Podcasts about hmg coa

This video explores the significant potential of bergamot, particularly its Bergamot Polyphenolic Fraction (BPF), in managing cholesterol levels, based on a review in Nutrients. Bergamot primarily lowers cholesterol by inhibiting HMG-CoA reductase, the same enzyme targeted by statins, with compounds like brutieridin and melitidin playing a key role ; in vitro studies have shown up to a 30-40% reduction in cholesterol synthesis in liver cells. Clinical trials demonstrate notable LDL-C reductions, for example, 500 mg/day of BPF decreased LDL-C by 24.1% in 30 days , while 1000 mg/day lowered LDL-C by 40.8%. Doses up to 1300 mg/day have resulted in LDL-C reductions of 37.7% over 120 days in patients with metabolic syndrome.Regarding safety, bergamot has generally been well-tolerated in human trials lasting up to 120 days, with no significant adverse effects reported. Animal studies also indicate a good safety profile, with doses up to 150 mg/kg/day of BPF showing no liver, kidney, or blood toxicity. Even in statin-intolerant patients, 1500 mg/day of bergamot extract showed favorable results without adverse effects in one study. However, it's important to note that data on long-term safety and use at higher doses are still limited. Caution is advised for individuals on multiple medications due to the potential for drug-nutraceutical interactions, which are not yet fully understood.Disclaimers:"This information is for educational purposes only and should not be interpreted as medical advice.""The review discusses findings from preclinical studies and clinical trials. While short-term human studies (up to 120 days) suggest bergamot is generally well-tolerated , comprehensive long-term safety data, especially at higher doses, is still emerging. The effects of bergamot can vary based on the individual, the formulation, and dosage.""Always consult with a qualified healthcare professional before making any changes to your diet, supplement regimen, or treatment plan, particularly if you have a medical condition, are taking medications (especially for cholesterol or other cardiovascular issues), or are considering bergamot supplementation. Discuss potential interactions if you are on polypharmacy.""This channel does not provide medical advice."#BergamotCholesterol #NutraceuticalSafety #LipidManagement #HeartHealthSupplements #BergamotCarpenito M, Coletti F, Muscoli S, Guarino L, Di Cristo A, Cammalleri V, Mega S, Emerenziani S, Cicala M, Fanali C, et al. Unveiling the Power of Bergamot: Beyond Lipid-Lowering Effects. Nutrients. 2025; 17(11):1871. https://doi.org/10.3390/nu17111871Alchepharma,Ralph Turchiano,Bergamot cholesterol reduction,bergamot safety profile,bergamot side effects,bergamot HMG-CoA reductase,bergamot triglycerides,bergamot clinical trials cholesterol,safe cholesterol supplements,natural cholesterol lowering,bergamot long-term use,bergamot dosage for cholesterol,bergamot vascular benefits,bergamot antioxidant heart,bergamot and statins,small dense LDL reduction,dyslipidemia nutraceuticals,bergamot mechanisms of action

This AANEM podcast features Dr. Joome Suh, a neurologist and neuromuscular specialist at Brigham and Women's Hospital, interviewed by neuromuscular fellow Dr. Nadia Khalil. They discuss HMG-CoA reductase immune-mediated necrotizing myopathy (HMGCR IMNM), a rare autoimmune muscle disease often associated with statin use. The discussion covers clinical presentation, epidemiologic considerations, histopathologic findings, and treatment approaches, with special focus on Dr. Suh's recent research published in Muscle and Nerve with co-author Dr. Anthony Amato. Their study found that patients receiving maintenance IVIG as part of their regimen were more likely to have a normal CK at 6 months and the daily prednisone-equivalent was lower. A sub-group analysis suggested IVIG as monotherapy is effective.

This podcast covers the cellular uses of cholesterol and a brief summary of its biosyntthesis and its regulation by intracellular levels of cholesterol. Check out the podcast on regulation of HMG CoA reductase below: https://youtu.be/FNSr3G6OTBs?si=da3V5SkXGkM8STsZ Also check out how statins reduce plasma cholesterol below: https://youtu.be/HrwI02Ww3Ew Also check out the he complete podcast on Regulation of Cholesterol Biosynthesis below: https://youtu.be/K1i3P3KPN3g

Welcome to my podcast. I am Doctor Warrick Bishop, and I want to help you to live as well as possible for as long as possible. I'm a practising cardiologist, best-selling author, keynote speaker, and the creator of The Healthy Heart Network. I have over 20 years as a specialist cardiologist and a private practice of over 10,000 patients. In this podcast, Warrick Bishop discusses the biochemical processes involved in statin therapy, particularly how it affects cholesterol production. He explains the conversion pathway from acetyl CoA to HMG CoA, mevalonic acid, and ultimately cholesterol. The conversation highlights the role of coenzyme Q10 (ubiquinone), which is essential for energy formation in cells and may be linked to muscle-related side effects from statins. A recent study from 2022 investigated the relationship between coenzyme Q10 levels and statin-related muscle symptoms but found no significant correlation or benefit from supplementation. Despite this, Bishop suggests that individual patients might still benefit from trying coenzyme Q10. He also introduces benberdomic acid, a new agent that works upstream of the statin pathway and may provide an alternative for those experiencing muscle aches due to statin use. The podcast encourages listeners to consider their experiences with these treatments and to reach out with feedback or suggestions for future topics. Bishop concludes with a positive message about living well.

Link to Buck's Results: https://drive.google.com/file/d/19BJaZNYwBxlPx4nR9695Q2NC3nNpgW6y/view?usp=sharing  https://drive.google.com/file/d/1br1ikAJKmgKev9X3jkS7nUPdXpAqMzYd/view?usp=sharing Section 1: Overview of Cholesterol Metabolism Cholesterol in the Body: Cholesterol is essential for cell membrane integrity, hormone synthesis, and bile acid production. It is produced endogenously in the liver and absorbed exogenously from dietary sources. Endogenous Production: Cholesterol is synthesized in the liver through the mevalonate pathway. Key intermediates: Lathosterol and Desmosterol, indicators of cholesterol production rate. Exogenous Absorption: Dietary cholesterol is absorbed in the intestines along with plant sterols like Beta-sitosterol and Campesterol. These sterols compete with cholesterol for absorption, reflecting dietary cholesterol absorption levels. Section 2: Detailed Analysis of the Test Components Production Markers: Lathosterol: Precursor in the cholesterol biosynthesis pathway. Elevated levels indicate increased hepatic cholesterol synthesis (overproduction). Example: Lathosterol level of 329 µmol x 100/mmol in my study indicates hyperactive cholesterol production. Desmosterol: Another precursor in the synthesis pathway, contributing to total cholesterol production. High levels reinforce the diagnosis of increased cholesterol production. Example: Desmosterol level of 74 µmol x 100/mmol in my study supports elevated production. Absorption Markers: Beta-sitosterol: Plant sterol absorbed in the intestines, competes with cholesterol. High levels suggest increased absorption of dietary cholesterol. Example: Beta-sitosterol level of 120 µmol x 100/mmol indicates borderline absorption. Campesterol: Similar to Beta-sitosterol, reflects cholesterol absorption efficiency. Elevated levels indicate increased absorption. Example: Campesterol level of 113 µmol x 100/mmol within normal limits but suggests absorption could be a factor. Cholesterol Balance Score: Ratio of production to absorption markers. A higher score indicates predominant cholesterol production; a lower score indicates absorption as the main issue. Example: Score of 2.4 suggests overproduction is the dominant issue. Section 3: Clinical Implications and Treatment Strategies (10 minutes) Frequency of Overproduction vs. Overabsorption: Common to see patients with either overproduction or overabsorption, but less commonly both. Overproducers: Significant portion of hypercholesterolemia patients, especially those with genetic conditions like Familial Hypercholesterolemia. Overabsorbers: Often have high-cholesterol diets or genetic predispositions. Treatment Implications: Overproducers: Statins are first-line treatment; they inhibit HMG-CoA reductase in cholesterol synthesis. Overabsorbers: Ezetimibe, which inhibits intestinal cholesterol absorption, can be effective. Combination Therapy: Considered for mixed dyslipidemia cases. Case Examples: Example of a patient with high production markers but borderline absorption: Statin therapy may be appropriate, with potential addition of Ezetimibe. Example of a patient who is a high absorber but not a high producer: Dietary changes and Ezetimibe might suffice without statins. Section 4: Physiological Mechanisms and Genetic Considerations Pathophysiology of Cholesterol Production: Overproduction may result from genetic mutations (LDL receptor or PCSK9) or conditions like insulin resistance. Pathophysiology of Cholesterol Absorption: Increased absorption could be due to genetic polymorphisms (NPC1L1 gene), leading to higher dietary cholesterol absorption. Section 5: Practical Application in Clinical Practice Incorporating the Test into Clinical Workflow: Integrate the Boston Heart Cholesterol Balance Test for patients with unexplained hypercholesterolemia or non-responders to standard therapy. Tailor treatment based on whether a patient is an overproducer, an overabsorber, or both. Patient Communication: Explain test results in an understandable way, emphasizing personalized treatment plans.

On this episode, we continue with the Top 200 Drugs podcast. We cover the basics of the following drugs: tizanidine, risperidone, ramipril, pravastatin, and terazosin. Tizanidine is a skeletal muscle relaxant that has drug interactions via CYP2D6 Risperidone is a 2nd generation antipsychotic. Be on the lookout for EPS, hyperprolactinemia, sedation, and metabolic syndrome. Ramipril is an antihypertensive agent that is an ACE Inhibitor. Cough and hyperkalemia are two important adverse effects. Pravastatin is an HMG-CoA reductase inhibitor that lowers LDL levels. It isn't as potent as other statins and I discuss this on the podcast episode. Terazosin is a non-selective alpha-blocker that may be used for BPH and hypertension.

This week, Paul shares his most recent set of bloodwork in totality. He shares what he decides to order and why, and what bloodwork you may consider getting yourself. He also unpacks the importance of cortisol to DHEA sulphate radio and his cholesterol results. 00:00:00 Podcast begins 00:01:40 Traditional bloodwork  00:05:40 MTHFR polymorphism: Does Paul take supplements? 00:10:10 Glucose & creatine 00:14:10 Electrolytes & insulin 00:23:10 Thyroid panel 00:26:18 Cortisol to DHEA sulphate ratio 00:32:20 Cholesterol panel 00:46:10 Hormones & Other results 00:50:20 Iron panel 00:52:40 What bloodwork should you get? References: July 2022 Bloodwork: https://www.youtube.com/watch?v=NuD9lWHMup8&t=669s August 2022 Bloodwork: https://www.youtube.com/watch?v=1br0cDkYv3Y December 2022 Bloodwork: https://www.youtube.com/watch?v=LQE3mrwaE8c March 2023 Bloodwork: https://www.youtube.com/watch?v=vonHW14TTdg DEXA scan reveals “side effects” of red meat: https://www.youtube.com/shorts/ZgRoz60ugnc Cortisol, DHEA sulphate, their ratio, and all-cause and cause-specific mortality in the Vietnam Experience Study: https://pubmed.ncbi.nlm.nih.gov/20498139/ Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies: https://pubmed.ncbi.nlm.nih.gov/7270479/ Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart disease: the Kitava study: https://pubmed.ncbi.nlm.nih.gov/8077891/ The effect of HMG-CoA reductase inhibitors on cognition in patients with Alzheimer's dementia: a prospective withdrawal and rechallenge pilot study: https://pubmed.ncbi.nlm.nih.gov/22921881/ Lipid profile of term infants on exclusive breastfeeding and mixed feeding: a comparative study: https://pubmed.ncbi.nlm.nih.gov/17327867/ Total cholesterol and all-cause mortality by sex and age: a prospective cohort study among 12.8 million adults: https://www.nature.com/articles/s41598-018-38461-y Low-Density Lipoprotein Cholesterol Is Predominantly Associated With Atherosclerotic Cardiovascular Disease Events in Patients With Evidence of Coronary Atherosclerosis: The Western Denmark Heart Registry: https://pubmed.ncbi.nlm.nih.gov/36621817/ Get your bloodwork from ultalabs.com

In this episode, we review the pharmacology, indications, adverse effects, monitoring, and unique drug characteristics of HMG CoA reductase inhibitors (“statins”). Key Concepts Statins reduce LDL cholesterol by 20-60% (depending on the dose and statin potency). They have modest favorable effects on HDL and triglycerides. Clinically, statins reduce the risk of major adverse cardiac events by about 30% depending on the statin potency. There are four main groups of patients who are indicated for a statin: LDL >= 190 mg/dL, diabetes with age 40-75 years with LDL 70-189 mg/dL, those with an elevated 10-year ASCVD risk of > 7.5% (or possibly > 5%), and those who have had an ASCVD event (“secondary prevention”). Atorvastatin, lovastatin, and simvastatin heavily rely on CYP 3A4 metabolism and tend to be most susceptible to drug interactions compared to the other statins. When a statin is started, baseline lipid panel and liver function tests should be obtained. After 4-12 weeks, a lipid panel should be repeated. Liver function and creatine kinase testing should only be done if a patient has a symptom (e.g. jaundice, right upper quadrant pain, muscle pain or weakness, dark urine, etc.) References Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;139(25):e1082-e1143. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000625

Links mentioned in the episode:www.betterwithcarbo.com/guideEp 14: Is Your Morning Brew the Secret Weapon Against Inflammation?Introduction: Hello and welcome to another episode of Inflamed in the Brain. I'm Krissy, your host, and friendly neighborhood Dietitian. Ever found yourself in a dinner dilemma? Well, I sure did the other day, and it led me to a breakfast-for-dinner solution. Today, I want to dive into a topic that's been a personal favorite of mine to debunk – the whole egg and cholesterol myth.Setting the Scene: Eggs, my go-to protein source, have often been the center of controversy. From fears about fat content to concerns about cholesterol, eggs have faced it all. Today, let's unravel the intricacies surrounding cholesterol, a topic closely tied to the egg debate.The Cholesterol Conundrum: Cholesterol has long been portrayed as the villain linked to heart disease. The American Heart Association advocated for a low-fat diet to curb cholesterol, yet high cholesterol remains prevalent. Approximately 86 million US adults had high cholesterol in 2020, prompting the need for a new approach.The Importance of Cholesterol: Contrary to its bad reputation, cholesterol is essential for health. It plays a vital role in hormone production, bile synthesis for fat digestion, and forms the basic structure of cell membranes. Think of it as the necessary foundation for your body's cells.Cholesterol Production and Transportation: Understanding how cholesterol is made and transported is crucial. Cholesterol is produced through the breakdown of fats or glucose, generating Acetyl CoA, a key player in the cholesterol-making process. LDL and HDL, often labeled as bad and good cholesterol, are lipoproteins carrying cholesterol through the bloodstream.LDL's Role and Concerns: LDL, responsible for transporting cholesterol, can become problematic in an inflammatory state. Frequent damage to blood vessel linings triggers LDL's healing response, leading to potential issues. Smoking, toxins, stress, and poor diets exacerbate LDL-related concerns. Research indicates that LDL particle size matters; small, dense particles pose more significant risks than larger, fluffier ones.Fructose and LDL Particle Size: Recent studies suggest that fructose may influence LDL particle size, making them smaller. However, it's crucial to differentiate naturally occurring fructose in foods like honey, mangoes, and grapes from the concentrated fructose in processed foods, notably high-fructose corn syrup.The Egg Solution: Dispelling myths, there's no reason to avoid whole eggs. In fact, whole eggs can decrease small LDL particles and increase protective HDL particles. Packed with nutrients like vitamin D, E, choline, and folate, eggs contribute to a balanced diet and support overall health.Blood Sugar Management: Managing blood sugar is key, especially for those concerned about cholesterol. Statins, prescribed for high cholesterol, target the HMG-CoA reductase enzyme. Insulin, influenced by a high-glycemic diet, can spike blood sugar, contributing to increased cholesterol production.Conclusion and Takeaways: In conclusion, eggs are not the enemy. They're a versatile, nutrient-packed option that, when enjoyed in balance, can be part of a heart-healthy diet. Remember, the quality of eggs matters, so opt for pasture-raised options with deep orange yolks. If cholesterol concerns you, focus on blood sugar management, and I'm here to guide you.Remember, fat, cholesterol, and eggs aren't the adversaries; itFollow along: https://betterwithcarbo.com/ Instagram

Suivez Romain dans son aventure internet pour en apprendre plus sur le cholestérol et les statines ! Un sujet dont on parle tous les jours ! Dans mise en scène aussi claire que drôle, Romain vous parle de la synthèse du cholestérol, de son utilité, du mécanisme d'action des statines et de l'histoire de leurs découvertes. Un épisode très complet qui vous apprendra certainement quelque chose. Temps d'écoute 13 min ! Bonne écoute !    

Dr. Mark Sherwood is a Naturopathic Doctor (ND) who operates a full-time wellness-based medical practice in Tulsa, OK called The Functional Medical Institute. Dr. Mark treated 10,000+ patients with Covid with zero deaths! Dr. Mark has completed training and certifications in age management, nutrigenetics, nutrigenomics, peptide therapy, hormone therapy, stress management, GI health, and immunology. All products, books, and supplements mentioned are available at https://www.ashleydeeley.com/mark⁠ 17:36: The size of your heart AND the size of your stomach (it may surprise you) 18:25: How many calories do you need? (And why calorie counting is a waste of time) 22:53: What ingredients or food to avoid 24:08: Cholesterol is good 24:35: What is LDL? 25:08: Worst thing to happen to American health 25:52: Statins Statin drugs knock off HMG-COA (study here), 3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase Inhibitors Hydroxymethylglutaryl-CoA (HMG-CoA) (pubmed) 26:30: When you lose hormones, you lose bone density, muscle, immune system resilience, and body fat goes up! 26:42: LDL is NOT bad 27:12: Cholesterol panel (do not focus on AMOUNT) is worthless 27:56: Cholesterol markers to look at: Oxidized LDL Lp-PLA2 (pressurization of vessel wall) Asymmetric Dimethylarginine (ADMA) (vascular stiffness) Lipoprotein Fractionation 34:52: Medicines don't provide healing; they're designed to manage the disease process 35:04: God did not make us vaccine or medication deficient 36:39: Dr. Mark treated 10,000+ patients with Covid with zero deaths 37:54: Ideas and suppplements for Covid included: Colostrum (link here) Broccoli Sprout Powder (link here) Vitamins A,D,E,K, and C (link here) Omega fatty acids Glutathione (precursor to glutathione is NAC, which I recommended over glutathione as your stomach acid will likely destroy liposomal glutathione. Best to have glutathione administered through IV) 45:25: Diagnosed with an illness or disease...? (Type II Diabetic) Once that diagnostic code is in your chart, it will stay in your health records and follow you forever. It can effect your health insurance and life insurance here and evermore 46:20: Thyroid conditions (Hashimoto's) 47:04: You CAN reverse thyroid disfunction (can take up to six months). Other autoimmune disorders can also be reversed 48:20: Thyroid medications are synthetic. Synthroid and Levothyroxine (T4 only medications) 49:30: Need a full thyroid panel to determine how thyroid is truly functioning: Free T4 Free T3 TPO antibodies (peroxidase) Reverse T3 TSH 51:06: Armour Thyroid and NP Thyroid medications are desiccated thyroid medications and therefore superior to synethic medications 52:17: Iodine (link here) 52:26: Mark recommends: 7.5 milligrams of potassium iodide 5 milligrams of iodine Totaling 12.5 milligrams (good combo for thyroid support) 52:42: Iodine is breast and prostate protective 53:05: Desiccated thyroid as a tool for longevity? 53:27: Inflammation is part of every disease process 54:16: Grass-fed, grass-finished liver (dense with micronutrients) 55:48: Supps: Vitamin D (anything test result less than 50 is not ideal) (link here); 1,000-2,000 IUD daily + MUST BE PAIRED WITH K2 Omega 3 fatty acids 1:02:56: Dr. Nathan Bryan and Nitric Oxide (NO2U) 1:06:10: Osteopenia (and reversing osteoperosis) 1:08:08: Magnesium 1:17:06: Perimenopause (1:28:13: sleep better) 1:20:31: Water supply full of birth control pills & statins (water filter) 1:21:16: Whole house water filter General Ionics (only available in Oklahoma) 1:22:33: Mold free, organic coffee 1:23:30: Theory around 'cheating' 1:25:33: My friend April and her chiropractic husband (Colorado) 1:26:55: Blue blockers, salt lamp 1:33:37: Sleep better Webinar on health & hormones: register here Where to find Dr. Mark: Website Instagram Facebook Twitter YouTube Phone: 918-748-3640 Address: 6048 S Sheridan Rd Tulsa, OK 74145 BONUS MATERIAL visit: https://www.ashleydeeley.com/mark

Oversiktsepisode. Myositt del 2a: immunmediert nekrotiserende myopati. Gjest: Marte Sæverås, lungelege og seksjonsoverlege ved Diagnostisk senter, Stavanger universitetssjukehus.Autoantistoff omtalt i episoden: anti-SRP, anti-HMG CoA reduktase (anti-HMGCR)Abstract om internasjonale anbefalinger for malignitetsscreening ved idiopatisk inflammatorisk myopati.(Første sesong av podcasten er finansiert av Norsk revmatologisk forening) Hosted on Acast. See acast.com/privacy for more information.

Oversiktsepisode. Idiopatisk inflammatorisk myopati (IIM, også kalt "myositt") del 1: Jens snakker generelt om IIM. Gjest: Marte Sæverås, lungelege og seksjonsoverlege ved Diagnostisk senter, Stavanger universitetssjukehus.Dette er en trilogi om IIM: I denne episoden presenteres undergrupper (som polymyositt (PM), dermatomyositt (DM), antisyntetasesyndrom (ASS) og immunmediert nekrotiserende myopati (IMNM)), samt overordnet informasjon om manifestasjoner og utredning (herunder myosittspesifikke autoantistoffer (MSA)). I neste episode går vi mer i detalj av de ulike undertypene. I siste episode (ekspertepisode) snakker vi om tips og triks om utredning og behandling av IIMBegreper som nevnes i episoden: (1) Utslett ved DM: heliotropt utslett, Gottronske papler, Gottrons tegn, V-tegn, sjaltegn, hylstertegn; (2) Hudforandring ved ASS: mekanikerhender; (3) MSA forbundet med DM: anti-Mi2, anti-SAE, anti-NXP2, anti-TIF1, anti-MDA5; (4) MSA forbundet med ASS: "antisyntetaseantistoffer" (anti-Jo1, anti-PL7, anti-PL12, og noen flere (OJ, EJ, KS, Zo, YRS)); (5) MSA forbundet med IMNM: anti-HMG CoA reduktase, anti-SRP.Første sesong av podcasten er finansiert gjennom et stipend av Norsk revmatologisk forening. Hosted on Acast. See acast.com/privacy for more information.

El colesterol es una molécula fundamental para la vida es el precursor del cortisol, de la vitamina D, de las sales biliares, de hormonas y encima forma parte de las membranas celulares, es una molécula grasa y como tal no se disuelve en un medio acuoso como es la sangre, la fórmula que utiliza para circular es unirse a proteínas formando las llamadas lipoproteínas, las más conocidas son las LDL y las HDL.La importancia del colesterol como parámetro depende además del estado de salud de cada uno, no es lo mismo para una persona sana que para un diabético o una persona con problemas hepáticos o de tiroides, o un fumador cuyo riesgo cardiovascular ya es elevado.Mucho se ha hablado y escrito sobre el colesterol en estos tiempos, que si no es tan importante , que si no está tan relacionado con el riesgo cardiovascular, que si solo el colesterol oxidado supone un verdadero riesgo… Lo importante es que si nuestra dieta es buena y llevamos una vida sana y no tenemos patología alguna el colesterol debe estar en niveles normales.La tendencia hasta ahora era utilizar un tipo de medicamentos llamados estatinas, que fácil es tomarse una pastillita que nos baje el colesterol y ya está y no tener que prescindir de esos quesos tan divinos que tenemos, ni de embutidos deliciosos; sin embargo , lo que hay que hacer en realidad es una buena dieta libre de grasas animales, embutidos, quesos, mantequilla, bollería y pastelería industrial , fritos etc… y ejercicio; vamos, lo que va a requerir mayor esfuerzo por nuestra parte, pero mejores recompensas.Debemos tener en cuenta que una parte del colesterol que circula por nuestras venas es de la dieta pero otra parte es de fabricación propia, aunque eso no es excusa para no probar inicialmente con la dieta a ver si conseguimos controlarlo.. Las estatinas deben tomarse siempre por la noche puesto que son más eficaces , no deben mezclarse nunca con algunos antifúngicos ni con zumo de pomelo(zumo de pomelo y medicamentos: lo que hay que saber)y curiosamente el salvado de avena disminuye su efectividad.Por suerte, aún nos quedan recursos, el médico probablemente nos prescriba las famosas estatinas ,un grupo de medicamentos que incluye simvastatina, atorvastatina, lovastatina, rosuvastatina… Son medicamentos ampliamente utilizados y relativamente seguros para la mayoría de las personas. Actualmente la más recetada es la simvastatina a pesar de su poder hipolipemiante ligeramente inferior tiene una mejor relación coste-eficacia.Estos medicamentos lo que hacen es inhibir la síntesis de colesterol que se lleva a cabo dentro del hígado , inhibiendo un enzima llamado acetilCoa reductasa, por esta misma vía fabricamos también el famoso Coenzima Q que realiza un papel fundamental en la prevención de producción de radicales libres, existen pacientes con unas características genéticas determinadas que hacen que cuando toman simvastatina ésta no penetre en el hígado , se queda en sangre y va hacia el músculo provocando dolores musculares; si a la vez se toman inhibidores del metabolismo como fluconazol, fibratos o zumo de pomelo, entre otros, el problema se agrava, y si tomamos ibuprofeno por nuestros dolores musculares causados por la simvastatina , en realidad lo que estamos es empeorando el cuadro porque el ibuprofeno es inhibidor de la entrada de las estatinas en el hígado, es decir entre que la misma estatina inhibe no solo la síntesis de colesterol sino también de coenzima Q y a consecuencia baja la producción de ATP y de energía necesaria para los músculos, y tomamos el ibuprofeno acabamos generando un cuadro importante de miopatía y dolores intensos musculares que pueden llegar a confundirse incluso con la fibromialgia.En resumen las estatinas últimamente están algo cuestionadas por varias razones:- Algunas pueden general dolores musculares.- Provocan un déficit de coenzima Q que debe compensarse con suplementos de calidad en dosis adecuadas.- Las estatinas no se recomiendan para mujeres embarazadas.- No deben utilizarse en personas que sufren enfermedades hepáticas. Y entonces ¿Qué hacemos? Si con la dieta no baja , no podemos tomar estatinas ¿Qué nos queda?Los productos naturales…Pero mucho cuidado! abundan los engaños, los suplementos deben ser de calidad contrastada. ¿QUE CONTIENEN ESTOS SUPLEMENTOS?LEVADURA ROJASe utiliza desde hace muchos años, es eficaz en los casos de hipercolesterolemia leve gracias a los múltiples componentes que presenta y concretamente a la Monacolina K, una sustancia responsable del bloqueo de la síntesis del colesterol en el hígado. Un estudio efectuado en 324 sujetos dislipidémicos puso en evidencia, después de 8 semanas, una disminución del 23% del colesterol total, del 31% de las LDL y del 34% de los triglicéridos, mientras los niveles de HDL evidenciaban un aumento del 20%.Sin embargo, los suplementos con levadura roja de arroz son muy susceptibles de falsificación puesto que se elabora fermentando la levadura Monascus purpureus del arroz a una temperatura controlada cuidadosamente y en condiciones de crecimiento muy controladas, es muy importante que este proceso se produzca correctamente pues sino se crean subproductos que pueden dañar el hígado, lo que más preocupa es la calidad del suplemento por mala elaboración y también se han encontrado suplementos de levadura roja de arroz que llevaban estatinas añadidas, por desgracia el control sanitario de este tipo de productos es insuficiente en muchas ocasiones. Hay muchos estudios por hacer pero si es de calidad y el fabricante de confianza y con los registros adecuados es más difícil que nos equivoquemos. La fermentación lenta y en condiciones controladas encarece el producto por eso hay tal variabilidad de precio en este tipo de suplementos.COENZIMA Q10Llamado también ubiquinone, es estructuralmente similar a la Vitamina K y a la Vitamina E., tiene actividad antioxidante y está implicado en la síntesis de elastina y colágeno , en un correcto funcionamiento muscular, sobre todo cuando se toman estatinas, que reducen sus niveles y, en algunos casos, provocan dolores musculares, ya que su vía de síntesis es la misma en la que actúan las estatinas. El 22% de los españoles consumen este tipo de medicamentos, estas personas son las primeras que deberían suplementarse con coenzima Q, podríamos tomarlo con la alimentación pero por desgracia ,las mayores cantidades se encuentran en alimentos que no solemos comer , como las vísceras, para conseguir cantidades necesarias de Q10 tendríamos que tomar medio kilo de sardinas ,por ejemplo.las dietas vegetarianas casi todas son deficitarias en q10. OMEGA 3En realidad, los omega3 sirven para prevenir el riesgo cardiovascular; sin embargo, no está comprobado que bajen el colesterol, POLICOSANOLESLos Policosanoles son sustancias naturales aisladas y purificadas por sustancias cerosas de la caña de azúcar (Saccharum officinarum L.). Poseen propiedades hipocolesterolemiantes, aumentan los niveles hemáticos de colesterol HDL y reducen al mismo tiempo los niveles hemáticos de colesterol total y LDL, gracias a la reducción del enzima HMG-CoA reductasa, fundamental para la síntesis del LDL.BERBERINAExiste cierta evidencia de que la berberina puede ayudar a disminuir los niveles de colesterol en personas con colesterol alto. La ingesta de 500 mg de berberina 1 o dos veces por día durante 3 meses parece reducir el colesterol de lipoproteína de baja densidad (LDL o malo) y los niveles de triglicéridos en personas con colesterol alto. La Berberina es una sustancia natural extraída de la corteza de Berberis aristata, un arbusto originario del Himalaya y del Nepal que posee una acción favorecedora del control de los triglicéridos plasmáticos y ayuda a mantener los niveles de colesterol plasmático.ASTAXANTINALa Astaxantina es un carotenoide cuya fuente vegetal más importante es un alga unicelular de agua dulce que produce de forma autónoma astaxantina cuando las condiciones ambientales inducen un estrés oxidativo. La Astaxantina es el antioxidante más potente que se conoce. Su poder antioxidante está considerado 500 veces superior al de la Vitamina E. También es de gran utilidad en problemas oculares como la degeneración macular. Tiene capacidad para captar los radicales libres de todos los tipos lo cual es un ventaja desde para problemas cardiovasculares como para problemas de piel.ÁCIDO FÓLICOEl Ácido Fólico es una vitamina hidrosoluble del grupo B. Es necesaria para las reacciones de síntesis, de reparación y de metilación del ADN. Es fundamental para el control de los valores de la homocisteína, un aminoácido derivado de la metionina que, si es excesiva, lleva a un aumento del riesgo cardiovascular. Hay muchos más aunque éstos son los más importantes y efectivos. En definitiva existen muchos productos naturales que nos pueden ayudar a bajar nuestro colesterol cuando sus niveles son elevados y es suficiente con bajar entre 15-25% , algunos contienen todos estos componentes citados que actúan de manera sinérgica, en otras ocasiones los medicamentos son necesarios y por supuesto debemos tomarlos tal como nos los prescribe el médico aunque se complementen con otros productos que pueden minimizar sus problemas.

Episode 112: Statins in Primary CareDr. Tiwana explains the use of statins for the primary prevention of cardiovascular disease.Written by Ripandeep Tiwana, MD (Post-Doctoral Research Fellow at Cedar Sinai Medical Center – Heart Institute). Edition of text and comments by Hector Arreaza, MD.____________________________________________You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Definition.Statins commonly referred to as lipid-lowering medications, are important in primary care as they serve multiple long-term benefits than just lipid lowering alone. They are HMG-CoA reductase inhibitors. As a refresher, this is the rate-controlling enzyme of the metabolic pathway that produces cholesterol. This enzyme is more active at night, so statins are recommended to be taken at bedtime instead of during the day. Statins are most effective at lowering LDL cholesterol. However, they also help lower triglycerides and raise HDL cholesterol.Statins are not limited to just patients with hyperlipidemia. They reduce illness and mortality in those who have diabetes, have a history of cardiovascular disease (including heart attack, stroke, peripheral arterial disease), or are simply at high risk for cardiovascular disease. Statins are used for primary and secondary prevention.Types of statins.How do we determine which statin our patients need?First, we need to know that not all statins are created equal. They vary by intensity and potency thus, and they are categorized as either low, moderate, or high intensity.Several statins are available for use in the United States. They include Atorvastatin (Lipitor), Fluvastatin (Lescol XL), Lovastatin (Altoprev), Pitavastatin (Livalo, Zypitamag), Pravastatin (Pravachol), Rosuvastatin (Crestor, Ezallor), Simvastatin (Zocor)Commonly used in clinics: Simvastatin, Atorvastatin, and Rosuvastatin.Statin Dosing and ACC/AHA Classification of Intensity                                  Low-intensity                                   Moderate-intensity                                     High-intensityAtorvastatin              NA 1                                                          10 to 20 mg                                                   40 to 80 mgFluvastatin                20 to 40 mg                                          40 mg 2×/day; XL 80 mg                                NALovastatin                 20 mg                                                       40 mg                                                                         NAPitavastatin               1 mg                                                          2 to 4 mg                                                                   NARosuvastatin             NA                                                            5 to 10 mg                                                          20 to 40 mgSimvastatin                10 mg                                                      20 to 40 mg                                                             NAOf note, atorvastatin and rosuvastatin are only for moderate or high-intensity use, and do not use simvastatin 80 mg.Identifying patients at risk.How do we determine who needs statin therapy?Once we become familiar with the different statins, we must figure out which intensity is advised for our patient. Recommendations for statin therapy are based on guidelines from The U.S. Preventive Services Task Force (USPSTF), American Diabetes Association (ADA), and the American College of Cardiology/American Heart Association (ACC/AHA) which recommend utilizing the ASCVD risk calculator in those patients who do not already have established cardiovascular disease.ASCVD stands for atherosclerotic cardiovascular disease, defined as coronary heart disease, cerebrovascular disease, or peripheral arterial disease presumed to be of atherosclerotic origin. ASCVD remains a leading cause of morbidity and mortality in the United States, especially in individuals with diabetes.The ASCVD risk score determines a patient's 10-year risk of cardiovascular complications, such as a myocardial infarction or stroke. This risk estimate considers age, sex, race, cholesterol levels, use of blood pressure medication, diabetic status, and smoking status. Regarding age, this calculator only applies to the age range of 40-79 as there is insufficient data to predict risk outside this age group.There are several online and mobile applications available to calculate this score. Once calculated it gives a recommendation for which intensity statin to use. However, as this is a recommendation, it is essential to use your own clinical judgment to decide what is best for your individual patient. Please refer to the above table as a reference for which statin and dose you may consider using.Keeping the above calculator in mind, additional statin guidelines are recommended by the ACC:Patients ages 20-75 years and LDL-C ≥190 mg/dl use high-intensity statin without risk assessment. (You do not need the calculator.)People with type 2 diabetes and aged 40-75 years use moderate-intensity statins, and risk estimate to consider high-intensity statins. (It means moderate for all diabetics older than 40, high for some.)Age >75 years, clinical assessment, and risk discussion. Age 40-75 years and LDL-C ≥70 mg/dl and 10%. Grade B recommendation: prescribe a statin for the primary prevention of CVD.Grade C – 40-75 years with >= 1 cardiovascular risk factor AND estimated 10-year ASCVD risk 7.5-10%. Grade C recommendation: selectively offer a statin for the primary prevention of CVD. The likelihood of benefit is smaller in this group than in persons with a 10-year risk of 10% or greater.Grade I - The USPSTF found insufficient evidence to recommend for or against initiating a statin for the primary prevention of CVD events and mortality in adults 76 years or older.The USPSTF is also very clear regarding the intensity of statin therapy. They explained that there is limited data directly comparing the effects of different statin intensities on health outcomes. Most of the trials they reviewed used moderate-intensity statin therapy. They conclude that moderate-intensity statin therapy seems reasonable for most persons' primary prevention of CVD.The USPSTF has a broader recommendation, whereas the ACC guidelines are more detailed and individualized and provide guidance on the recommended intensity of statin therapy.Labs needed.Establish baseline labs for serum creatinine, LFTs, and CK only if there is a myopathy risk. Routine monitoring of LFTs, serum creatinine, and CK is unnecessary; only check if clinically indicated.A lipid panel should be checked in 6-8 weeks, and the patient should monitor themselves for any side effects, including myalgias. If LDL-C reduction is adequate (≥30% reduction with intermediate statins and 50% with high-intensity statins), regular interval monitoring of risk factors and compliance with statin therapy is necessary to sustain long-term benefit.Side effects and contraindications.Some common side effects include URI-like symptoms, headache, UTI, and diarrhea. Some patients are very hesitant to take any medications. Warning about side effects may decrease compliance. Major  contraindications for statin therapy include active liver disease, muscle disorders, pregnancy, and breastfeeding.Special considerations.Chronic kidney disease: The preferred statins for CKD with severe renal impairment are atorvastatin and fluvastatin because they do not require dose adjustment. Pravastatin would be a second choice.Chronic liver disease: Statins are contraindicated in patients with decompensated cirrhosis or acute liver failure. Abstinence from alcohol is critical in patients with chronic liver disease who are taking statins. Pravastatin and rosuvastatin are the preferred agents. Check lipid levels to determine if LDL-C reduction is accomplished with no changes in aminotransferases. You may consider stopping, increasing dose, or changing statin as you discuss the risks vs. benefits with your patient.Conclusion: Simply put, if a patient has an LDL of greater than 190, is a diabetic, has an established history of cardiovascular disease, or is at risk for it, then the patient should ideally be taking a statin unless there is a contraindication, allergy, or other special circumstance that limits him/her from doing so. If you have patients that apply to any of the above scenarios and are not already on a statin, determine their risk, and consider starting them on a statin “stat” to reduce morbidity and mortality. On the other hand, be mindful of overprescribing. Do not prescribe statins to patients who do not meet the above criteria.________________________________________Now we conclude our episode number 113, “Statins in Primary Care.” Statins are powerful medications for the prevention of cardiovascular disease. Do not forget to recommend non-pharmacologic measures such as healthy eating and physical activity, but let's also consider adding a statin to patients who are at moderate to high risk for cardiovascular disease.This week we thank Hector Arreaza and Ripandeep Tiwana. Audio by Adrianne Silva.Even without trying, every night, you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you; send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week!______________________________________References:1. Statins, U.S. Food & Drug Administration, 2014, December 16, fda.gov, https://www.fda.gov/drugs/information-drug-class/statins, accessed September 14, 2022.2. Chou R, Cantor A, Dana T, et al. Statin Use for the Primary Prevention of Cardiovascular Disease in Adults: A Systematic Review for the U.S. Preventive Services Task Force [Internet]. Rockville (MD): Agency for Healthcare Research and Quality (US); 2022 Aug. (Evidence Synthesis, No. 219.) Available from: https://www.ncbi.nlm.nih.gov/books/NBK583661/3. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol 2019; March 17. https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2019/03/07/16/00/2019-acc-aha-guideline-on-primary-prevention-gl-prevention. 4. ASCVD Risk Estimator Plus, published by the American College of Cardiology, https://tools.acc.org/ascvd-risk-estimator-plus/#!/calculate/estimate/, accessed September 14, 2022.5. Statin Use for the Primary Prevention of Cardiovascular Disease in Adults: Preventive Medication, U.S. Preventive Services Task Force, Final Recommendation Statement, 2022, August 23. https://uspreventiveservicestaskforce.org/uspstf/recommendation/statin-use-in-adults-preventive-medication6.  Videvo. “Distinction.” Https://Www.videvo.net/Royalty-Free-Music-Track/Distinction/227882/, Https://Www.videvo.net/, https://www.videvo.net/royalty-free-music-track/distinction/227882/. Accessed 26 Sept. 2022.

HOUR 2 Magnesium- A Key Mineral for Cardiovascular Health– Carolyn Dean MD ND  Heart disease has become a dreaded condition because most people know it means a handful of medications and the certain knowledge that things are only going to get worse. But what if heart disease has a strong element of magnesium deficiency? What if you have magnesium deficiency and not heart disease? Magnesium deficiency is very common in people with a compromised cardiovascular system. In hospitals magnesium is administered for acute myocardial infarction and cardiac arrhythmia. Like any other muscle, the heart requires magnesium. Magnesium is also used to treat angina, or chest pain.  In your local clinic or practitioner's office, their response to magnesium deficiency may be a little different. Magnesium's role in preventing heart disease and strokes is accepted for acute conditions, with the use of IV magnesium,  yet many cardiologists do not recognize and respond to magnesium deficiency conditions in their primary care protocols.  After all, your doctor probably thinks magnesium pill is a laxative and certainly won't do an ionized magnesium blood test to find out how much magnesium is in your cells working away at 1,000 enzyme processes and involved with 80% of known metabolic functions many of which contribute to cardiovascular health.  An average of 1,671 American's die suddenly and unexpectedly of a heart attack every day. This is a pandemic! Millions of people are unaware they are walking on a very thin edge of the same health conditions as those who have transitioned- with high cholesterol, high blood pressure, and on several medications to avoid having a heart attack. Yet the treatments for high blood pressure, high cholesterol, and high blood sugar all deplete magnesium and cause worsening of these life-threatening cardiovascular conditions.  Magnesium acts by the same mechanisms as statin drugs to lower cholesterol.   Every metabolic activity in the body depends on enzymes. Making cholesterol, for example, requires a specific enzyme called HMG-CoA reductase. Magnesium slows down this enzymatic reaction when you have enough cholesterol.  HMG-CoA reductase is the same enzyme that statin drugs block. The mechanisms are nearly the same; however, magnesium is the natural way that the body has evolved to balance cholesterol when it reaches a certain level, whereas statin drugs are used to destroy the whole process.  This means that if sufficient magnesium is present in the body, cholesterol will be limited to its necessary functions—the production of hormones and the maintenance of cell membranes—and will not be produced in excess. Magnesium is also responsible for several other lipid-altering functions that are not even shared by statin drugs. Magnesium is necessary for the activity of an enzyme that lowers LDL, the “bad” cholesterol; it also lowers triglycerides and raises the “good” cholesterol, HDL. Another magnesium-dependent enzyme converts omega-3 and omega- 6 essential fatty acids into prostaglandins, which are required for heart and overall health.  At least 18 human studies have verified that magnesium supplements can have an extremely beneficial effect on lipids. In these studies, total cholesterol levels were reduced by 6 to 23 percent; LDL (bad) cholesterol were lowered by 10 to 18 percent; triglycerides fell by 10 to 42 percent; and HDL (good) cholesterol rose by 4 to 11 percent. Furthermore, the studies showed that low magnesium levels are associated with higher levels of “bad” cholesterol and high magnesium levels indicate an increase in “good” cholesterol.  In addition to the ‘traditional' form of heart disease, heart rhythm issues plague many Americans as well.  Atrial fibrillation is the most commonly diagnosed heart arrhythmia, reaching epidemic proportions. In the US, AFib hospitalizations increased by 23% between 2000 and 2010.  In 2010 there were about 5.2 million people with A-Fib; that number is expected to escalate to 12.1 million cases in 2030.  Fortunately for us, Dr. Carolyn Dean has a pretty good idea of what's going on and how to help millions of American's suffering with magnesium deficiency symptoms that affect the structure and function of the cardiovascular system. Dr. Carolyn Dean has been helping educate the public and practitioners about the role of magnesium in proper heart function and, in Dan's case, while he was waiting to see his doctor he learned quite a bit about how magnesium could support his health:  Hi, Dr. Dean. Three months ago, I was diagnosed with Atrial Fibrillation by my General Practitioner. I am not on drugs yet and I have been referred to a highly reputable cardiologist here in Northern California who has me wearing a heart monitor for two weeks to see what's going on with the a-fib.  I am having to wait 2 months to meet with him to get the results and what he wants me to do for treatment. In the meantime, I found your booklet on A-Fib. This was very encouraging to read and I have started taking ReMag. I have noticed the heart palpitations when taking the magnesium are less or not at all and I have some days that are normal. I have had the RBC blood test and yes, my magnesium was low. I also had a cardio ultra sound and my heart is normal. I am very grateful to be making progress with ReMag and have more hope than before that I will be okay. Dan  The booklet on AFib is now called Heart Health and is a free download at www.drcarolyndeanlive.com.   Tonight on Dr. Carolyn Dean LIVE we'll be talking with Dr. Carolyn Dean about Magnesium – A Key Mineral for Cardiovascular Health -  along with a wide range of health topics and safe solutions. You will love hearing the beneficial interactions with callers and hosts alike including the body/mind connection, identifying the ‘conflict' in the ‘conflict basis' of disease and much more!!  About Dr. Carolyn Dean    Dr. Carolyn Dean MD ND has been featured on national media for over 30 years offering practical strategies to improve health, vitality, and well-being the natural way. As a medical doctor, naturopath, certified clinical nutritionist and master of many modalities including acupuncture and homeopathy, Dr. Carolyn Dean MD ND has authored over 33 books and 100 publications including The Magnesium Miracle, 3rd Edition, Hormone Balance, Future Health Now Encyclopedia and Heart Health. Please note that the information and opinions expressed on these broadcasts are not designed to constitute advice or recommendations as to any disease, ailment, or physical condition. You should not act or rely upon any information contained in these broadcasts without seeking the advice of your personal physician. If you have any questions about the information or opinions expressed during these broadcasts, please contact your doctor.  Video Version:  https://youtu.be/hHieNnRwnK0 Disclosure: Dr. Dean does have a financial interest in the sale of all the Completement Formulas.  Call in and Chat with Dr. Dean during Live Show with Video Stream: Call 646-558-8656   ID: 8836953587 press #.  To Ask a Question press *9 to raise your hand  Dr. Dean takes questions via email. Please write questions@drcarolyndeanlive.com We will be glad to respond to your email  Learn more about Dr. Carolyn here: https://drcarolyndeanlive.com   Chatline on Station: http://bit.ly/Dreamvisions7Radio_Network 

HOUR 1 Magnesium- A Key Mineral for Cardiovascular Health– Carolyn Dean MD ND  Heart disease has become a dreaded condition because most people know it means a handful of medications and the certain knowledge that things are only going to get worse. But what if heart disease has a strong element of magnesium deficiency? What if you have magnesium deficiency and not heart disease? Magnesium deficiency is very common in people with a compromised cardiovascular system. In hospitals magnesium is administered for acute myocardial infarction and cardiac arrhythmia. Like any other muscle, the heart requires magnesium. Magnesium is also used to treat angina, or chest pain.  In your local clinic or practitioner's office, their response to magnesium deficiency may be a little different. Magnesium's role in preventing heart disease and strokes is accepted for acute conditions, with the use of IV magnesium,  yet many cardiologists do not recognize and respond to magnesium deficiency conditions in their primary care protocols.  After all, your doctor probably thinks magnesium pill is a laxative and certainly won't do an ionized magnesium blood test to find out how much magnesium is in your cells working away at 1,000 enzyme processes and involved with 80% of known metabolic functions many of which contribute to cardiovascular health.  An average of 1,671 American's die suddenly and unexpectedly of a heart attack every day. This is a pandemic! Millions of people are unaware they are walking on a very thin edge of the same health conditions as those who have transitioned- with high cholesterol, high blood pressure, and on several medications to avoid having a heart attack. Yet the treatments for high blood pressure, high cholesterol, and high blood sugar all deplete magnesium and cause worsening of these life-threatening cardiovascular conditions.  Magnesium acts by the same mechanisms as statin drugs to lower cholesterol.   Every metabolic activity in the body depends on enzymes. Making cholesterol, for example, requires a specific enzyme called HMG-CoA reductase. Magnesium slows down this enzymatic reaction when you have enough cholesterol.  HMG-CoA reductase is the same enzyme that statin drugs block. The mechanisms are nearly the same; however, magnesium is the natural way that the body has evolved to balance cholesterol when it reaches a certain level, whereas statin drugs are used to destroy the whole process.  This means that if sufficient magnesium is present in the body, cholesterol will be limited to its necessary functions—the production of hormones and the maintenance of cell membranes—and will not be produced in excess. Magnesium is also responsible for several other lipid-altering functions that are not even shared by statin drugs. Magnesium is necessary for the activity of an enzyme that lowers LDL, the “bad” cholesterol; it also lowers triglycerides and raises the “good” cholesterol, HDL. Another magnesium-dependent enzyme converts omega-3 and omega- 6 essential fatty acids into prostaglandins, which are required for heart and overall health.  At least 18 human studies have verified that magnesium supplements can have an extremely beneficial effect on lipids. In these studies, total cholesterol levels were reduced by 6 to 23 percent; LDL (bad) cholesterol were lowered by 10 to 18 percent; triglycerides fell by 10 to 42 percent; and HDL (good) cholesterol rose by 4 to 11 percent. Furthermore, the studies showed that low magnesium levels are associated with higher levels of “bad” cholesterol and high magnesium levels indicate an increase in “good” cholesterol.  In addition to the ‘traditional' form of heart disease, heart rhythm issues plague many Americans as well.  Atrial fibrillation is the most commonly diagnosed heart arrhythmia, reaching epidemic proportions. In the US, AFib hospitalizations increased by 23% between 2000 and 2010.  In 2010 there were about 5.2 million people with A-Fib; that number is expected to escalate to 12.1 million cases in 2030.  Fortunately for us, Dr. Carolyn Dean has a pretty good idea of what's going on and how to help millions of American's suffering with magnesium deficiency symptoms that affect the structure and function of the cardiovascular system. Dr. Carolyn Dean has been helping educate the public and practitioners about the role of magnesium in proper heart function and, in Dan's case, while he was waiting to see his doctor he learned quite a bit about how magnesium could support his health:  Hi, Dr. Dean. Three months ago, I was diagnosed with Atrial Fibrillation by my General Practitioner. I am not on drugs yet and I have been referred to a highly reputable cardiologist here in Northern California who has me wearing a heart monitor for two weeks to see what's going on with the a-fib.  I am having to wait 2 months to meet with him to get the results and what he wants me to do for treatment. In the meantime, I found your booklet on A-Fib. This was very encouraging to read and I have started taking ReMag. I have noticed the heart palpitations when taking the magnesium are less or not at all and I have some days that are normal. I have had the RBC blood test and yes, my magnesium was low. I also had a cardio ultra sound and my heart is normal. I am very grateful to be making progress with ReMag and have more hope than before that I will be okay. Dan  The booklet on AFib is now called Heart Health and is a free download at www.drcarolyndeanlive.com.   Tonight on Dr. Carolyn Dean LIVE we'll be talking with Dr. Carolyn Dean about Magnesium – A Key Mineral for Cardiovascular Health -  along with a wide range of health topics and safe solutions. You will love hearing the beneficial interactions with callers and hosts alike including the body/mind connection, identifying the ‘conflict' in the ‘conflict basis' of disease and much more!!  About Dr. Carolyn Dean    Dr. Carolyn Dean MD ND has been featured on national media for over 30 years offering practical strategies to improve health, vitality, and well-being the natural way. As a medical doctor, naturopath, certified clinical nutritionist and master of many modalities including acupuncture and homeopathy, Dr. Carolyn Dean MD ND has authored over 33 books and 100 publications including The Magnesium Miracle, 3rd Edition, Hormone Balance, Future Health Now Encyclopedia and Heart Health. Please note that the information and opinions expressed on these broadcasts are not designed to constitute advice or recommendations as to any disease, ailment, or physical condition. You should not act or rely upon any information contained in these broadcasts without seeking the advice of your personal physician. If you have any questions about the information or opinions expressed during these broadcasts, please contact your doctor.  Video Version:  https://youtu.be/hHieNnRwnK0 Disclosure: Dr. Dean does have a financial interest in the sale of all the Completement Formulas.  Call in and Chat with Dr. Dean during Live Show with Video Stream: Call 646-558-8656   ID: 8836953587 press #.  To Ask a Question press *9 to raise your hand  Dr. Dean takes questions via email. Please write questions@drcarolyndeanlive.com We will be glad to respond to your email  Learn more about Dr. Carolyn here: https://drcarolyndeanlive.com   Chatline on Station: http://bit.ly/Dreamvisions7Radio_Network 

This podcast covers the regulation of HMG CoA reductase by hormones, cholesterol and statins. This biochemistry content may be useful to premedical and medical students. --- Send in a voice message: https://anchor.fm/a-j-ghalayini/message

Rosuvastatin is an antilipemic agent that works through the inhibition of the rate limiting enzyme in cholesterol synthesis (HMG CoA reductase). It is used in the management of dyslipidemia as well as having benefits in cardiovascular event prevention. The typical dosing range when treating dyslipidemia is between 5-40 mg PO qd. The max dose is 40 mg/day. Dose adjustments are made every 2-4 weeks after initiating between 10-20 mg PO qd. Some concerns are to avoid red yeast rice due to the similarity to the medication lovastatin, avoid use during pregnancy and breastfeeding, and dose at the lower end of the therapeutic range in Asian American patients due to higher levels being present which could lead to an increased risk for toxicity. The most common side effects are headache, abdominal pain, nausea, joint pain, and weakness. Go to DrugCardsDaily.com for episode show notes which consist of the drug summary, quiz, and link to the drug card for FREE! Please SUBSCRIBE, FOLLOW, and RATE on Spotify, Apple Podcasts, or wherever your favorite place to listen to podcasts are. The main goal is to go over the Top 200 Drugs with the occasional drug of interest. Also, if you'd like to say hello, suggest a drug, or leave some feedback I'd really appreciate hearing from you! Leave a voice message at anchor.fm/drugcardsdaily or find me on twitter @drugcardsdaily --- Send in a voice message: https://anchor.fm/drugcardsdaily/message

Learn from the experts about immune mediated neurological toxicities. Join our hosts Dr. Afreen Shariff and Dr. Tian Zhang as they discuss with guest expert and Neurologist Dr. Andrew Mammen. Andrew Mammen, M.D., Ph.D., joined NIAMS as Muscle Disease Unit Leader in the Laboratory of Muscle Stem Cells and Gene Regulation in 2014. He obtained his medical degree and Ph.D. in neuroscience at Johns Hopkins in 2000, where he subsequently completed his medicine internship, neurology residency, and neuromuscular fellowship. Prior to his appointment at NIH, he was Associate Professor of Neurology and Medicine at the Johns Hopkins University School of Medicine. He co-founded the Johns Hopkins Myositis Center in 2007, where he continues to see myositis patients as an adjunct faculty member. Dr. Mammen and his colleagues at Hopkins discovered a novel form of autoimmune myopathy associated with statin use and autoantibodies recognizing HMG-CoA reductase, the pharmacologic target of statins. In addition to clinical studies involving myositis patients, his current laboratory research interests include defining pathogenic mechanisms in the various forms of autoimmune myopathy and understanding the role of myositis autoantigens in muscle regeneration.

Simvastatin is used to slow the progress of heart disease as well as lowering cholesterol in patients. It is also known by the brand name of Zocor. Simvastatin works by affecting the rate-limiting step in cholesterol synthesis. It is a competitive inhibitor of the HMG-CoA reductase enzyme. There are also other benefits such as reducing inflammation and coronary plaque sites, inhibiting platelet aggregation, as well as having an anticoagulant effect. Simvastatin is contraindicated in pregnancy and should be stopped immediately if pregnancy is suspected. Some serious side effects to be aware of are rhabdomyolysis; muscle pain, tenderness, and weakness, and dark urine. Common monitoring parameters for patients on simvastatin are lipid panels, pregnancy, hepatic transaminase levels, and CPK. In order to get the best benefit from simvastatin it is recommended to be taken in the evening. Go to DrugCardsDaily.com for my episode show notes which will contain a drug summary, quiz, and a link to FREE drug card sheets. SUBSCRIBE on Spotify or Apple Podcasts or search for us on your favorite place to listen to podcasts. I will go over the Top 100-200 Drugs as well as throwing in some recently released drugs that peak my interest. Also, if you'd like to say hello, suggest a drug, or leave any constructive feedback on the show I'd really appreciate it! Leave a voice message at anchor.fm/drugcardsdaily or message us through twitter @drugcardsdaily --- Send in a voice message: https://anchor.fm/drugcardsdaily/message

Today we'll be covering Dyslipidemia, going along with this month's theme, Cardiology. If you haven't listened to our podcast before, each week we have a case-based discussion about a medical topic to help you study for the pediatric medicine board exam. Episodes are released every weekend, and the case is then reviewed and reinforced on social media throughout the week.   Follow the podcast on social media: Facebook- @portablepeds (www.facebook.com/portablepeds) Twitter- @portablepeds (www.twitter.com/portablepeds)   We'd love to hear from you via email at portablepeds@gmail.com!   Also, feel free to visit our website, www.portablepeds.com, for more content.   Today's Case:   An 11 year old presents to your office for a routine well child check.  In discussing their diet, you find that they are eating foods high in saturated fat and low in fiber.  Their BMI is 31, and they have not yet reached puberty.  They have a family history of a myocardial infarction in their maternal grandfather at the age of 48.  You perform a routine lipid screening profile, and their LDL level is 170mg/dL.  You recommend dietary modifications, and six months later you repeat an LDL level, which is now 165mg/dL. What is the most appropriate next step?   Do nothing; their LDL will continue to naturally decrease through puberty Repeat a level in 6 months as their LDL level is below the treatment threshold Continue dietary modifications only, as there are no FDA approved medications for adolescents with dyslipidemia  Start an HMG-CoA reductase inhibitor Start a cholesterol absorption blocker   We would like to give an enormous thank you to Zack Goldmann for designing this podcast's logo and accompanying artwork. You can find more of his work at www.zackgoldmann.com.   The intro and outro of this podcast is a public domain song obtained from scottholmesmusic.com.   Intro/Outro- Hotshot by Scott Holmes   Disclaimer: This podcast is intended for healthcare professionals. The information presented is for general educational purposes only and should NOT be used as professional medical advice or for the diagnosis or treatment of medical conditions.   The views and opinions expressed do not represent the views and opinions of our employer or any affiliated institution. Expressed opinions are based on specific facts, under certain conditions, and subject to certain assumptions and should not be used or relied upon for any other purpose, including, but not limited to, the diagnosis or treatment of medical conditions or in any legal proceeding. Full terms and conditions can be found at portablepeds.com.   Thanks for listening! As always, please Rate and Review this podcast on Apple Podcasts, Facebook, or your favorite podcasting platform. Also, Subscribe to get all the latest episodes, and Share this episode with someone you think would enjoy it! Hope to see you real soon!

Edit: an apology form Nick - "Apologies to everyone. At 34:30 I made a false statement when I said HMG-CoA reductase inhibition could inhibit ketone production directly. It is not the RLE in ketogenesis. There are indirect mechanisms potentially at play, but that enzyme is downstream of the divergence point in ketone and cholesterol metabolism. I was questioning the thought as it came to mind and regret the impulsive speculation. My sincerest apologies. That's embarrassing." What a treat to spend some time with Nick Norwitz PhD.  He just graduated from Oxford with a PhD in neuro-metabolism and now he is about to embark on his MD at Harvard.  But this is not about his academic achievements, impressive as they are, rather it is about his immense battles with numerous chronic conditions that led him down the path to discovering keto.  When he was younger he never put on weight and was as carefree as most kids are until the end of high school when he started to develop osteoporosis, which was super weird for a male of his age.  By the end of college he developed ulcerative colitis.  He went to Oxford to pursue his PhD and had a huge flare up soon after arriving ending up in a hospital in a strange country where no one knew what was wrong with him.  So he started doing a bunch of research and he voraciously consumed scientific papers about carb reduction and the ketogenic diet and, although still skeptical, he decided to go for it. Within a week his colitis disappeared.  So he titrated off his meds over time and feels confident that his colitis is gone.  He is totally excited about this to the point that he is worried about getting expelled from Harvard for calling out his professors on this stuff. We went on to talk about the new Society of Metabolic Practitioners (SMHP), a non-profit in which Nick is very active and even ended up in a pretty scientific discussion about cholesterol.  We made mention of his new YouTube testimonial video he put out and he talked about his book and referred to a bunch of papers so I have put a few interesting links down below here. Nick's YouTube Video   Nick's New Book Page    Amazon Pre-order Note, pre-orders up-rank it on Amazon and help bump down calorie counting low-fat style books ;)   YouTube Sample, Omega3s   Three selected peer-reviewed papers: 1. Keto Diet & Lipid Panel 2. Keto Diet Mental Health 3. Alzheimer's and insulin resistance

Red yeast rice has been used for centuries in Chinese medicine. It has been shown to decrease cholesterol. It includes HMG-CoA reductase materials. In fact, statins were originally developed from Monacolins, the fungus used to make red yeast rice. The FDA declared Monacolin products as a drug and tried to stop the sale of supplements containing it. This decision went to court and was overturned by the US Court of Appeals. They actually typically contain 10-20 mg of monacolins. Mevachor, made by Merck from red yeast rice, contains 20-80 mg of monacolins. So you're taking the same thing but usually at a lower dose. Side effects are the same: liver function problems, muscle breakdown. I prefer to use better statins at far lower doses. And I don't appreciate the patent formula product salesmen all over the web saying, "my product, XXX, is safer, more effective, and contains the exact right combination..... blah, blah, blah."For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources: PrevMed's blogsPrevMed's websitePrevMed's YouTube channelPrevMed's Facebook page

CoQ10 stands for coenzyme Q10. It is used for ATP, which is in turn critical to cell respiration which provides over 90% of human cell energy. Ubiquinol is the reduced alcohol form of CoQ10. It's supposed to be the most effective and easily absorbed form. On the other hand, ubiquinone is the oxidized ketone form. Statins are HMG-CoA reductase inhibitors. When they stop cholesterol production, they also decrease CoQ10 production. There is a lot of great research on ubiquinone & ubiquinol. However, the study results conflict. There seems to be evidence that we can elevate our levels of CoQ10. But it's not so clear that it works. Part of the evidence is that it's difficult to assume an improvement in biological status based on mitochondrial improvement. That in turn requires assumptions that lung, heart, and vascular functions are not the actual rate-limiting problem. For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources: PrevMed's article on CoQ10PrevMed's websitePrevMed's YouTube channelPrevMed's Facebook page

2020年11月2日 星期一 第1期FDA 淀粉样变心肌病的新药上市LANCET 肾去神经支配术治疗高血压的新研究Science Advance 四维心脏补片治疗缺血性心肌病他法米迪（tafamidis）2019年5月，他法米迪（tafamidis）被FDA批准用于治疗家族性或野生型甲状腺素运载蛋白介导（ATTR型）的淀粉样变心肌病。淀粉样变心肌病是一种淀粉样原纤维在心脏细胞外区沉积导致的疾病，其中约95%是由甲状腺素运载蛋白介导的（ATTR型）、或由免疫球蛋白轻链介导的（AL型）。淀粉样变性可累及多个脏器，其中心脏受累可导致心力衰竭、心律失常和死亡。他法米迪在甲状腺素结合位点与甲状腺素运载蛋白结合，稳定化合物、防止四聚体分离和淀粉样物质生成。《ATTR-ACT研究：他法米迪治疗ATTR型淀粉样变心肌病》New England Journal of Medicine，2018年9月 (1)这个多中心、国际、双盲、安慰剂对照、3期试验中，纳入441名患者ATTR型淀粉样心肌病患者，分别接受他法米迪80mg、他法米迪20mg或安慰剂治疗30个月。接受他法米迪治疗的患者的全因死亡率和心血管相关的住院率显著低于安慰剂组（P

In Part 2 of his talk, DeBose-Boyd introduces a rare genetic disorder known as Schnyder Corneal Dystrophy (SCD). SCD is characterized by accumulation of cholesterol in the corneas of affected individuals, indicating that the genetic defect in SCD may affect cholesterol synthesis. Mutations in the UBIAD1 gene cause SCD – therefore, DeBose-Boyd's lab sought to understand the role of UBIAD1 in regulation of cholesterol metabolism. They found that UBIAD1 acts as a sensor for levels of the metabolite GGpp, which enhances sterol-mediated ERAD of HMG CoA reductase. In the presence of GGpp, UBIAD1 releases HMG CoA reductase, leading to its proteasomal degradation. DeBose-Boyd's lab also discovered a fascinating spatial regulation of UBIAD1, whereby binding of UBIAD1 to GGpp causes UBIAD1 to accumulate in the Golgi apparatus and away from HMG CoA reductase in the ER. Finally, his group found that the SCD-associated mutation N102S in UBIAD1 inhibits the interaction between UBIAD1 and GGpp, such that mutant UBIAD1 is unable to translocate from the ER to the Golgi in the presence of high GGpp.

Regulation of cholesterol synthesis is very important: cholesterol is a component of cell membranes and a precursor of steroid hormones and bile acids, yet high levels of cholesterol can be toxic to cells and can contribute to heart disease. Cells in our body obtain cholesterol one of two ways – by taking it up from the bloodstream (via low-density lipoprotein or LDL) or by synthesizing it intracellularly. In Part 1 of his iBioSeminar, Dr. Russell DeBose-Boyd provides an overview of cholesterol regulation with a focus on HMG CoA reductase, the rate-limiting enzyme of cholesterol synthesis. He describes how the effects of statins, drugs prescribed to lower LDL in the blood, are blunted due to the disruption of feedback control of HMG CoA reductase. In the presence of sterols, HMG CoA reductase protein stability is decreased. This sterol-accelerated degradation of HMG CoA reductase is dependent on the enzyme's membrane domain in a process known as ER-associated degradation (ERAD). DeBose-Boyd describes his lab's contributions to a model of HMG CoA reductase ERAD in which polyubiquitination of the enzyme in response to sterols is mediated by two proteins, Insig-1 and Insig-2, leading to its ERAD by the 26S proteasome.

In Part 2 of his talk, DeBose-Boyd introduces a rare genetic disorder known as Schnyder Corneal Dystrophy (SCD). SCD is characterized by accumulation of cholesterol in the corneas of affected individuals, indicating that the genetic defect in SCD may affect cholesterol synthesis. Mutations in the UBIAD1 gene cause SCD – therefore, DeBose-Boyd’s lab sought to understand the role of UBIAD1 in regulation of cholesterol metabolism. They found that UBIAD1 acts as a sensor for levels of the metabolite GGpp, which enhances sterol-mediated ERAD of HMG CoA reductase. In the presence of GGpp, UBIAD1 releases HMG CoA reductase, leading to its proteasomal degradation. DeBose-Boyd’s lab also discovered a fascinating spatial regulation of UBIAD1, whereby binding of UBIAD1 to GGpp causes UBIAD1 to accumulate in the Golgi apparatus and away from HMG CoA reductase in the ER. Finally, his group found that the SCD-associated mutation N102S in UBIAD1 inhibits the interaction between UBIAD1 and GGpp, such that mutant UBIAD1 is unable to translocate from the ER to the Golgi in the presence of high GGpp.

Regulation of cholesterol synthesis is very important: cholesterol is a component of cell membranes and a precursor of steroid hormones and bile acids, yet high levels of cholesterol can be toxic to cells and can contribute to heart disease. Cells in our body obtain cholesterol one of two ways – by taking it up from the bloodstream (via low-density lipoprotein or LDL) or by synthesizing it intracellularly. In Part 1 of his iBioSeminar, Dr. Russell DeBose-Boyd provides an overview of cholesterol regulation with a focus on HMG CoA reductase, the rate-limiting enzyme of cholesterol synthesis. He describes how the effects of statins, drugs prescribed to lower LDL in the blood, are blunted due to the disruption of feedback control of HMG CoA reductase. In the presence of sterols, HMG CoA reductase protein stability is decreased. This sterol-accelerated degradation of HMG CoA reductase is dependent on the enzyme’s membrane domain in a process known as ER-associated degradation (ERAD). DeBose-Boyd describes his lab’s contributions to a model of HMG CoA reductase ERAD in which polyubiquitination of the enzyme in response to sterols is mediated by two proteins, Insig-1 and Insig-2, leading to its ERAD by the 26S proteasome.

HOUR 1September is Atrial Fibrillation Month -- Carolyn Dean MD ND September is Atrial Fibrillation Awareness Month although in Dr. Dean’s world we say Atrial Fibrillation is a Magnesium Deficiency Awareness Month. While hospital departments and health organizations want you to know about the drug and surgical treatment for AFib, on tonight’s radio show we focus on magnesium and mineral deficiencies that may trigger AFib and other heart rhythm abnormalities. Magnesium deficiency is very common in people with a compromised cardiovascular system. However, magnesium deficiency itself can mimic cardiovascular symptoms. In some hospitals, magnesium is administered for acute myocardial infarction and cardiac arrhythmia. Like any other muscle, the heart requires magnesium. Magnesium’s role in preventing heart disease and strokes is accepted in these hospitals for acute conditions, yet most cardiologists and family doctors do not recognize and respond to magnesium deficiency conditions in their primary care protocols.   An average of 1,671 American’s die suddenly and unexpectedly of a heart attack every day. Millions of people around the world are in the same position as those who have recently transitioned – with high cholesterol, high blood pressure and on several medications to avoid having a heart attack. Yet the treatments for high blood pressure, high cholesterol, and high blood sugar all deplete magnesium and cause worsening of these three very common conditions. Magnesium acts by the same mechanisms as statin drugs to lower cholesterol. Every metabolic activity in the body depends on enzymes. Making cholesterol, for example, requires a specific enzyme called HMG-CoA reductase. Magnesium slows down this enzymatic reaction when it is present in sufficient quantities. It’s the same enzyme that statin drugs target and inhibit. However, magnesium is the natural way that the body has evolved to control cholesterol when it reaches a certain level, whereas statin drugs are used to destroy the whole process. This means that if sufficient magnesium is present in the body, cholesterol will be limited to its necessary functions—the production of hormones and the maintenance of cell membranes—and will not be produced in excess. Magnesium is also responsible for several other lipid-altering functions that are not even shared by statin drugs. Magnesium is necessary for the activity of an enzyme that lowers LDL, the “bad” cholesterol; it also lowers triglycerides and raises the “good” cholesterol, HDL. Another magnesium-dependent enzyme converts omega-3 and omega- 6 essential fatty acids into prostaglandins, which are required for heart and overall health. In addition to the ‘traditional’ form of heart disease, heart rhythm issues plague many Americans.  Atrial fibrillation is the most commonly diagnosed heart arrhythmia, reaching epidemic proportions. In the US, AFib hospitalizations increased by 23% between 2000 and 2010.  In 2010 there were about 5.2 million people with AFib; that number is expected to escalate to 12.1 million cases in 2030. Fortunately for us, Dr. Carolyn Dean has a pretty good idea of what’s going on and how to help millions of American’s suffering with magnesium deficiency symptoms that affect the structure and function of the cardiovascular system. Dr. Carolyn Dean has been helping educate the public and practitioners about the role of magnesium in proper heart function and, in Dan’s case, while he was waiting to see his doctor, he learned quite a bit about how ReMag could support his health. However, Dr. Dean would encourage Dan to also take Pico Potassium, Whole C ReSet, and our D3-K2 ReSet to ReSet his Heart. Hi, Dr. Dean. Three months ago, I was diagnosed with Atrial Fibrillation by my General Practitioner. I am not on drugs yet and I have been referred to a highly reputable cardiologist here in Northern California who has me wearing a heart monitor for two weeks to see what’s going on with the AFib. I am having to wait 2 months to meet with him to get the results and what he wants me to do for treatment. In the meantime, I found your booklet called Heart Health. This was very encouraging to read and I have started taking ReMag. I have noticed the heart palpitations when taking the magnesium are less or not at all and I have some days that are normal. I have had the RBC blood test and yes, my magnesium was low. I also had a cardio ultra sound and my heart is normal. I am very grateful to be making progress and have more hope than before that I will be okay. Dan Call in and Chat with Dr. Dean during Live Show with Video Stream: Call 646-558-8656   ID: 8836953587 press #.  To Ask a Question press *9 to raise your hand Dr. Dean takes questions via email. Please write questions@drcarolyndeanlive.comWe will be glad to respond to your email Learn more about Dr. Carolyn here: https://drcarolyndeanlive.com  

HOUR 2September is Atrial Fibrillation Month -- Carolyn Dean MD ND September is Atrial Fibrillation Awareness Month although in Dr. Dean’s world we say Atrial Fibrillation is a Magnesium Deficiency Awareness Month. While hospital departments and health organizations want you to know about the drug and surgical treatment for AFib, on tonight’s radio show we focus on magnesium and mineral deficiencies that may trigger AFib and other heart rhythm abnormalities. Magnesium deficiency is very common in people with a compromised cardiovascular system. However, magnesium deficiency itself can mimic cardiovascular symptoms. In some hospitals, magnesium is administered for acute myocardial infarction and cardiac arrhythmia. Like any other muscle, the heart requires magnesium. Magnesium’s role in preventing heart disease and strokes is accepted in these hospitals for acute conditions, yet most cardiologists and family doctors do not recognize and respond to magnesium deficiency conditions in their primary care protocols.   An average of 1,671 American’s die suddenly and unexpectedly of a heart attack every day. Millions of people around the world are in the same position as those who have recently transitioned – with high cholesterol, high blood pressure and on several medications to avoid having a heart attack. Yet the treatments for high blood pressure, high cholesterol, and high blood sugar all deplete magnesium and cause worsening of these three very common conditions. Magnesium acts by the same mechanisms as statin drugs to lower cholesterol. Every metabolic activity in the body depends on enzymes. Making cholesterol, for example, requires a specific enzyme called HMG-CoA reductase. Magnesium slows down this enzymatic reaction when it is present in sufficient quantities. It’s the same enzyme that statin drugs target and inhibit. However, magnesium is the natural way that the body has evolved to control cholesterol when it reaches a certain level, whereas statin drugs are used to destroy the whole process. This means that if sufficient magnesium is present in the body, cholesterol will be limited to its necessary functions—the production of hormones and the maintenance of cell membranes—and will not be produced in excess. Magnesium is also responsible for several other lipid-altering functions that are not even shared by statin drugs. Magnesium is necessary for the activity of an enzyme that lowers LDL, the “bad” cholesterol; it also lowers triglycerides and raises the “good” cholesterol, HDL. Another magnesium-dependent enzyme converts omega-3 and omega- 6 essential fatty acids into prostaglandins, which are required for heart and overall health. In addition to the ‘traditional’ form of heart disease, heart rhythm issues plague many Americans.  Atrial fibrillation is the most commonly diagnosed heart arrhythmia, reaching epidemic proportions. In the US, AFib hospitalizations increased by 23% between 2000 and 2010.  In 2010 there were about 5.2 million people with AFib; that number is expected to escalate to 12.1 million cases in 2030. Fortunately for us, Dr. Carolyn Dean has a pretty good idea of what’s going on and how to help millions of American’s suffering with magnesium deficiency symptoms that affect the structure and function of the cardiovascular system. Dr. Carolyn Dean has been helping educate the public and practitioners about the role of magnesium in proper heart function and, in Dan’s case, while he was waiting to see his doctor, he learned quite a bit about how ReMag could support his health. However, Dr. Dean would encourage Dan to also take Pico Potassium, Whole C ReSet, and our D3-K2 ReSet to ReSet his Heart. Hi, Dr. Dean. Three months ago, I was diagnosed with Atrial Fibrillation by my General Practitioner. I am not on drugs yet and I have been referred to a highly reputable cardiologist here in Northern California who has me wearing a heart monitor for two weeks to see what’s going on with the AFib. I am having to wait 2 months to meet with him to get the results and what he wants me to do for treatment. In the meantime, I found your booklet called Heart Health. This was very encouraging to read and I have started taking ReMag. I have noticed the heart palpitations when taking the magnesium are less or not at all and I have some days that are normal. I have had the RBC blood test and yes, my magnesium was low. I also had a cardio ultra sound and my heart is normal. I am very grateful to be making progress and have more hope than before that I will be okay. Dan Call in and Chat with Dr. Dean during Live Show with Video Stream: Call 646-558-8656   ID: 8836953587 press #.  To Ask a Question press *9 to raise your hand Dr. Dean takes questions via email. Please write questions@drcarolyndeanlive.comWe will be glad to respond to your email Learn more about Dr. Carolyn here: https://drcarolyndeanlive.com  

Patients with very high levels of serum triglycerides (greater than 1000 mg/dL) are at risk for pancreatitis. Most patients with congenital abnormalities in triglyceride metabolism present in childhood. By way of contrast, hypertriglyceridemia-induced pancreatitis in adults is often due to an acquired lipid metabolism problem. Although, there are no clear triglyceride levels that predict pancreatitis, most clinicians treat fasting levels above 500 mg/dL. The risk of pancreatitis here may be more related to the triglyceride level following consumption of a fatty meal. Thus, because postprandial increases in triglyceride are inevitable if fat-containing foods are eaten, fasting triglyceride levels in persons prone to pancreatitis should be kept below that level. The primary treatment for high triglyceride levels is dietary and calls for reduced consumption of alcohol, simple sugars, and refined starches as well as saturated and trans fatty acids. In patients with fasting triglycerides greater than or equal to 500 mg/dL despite adequate dietary compliance, a triglyceride lowering drug such as niacin, a fibric acid derivative, an omega-3-acid ethyl ester, or an HMG-CoA reductase inhibitor may be helpful. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app

Proper mold/mycotoxin testing, Fasted BJJ, Statins vs PSK9 inhibitors for high LDLs, Best Conventional Meat Cut, Keto and breastfeeding Make your health an act of rebellion. Join The Healthy Rebellion Please Subscribe and Review: Apple Podcasts | RSS  Submit your questions for the podcast here   Show Notes: ---- News topic du jour: Original UN tweet I talked about seems to be deleted/removed: https://www.stockjournal.com.au/story/6855807/un-told-to-stick-to-knitting-after-urging-people-to-eat-less-meat/ https://www.beefcentral.com/news/un-removes-meat-worse-than-oil-tweet/ ---- 1. Proper mold/mycotoxin testing [17:20] Scott says: Hello Robb and Nicki, I've been struggling with mycotoxins/Lyme.  I read Toxic by Dr. Nathan last October when my doctor diagnosed.  I am wondering can you recommend a company that can test for ERMI and do the plate testing.  I live in a 1 bedroom apartment.  I had testing done in October but was not as informed at that time and it was a company that did the basic air quality although even that did have some positives as well as my 1st GPL urine test and most recent one this month.  I live in Oak Park, IL which is a suburb of Chicago.  Thank you in advance for your time and information. With gratitude, Scott Davis 2. Fasted BJJ [19:43] Eric says: Hi Robb and Nicki, First, thanks for all that both of you do. I’m a listener since episode one of The Paleo Solution Podcast and continue to refer my personal training clients to all of your content, new and old. Ok, context first. I’ve been a time restricted eater for about a year and half and have had great results. Monday-Saturday I run an 18:6 protocol and Sunday’s are 16:8. Whether it’s 6am or towards the end of the TRE window, I feel good and perform well when I have a strength or sprint workout. Next week I start no gi BJJ from 11:30-1pm Tues/Thurs. I typically end my TRE around 12:30 or so but am wondering how BJJ workouts will play out. Should I supplement with quality sea salt and/or other electrolytes since they have little or no impact on most types of fasting (per Dr. Rhonda Patrick)? Of course I’m going to give it a whirl and see how it goes but just curious in case I end up needing something. Again, thanks and keep up the great work! 3. Statins vs PSK9 inhibitors for high LDLs [24:42] Dr. Mandal says: Hey Robb and Nicki. I shot this question off to the Peter Atia podcast also cause I'd be genuinely intrigued how someone with your biochemistry background would approach this problem, I know you can't give medical advice, but just wondering what ideas you'd have about treating someone like myself with an elevated LDL particle count who has an APOE3/E4 genotype. The LDL particle count did improve with a 3 times a week dosing with Lipitor 10mg. However, since statins work by diminishing the output of total cholesterol by inhibiting HMG-CoA reductase would long term use of a statin eventually be detrimental to someone who is more prone to Alzheimer's dementia with an APOE3/E4 genotype? Would a PSK9 inhibitor be a better choice since it works by removing LDL particles? Additionally, total cholesterol, triglyceride, HDL levels, and inflammatory markers are excellent and are controlled with a targeted keto-ish diet (

生物科技驱动制药创新的历程来自青侨阳光主播：小陆https://xueqiu.com/3770558188/150465923 医药行业里的新机会，是供给还是需求在驱动呢？ 其实，供给驱动是在寻找【改写游戏规则】的技术，而需求驱动呢，则是在寻找【远未满足的迫切需求】。最好的状况，是用技术去满足需求。我们更关注供给驱动，因为，如果仅仅有需求，不一定找得到技术和供给。但只要技术够颠覆，创新供给够颠覆，迟早能找到释放价值的地方、合适的使用场景。 今天，我们就来简单梳理一下，生物科技是如何驱动生物药和化学药的创新发展的。 首先先说生物药。在过去几十年，生物药技术驱动的核心是什么？当然就是——生物科技。在几十年的时间里，生物科技在医药行业有了层层突破。 简单回顾一下历史—— 50年代的时候，DNA双螺旋模型被提出，分子生物学诞生。DNA双螺旋模型简洁地解释了众多复杂现象，震撼学界，由此也获得资源和市场的青睐，加速了学科发展。 70年代，内切酶、连接酶、质粒、PCR都出来了，微生物研究也越来越清晰。产业化尝试也从这个阶段开始。 80年代，基因泰克生长激素、胰岛素相继获批，多肽药物进入爆发期。多肽药物最先爆发，它没有人源化免疫原性的问题，用大肠杆菌就可以。1975年，抗体开始尝试产业化，1983年，第一个抗体药物上市了。80年代就有了抗体，但2000年左右才真正爆发，正是因为免疫原性。 90年代后，人源化逐渐被突破，单抗开始爆发，因为最初的限制瓶颈被解决了。单抗行业刚打开的时候，大家尽情的去筛临床价值好的靶点，比如现在的药王阿达木单抗，未来的药王pd1单抗，一个是下调免疫系统治疗自身免疫性疾病，一个是上调免疫系统治疗肿瘤。但是，胞外靶点毕竟是有限的，筛到一定程度，好靶点就筛的差不多了。 抗体要进一步创新，要提高临床效果，更多是在现有靶点上的精耕细作。所以工程抗体是一个必然趋势，双抗、ADC、合成生物学都是其中的重要细分。 抗体之后，接下来一波比较大的浪潮，我们称之为入胞时代。抗体比多肽难，时间轴上对应的爆发时间点也晚些，但入胞的技术比抗体更难。多肽、抗体针对胞外的蛋白，难度小很多。但90%以上的生命过程在细胞内，而且蛋白只是下游功能元件，胞外远比不上核酸调控的效果。 令人振奋的是，入胞相关的前沿性基础研究在过去几年，随着技术的突破也有了新发展。2010、2015年后，入胞技术逐渐成熟，第一个真正有显著临床优势的基因疗法、第一款RNAi疗法药物相继获批。NGB-也就是下一代生物技术成为一个很大的浪潮。 接下来，我们看下：过去几十年，化学药技术驱动的核心是什么？答案同样是生物科技。为什么这么说呢？大家都熟悉青霉素、二甲双胍，但很难说清它们对应的靶点。因为以前化药的发现和研发，都是基于某种现象来反向筛选。比如，发现菌落周围不长菌，根据这个现象反向推导回溯，找到青霉素，更像盲筛的过程。 但70到80年代间，随着分子生物学的渗透，化药的研发过程被极大的颠覆。生物学带来“靶点”的概念，照着靶点来开发药物，极大提升了小分子化药的成功率。 很多创新药出现在八、九十年代之后，一方面是因为这个时期有一些关键的政治决策颁布出台，比如1984年颁布的“Hatch-Waxman法案“在美国医药产业百年发展历程中具有里程碑意义。但更重要的一方面是生物科技的进步。生物科技改写了小分子化药的研发格局，也促进了生物药的发展。 从80到90年代开始，HMG-CoA的靶点带来了一批的他汀；ACEI和ARB的靶点带来了普利类、沙坦类。再到2000年后，肿瘤驱动基因的概念被验证，开山之作就是诺华的格列卫，也就是伊马替尼，靶向BCR-ABL融合蛋白。大家发现某些肿瘤的发生也是受核心基因所驱动，抑制了融合蛋白BCR-ABL，急淋白血病就得到了极好的控制。 之后，一批小分子抗肿瘤药物奔涌而出。很多小分子靶向药物其实就是酪氨酸激酶抑制剂也就是我们常听说的TKI。比如典型的在膜上的EGFR，贝达的埃克替尼；在胞内的BTK抑制剂，诺诚健华的奥布替尼；JAK抑制剂，辉瑞托法替尼等。还有一类较大的多靶点激酶抑制剂，比如恒瑞的阿帕替尼。这也是一个比较大的浪潮，相关的上市公司非常多。 回顾整个发展历程，分子生物学对整个生物制药有着重大影响。 化药的发现是基于生物的靶点，生物药更是基于生物科技。过去生物制药领域出现众多机会，生物科技功不可没。很多时候，表面看上去是公司个体的成就，实际上都是技术与时代发展的烙印。对于医药行业的投资者来说，值得庆幸的是：往前看，生物技术的大潮仍将汹涌，技术创新与突破仍将不断。

生物科技驱动制药创新的历程来自青侨阳光主播：小陆https://xueqiu.com/3770558188/150465923 医药行业里的新机会，是供给还是需求在驱动呢？ 其实，供给驱动是在寻找【改写游戏规则】的技术，而需求驱动呢，则是在寻找【远未满足的迫切需求】。最好的状况，是用技术去满足需求。我们更关注供给驱动，因为，如果仅仅有需求，不一定找得到技术和供给。但只要技术够颠覆，创新供给够颠覆，迟早能找到释放价值的地方、合适的使用场景。 今天，我们就来简单梳理一下，生物科技是如何驱动生物药和化学药的创新发展的。 首先先说生物药。在过去几十年，生物药技术驱动的核心是什么？当然就是——生物科技。在几十年的时间里，生物科技在医药行业有了层层突破。 简单回顾一下历史—— 50年代的时候，DNA双螺旋模型被提出，分子生物学诞生。DNA双螺旋模型简洁地解释了众多复杂现象，震撼学界，由此也获得资源和市场的青睐，加速了学科发展。 70年代，内切酶、连接酶、质粒、PCR都出来了，微生物研究也越来越清晰。产业化尝试也从这个阶段开始。 80年代，基因泰克生长激素、胰岛素相继获批，多肽药物进入爆发期。多肽药物最先爆发，它没有人源化免疫原性的问题，用大肠杆菌就可以。1975年，抗体开始尝试产业化，1983年，第一个抗体药物上市了。80年代就有了抗体，但2000年左右才真正爆发，正是因为免疫原性。 90年代后，人源化逐渐被突破，单抗开始爆发，因为最初的限制瓶颈被解决了。单抗行业刚打开的时候，大家尽情的去筛临床价值好的靶点，比如现在的药王阿达木单抗，未来的药王pd1单抗，一个是下调免疫系统治疗自身免疫性疾病，一个是上调免疫系统治疗肿瘤。但是，胞外靶点毕竟是有限的，筛到一定程度，好靶点就筛的差不多了。 抗体要进一步创新，要提高临床效果，更多是在现有靶点上的精耕细作。所以工程抗体是一个必然趋势，双抗、ADC、合成生物学都是其中的重要细分。 抗体之后，接下来一波比较大的浪潮，我们称之为入胞时代。抗体比多肽难，时间轴上对应的爆发时间点也晚些，但入胞的技术比抗体更难。多肽、抗体针对胞外的蛋白，难度小很多。但90%以上的生命过程在细胞内，而且蛋白只是下游功能元件，胞外远比不上核酸调控的效果。 令人振奋的是，入胞相关的前沿性基础研究在过去几年，随着技术的突破也有了新发展。2010、2015年后，入胞技术逐渐成熟，第一个真正有显著临床优势的基因疗法、第一款RNAi疗法药物相继获批。NGB-也就是下一代生物技术成为一个很大的浪潮。 接下来，我们看下：过去几十年，化学药技术驱动的核心是什么？答案同样是生物科技。为什么这么说呢？大家都熟悉青霉素、二甲双胍，但很难说清它们对应的靶点。因为以前化药的发现和研发，都是基于某种现象来反向筛选。比如，发现菌落周围不长菌，根据这个现象反向推导回溯，找到青霉素，更像盲筛的过程。 但70到80年代间，随着分子生物学的渗透，化药的研发过程被极大的颠覆。生物学带来“靶点”的概念，照着靶点来开发药物，极大提升了小分子化药的成功率。 很多创新药出现在八、九十年代之后，一方面是因为这个时期有一些关键的政治决策颁布出台，比如1984年颁布的“Hatch-Waxman法案“在美国医药产业百年发展历程中具有里程碑意义。但更重要的一方面是生物科技的进步。生物科技改写了小分子化药的研发格局，也促进了生物药的发展。 从80到90年代开始，HMG-CoA的靶点带来了一批的他汀；ACEI和ARB的靶点带来了普利类、沙坦类。再到2000年后，肿瘤驱动基因的概念被验证，开山之作就是诺华的格列卫，也就是伊马替尼，靶向BCR-ABL融合蛋白。大家发现某些肿瘤的发生也是受核心基因所驱动，抑制了融合蛋白BCR-ABL，急淋白血病就得到了极好的控制。 之后，一批小分子抗肿瘤药物奔涌而出。很多小分子靶向药物其实就是酪氨酸激酶抑制剂也就是我们常听说的TKI。比如典型的在膜上的EGFR，贝达的埃克替尼；在胞内的BTK抑制剂，诺诚健华的奥布替尼；JAK抑制剂，辉瑞托法替尼等。还有一类较大的多靶点激酶抑制剂，比如恒瑞的阿帕替尼。这也是一个比较大的浪潮，相关的上市公司非常多。 回顾整个发展历程，分子生物学对整个生物制药有着重大影响。 化药的发现是基于生物的靶点，生物药更是基于生物科技。过去生物制药领域出现众多机会，生物科技功不可没。很多时候，表面看上去是公司个体的成就，实际上都是技术与时代发展的烙印。对于医药行业的投资者来说，值得庆幸的是：往前看，生物技术的大潮仍将汹涌，技术创新与突破仍将不断。

Many studies show magnesiums positive rolee in the reduction of cholesterol. We have known for many decades that magnesium helps with hypertension as a natural calcium channel blocker, but know studies show that magnesium also is nature's statin--without the harmful effects of statins.HMG-CoA reductase is the enzyme that regulates cholesterol production. This enzyme is highly dependent on magnesium. How does magnesium's water-bearing natural viscosity play into this? Lets find out.For Transdermal Magnesium in Glass bottles "Zechstein Inside®" for only 3$ a week or for our free health tips, books or podcasts come check us out at : theheartoftradition.comFor 10% off try the promo code : HEART10

Statins are some of the most commonly prescribed cholesterol-lowering drugs. They act by inhibiting HMG-CoA reductase, the main enzyme in the synthesis of cholesterol. Earlier studies have shown that statins have an osteoprotective effect: a recently published paper has shown that there is a dose-dependent relationship between different kinds of statins with diagnosis of osteoporosis. "We could find an underrepresentation of osteoporosis in low-dose and an overrepresentation in high-dose statin treatment," says first author Dr. Michael Leutner, MSc PhD (Department of Internal Medicine 3, Division of Endocrinology and Metabolism, Medical University of Vienna), who discusses the details of his study with Dr. Paul Studenic in this podcast. Read the paper: https://ard.bmj.com/content/78/12/1706

Editor's Summary by Howard Bauchner, MD, Editor in Chief of JAMA, the Journal of the American Medical Association, for the February 18, 2020 issue

脂質異常症(HMG-CoA還元酵素阻害薬)の商品名、一般名の音読です。

HMG-COA reductase regulation via phosphorylation and Dephosphorylation --- Support this podcast: https://anchor.fm/kamesa-anota/support

Statistics indicate that hearing loss is on the rise. In this interview, board certified otolaryngologist Dr. Ford D. Albritton IV describes the magnitude of the problem, as well as the research associated with key nutrients that can help reduce the risk of hearing loss. It's critical that all practitioners, not just hearing specialists, put this topic on their radar so they can help patients who already have hearing loss and those who are at risk.   About the Expert Ford D Albritton IV, MD, FACS, is the director of sinus surgery at the Sinus and Respiratory Disease Center at the Texas Institute for Surgery. He has served as chairman of the board of directors at the Texas Institute for Surgery and chairman of the Department of Otolaryngology-Head & Neck Surgery at the Texas Health Presbyterian Hospital of Dallas. Innovation and creative solutions to long standing problems in his field have been a focus of his practice since completing his training at the Emory University School of Medicine. He holds patents in the fields of nutritional compounds for targeting prevention of sensorineural hearing loss based on research initiated in the early 2000s. He also holds patents and expertise in the field of sinus disease and surgery with several publications to his credit. He remains active in clinical research and has been requested as a lecturer on the subject for surgeons domestically and internationally. Current interest exists in linking dietary methods of hearing preservation to cognitive function maintenance in patients with hearing disability, defining intervention strategy, and establishing modes of prevention. Transcript Karolyn Gazella: Hello, I'm Karolyn Gazella, the publisher of the Natural Medicine Journal. Today we have a fascinating topic. We'll be talking about how certain nutrients can help reduce the risk of developing hearing loss, and we have the perfect expert to help us with this topic. Dr. Ford Albritton, IV is a board certified otolaryngologist with the Sinus and Respiratory Disease Center at the Texas Institute. Dr. Albritton, thank you so much for joining me. Ford Albritton, IV: It's my pleasure, Karolyn. Thanks for having me. Gazella: Yeah. So, how common is hearing loss, and have we actually seen an increase over the past decade or so? Albritton: Hearing loss is incredibly common, and it's been pretty consistent if we look at the prevalence. The National Institutes of Health actually has its own group that looks at communication disorders, and they estimate the prevalence of about 15% of residents in the US having a diagnosis of hearing loss, and currently that puts us at about 38 to 40 million. And you asked the question has there been an increase, and it's sort of a tricky answer. Yes, there's been an increase, but so has the population increased. In 1971, that number was 13.2 million and basically one third the current number. So, why are we seeing such an increase? Well, it's a combination of population growth and the basic dynamics of our population age. If we look at aging as a criteria for hearing loss, we can compare people that are between the ages of 45 and 54. Only about 2% of those people are going to have a diagnosis of hearing loss, but if we go up to 75 years or older, almost one half to two thirds of the population will be having a hearing loss diagnosis depending on the studies you look at. And the World Health Organization has currently estimated hearing loss at about 466 million, but by 2050 they do predict that number should hit 900 million. So, there's certainly an increase, but it's tricky to say that that's because of something changing in the environment or our susceptibility is increasing, and their point of fact is a few years ago, pediatrics journals documented that adolescents were having an increased rate of hearing loss from comparing data between '94 and 2006. They reviewed that data again in 2010 and found that that was just simply a statistical error and that they had erroneously just compared two points of data instead of contiguous and that actually the rate of hearing loss has not increased in that age group. Gazella: Okay, that's interesting. So, what is considered a normal hearing range, and at what range does there begin to be a problem? Albritton: The way we measure hearing is using something called an audiogram or audiometry, and it measures sound intensity. The official measurement unit is called the decibel, which is a logarithmic measurement of sound intensity, and we define normal hearing as a threshold where a subject can recognize a presented tone at a specific frequency less than 20 decibels. So, if you're presented a tone at a low frequency or a high frequency and you can perceive it, recognize it at a sound energy level quieter or equal to 20 decibels, that's normal. Furthermore, we use some tricks of averaging and statistics to have some simple ways of measuring. Like we will average two tones or three tones or pitches on the hearing test and come up with a number of sound intensity, and we consider anything less than 20 normal, and anything above 25 we start to believe is abnormal and probably would benefit from some sort of intervention. Gazella: Okay, great. So, let's talk a little bit about risk factor. Who's at risk of developing hearing loss? Albritton: Probably a number one factor is family history. So, genetics play a larger role than we really can appreciate at this point in our mapping of the human genome, but family history is probably the most important question we ask patients into mapping their risk for hearing loss. The second one would be noise exposures, people with a high occupational noise exposure. OSHA measures that as greater than eight hours exposed at 90 decibels, so noise exposure at that rate can cause hearing loss. And then drugs; certain chemotherapy agents, some antibiotics are notorious for being toxic to the inner ear. Certain infections; one of the great benefits of immunizations and the reason we recommend immunizations is to prevent some of these preventable causes of hearing loss. Maternal infection of mumps, measles, rubella, for instance, can have devastating consequences on a fetal ear development and could have consequent hearing loss. And then finally, sort of our chronic illnesses, diabetes, hypertension, heart disease can compromise blood flow and health to the inner ear causing problems. Inflammatory conditions such as rheumatoid arthritis, certain inner ear inflammatory conditions can also cause problems. So, it's a pretty broad area of the things that can cause hearing loss, but the biggest risk, again, being family history. Gazella: So, when we think of hearing loss, it's understood that it obviously affects communication and how we communicate with each other, but does hearing loss have any physical impact on a patient's life? Albritton: That's an interesting question, and I think that 20 years ago we probably would not have directly thought so. It obviously does affect sense of wellbeing and ability to interact with others, but it can affect a lot of other things. An interesting study from last February demonstrated a correlation of hearing impairment severity and the incidence of fractures to the radial forearm, to the hip, to the spine, and it showed that patients with severe hearing impairment actually had an increased risk of fracture that was greater than the normal hearing group, and basically you had 1.4 to 1.6 greater risk of having one of those types of fracture from a fall if your hearing was severely affected. There's lots of further digging that needs to be explored such as severe hearing loss also contribute to injuries to the balance system. That's sort of outside the scope of the research at this time. But really the most newsworthy research in the past decade is focused on the correlation of hearing loss, severity of the hearing loss, with cognitive impairment and dementia. In 2013, a paper out of Johns Hopkins authored by Dr. Lin out of their department of otolaryngology and his colleagues demonstrated in just under 2000 patients that patients with a pure-tone average, that's that average we discussed earlier, of several frequencies of over 25 decibels, they had rates in decline in their cognitive function testing that was 30% to 40% greater than their normal hearing peers. And not only that, there was a linear relation between the hearing loss severity and the degree of decrease in their cognitive function test scores. So, that data really set off alarm bells, and health organizations throughout the world, the British health system, the French health system, Danes, Italians began looking at their population, and probably the most robust examination has been the English, many thousands of patients, have agreed with this information. They put a cognitive impairment risk of 1.6 times greater than normal hearing population with hearing impairment. Interestingly, some of these studies took the next step and tried to assess, well, if we do something for the hearing, such as a hearing aid or a Cochlear implant, something that will restore hearing, does that make a difference in the cognitive impairment testing? And it actually does. An Italian study was one of the preliminary studies to look at this, and they demonstrated that either a hearing aid or a Cochlear implant could actually reverse some of this cognitive impairment seen on the testing with improved scores. The French study was pretty astounding in terms of its result. Greater than 80% of their lowest scoring cognitive impairment patients tested, they showed improvement after the Cochlear implant, which was quite surprising. So, there's a question as to how hearing loss, how is this leading to dementia? And I don't think we fully understand that yet, though there are some hypotheses, and Dr. Lin laid out about four of these. First one being is there some common physiologic pathway that's contributing to both brain damage and inner ear damage? Something like blood pressure elevations where we see some chronic ischemic changes to the brain on MRIs or diabetes or something along those lines. The second theory is something called the cognitive load theory. Basically, it surmises that the effort of constantly trying to comprehend what is being heard takes memory resources, whether it be a neurotransmitter or other nutritive resources, and the chronicity and cumulative nature of this leads to issues and errors in ongoing brain function, the ability to maintain memories in an ongoing manner. A third theory is that hearing loss may affect brain structure. We do know that in brains of patients without stimulation, stroke patients, et cetera, that there's certain areas of the brain that shrink, and it isn't necessarily that we lose cells there, but there are some changes in the simple [inaudible 00:11:38] of those cells and that hearing loss patients do appear to show some of those similar findings on their MRIs. And then finally, social isolation. We know that social isolation happens with hearing loss, and we also know that social isolation is a known risk for cognitive impairment. One theory that a lot of fellow ENTs and otolaryngologists specializing in ear have known about since the '90s is that if we fit a patient with hearing aids earlier, they do better long term, and a large study in the VA looking at World War II veterans in the '90s established that patients that obtained hearing aids earlier did better with those hearing aids long term. They were able to accurately repeat words presented to them at a higher rate than their peers who had not obtained a hearing aid and had similar hearing test results. They would have basically the same level of hearing loss, but their ability to interpret speech was impaired, and the ability for the hearing aid to function with those patients was just suboptimal and were not able to get the same level of functionality from their hearing aid. And what the theory was is that the stimulation of certain areas of the cortical brain kept those areas healthy and functioning and that the old use it or lose it hypothesis, the patients who weren't using it did not maintain that brain and it therefore degenerated, never to really fully improve. This takes it to another level and seems to suggest that it's not just those areas of brain corresponding to speech recognition; it's rather the brain as a whole that is suffering from the lack of input. Gazella: Yeah. Early intervention is always best, so that makes a lot of sense. Now, you mentioned social isolation. Are there other areas that are affected with hearing loss that negatively impact the quality of the life of the patient? Albritton: Well, I'm sure that there are, and I'm sure that we're going to discover more, but I think the most obvious is isolation and its consequential potential for depression. People that can't hear, they eventually will isolate themselves in social situations because it just becomes too embarrassing or futile for them to continue trying to participate in a conversation they can't hear. And I think we all can appreciate what that feels like. If we've ever been to a noisy restaurant and we can't hear the conversation across the table or slightly away from us, we tend to withdraw. Imagine that for patients with significant hearing loss being a daily ongoing issue, and that ends up contributing to further self-isolation, but depression, and several studies have demonstrated that there is an increased incidence of associated depression with hearing loss. Gazella: Yeah, that makes a lot of sense. Now, you mentioned genetics. So, what is the difference between hereditary hearing loss and age-related hearing loss? Albritton: I would suggest that almost all forms of hearing loss that we attribute to age probably have some genetic component. As we look at just genetic programming for your resilience, your resilience of your skin, your eyes, your hair, your ears, all of those things are sort of pre-programmed, and most people accept multi-hit hypothesis to hearing loss. In other words, that it's not one thing; it's a multitude of things over time that lead to the cumulative and irreparable damage and that there are certain susceptibilities imparted by our genetics. So, we would guess that most age-related hearing loss does have some genetic, if not total genetic, predisposition, and the fact that it's not 100% of patients over the age of 75 with hearing loss, rather one half to two thirds, sort of backs that up. But in terms of congenital or hereditary hearing loss, there are certain conditions and syndromes which we know are hearing loss related, and we can diagnose those fairly young. It's the patients over the age of 40, 50, 60 that we're less able to determine. And there are some studies, though, that have looked at what we term age-related hearing loss and looked at their genetics and have identified some mutations that are fairly specific for a family group but not universally represented in other genomic studies, and they show up in certain areas of the gene pool where we know that genes dedicated to hearing messaging are present. So, there's probably a multitude of issues with mutations over our family histories that does lead to the age-related hearing loss, so I would look at them mostly in the same way. Gazella: Yeah. It'll be interesting to see how that research kind of plays out from an epigenetic standpoint. Now, there's early evidence showing that antioxidants, specifically beta-carotene, vitamins A, C, and E and magnesium can be protective. Tell us about that research. Albritton: Sure. I want to add one more little point to the last question as it'll tie into this. We do know that insulin-like growth factor 1 is something that's important in our homeostasis and our ability to fight off reactive oxygen species or free radicals, and some studies have demonstrated that this decreases with age, and some other studies have taken it a step further and looked at does this have a role in some of the age-related hearing loss, and it does appear to have some role in that. So, it's been a natural thing for antioxidants to have been targeted as a potential therapeutic arm against the aging of the ear. You mentioned vitamin A, C, E, magnesium, and I would caution drawing conclusions to these individual compounds at this time because the data is really all over the place. There are numerous studies in mice that have demonstrated some general improvements using a group of different antioxidants versus control groups. Some of those antioxidants include things like cysteine or acetylcarnitine. Longitudinal studies, though, looking at humans with vitamins A, E, C, B12, folate have showed different results. For instance, in men, they didn't find any difference with any of those vitamins used except in men over the age of 60 they did note that folate may have given some protective benefit. In women, they found that vitamin A and folate also helped not necessarily an age dependent result, but this is interesting; vitamin C, which has been shown to be helpful in some animal models, was actually harmful and actually worsened things in some women studies. We know that folate is an effective cofactor. We know that it helps balance out homocysteine levels, which can protect ischemic vascular damage, so that makes sense to us that it would work. The roles of vitamin C are just straight antioxidant properties, so that suggests that there's something more than just straight antioxidant benefits. One interesting study in Finland that was done about 10 years ago, and they call it the disco study, and it wasn't a very large study; about 20 people were given either an antioxidant vitamin or a placebo. They had their hearing tested before a night exposed to loud music and then they had their hearing tested short term and long term afterwards, and they definitively showed that the group with the antioxidants had less impact from the noise exposure than the control group. Gazella: That's interesting. I like they called it the disco study. That speaks to the era or the timing of that study, I think. So, when we're talking about studies, the research that I read I believe also included magnesium. What would be the connection with magnesium and why would magnesium help our ears? Am I correct? Was magnesium a part of that study? Albritton: Magnesium's a part in several of these studies, and magnesium and the metals probably have a bigger role in enzymatic cofactor, enzymes that can control either the release of certain natural antioxidants or enzymes that have some role in keeping a biochemical process in its favorable state as opposed to going to its unfavorable state. Those metals are essential to these enzymes functioning theoretically, and yes, in some military studies, the use of magnesium has been shown to be effective. Gazella: Now, you mentioned a lot of nutrients, A, C, E, just talked about magnesium. Is the combination of nutrients important and are there other nutrients that you wish researchers would be looking at? Albritton: Now, you're getting to what my interest is. I think yes. I think very much there is combination therapy that makes a difference. I think we're still trying to figure out what that precisely is. There are a host of readily available organic compounds that are something we may have picked up through ethnobotany or traditional Chinese medicine or just from the vitamin industry at large, but we have found that several of these compounds do appear to help in the protection of the inner ear, the heart, the kidney, et cetera. One of those is N-acetylcysteine in rat models, which has proven to be effective at protecting the outer hair cells of the inner ear, and one of the methods we think it works is just by scavenging the free radicals, but it does turn on the body's natural production of glutathione synthesis. So, it doesn't just target the free radicals with its own ability to neutralize them. It actually turns on the body's ability to keep producing those free radical fighters. But there's something else that goes on. It seems to regulate the nitric oxide in the inner ear, and one of the things that nitric oxide can do is, depending on its concentrations, it can trigger a cell to commit cell suicide. We call that apoptosis. In damage that may be sublethal, damage that shouldn't cause a cell to destroy itself, sometimes that misregulation allows the nitric oxide to get so high that it ends up allowing that cell to die. And as you may or may not know, these cells can't regenerate at this time, and so that regulation of the nitric oxide is one unexpected benefit of the N-acetylcysteine. And that's something we see in several other compounds. Some compounds, for instance ... I'm just going to give you a brief list. Resveratrol. We know resveratrol as a miracle compound that has some anti-aging properties in animals, turns on some anti-aging genes, but we found in several studies that it has a highly effective role in reducing inner ear damage in animal studies. It has not been studied in humans to date. We believe that's a real key chemical. CoQ10 has been also very effective in guinea pig models. We know that the mitochondria stabilization appears to be important, and CoQ10 is important in the function of our energy production in the mitochondria. Replacement does appear to have beneficial effects. One independent observation as I see patients in my office all the time with a balance disorder that we can attribute to a medication being used for their high cholesterol, and a class of medications HMG-CoA reductase inhibitors, such as the statin drugs, are notorious for depleting the body's natural production of CoQ10. So, replacement of that in patients has helped with balance preservation, and anything that helps balance preservation we can assume is also working in other areas of the inner ear as well. There are a number of elements and compounds that we discussed. We put together in 2006 a group of compounds we thought were going to be important that included the resveratrol, the N-acetylcysteine, N-acetyl-carnitine, alpha lipoic acid, green tea extracts, flavonoids from citrus, the CoQ10, B complex, and the trace minerals such as selenium, manganese, magnesium, and have found that to be effective in some pilot studies that we have performed on patients with their hearing loss showing some actual improvement in their hearing using the compound versus not using the compounds. We've not had the opportunity yet to complete a double blinded study at this time, but there is certain promise with this. I think the holy grail is a compound that would be able to be taken on a daily basis that would offer protective benefits to the whole body, not just the inner ear. Gazella: Right, and when you're talking about protection, you're even talking about protection in a patient that has some hearing loss; that it can also work in that patient population. Albritton: Yes. In fact, our pilot study really only targeted patients with hearing loss. We compared patients that had many years of hearing loss, and we had multiple hearing tests on them and then started therapy with them and measured several hearing tests on the medication, were able to compare their hearing test pre and post, and were able to make those comparisons based on a preexisting condition. And so we did see some improvements in patients with existing hearing loss. Gazella: What about reversal? Is that on the radar or is that a little bit too pie in the sky to actually reverse damage, to have a hearing be regained? Albritton: There's research being done in terms of hair cell regeneration. That's several decades away at best. That, if it does prove possible, would reverse it. Now, in terms of nutritional therapy, that's an unknown. We don't have the data yet to determine that. I think it is promising that we can see improvements in cognitive function with hearing aids and with Cochlear implants, but we can't know that by correcting some of the metabolic issues or protecting the interior from damage from its own physiologic stressors or noise exposures whether that's going to actually reverse the hearing loss that has occurred. I think that's probably pretty hopeful on our parts, but never rule anything out. Gazella: Yeah. Yeah, that's for sure. Now, given how common hearing loss is, it's likely that the readers of our journal have patients in their practice who are at risk. So, in addition to the nutrients that you mentioned, what else should doctors be recommending to their patients to help protect hearing? Albritton: I think first and foremost is recognize how common of a condition this is and screen for it. Ask patients, "Have you had any problems hearing? Has your spouse indicated that you may be having trouble hearing you?" It's interesting that spouses tend to be the ones that send patients for hearing tests more often than the patient seeks testing on their own. And it's a known fact that only one in five patients with hearing loss is going to seek help for it on their own typically. It can take 10 years or so before patients seek help for the symptoms. So, it can lay dormant, it can be hiding and be attributed to mumbling or volume not being turned up loud enough before a patient truly begins to embrace there may be a problem they need to evaluate. Refer patients for hearing tests if there is a presumed hearing loss or if there's a family history of hearing loss. Any patient that is on those medications, chemotherapy drugs, certain types of antibiotics, those patients should be monitored. One other thing that I think is very important and I think most practitioners are very good about doing, but let's remind them that noise exposure can be prevented. If you can't prevent the noise exposure, then protect yourself from it and that people that have hobbies or occupational risks should be wearing some degree of hearing protection, and just like smoking cessation's important for us to counsel, the use and adoption of protective devices should be something we continually discuss at our meetings with these patients. Gazella: Yeah, it's such a good point that you bring up that one in five seek help on their own and a lot just kind of let it go, let it go, and yet early detection, the earlier it's caught, the better off they'll be. So, I'm so glad that we're putting this on the radar of the doctors who are reading our journal. This has been very interesting, and I really appreciate you for joining me today. Albritton: Well, thank you. It's been a pleasure. Gazella: Have a great day. Albritton: You as well.

This episode will discuss six simple ways you can reduce your risk of getting cataracts.  You can contact us at yopi@post.com You can also read this episode on our blog at www.yopistudio.com Feel free to check us out daily at the following and see what we are up to.   https://twitter.com/Dauricee https://www.facebook.com/yopistudio/ https://www.facebook.com/Louisiana-Entertainment-Association-671304786265477/ To learn more about our topic, here is a list of references to guide you.  R J Gerson, H L Allen, G R Lankas, J S MacDonald, A W Alberts, D L Bokelman. The toxicity of a fluorinated-biphenyl HMG-CoA reductase inhibitor in beagle dogs.Fundam Appl Toxicol. 1991 Feb ;16(2):320-9. PMID: 2055362  Julia Hippisley-Cox, Carol Coupland. Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database. BMJ. 2010;340:c2197. Epub 2010 May 20. PMID: 20488911  R G Schlienger, W E Haefeli, H Jick, C R Meier. Risk of cataract in patients treated with statins. Arch Intern Med. 2001 Sep 10; 161(16):2021-6. PMID: 11525705  S Awasthi, S K Srivatava, J T Piper, S S Singhal, M Chaubey, Y C Awasthi. Curcumin protects against 4-hydroxy-2-trans-nonenal-induced cataract formation in rat lenses. Am J Clin Nutr. 1996 Nov;64(5):761-6. PMID: 8901798  Palla Suryanarayana, Kamala Krishnaswamy, Geereddy Bhanuprakash Reddy. Effect of curcumin on galactose-induced cataractogenesis in rats. Mol Vis. 2003 Jun 9;9:223-30. PMID: 12802258  R Manikandan, R Thiagarajan, S Beulaja, G Sudhandiran, M Arumugam. Effect of curcumin on selenite-induced cataractogenesis in Wistar rat pups. Curr Eye Res. 2010 Feb;35(2):122-9. PMID: 20136422  Ramar Manikandan, Raman Thiagarajan, Sivagnanam Beulaja, Ganapasam Sudhandiran, Munuswamy Arumugam. Curcumin prevents free radical-mediated cataractogenesis through modulations in lens calcium. Free Radic Biol Med. 2010 Feb 15;48(4):483-92. Epub 2009 Dec 10. PMID: 19932168  R Manikandan, R Thiagarajan, S Beulaja, S Chindhu, K Mariammal, G Sudhandiran, M Arumugam. Anti-cataractogenic effect of curcumin and aminoguanidine against selenium-induced oxidative stress in the eye lens of Wistar rat pups: An in vitro study using an isolated lens. Chem Biol Interact. 2009 Oct 7;181(2):202-9. Epub 2009 May 27. PMID: 19481068  S Padmaja, T N Raju. Antioxidant effect of curcumin ina selenium-induced cataract of Wistar rats. Indian J Exp Biol. 2004 Jun;42(6):601-3. PMID: 15260112  B Olmedilla, F Granado, I Blanco, M Vaquero. Lutein, but not alpha-tocopherol, supplementation improves visual function in patients with age-related cataracts: a 2-y double-blind, placebo-controlled pilot study. Nutrition. 2003 Jan;19(1):21-4.PMID: 12507634  Andrea Basso, Giuliana Rossolini, Anna Piantanelli, Domenico Amici, Isabella Calzuola, Loretta Mancinelli, Valeria Marsili, Gian Luigi Gianfranceschi. Aging reversibility: from thymus graft to vegetable extract treatment-- application to cure an age-associated pathology. Biogerontology. 2005;6(4):245-53. PMID: 16333758 https://www.researchgate.net/publication/44574408_Alcohol_Use_and_Cataract    

Statins, also known as HMG-CoA reductase inhibitors, are a class of lipid-lowering medications. Should you take them or not? Dr. Greg shares with us the dubious nature of these frequently prescribed drugs so that you can make an informed decision as to whether or not they're right for you. Send your questions to: askdrpatrick@twwclinics.com Find a clinic: https://twwclinics.com/clinics/ Find a lab test: http://www.twwlabs.com/ FACEBOOK: https://www.facebook.com/TheHormoneWh… https://www.facebook.com/TheWellnessWay/

This podcast reviews HMG COA reductase inhibiors or "Statins" for hypercholesterolemia. Use, action, and easy to remember tips for side-effects are reviewed.

Carl Franklin and Richard Morris talk to Amber O'Hearn about being a carnivore, evolution, sleep, ketogenic metabolism, and a few other tasty nuggets you won't want to miss! Errata Richard forgot to mention when working with Transglutaminase .. wear food prep gloves. Amber sent us a piece of errata. She writes: In our podcast, Carl asks me if babies *have* to be in ketosis to build brains, and I say yes, but that's not true. That is, the primary way that babies build fat and cholesterol in the brain in normal conditions *is* out of ketone bodies, though a small proportion is also made from glucose. I have a few references on this point in the talk transcript on my blog. The critical question is: What happens if there are no ketones to be had and only glucose? The answer seems to be that glucose will suffice. There is a rare inborn error of metabolism called HMG-CoA lyase deficiency, which prevents the body from making ketones. A paper by another brilliant Morris ( Cerebral ketone body metabolism ) reports that people afflicted with this have white matter abnormalities, but no noticeable loss of function, except of course, they can't go without food for long. This suggests that in cases where there are no circulating ketones, the glucose alternative pathway will take over, and get at least an adequate brain constructed. It occurs to me that children with this condition may be perfect candidates for the therapeutic use of ketones esters, provided the condition doesn't somehow prevent their use. "Given the importance of KBs [ketone bodies] as substrates for myelination, one might expect disorders of ketogenesis to be associated with cerebral white-matter abnormalities. Magnetic resonance imaging has, indeed, shown diffuse mildly increased signal in the white matter of patients with HMG-CoA lyase deficiency. Superimposed on this are foci of more abnormal signal. In most cases, multiple lesions have been present, varying in size from a few millimetres to large confluent areas; as well as in the cerebral hemispheres, they have been reported in the internal capsule and brainstem but not in the corpus callosum or cerebellar white matter. Despite the imaging abnormalities, most patients have had no neurological problems and normal or slightly below average intelligence. The findings would be compatible with hypomyelination, caused by the lack of KB."

I continue to be horrified by guidelines issued by the American Heart Association and American College of Cardiology, which speak of giving statin drugs to healthy people. Meanwhile, draft recommendations from the US Preventive Task Force have issued new directives claiming that healthy people should be taking statin drugs as a “preventative against possible future illness.” Their main plan is to see one third of all adults in the United States are put on statin drugs—44% of all men and 22% of all women—even if none of these people have ever had a previous heart attack or stroke. Statins are the most widely prescribed drugs on the market. One in four Americans over 45 are already on statins, despite more than 900 studies reporting dangerous side effects from these drugs. These range from heightened risks of cancer and diabetes to sexual problems, neuropathy, and liver dysfunction, as well as immune system suppression, and even a higher risk of cataracts. In Britain too, statins are the most commonly prescribed drugs, costing the NMS £450 million a year. Now 40% of adults (175 million people) are being advised to take the drug. If the new directives are put into practice by the UK medical establishment—as they are likely to be—the numbers of men and women being prescribed statins could well become legion. What are statins anyway? Statins are a group of drugs prescribed to lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver. Statins have many different names, such as Lipitor, Lescol, Mevacor, Altocor, and Zocor. These drugs are prescribed on the assumption that they will lower the risks of cardiovascular events and strokes. The new directives assert that, if given to healthy people, they could help protect the population from heart attacks and strokes at some time in the future. Happily, a growing number of cardiologists are strongly opposed to the new directives. What's the problem with statins? Plenty: • They deplete your body of CoQ10, which is essential for every cell in your body, and ubiquinol. Both CoQ10 and ubiquinol keep the so-called bad cholesterol from doing harm to your body. However, very few mainstream doctors are ever aware of these dangers. One exception is cardiologist Steven Sinatra, founder of the New England Heart Center. Sinatra recommends that anyone taking statins should take between 100 and 200 mg of CoQ10 or ubiquinol each day as protection. • Statins lower Vitamin K2 in the body. This puts you at risk of deficiency of this vitamin, which contributes to chronic diseases, such as osteoporosis, cancer, and brain disease. • Long-term statin use—10 years or so—has been shown to increase your risk of diabetes, neurogenerative diseases, musculoskeletal problems, and even cataracts.

I continue to be horrified by guidelines issued by the American Heart Association and American College of Cardiology, which speak of giving statin drugs to healthy people. Meanwhile, draft recommendations from the US Preventive Task Force have issued new directives claiming that healthy people should be taking statin drugs as a “preventative against possible future illness.” Their main plan is to see one third of all adults in the United States are put on statin drugs—44% of all men and 22% of all women—even if none of these people have ever had a previous heart attack or stroke. Statins are the most widely prescribed drugs on the market. One in four Americans over 45 are already on statins, despite more than 900 studies reporting dangerous side effects from these drugs. These range from heightened risks of cancer and diabetes to sexual problems, neuropathy, and liver dysfunction, as well as immune system suppression, and even a higher risk of cataracts. In Britain too, statins are the most commonly prescribed drugs, costing the NMS £450 million a year. Now 40% of adults (175 million people) are being advised to take the drug. If the new directives are put into practice by the UK medical establishment—as they are likely to be—the numbers of men and women being prescribed statins could well become legion. What are statins anyway? Statins are a group of drugs prescribed to lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver. Statins have many different names, such as Lipitor, Lescol, Mevacor, Altocor, and Zocor. These drugs are prescribed on the assumption that they will lower the risks of cardiovascular events and strokes. The new directives assert that, if given to healthy people, they could help protect the population from heart attacks and strokes at some time in the future. Happily, a growing number of cardiologists are strongly opposed to the new directives. What’s the problem with statins? Plenty: They deplete your body of CoQ10, which is essential for every cell in your body, and ubiquinol. Both CoQ10 and ubiquinol keep the so-called bad cholesterol from doing harm to your body. However, very few mainstream doctors are ever aware of these dangers. One exception is cardiologist Steven Sinatra, founder of the New England Heart Center. Sinatra recommends that anyone taking statins should take between 100 and 200 mg of CoQ10 or ubiquinol each day as protection. Statins lower Vitamin K2 in the body. This puts you at risk of deficiency of this vitamin, which contributes to chronic diseases, such as osteoporosis, cancer, and brain disease. Long-term statin use—10 years or so—has been shown to increase your risk of diabetes, neurogenerative diseases, musculoskeletal problems, and even cataracts. Dr. Eric Topol, highly respected cardiologist and Professor of Genomics at Scripps Research Institute in California, wrote an excellent article for The New York Times Opinion Page in which he warns: “We’re overdosing on cholesterol-lowering statins.” Topol is especially concerned about the sharp increase in the prevalence of Type 2 Diabetes that is occurring in people using them. He writes: “Statins have been available since the 1980s but their risk of inducing diabetes did not surface for nearly 20 years. When all the data available from multiple studies was pooled in 2010 for more than 91,000 patients randomly assigned to be treated with a statin or a sugar pill (placebo), the risk of developing diabetes with any statin was one in every 255 patients treated. But this figure is misleading since it includes weaker statins like Pravachol and Mevacor—which were introduced earlier and do not carry any clear-cut risk. It is only with the more potent statins—Zocor (now known as simvastatin), Lipitor (atorvastatin), and Crestor (rosuvastatin)—particularly at higher doses—that the risk of diabetes shows up. The cause and effect was unequivocal because the multiple large trials of the more potent statins had a consistent excess of diabetes.” Meanwhile, a recent study by Jean A. McDougall and her colleagues in the Journal of Cancer Epidemiology, Biomarkers & Prevention reveals that long-term use of statins increases the risk of both lobular and ductal breast cancer in women between 55 and 74. I am no doctor, but what I have learned during my more than forty years of writing and broadcasting on health is this: When a body is restored to healthy functioning naturally, the need for medication is either dramatically reduced or, more often than not, eliminated altogether. Statins, like most pharmaceuticals, only mask symptoms—they do not heal. Only nature can heal from within. My advice to anyone thinking of accepting the new directives is this: Before you agree to take statins, research the implications of doing so. Learn as much as you can about statin drugs. There are excellent natural alternatives, such as inexpensive dietary changes. So, if your doctor wants to prescribe statins for you, you can be sure you have done your homework. Then you’ll know yourself if these drugs are appropriate for you. Chances are they are not. Here are a few recommendations for where to start your research: U-T San Diego “Doctors assail new guidelines for statins: 18 November, 2013 Cancer Epidemiology, Biomarkers & Prevention; Published Online First July 5, 2013; doi: 10.1158/1055-9965.EPI-13-0414 http://www.greenmedinfo.com/toxic-ingredient/statin-drugs. This is an excellent compilation of dangers from statin drugs, with links to abstracts. www.ncbi.nlm.nih.gov/pubmed/24052188 Association of statin use with cataracts: a propensity score-matched analysis. This is a good source of information on the use of statins for the elderly. A. Sultan and N. Hynes, "The Ugly Side of Statins. Systemic Appraisal of the Contemporary Un-Known Unknowns," Open Journal of Endocrine and Metabolic Diseases, Vol. 3 No. 3, 2013, pp. 179-185. doi: 10.4236/ojemd.2013.33025.

I continue to be horrified by guidelines issued by the American Heart Association and American College of Cardiology, which speak of giving statin drugs to healthy people. Meanwhile, draft recommendations from the US Preventive Task Force have issued new directives claiming that healthy people should be taking statin drugs as a “preventative against possible future illness.” Their main plan is to see one third of all adults in the United States are put on statin drugs—44% of all men and 22% of all women—even if none of these people have ever had a previous heart attack or stroke. Statins are the most widely prescribed drugs on the market. One in four Americans over 45 are already on statins, despite more than 900 studies reporting dangerous side effects from these drugs. These range from heightened risks of cancer and diabetes to sexual problems, neuropathy, and liver dysfunction, as well as immune system suppression, and even a higher risk of cataracts. In Britain too, statins are the most commonly prescribed drugs, costing the NMS £450 million a year. Now 40% of adults (175 million people) are being advised to take the drug. If the new directives are put into practice by the UK medical establishment—as they are likely to be—the numbers of men and women being prescribed statins could well become legion. What are statins anyway? Statins are a group of drugs prescribed to lower cholesterol levels by inhibiting the enzyme HMG-CoA reductase, which plays a central role in the production of cholesterol in the liver. Statins have many different names, such as Lipitor, Lescol, Mevacor, Altocor, and Zocor. These drugs are prescribed on the assumption that they will lower the risks of cardiovascular events and strokes. The new directives assert that, if given to healthy people, they could help protect the population from heart attacks and strokes at some time in the future. Happily, a growing number of cardiologists are strongly opposed to the new directives. What’s the problem with statins? Plenty: They deplete your body of CoQ10, which is essential for every cell in your body, and ubiquinol. Both CoQ10 and ubiquinol keep the so-called bad cholesterol from doing harm to your body. However, very few mainstream doctors are ever aware of these dangers. One exception is cardiologist Steven Sinatra, founder of the New England Heart Center. Sinatra recommends that anyone taking statins should take between 100 and 200 mg of CoQ10 or ubiquinol each day as protection. Statins lower Vitamin K2 in the body. This puts you at risk of deficiency of this vitamin, which contributes to chronic diseases, such as osteoporosis, cancer, and brain disease. Long-term statin use—10 years or so—has been shown to increase your risk of diabetes, neurogenerative diseases, musculoskeletal problems, and even cataracts. Dr. Eric Topol, highly respected cardiologist and Professor of Genomics at Scripps Research Institute in California, wrote an excellent article for The New York Times Opinion Page in which he warns: “We’re overdosing on cholesterol-lowering statins.” Topol is especially concerned about the sharp increase in the prevalence of Type 2 Diabetes that is occurring in people using them. He writes: “Statins have been available since the 1980s but their risk of inducing diabetes did not surface for nearly 20 years. When all the data available from multiple studies was pooled in 2010 for more than 91,000 patients randomly assigned to be treated with a statin or a sugar pill (placebo), the risk of developing diabetes with any statin was one in every 255 patients treated. But this figure is misleading since it includes weaker statins like Pravachol and Mevacor—which were introduced earlier and do not carry any clear-cut risk. It is only with the more potent statins—Zocor (now known as simvastatin), Lipitor (atorvastatin), and Crestor (rosuvastatin)—particularly at higher doses—that the risk of diabetes shows up. The cause and effect was unequivocal because the multiple large trials of the more potent statins had a consistent excess of diabetes.” Meanwhile, a recent study by Jean A. McDougall and her colleagues in the Journal of Cancer Epidemiology, Biomarkers & Prevention reveals that long-term use of statins increases the risk of both lobular and ductal breast cancer in women between 55 and 74. I am no doctor, but what I have learned during my more than forty years of writing and broadcasting on health is this: When a body is restored to healthy functioning naturally, the need for medication is either dramatically reduced or, more often than not, eliminated altogether. Statins, like most pharmaceuticals, only mask symptoms—they do not heal. Only nature can heal from within. My advice to anyone thinking of accepting the new directives is this: Before you agree to take statins, research the implications of doing so. Learn as much as you can about statin drugs. There are excellent natural alternatives, such as inexpensive dietary changes. So, if your doctor wants to prescribe statins for you, you can be sure you have done your homework. Then you’ll know yourself if these drugs are appropriate for you. Chances are they are not. Here are a few recommendations for where to start your research: U-T San Diego “Doctors assail new guidelines for statins: 18 November, 2013 Cancer Epidemiology, Biomarkers & Prevention; Published Online First July 5, 2013; doi: 10.1158/1055-9965.EPI-13-0414 http://www.greenmedinfo.com/toxic-ingredient/statin-drugs. This is an excellent compilation of dangers from statin drugs, with links to abstracts. www.ncbi.nlm.nih.gov/pubmed/24052188 Association of statin use with cataracts: a propensity score-matched analysis. This is a good source of information on the use of statins for the elderly. A. Sultan and N. Hynes, "The Ugly Side of Statins. Systemic Appraisal of the Contemporary Un-Known Unknowns," Open Journal of Endocrine and Metabolic Diseases, Vol. 3 No. 3, 2013, pp. 179-185. doi: 10.4236/ojemd.2013.33025.

Das multiple Myelom ist eine Erkrankung, bei der terminal differenzierte Plasmazellen das Knochenmark infiltrieren, wodurch das typische klinische Bild eines Myelompatienten zustande kommt. In den letzten Jahren haben sich die Hinweise gehäuft, dass die Bindung der Myelomzellen im Knochenmark an Stromazellen die Chemosensitivität der Myelomzellen vermindert und somit zur „de-novo drug resistance" beiträgt. Das primäre Ziel dieser Arbeit war es, ein Zellmodell zu entwerfen, mit welchem die Untersuchung der Interaktionen von Stromazelle und Myelomzelle und damit der zelladhäsionsabhängigen Zytostatikaresistenz (CAM-DR) möglich ist. Darüber hinaus sollte diese Zytostatikaresistenz charakterisiert und mögliche molekulare Therapietargets identifiziert werden, welche eine Verhinderung von CAM-DR ermöglichen. Da das etablierte Kokulturmodell auf einer Kultur mit der Stromazelllinie HS-5 beruhte, wurde diese zuerst bezüglich der Oberflächenmarker und des Apoptoseverhaltens charakterisiert. Es wurde gezeigt, dass sich primäre Stromazellen aus Knochenmarksspiraten und die Stromazelllinie HS-5 zwar in ihrer Chemosensibilität unterscheiden, sie prinzipiell jedoch gleich reagieren. Beide lösen bei einer direkten Kokultur mit Myelomzellen im selben Maße CAMDR in den Myelomzellen aus. Die anschließende Charakterisierung von CAM-DR bewies, dass CAM-DR nicht zelllinienspezifisch und nicht zytostatikaspezifisch ist. HS-5-Zellen verhinderten nicht nur die Entstehung von später sondern auch von früher Apoptose. Es zeigte sich, dass das Ausmaß von CAM-DR maßgeblich von der Dauer der Kokultivierung abhängt. Des Weiteren stellte sich heraus, dass in diesem Zellmodell die von den HS-5-Zellen sezernierten Zytokine keinen Einfluss auf die Apoptoseinduktion hatten. Konsequenterweise wurden die Oberflächenantigene auf den Myelomzellen und den Stromazellen quantifiziert und teilweise deren Alteration nach einer Inkubation mit Zytostatika festgestellt. Sowohl eine Blockade der wichtigsten Integrine VLA-4 und LFA-1 als die Modulation der wichtigsten Signalwege konnte CAM-DR zwar teilweise, aber nicht vollkommen verhindern. Allein Vertreter der Statine, Simvastatin und Lovastatin, konnten CAM-DR drastisch reduzieren. Wie weiterhin gezeigt werden konnte, lag dies nicht an einer verminderten Expression von Oberflächenintegrinen, einer verminderten Zytokinsekretion der Stromazellen oder einer verstärkten Deadhäsion der Myelomzellen von den Stromazellen, sondern an der Hemmung der Geranylgeraniolpyrophosphatsynthese. Wir wiesen nach, daß Statine in der Kokultur über die Hemmung des HMG-CoA-Reduktase/GG-PP/Rho/Rho-kinase-Signalwegs wirken. Dies wurde in weiteren Experimenten, in denen selektiv die Geranylgeranioltransferase mittels GGTI-298 und die Rho-Kinase mit Y-27632 gehemmt wurden, bestätigt. Die Ergebnisse der vorliegenden Arbeit können als Grundlage für einen potentiellen Einsatz von Statinen in der Therapie des multiplen Myeloms dienen, denn bezüglich des dargestellten Signalwegs wirken die Statine bereits im subtoxischen Bereich. Die weitere Erforschung von CAM-DR und deren assoziierte Signalwege bei anderen Tumorentitäten sowie die Evaluation der klinischen Relevanz der Gabe von Statinen zur Blockade von CAM-DR ergeben sich als wichtige nächste Schritte als Konsequenz der vorliegenden Arbeit.

Sowohl für die Inhibierung der Apoptose zur Plaquestabilisierung, wie auch für eine selektive Induktion von Apoptose in Zellen der Neointima zur Restenose-prävention ist ein besseres Verständnis der Apoptoseregulation in glatten Gefäßmuskelzellen erforderlich. In dieser Arbeit wurden glatte Gefäßmuskelzellen aus Media und Neointima der Ratte im Hinblick auf ihre Empfindlichkeit auf Statinbehandlung untersucht. Diese Zellen repräsentieren ein gut charakterisiertes und breit verwendetes Modell. Die Ergebnisse basieren auf Versuchen mit Zellkulturen und können als Grundlage für Versuche mit menschlichen Zellen und/oder weitere Tierexperimente betrachtet werden. Man kann Folgendes zusammenfassen: A). Statine induzieren in vitro Apoptose sowohl in Media als auch in Neointima glatter Gefäßmuskelzellen. Diesen Effekt beobachtet man nur bei den lipophilen Statinen Lovastatin, Simvastatin und Fluvastatin. Das hydrophile Pravastatin zeigt keinen Effekt. Die Apoptoseinduktion in glatten Gefäßmuskelzellen aus der Media war gering bei serumfreien Bedingungen. B). Die Neointima Zellen sind im Vergleich zu den Media Zellen sowohl bei serumhaltigen, als auch unter serumfreien Bedingungen deutlich empfindlicher auf Apoptoseinduktion durch Statine. C). Eine mögliche Erklärung für die beobachteten Unterschiede könnte in der niedrigeren Expression des antiapoptotischen Proteins cIAP-1 in Neointima Zellen liegen. Dank der Ergebnisse dieser Versuche könnten neue effektive Strategien zur Prävention der Restenose nach Ballonangioplastie entwickelt werden, z.B. durch die lokale Anwendung lipophiler Statine mittels entsprechender Stentbeschich-tung.