry Watchman.

Adrian Black and Mr. P talk Culture & Health from southern China's megalopolis, Shenzhen. Intro to the Artists-Who are you? What do you hope to accomplish? What shaped you into the person/artist that you are? What sort of experiences bonded you to this path that you'd like to share? "Intro to MiVa"- What is this MiVa thing? How is it different from what's out there already? G6PD awareness "Seeing things clearly"-How has living overseas affected your relationship to identity politics? What were you able to get as a globe-trotter that you're unable to get living in your "home/native" land? "Culture Corner (not really....I just made that name up)"- Reflections on how witnessing US culture (clearly the State's largest and most valuable export) impacts you/me/us” "Shenzhen Social Culture"-So much to talk about here. What's the most impactful parts of living in SZ? What do you notice here that you haven't seen anywhere else in the world? What do you feel is important for people not in SZ to know about the place/your experiences here?

Session 07 We often associate biochemistry with undergrad, but biochemistry is present in many specialties! Let’s dive into the types of biochem questions you may see! We're joined once again by Dr. Andrea Paul from Board Vitals as we help you prepare for your first board exam so you have what it takes to score high and match into your specialty of choice. Use the promo code BOARDROUNDS to save 15% on your QBank purchase. [03:30] Why Biochemistry? Biochemistry is more applicable to some specialties than others. But just basic genetics and metabolic diseases, for instance, are seen in many specialties. Biochemistry comes into play especially when you talk about metabolic diseases. Hence, it's a commonly tested subject on the exam, more than the other basic science components. [04:41] Question for this Week: A healthy married couple has a child who develops clinical symptoms of what you suspect to be a rare disease. Genetic testing revealed the patient's mother carries the mutated gene, but the father is not a carrier. However, the father's brother had the same disease, which has also occurred in one of his sisters' sons. This pattern is characteristic of which of the following diseases? Note from Andrea: The question is drawing you a pedigree. You can jot down a little diagram of pedigree for yourself as you're going through it. You have to figure out the pattern from the pedigree but know which diseases of the options fit that pattern of inheritance. Answer choices: (A) G6PD (B) Cystic fibrosis (C) Phenylketonuria (PKU) (D) Alpha-1 antitrypsin deficiency (E) Tay-Sachs Disease [05:50] The Thought Process Behind the Answer Once you've drawn that pedigree and determined what the inheritance pattern is, you can go through each option and cross out what doesn't fit or jot down what pattern each one has. In this case, the couple is healthy and not showing any disease. But the one child does and the father is not a carrier. This gives you another hint. So if he's not a carrier, how is that possible if the child is showing the disease? Then you're seeing that it's present in the father's brother and one of the sisters' sons. Here, you can see a distinctive pattern where this is not an autosomal recessive type pattern. This leads you to a dominant X-linked route. As you draw this out, you will start to see the pattern where the children follow up to them. The mother is a carrier, the father is not. And the child has the disease. It's likely that the child is a male because they're receiving only an X from the mom. So this would be an X-linked pattern. Now, you would only see one that follows that X-linked disease – G6PD Looking at patterns and pedigrees can really help you. Another algorithm Andrea found helpful is to ask: does the child with the disease have a parent with a disease. If no, then you're skipping a lot of things. You're left here with X-linked recessive which is 50% more common than a male child. Therefore, it's an X-linked recessive disease. [11:02] Tips and Tricks to Help You Memorize and Understand Better Most students are using mnemonics to remember all of the X-linked recessive diseases. This is most common for autosomal recessive or autosomal dominant. There's no way to think through them in a way that doesn't require memorization. The names of the disease don't really help in this case. All this being said, Andrea recommends using mnemonics. You can also use visual mnemonics you can look at or silly drawings to help you remember stuff. [12:37] Other Possible Questions Probably, if the question talked about a food that this person that this person may develop symptoms with, then you could probably remove some answer choices out. For example, G6PD is one of those diseases. If it's cystic fibrosis, they could ask what microbe commonly infects patients with this disorder. Or they could ask a treatment for that disorder. [14:00] Other Patterns Students Should Know About One pattern would be X-linked dominant. In this case, you would not see skipping of generations unlike what's in the above question. You would also see male and female as affected equally since the disease of the X chromosomes is dominant. So you think of diseases like X-linked dominant Alport syndrome or hypophosphatemic rickets. Another interesting inheritance pattern is mitochondrial where males and females are affected equally. It would skip generations but it is only transmitted from an affected female because mitochondrial diseases come from the maternal side always. And you would see a different pattern and all of the offspring would be affected – something you wouldn't see in the other types. Autosomal dominant, you would also see male and female as affected and not skipping generations. For instance, if two parents without the disease have a child with the disease, you'd think that the only way this could be autosomal dominant is there's a new mutation or there's some type of reduced penetrants or maybe the parent has the gene but just phenotypically normal. Otherwise, you would see this in every offspring because it's a dominant disease. Autosomal recessive is the opposite where you see skipping of generations. For example, if you have a couple both carrying the gene without any signs of disease, there would be 25% the child is born with two normal genes from the parents, 50% chance that they have one normal and one abnormal gene, and 25% that they would receive both. Since it's recessive that's the only case where you would see disease such as cystic fibrosis, thalassemia, sickle cell anemia, or PKU (of which some are shown in the answer choices above). Spinal muscular atrophy would be a more popular disease here, which my daughter has but me and my wife don't have, which makes us both carriers. This is going to be more popular to start talking about it on medical school and the boards because it's one of the first diseases out there that will be cured with gene therapy. [17:45] Board Vitals If you're interested in the QBank and how Board Vitals can help you prepare the best way you can for your Step 1 or Level 1, check out their site and use the promo code BOARDROUNDS to save 15% off of your QBank purchase. Links: Board Vitals (promo code: BOARDROUNDS)

“Genotype–Phenotype Correlations of Glucose-6-Phosphate–Deficient Variants Throughout an Activity Distribution” was published in the May 2018 issue of The Journal of Applied Laboratory Medicine.  This work examines G6PD mutations across a range of enzyme activities and seeks to establish enzyme activity cutoffs that could be implemented to rule out G6PD deficiency.

This week we answer your questions about laryngomalacia, noise sensitivity and G6PD deficiency. We also consider the recent test flight of Falcon Heavy and how watching a rocket launch can ignite a child’s love of science. We hope you can join us!

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Most newborns will have some jaundice.  Most jaundice is benign. So, how can we sort through the various presentations and keep our newborns safe? Pathologic Jaundice When a baby is born with jaundice, it’s always bad.  This is pathologic jaundice, and it’s almost always caught before the baby goes home.  Think about ABO-incompatbility, G6PD deficiency, Crigler-Najjar, metabolic disturbances, and infections to name a few.  Newborns are typically screened and managed. Physiologic Jaundice Physiologic jaundice, on the other hand, is usually fine, until it’s not. All babies have some inclination to develop jaundice.  Their livers are immature.  They may get a little dehydrated, especially if mother’s milk is late to come in.  In today’s practice, we are challenged to catch those at risk for developing complications from rising bilirubin levels. Hyperbilirubinemia is the result of at least one of three processes: you make too much, you don’t process it enough, or you don’t get rid of it fast enough. Increased production Bilirubin mostly comes from the recycling of red blood cells. Heme is broken down in in the liver and spleen to biliverdin then bilirubin. Normal, full term babies without jaundice run a little high -- bilirubin production is two to three times higher than in adults, because they are born with a higher hematocrit.  Also, fetal hemoglobin is great at holding on to oxygen, but has a shorter life span, and high turn-over rate, producing more bilirubin. Impaired conjugation Think of bilirubin as your email.  Unconjugated bilirubin is your unread email.  To process it or get rid of it – you have to open it.  Of course, the more unread messages that accumulate, the more unwell you feel. Conjugated bilirubin is your opened and processed email.  So much easier to sort out, deal with, and get rid of. Decreased excretion Both unread email and unconjugated bilirubin continue to float around in your inbox.  Unconjugated bilirubin keeps getting reabsorbed in the intestinal mucosa through enterohepatic circulation. Processed email and conjugated bilirubin are easier to sort out.  Conjugated bilirubin is water soluble, so it goes right into the read folder in your gallbladder, and is excreted off your inbox.  Later on down the line in the intestine, conjugated bilirubin can’t be reabsorbed through the intestinal mucosa.  Like when you open an email and forget about it – it passes on through, out of your system. Newborns are terrible at answering emails.  There is a lot of unread unconjugated bilirubin is floating around.  The liver and spleen are just not able to keep up. Also, newborns have a double-whammy administrative load.  Normally, bacteria in the gut can further break down conjugated bilirubin to urobilin and get excreted in the urine.  The infant’s gut is relatively sterile, so no admin assistance there.  Just to add to the workload a poor little newborn has to do – he is being sabotaged by extra beta-glucuronidase which will take his hard-earned conjugated bilirubin and unconjugate it again, then recycle it, just like email you “mark as unread”. How Does this All Go Down? The recommended followup is 48 hours after discharge from the nursery for a routine bilirubin check, often in clinic, and often via the transcutaneous route. More Specifically: Infant Discharged Should Be Seen by Age Before age 24 h 72 h Between 24 and 48 h 96 h Between 48 and 72 h 120 h The neonate will end up in your ED off hours, if there is concern, if his status deteriorates, or simply by chance.  We need to know how to manage this presentation, because time is of the essence to avoid complications if hyperbilirubinemia is present. Critical Action #1: Assess risk for developing severe hyperbilirubinemia. This will tell you: check now in ED or defer to clinic (default is to check). Risk Factors for Developing Hyperbilirubinemia Total serum bilirubin/Transcutaneous bilirubin in high-risk zone Jaundice in first 24 hours ABO incompatibility with positive direct Coombs, known hemolytic disease, or elevated ETCO Gestational age 35-36 weeks Prior sibling had phototherapy Cephalohematoma or bruising Exclusive breastfeeding, especially with poor feeding or weight loss East Asian Race Critical Action #2 Check bilirubin and match this with how old the child is -- in hours of life -- at the time of bilirubin measurement. This will tell you: home or admission. Use the Bilitool or Bhutani Nomogram (below).   Can I go Home Now? Risk Stratification for Developing Severe Hyperbilirubinemia. Bhutani et al. Pediatrics. 1999. In general, babies at low-risk and low-intermediate risk can go home (see below).  Babies at high-intermediate or high risk are admitted (see below). Critical Action #3: Assess risk for developing subsequent neurotoxicity. This will tell you: a) phototherapy or b) exchange transfusion     Phototherapy Now?     Exchange Transfusion Now? Threshold for Initiating Exchange Transfusion by Risk Stratum. Bhutani et al. Pediatrics. 1999. Home care The neonate who is safe to go home is well appearing, and not dehydrated.  His total bilirubin is in the low to low-intermediate risk for developing severe hyperbilirubinemia, and he is not at high risk for neurotoxicity based on risk factors. Babies need to stay hydrated.  Breast feeding mothers need encouragement and need to offer feeds 8-12 times/day – an exhausting regimen.  The main message is: stick with it.  Make sure to enlist the family's help and support to keep Mom hydrated, eating well, and resting whenever she can.  Supplementing with formula or expressed breast milk is not routinely needed.  Be explicit that the neonate should not receive water or sugar water – it can cause dangerous hyponatremia.  A moment of solid precautionary advice could avert a disaster in the making. The child’s pediatrician will help more with this, and you can remind nursing mothers of the excellent La Leche League – an international group for breastfeeding support.  They have local groups everywhere, including a hotline to call. Nursery Care If the baby is at high intermediate or high risk for hyperbilirubinemia, then he should be admitted for hydration, often IV.  Most babies with hyperbilirubinemia are dehydrated, which just exacerbates the problem. Bililights or biliblankets, provide the baby with the right blue spectrum of light to isomerize bilirubin to the more soluble form.  Traditionally, we have thought them to be more effective or safer than filtered sunlight.  A recent randomized control trial by Slusher et al. in the New England Journal of Medicine compared filtered sunlight versus conventional phototherapy for safety and efficacy in a resource-poor environment.  These were all term babies with clinically significant jaundice in Nigeria.  To standardize the intervention, they used commercial phototherapy canopies that remove most UV rays. None of them became dehydrated or became sunburned.  The filtered sunlight resulted in a 93% successful treatment versus 90% for conventional phototherapy.  My take away: we now have some evidence basis for using filtered sunlight as an adjunct for babies well enough to go home. Critical Care Although rare, the critically ill neonate with hyperbilirubinemia requires immediate intervention. He will be dehydrated – possibly in shock.  He will be irritable. Or, he may just have a dangerously high bilirubin level – at any minute he could develop bilirubin induced neurologic dysfunction, or BIND, especially when bilirubin concentrations reach or surpass 25 mg/dL (428 micromol/L).  The bilirubin is so concentrated that it leeches past the blood brain barrier and causes neuronal apoptosis.  BIND is a spectrum from acute bilirubin encephalopathy to kernicterus, all involving some disorder in vision, hearing, and later gait, speech, and cognition. Acute bilirubin encephalopathy starts subtly.  The neonate may be sleepy but hypotonic or have a high-pitched cry; he maybe irritable or inconsolable, jittery or lethergic. The dehydration and neurologic dysfnction from the hyperbilirubinemia may even cause fever.  Check the bilirubin in any neonate you are working up for sepsis. Acute bilirubin encephalopathy may progress to an abnormal neurologic exam, seizures, apnea, or coma. Kernicterus is the final, permanent result of bilirubin encephalpathy.  The child may have choreoathetoid cerebral palsy with chorea, tremor, ballismus, and dystonia.  He may have sensorineural hearting loss, or cognitive dysfunction. It is for this reason that any child sick enough to be admitted should be considered for exchange transfusion.  Most babies need just a little gentle rehydration and bililights, but to be sure, the admitting team will look at a separate nomogram to gage the child’s risk and decide whether to pull the trigger on exchange transfusion.  For our purposes, a ballpark estimate is that if the total serum bilirubin is 5 mg/dL above the phototherapy threshold, or if they have any red flag signs or symptoms, then exchange transfusion should be started. Exchange transfusion involves taking small aliquots of blood from the baby and replacing them with donor blood.  It’s often a manual procedure, done with careful monitoring.  It can be done with any combination of umbilical arteries or veins with peripheral arteries or veins.  In general, arteries are the output, veins are for transfusion. The baby may need a double-volume exchange, which ends up replacing about 85% of circulating blood, a single-voume exchange, replacing about 60% of blood, or any fraction of that with apartial volume exchange.  It is a very delicate procedure that requires multiple hours and often multiple staff. For our pruposes, just be aware that the jaundiced baby in front of you may need escalation of his care. Summary Find out the hour of life of the baby at the time of bilirubin measurement.  Identify risk factors for developing severe hyperbilirubinemia and/or neurotoxicity The child with low to low-intermediate risk may be a good outpatient candidate provided he is well, not dehydrated, and follow-up is assured. The child with high-intermediate to high-risk for developing severe hyperbilirubinemia should be admitted for hydration, bililights, and/or assessment for exchange transfusion. The unwell child with or without current neurologic findings should have immediate exchange transfusion. References Benitz WE. Hospital Stay for Healthy Term Newborn Infants. Pediatrics. 2015; 135(5):948-53. Bhutani V et al. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics. 2004; 114(1). Bhutani VK, Wong RJ. Bilirubin Neurotoxicity in Preterm Infants: Risk and Prevention. J Clin Neonatol. 2013 Apr-Jun; 2(2): 61–69. Bosschaart N et al. Limitations and Opportunities of Transcutaneous Bilirubin Measurements. Pediatrics. 2012; 129(4). Colletti JE, Kothari S, Jackson DM, Kilgore KP, Barringer K. An emergency medicine approach to neonatal hyperbilirubinemia. Emerg Med Clin North Am. 2007 Nov;25(4):1117-35, vii. Gamaleldin R et al. Risk Factors for Neurotoxicity in Newborns With Severe Neonatal Hyperbilirubinemia. Pediatrics. 2011; 128(4):825-31. Lauer BJ, Spector ND. Hyperbilirubinemia in the Newborn. Pediatrics in Review. 2011; 32(8):341-9. Maisels J et al. Hyperbilirubinemia in the Newborn Infant ≥35 Weeks’ Gestation: An Update With Clarifications. Pediatrics. 2009; 124(4):1193-6. Smitherman H, Stark AR, Bhutani VK. Early recognition of neonatal hyperbilirubinemia and its emergent management.  Semin Fetal Neonatal Med. 2006 Jun;11(3):214-24. Vandborg PK, Hansen BM, Greisen G, Ebbesen F. Dose-response relationship of phototherapy for hyperbilirubinemia. Pediatrics. 2012 Aug;130(2):e352-7. This post and podcast are dedicated to Gita Pensa, MD, for her commitment to #FOAMed and passion for asynchronous learning and education innovation.

Professor Kevin Baird leads our Eijkman-Oxford Clinical Research Unit (EOCRU) in Jakarta, Indonesia. Delivering health care in Indonesia is a challenge, made more difficult by the geography and distances. Our EOCRU unit specialises in clinical trials on tropical infections, particularly Plasmodium vivax malaria. Current treatments with primaquine are effective but very toxic for patients with G6PD deficiency. Better point of care diagnostics can help us treat all patients safely.

Professor Kevin Baird leads our Eijkman-Oxford Clinical Research Unit (EOCRU) in Jakarta, Indonesia. Delivering health care in Indonesia is a challenge, made more difficult by the geography and distances. Our EOCRU unit specialises in clinical trials on tropical infections, particularly Plasmodium vivax malaria. Current treatments with primaquine are effective but very toxic for patients with G6PD deficiency. Better point of care diagnostics can help us treat all patients safely.

WiTThai ตอนนี้เป็นการเดินทางไปสัมภาษณ์ ศ.ดร.นพ.อิศรางค์ นุชประยูร ที่ภาควิชากุมารเวชศาสตร์ โรงพยาบาลจุฬาลงกรณ์ ในหัวข้อเรื่องความสัมพันธ์เชิงวิวัฒนาการระหว่างโรคมาลาเรีย ธาลัสซีเมีย และภาวะพร่องเอนไซม์ G6PD นอกจากนี้อาจารย์อิศรางค์ยังถ่ายทอดข้อคิดและประสบการณ์ในการทำงานวิจัย ตลอดจนการช่วยผู้ป่วยเด็กให้มองเห็นคุณค่าของชีวิต แทนที่จะท้อแท้ไปกับความเจ็บป่วยซึ่งเลือกเกิดไม่ได้ งานวิจัยที่พูดถึงในตอนนี้ได้รับคัดเลือกเป็นหนึ่งในงานวิจัยเด่นของสกว. ประจำปี 2553 Timestamp เริ่ม-ทักทาย เกริ่นนำ WiTThai 1:01-ภาพรวม WitThai ตอน “โรคาวิวัฒน์” กับ อ.อิศรางค์ นุชประยูร 1:53-เพลง WiTThai 3:52-แนะนำตัวทีมงาน และรายการ 7:02-มาลาเรีย (Malaria) 27:47-ธาลัสซีเมีย (Thalassemia) 36:00-ความสัมพันธ์ระหว่างธาลัสซีเมีย และมาลาเรีย 48:55-ภาวะพร่องเอนไซม์ G6PD (Glucose-6-phosphate dehydrogenase deficiency) 1:12:59-ความสัมพันธ์ระหว่างภาวะพร่องเอนไซม์ G6PD และมาลาเรีย 1:18:07-ฐานข้อมูลกับการทำวิจัย / งานวิจัยที่ตีพิมพ์ลงวารสาร Science 1:21:23-การทำงานวิจัยของ อ.อิศรางค์ นุชประยูร 1:26:18-โรคมะเร็งในเด็ก 1:28:24-เก็บกวาด WiTThai 1:30:10-โรคมะเร็งในเด็ก (ต่อ) / มูลนิธิสายธารแห่งความหวัง (Wishing Well Foundation) 1:44:29-ทิ้งท้าย สรุปจบ SHOW NOTE  WiTThai ตอนนี้ ฟีเจอริ่งผลงานของอ.อิศรางค์ นุชประยูร แห่งภาควิชากุมารเวชศาสตร์ คณะแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย (รวมทั้งคณะร่วมวิจัยอีกหลายท่าน) เนื้อหาว่าด้วยความสัมพันธ์อันน่าสนใจมากกกกกกกกกกกก ระหว่างมาลาเรีย ธาลัสซีเมีย ภาวะพร่องเอนไซม์ G6PD และกระบวนการวิวัฒนาการ อันนี้ลิงค์ไปยังเปเปอร์และการเผยแพร่ทางวิชาการต่างๆ ของอาจารย์นะครับ ภาวะพร่องเอนไซม์G6PD ในเอเชียตะวันออกเฉียงใต้ Glucose-6-phosphate dehydrogenase (G6PD) mutations in Thailand: G6PD Viangchan (871G>A) is the most common deficiency variant in the Thai population. (2002) G6PD Viangchan (871G>A) is the most common G6PD-deficient variant in the Cambodian population. (2005) Glucose-6-phosphate dehydrogenase mutations in Mon and Burmese of southern Myanmar (2008) Positively Selected G6PD-Mahidol Mutation Reduces Plasmodium vivax Density in Southeast Asians (2009) ลงวารสาร Science สไลด์ประกอบการบรรยายเรื่อง Prevalence of GDPD in Southeast Asians อันนี้ลิงค์ข่าวรับรางวัลงานวิจัยเด่นของสกว.ครับ https://www.youtube.com/watch?v=QiD3OaukeBU อันนี้ลิงค์ไปเฟซบุคเพจ มูลนิธิ Wishing Well Foundation   อันนี้ลิงค์ไปแบบสอบถาม feedback รายการ WiTThai ช่วยกันทำหน่อยนะคร้าบ ^ ^

يُسلَّط الضوء في هذه الومضة على الفروق الجوهرية بين أهم ثلاثة أمراض دم وراثية منتشرة في العالم العربي، وهي: الأنيميا المنجلية (sickle cell)، والثلاسيميا (thalassemia)، وأنيميا الفول (G6PD)

أهم ما يجب أنْ تعرفه عن نقص إنزيم الـ (G6PD) أو أنيميا الفول في دقائق معدودة وبلغة مُبَسَّطة

How do you classify hemolytic anemias? What are common signs and findings in these cases? Can you explain hereditary spherocytosis, G6PD deficiency or pyruvate kinase deficiency? Join us on the Common Rounds as we talk through intra and extravascular hemolysis!

Thu, 24 Jan 2008 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/8795/ https://edoc.ub.uni-muenchen.de/8795/1/Petropoulou_Theoni.pdf Petropoulou, Theoni ddc:600, dd

Background: Safe, effective and affordable drug combinations against falciparum malaria are urgently needed for the poor populations in malaria endemic countries. Methylene blue (MB) combined with chloroquine (CQ) has been considered as one promising new regimen. Objectives: The primary objective of this study was to evaluate the safety of CQ-MB in African children with uncomplicated falciparum malaria. Secondary objectives were to assess the efficacy and the acceptance of CQ-MB in a rural population of West Africa. Methods: In this hospital-based randomized controlled trial, 226 children ( 6 - 59 months) with uncomplicated falciparum malaria were treated in Burkina Faso. The children were 4: 1 randomized to CQ-MB (n = 181; 25 mg/kg CQ and 12 mg/kg MB over three days) or CQ ( n = 45; 25 mg/kg over three days) respectively. The primary outcome was the incidence of severe haemolysis or other serious adverse events (SAEs). Efficacy outcomes were defined according to the WHO 2003 classification system. Patients were hospitalized for four days and followed up until day 14. Results: No differences in the incidence of SAEs and other adverse events were observed between children treated with CQ-MB ( including 24 cases of G6PD deficiency) compared to children treated with CQ. There was no case of severe haemolysis and also no significant difference in mean haemoglobin between study groups. Treatment failure rates were 53.7% (95% CI [37.4%; 69.3%]) in the CQ group compared to 44.0% ( 95% CI [36.3%; 51.9%]) in the CQ-MB group. Conclusion: MB is safe for the treatment of uncomplicated falciparum malaria, even in G6PD deficient African children. However, the efficacy of the CQ-MB combination has not been sufficient at the MB dose used in this study. Future studies need to assess the efficacy of MB at higher doses and in combination with appropriate partner drugs.