Podcasts about ogtt

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter Ralph DeFronzo is a distinguished diabetes researcher and clinician whose groundbreaking work on insulin resistance has reshaped the understanding and treatment of type 2 diabetes. In this episode, Ralph shares insights from his five decades of research, including his pivotal role in bringing metformin to the U.S. and developing SGLT2 inhibitors. Ralph explores the impacts of insulin resistance on specific organs, the pharmacologic interventions available, and the gold-standard euglycemic clamp method for measuring insulin resistance. This episode is a masterclass in the pathophysiology and treatment of type 2 diabetes, featuring an in-depth discussion of GLP-1 receptor agonists, metformin, and a lesser-known class of drugs that opened Peter's eyes to new possibilities in diabetes care. We discuss: Metabolic disease as a foundational driver of chronic illness [4:00]; Defining insulin resistance: effects on glucose, fat, and protein metabolism, and how it varies between healthy, obese, and diabetic individuals [8:15]; The historical significance of the development of the euglycemic clamp technique for measuring insulin resistance [11:45]; How insulin affects different tissues: liver, muscle, and fat cells [15:00]; The different ways insulin resistance manifests in various tissues: Alzheimer's disease, cardiovascular disease, and more [25:00]; The dangers of hyperinsulinemia, and the importance of keeping insulin levels within a physiological range [29:00]; The challenges of identifying the genetic basis of insulin resistance and type 2 diabetes [37:00]; The “ominous octet”—a more comprehensive model of type 2 diabetes than the traditional triumvirate [45:45]; The kidneys' unexpected role in worsening diabetes, and how SGLT2 inhibitors were developed to treat diabetes [55:45]; How insulin resistance in the brain and neurocircuitry dysfunction contribute to overeating and metabolic disease [1:04:15]; Lipotoxicity: how overeating fuels insulin resistance and mitochondrial dysfunction [1:07:30]; Pioglitazone: an underappreciated and misunderstood treatment for insulin resistance [1:10:15]; Metformin: debunking the misconception that it is an insulin sensitizer and explaining its true mechanism of action [1:19:15]; Treating diabetes with triple therapy vs. the ADA approach: a better path for diabetes management [1:24:00]; GLP-1 agonists, the Qatar study, and rethinking diabetes treatment [1:31:30]; Using a hyperglycemic clamp to look for genes that cause diabetes [1:45:15]; The superiority of measuring C-peptide instead of insulin to assess beta-cell function [1:46:45]; How GLP-1-induced weight loss affects muscle mass, the benefits and risks of myostatin inhibitors, and the need for better methods of evaluating functional outcomes of increased muscle mass [1:51:30]; The growing crisis of childhood obesity and challenges in treating it [2:02:15]; The environmental and neurological factors driving the obesity epidemic [2:07:30]; The role of genetics, insulin signaling defects, and lipotoxicity in insulin resistance and diabetes treatment challenges [2:11:00]; The oral glucose tolerance test (OGTT): detecting early insulin resistance and beta cell dysfunction [2:18:30]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

On May 22, 2024, we summarized a then soon-to-be-released ACOG CPU on Screening for GDM in Pregnancy and Postpartum. That CPU was officially released July 2024. That update endorsed the possibility of immediate postpartum GTT testing with a 75-gram OGTT. Now, on September 19, 2024, authors from UT Houston have published a systematic review/meta-analysis on this subject. In this episode, we will review what this data is and what it isn't. Listen in for details.

Episode 2519 - On this Friday's show Vinnie Tortorich speaks with author Daniel Trevor and they discuss empowering yourself through health testing, lifestyle changes, and more. https://vinnietortorich.com/2024/07/empowering-yourself-with-daniel-trevor-episode-2519 PLEASE SUPPORT OUR SPONSORS YOU CAN WATCH ALL THE PODCAST EPISODES ON YOUTUBE - Empowering Yourself Daniel Trevor is the author of “The Unholy Trinity.” (2:00) He almost died of a heart attack at age 72 and he decided to research heart health. (3:30) He shares what happened to him that day. Being slim doesn't necessarily mean you are metabolically healthy. He investigated the most important lab tests the average person can do, without needing a doctor's prescription. (9:30) He recommends the OGTT (oral glucose tolerance test) with insulin. He learned what he was doing wrong in his nutrition. Another test is GGT (gamma-glutamyl transferase). Empowering yourself is important. The book is not only about how Daniel reversed his co-morbidities, but it's also an exposé on Big Food and Big Pharma. (25:30) The Unholy Trinity Carbs, sugars, and oils are what he calls “The Unholy Trinity.” (27:00) Vinnie shares his inspiration and deep dive behind his documentary “Beyond Impossible.”(32:00) Daniel did some research on a study called the Ischemia Trial. (42:00) The trial's goal was to show the effectiveness of certain invasive procedures for prevention; however, it only showed that lifestyle changes were more effective. Statins for primary prevention haven't proven to be effective. (50:00) You can find Daniel at his website You can download sample chapters. The book will also be made available in Vinnie's Book Club in the near future. There's a new NSNG® Foods promo code you can use: enter VINNIE and get 15% off! (25:00) The promo code ONLY works on the NSNG® Foods website, NOT on Amazon. Vinnie's new documentary "Dirty Keto" is out soon! Go to to get it at ! [the_ad id="20253"] PURCHASE BEYOND IMPOSSIBLE (2022) The documentary launched on January 11! Order it TODAY! This is Vinnie's third documentary in just over three years. Get it now on Apple TV (iTunes) and/or Amazon Video! Link to the film on Apple TV (iTunes):  Then, Share this link with friends, too! It's also now available on Amazon (the USA only for now)!  Visit my new Documentaries HQ to find my films everywhere: REVIEWS: Please submit your REVIEW after you watch my films. Your positive REVIEW does matter! FAT: A DOCUMENTARY 2 (2021) Visit my new Documentaries HQ to find my films everywhere: Then, please share my fact-based, health-focused documentary series with your friends and family. The more views, the better it ranks, so please watch it again with a new friend! REVIEWS: Please submit your REVIEW after you watch my films. Your positive REVIEW does matter! FAT: A DOCUMENTARY (2019) Visit my new Documentaries HQ to find my films everywhere: Then, please share my fact-based, health-focused documentary series with your friends and family. The more views, the better it ranks, so please watch it again with a new friend! REVIEWS: Please submit your REVIEW after you watch my films. Your positive REVIEW does matter!  

Daniel shares his incredible health journey - from battling type 2 diabetes, nonalcoholic fatty liver disease, and osteoporosis to overcoming a heart attack and undergoing a percutaneous coronary intervention, Daniel's story is both inspiring and eye-opening. During the podcast, Shawn and Daniel delve into the importance of comprehensive testing, like the OGTT with insulin, and address financial incentives behind common medical procedures like stents and bypass surgeries. Daniel provides a compelling critique of traditional dietary advice, advocating for an ancestral diet and highlighting the negative impacts of high fructose, sugar, and seed oils. Find out about Daniel's transformation through low-carb, keto, and carnivore diets, his success with intermittent fasting and fasted exercise, and the triumph he shares in his book, "Unholy Trinity." With endorsements from respected doctors and a top spot on Amazon for heart disease and diabetes, Daniel's story is not to be missed. Website: www.DanielTrevor.com Timestamps: 00:00 Trailer. 00:48 Introduction. 04:27 Daniel's dietary evolution and book. 07:34 Realization about misleading health information and its effects. 10:24 Ancel Keys. 14:34 Glycocalyx protection against LDL, damaged by smoking. 16:48 Doctor Phil talked about low-fat diet deception. 19:02 Surprising research findings. 21:53 Doctors lack knowledge of diabetes testing. 25:24 Exercise vs heart attack risk. 28:17 PCI procedure, statins, and ischemia trial. 29:56 Challenges of medical industry and gratitude expressed. 35:05 Addictions and diet. 36:50 Trinity of triumph: low carb, keto, carnivore. 41:47 False data and fake science. 44:39 Endorsements for book. 45:58 Selective, impactful testing. 49:05 How to avoid surprises. 51:35 Where to find Daniel. See open positions at Revero: https://jobs.lever.co/Revero/ Join Carnivore Diet for a free 30 day trial: https://carnivore.diet/join/ Carnivore Shirts: https://merch.carnivore.diet Subscribe to our Newsletter: https://carnivore.diet/subscribe/ . ‪#revero #shawnbaker #Carnivorediet #MeatHeals #HealthCreation   #humanfood #AnimalBased #ZeroCarb #DietCoach  #FatAdapted #Carnivore #sugarfree  ‪

Sitting is a new Tobacco. If you are sitting for a long time, you are likely to enter into a high risk zone of developing diabetes & other co-morbid diseases. So try to be physically active & if you are in a sitting job, try to get-up and move after every 1 hour. To check whether you are diabetic or not, get your Glycosylated Haemoglobin A1c (GHb%) test or Oral Glucose Tolerance Test (OGTT) with 75gm of glucose. OGTT is the gold standard for the diagnosis of diabetes, informed Dr. Sunil Gupta. Answering on a query online, Dr. Kavita expressed that calories distribution is different for different person and also depends on whether you are sedentary or moderate or hard worker. While answering a question on millets, she said that people with diabetes may consume millets as they are rich in fibre & micronutrients. The post prandial blood sugar spikes, can be controlled by splitting of meal or changing the order of the meals, she added. Diabetes is your life partner and one should take it's care with utmost personal attention, quoted Dr. Gupta. Recorded on 9th February 2024.

Sugar, Immune Health and Two Studies Let us start right out of the gate with two studies. #1: Here is the abstract from European Journal of Clinical Nutrition: "Milk contributes with saturated fat, but randomized controlled trials (RCT) on the effects of dairy on the risk of type 2 diabetes (T2D) where dairy is given as whole foods are scarce. The objective of our study was to investigate the long-term effects of semi-skimmed milk on insulin sensitivity and further to compare milk with sugar-sweetened soft drinks (SSSD). A secondary analysis of a 6-month RCT with 60 overweight and obese subjects randomly assigned to 1 L/d of either milk (1.5 g fat/100 mL), SSSD, non-calorie soft drink (NCSD), or water was conducted. Insulin sensitivity was evaluated by oral glucose tolerance test (OGTT) and plasma free fatty acids. Second, fasting blood lipids, blood pressure, and concentration of plasminogen activator inhibitor-1 were assessed......and more on antibiotic resistance. Enjoy, Dr. M

I grab the mic to discuss my latest lab test results and how I'm shocked that my ApoB came out much higher than anticipated. This is a protein that can be used to determine heart disease risk. I discuss the differences between Medicine 2.0 (attacking the issue after you have it) and Medicine 3.0 (preventing the issue before it occurs). Below are extra biomarkers that Dr. Peter Attia recommends we get tested. Coronary calcium scan A screening that looks for calcium deposits in the heart's arteries—to determine risk for cardiovascular disease. This test involves a CT scan of your heart, which is then used to give you a calcium score. The higher your score, the more likely you are to develop heart disease.  In addition to a standard annual blood test—which includes a basic metabolic panel and a complete blood count (CBC)—Attia also recommends five preventative tests: Biomarker Tests: Lipoprotein (a) (Lp(a)-P): Certain LPA gene expressions are linked to an increased risk for blood vessel diseases, stroke, and heart attack. You only need to get this test done once to uncover your genotype.  APOE Gene: This one time test can determine your risk for neurodegenerative diseases like Alzheimer's. ApoB: This test measures ApoB levels, the main protein found in the “bad” low-density lipoprotein (LDL) cholesterol, and can be used to determine heart disease risk. OGTT with insulin measurements: This test has more sensitivity and specificity than a typical A1C glucose test when used to diagnose pre-diabetes. ALT: This test can indicate fatty liver disease risk. When alanine transaminase (ALT)—an enzyme that is released when your liver is injured or damaged—levels are high, it may indicate that your liver isn't functioning optimally.

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter In this “Ask Me Anything” (AMA) episode, Peter dives deep into the critical topic of metabolic disease. He first sheds light on how poor metabolic health drives up the risk of developing other chronic diseases such as cardiovascular disease, cancer, neurodegenerative disease, and overall mortality. He explores the array of metrics and tests used to assess metabolic health, underscoring his preferred methodologies utilized with patients. Finally, Peter provides an overview of the factors one can manipulate in order to improve metabolic health. If you're not a subscriber and are listening on a podcast player, you'll only be able to hear a preview of the AMA. If you're a subscriber, you can now listen to this full episode on your private RSS feed or our website at the AMA #51 show notes page. If you are not a subscriber, you can learn more about the subscriber benefits here. We discuss: Importance of metabolic health and a primer on metabolic disease [1:30]; How poor metabolic health increases one's risk for other chronic diseases [6:00]; How useful is body weight and BMI for estimating metabolic health? [9:45]; Overview of various tests and metrics used to understand metabolic health [12:15]; Traditional biomarkers and how Peter's point of view may differ from the guidelines [15:00]; Lactate: insights into metabolic health through fasting and resting lactate levels [17:00]; Zone 2 output: an important functional test of metabolic health [20:00]; Cardiopulmonary exercise testing (CPET) [25:45]; Visceral adipose tissue (VAT): what is VAT and how does it impact health? [27:00]; Oral glucose tolerance test (OGTT): how it works and why it is such an important metric for assessing metabolic health [32:15]; The utility of a continuous glucose monitor (CGM) [40:45]; Liver function and NAFLD [42:15]; Sleep as an intervention [46:00]; Exercise as an intervention [53:15]; Diet and nutrition [59:00]; How reducing stress can improve metabolic health [1:05:15]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

Wollt ihr unsere Arbeit unterstützen?Carnitarier UGIBAN: DE98 7016 9388 0000 1849 42oder PAYPAL: info@carnitarier.de Herzlichen Dank an den WERBEPARTNER www.carnivoro.deMit dem Gutscheincode CARNITARIER erhältst du 5 % Rabatt auf die Produkte!Affiliate Link: www.carnivoro.de/carnitarierin Folge 112: Ketologix über Remission seines Typ 1 DiabetesLucas, 55, Diplom-Informatiker, von Ketologix erklärt uns im Interview wie er zunächst mit einer kohlenhydratreichen Ernährung seinen Typ 1 Diabetes regeln musste. Das ständige Messen und Zucker zuführen und Insulin spritzen wurde ihm allerdings so sehr zur Last. Auch die Tatsache, dass man mit Insulin so sehr zunimmt ging ihm gegen den Strich. Er versuchte die Gewichtszunahme zunächst mit Sport zu kompensieren, aber auch das erwies sich als unsäglich kompliziert und nahm ihm die Freude am Sport. So stieß er auf die ketogene Ernährung und war nach der Umstellung bereits sehr bald nur mehr auf das Basalinsulin angewiesen. Was für eine Erleichterung. Aber auch dieses Basalinsulin konnte er Stück für Stück reduzieren. So schaffte er es nach zwei Jahren ketogener Ernährung gänzlich auf Insulin zu verzichten. Seine Bauchspeicheldrüse arbeitete wieder besser und hatte sich wohl durch die ketogene Ernährung erholt. Er konnte somit, vermutlich auch durch die frühe Umstellung auf Keto, seinen Typ 1 Diabetes in Remission bringen. Des Weiteren geht es um Unterzucker mit und ohne ketogenen Stoffwechsel, um den Oralen Glucose Toleranz Test, um den Langzeitzucker HbA1C, Gluconeogenese, Alkoholkonsum in der Ketose, Verbesserung der Schuppenflechte durch Carnivore, kontinuierliche Glucosemessung CGM, Blutzuckerschwankungen, Typ 2 Diabetes, Remission nur solange die ketogene Ernährung beibehalten wird, LDL, HDL und Triglyceride, Lean Mass Hyper Responder, Essensideen mit Carnivore, Milchprodukte.Im Podcast empfiehlt Lucas das Buch „Dr. Bernstein's Diabetes Solution“ Lucas könnt ihr erreichen unter: www.instagram.com/ketologixwww.facebook.com/ketologix oder www.twitter.com/ketologix.  Fleischzeit ist der erste deutschsprachige Podcast rund um die carnivore Ernährung. Hier erfahrt ihr Tipps zur Umsetzung des carnivoren Lifestyles, wissenschaftliche Hintergründe zur Heilsamkeit sowie ökologische und ethische Informationen zum Fleischkonsum. Eine Übersicht über alle Folgen findet ihr hier: www.carnitarier.de/fleischzeitpodcastAndrea Siemoneit berichtet nach über drei Jahren carnivorer Ernährung über ihre Erfahrungen und Erkenntnisse. Außerdem interviewt sie andere Carnivoren und Wissenschaftler.Ihr findet sie auf Instagram unter @carnitarierinHandbuch der Carnivoren Ernährung: www.carnitarier.de/shop Haftungsausschluss:Alle Inhalte im Podcast werden von uns mit größter Sorgfalt recherchiert und publiziert. Dennoch übernehmen wir keine Haftung für die Richtigkeit, Vollständigkeit oder Aktualität der Informationen. Sie stellen unsere persönliche subjektive Meinung dar und ersetzen auch keine medizinische Diagnose oder ärztliche Beratung. Dasselbe gilt für unsere Gäste. Konsultieren Sie bei Fragen oder Beschwerden immer Ihren behandelnden Arzt.#carnitarier #carnetarier #carnivor #carnivoreernährung #carnivorediät #fleischbasiert #keto #lowcarb #ketogeneernährung #ketogeneernaehrung #paleo #paleoernährung #ohnezucker #zuckerfrei #paleodiät#typ1diabetes #diabetes #insulin #insulinspritzen #basalinsulin #unterzucker #ogtt #hba1c #gluconeogenese #alkohol #schuppenflechte #cgm #Blutzuckerschwankungen #dauerketose #remission #ldl #hdl #triglyceride 

Dr. Fiona McCulloch discusses Managing a Healthy Menopause at the Functional Medicine Discussion Group meeting on April 27, 2023 with moderator Dr. Ben Weitz. [If you enjoy this podcast, please give us a rating and review on Apple Podcasts, so more people will find The Rational Wellness Podcast. Also check out the video version on my WeitzChiro YouTube page.]    Podcast Highlights 5:35  Perimenopause usually starts around age 39 till 55 or so and this is when we start seeing irregular cycles and lots of symptoms and increases in chronic health risks.  Perimenopause is a time of fluctuation.  Women are born with all of the follicles in their ovaries for their entire life. the follicles house the eggs and each egg is housed by cells that make hormones.  Over the lifespan the pool of follicles decrease and when you get to the end of the reproductive years, there are far fewer follicles and hormones are released abnormally and inconsistently.  During a normal menstrual cycle the granulosis cells in the inner follicle make estrogen and when the egg comes out, it ovulated and the shell of the egg makes progesterone for two weeks.  During perimenopause we have follicles on their last legs and they make estrogen all the time but not in a normal pattern and there is almost no progesterone.  The adrenals do make small amounts of progesterone but the ovaries make massive amounts of progesterone.  Perimenopause is marked by wildly fluctuating wild estrogen levels up and down and pretty much no progesterone for the majority of the time. 10:37  Diagnosis of Perimenopause. The pituitary gland is involved with the complex control of ovulation.  When estrogen levels start to drop, the pituitary senses that and then sends FSH down to the ovary to make an egg and then you get increased estrogen.  When estrogen levels get irregular but generally higher, the brain will stop making FSH, so some measure FSH as a way to diagnose perimenopause. But FSH is not consistently low, so it is not a good way to diagnose perimenopause. The best way to diagnose perimenopause is not to test hormones but based on age and that the menstrual cycle gets shorter, irregular. Women will get insomnia, have mood changes, etc.  Testing can be useful for treatment but not for diagnosis.  Menopause is easy to diagnose, since it is diagnosed when it has been 12 months since the last period.  14:32  Stages of Perimenopause.  During the first stage of perimenopause, the cycles become shorter because there are less follicles and they make less anti-müllerian hormone, which slows them down from ovulating too early.  In the later stages of perimenopause we see highly unpredictable cycles and lots of heavy, long bleeding. Some of the common symptoms that may occur in menopause include hot flashes, insomnia, anxiety, depression, low libido, vaginal dryness, autoimmunity, insulin resistance, loss of bone density, increased cardiovascular risk, and increased Alzheimer's risk.    20:12  Hormone testing.  Different modalities of testing are more or less effective for different reasons. Serum or blood spot is the most common form of hormones testing and it is good at picking up topical estrogen, oral and vaginal hormones.  Topical progesterone is not seen very well in a serum test, but it is seen in a blood spot or in saliva testing.  Urine testing is good to look at the metabolites of estrogen and cortisol and Dr. McCulloch will typically use DUTCH testing.  But urine testing is not as good to monitor topical hormone replacement therapy or vaginal HRT, since this can end up in the urine directly.  Saliva is helpful to look at the diurnal rhythm of free cortisol and is good for picking up topical progesterone.  For saliva and blood spot testing she will use ZRT Labs. 24:28  Other labs that Dr. McCulloch will often order besides hormones include the following: 1. Lipids, 2. ApoB, 3. Homocysteine, 4. HOMA-IR, 5. HBA1C, 6. Glucose, 7. OGTT with insulin, 8.

View the Show Notes Page for This Episode Become a Member to Receive Exclusive Content Sign Up to Receive Peter's Weekly Newsletter In this “Ask Me Anything” (AMA) episode, Peter answers questions related to the leading cause of death in both men and women—atherosclerotic cardiovascular disease (ASCVD). He highlights the most important risk factors for ASCVD, such as apoB, LDL, hyperinsulinemia, and Lp(a), and explains the mechanism by which they confer risk and how these factors are interrelated. Peter also dives deep into the data around apoB to try to answer the question of how much residual risk is conferred for ASCVD through metabolic dysfunction once you correct for apoB. He also looks at the data around lifetime risk reduction of ASCVD in the context of low apoB. If you're not a subscriber and are listening on a podcast player, you'll only be able to hear a preview of the AMA. If you're a subscriber, you can now listen to this full episode on your private RSS feed or our website at the AMA #42 show notes page. If you are not a subscriber, you can learn more about the subscriber benefits here. We discuss: A racecar analogy for understanding atherosclerotic cardiovascular disease [2:00]; Defining and differentiating apoB and LDL-C [10:00]; The interrelated nature of insulin levels, apoB, triglycerides, and ASCVD parameters [13:00]; Another way that hyperinsulinemia plays a role in endothelial dysfunction [18:00]; Why Peter uses the oral glucose tolerance test (OGTT) with all patients [20:15]; Is there any evidence that hyperinsulinemia is an independent contributor to ASCVD? [23:00]; Thinking through risk in the context of high-fat diets resulting in improved metabolic metrics but with an elevation of apoB/LDL-C [27:30]; Thinking through risk in the context of low apoB but higher than normal triglyceride levels [32:15]; The importance of lowering apoB for reducing ASCVD risk [38:15]; Data on men and women with familial hypercholesterolemia that demonstrates the direct impact of high apoB and LDL-C on ASCVD risk [47:45]; Importance of starting prevention early, calcium scores, and explaining causality [52:30]; Defining Lp(a), its impact on ASCVD risk, and what you should know if you have high Lp(a) [56:30]; Lp(a) and ethnic differences in risk [1:00:30]; Why someone with elevated Lp(a) should consider being more aggressive with apoB lowering strategies [1:05:00]; Addressing the common feeling of hesitancy to taking a pharmacologic approach to lower ASCVD risk [1:07:15]; Peter's take on the 2022 Formula 1 season and thoughts on 2023 [1:15:15]; and More. Connect With Peter on Twitter, Instagram, Facebook and YouTube

On Episode 19 of the Stroke Alert Podcast, host Dr. Negar Asdaghi highlights two articles from the August 2022 issue of Stroke: “Direct to Angiosuite Versus Conventional Imaging in Suspected Large Vessel Occlusion” and “Recurrent Ischemic Stroke and Bleeding in Patients With AF Who Suffered an Acute Stroke While on Treatment With NOACs.” She also interviews Dr. Alexander Nave about “Combined Oral Triglyceride and Glucose Tolerance Test After Acute Ischemic Stroke to Predict Recurrent Vascular Events.” Dr. Negar Asdaghi:         Let's start with a few questions. 1) How much time do we actually save if we were to transfer all patients with suspected target vessel occlusion directly to the angiosuite and practically bypassing our current conventional imaging model? 2) What is the impact of an impaired metabolic state as measured by abnormal glucose and triglyceride tolerance tests on the risk of stroke recurrence in patients with ischemic stroke? 3) And finally, should we or should we not change the anticoagulant therapy of a patient with atrial fibrillation who suffered an ischemic stroke despite appropriate treatment with anticoagulation? We have the answers to these questions and much more in today's podcast because this is the best in Stroke. Stay with us. Dr. Negar Asdaghi:         Welcome back to another issue of the Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami Miller School of Medicine and your host for the monthly Stroke Alert Podcast. The August 2022 issue of Stroke contains a range of really stimulating articles. We have an interesting study titled "Individual and Joint Effects of Influenza-Like Illness and Vaccinations on Stroke in the Young," led by Dr. Amelia Boehme and colleagues from Columbia University, with its accompanying editorial on how influenza-like illness is associated with increased risk of stroke in the young and middle-aged population while vaccinations of any type is protective of this risk. In a different paper, as part of a population-based study out of Scotland, Dr. Rustam Al-Shahi Salman from University of Edinburgh and colleagues report on a positive association between the use of beta-blockers, especially propranolol, and a lower risk of cerebral cavernous malformation, or CCM, associated intracranial hemorrhage. This study's findings are very interesting and quite important, and I encourage you to review the growing literature to suggest how beta-blockers may, in fact, reduce the risk of CCM-related hemorrhages through their anti-angiogenic properties. Dr. Negar Asdaghi:         Later in the podcast, I have the great pleasure of interviewing Dr. Alexander Nave from Charité University Hospital in Berlin to discuss the relationship between having an impaired metabolic state in the setting of acute stroke and the risk of ischemic stroke recurrence, as we'll review the long-awaited results of the Berlin "Cream&Sugar" study, a very catchy title. But first, with these two articles. Dr. Negar Asdaghi:         Time to successful endovascular reperfusion is an important predictor of clinical outcomes in patients with acute ischemic stroke related to a large vessel occlusion. And for years, we've known that the faster we're able to open the affected artery, the better the ischemic stroke outcomes are. Correspondingly, systems of care have adapted to various requirements of this so-called rapid workflow to ensure that all necessary pre-reperfusion steps are completed as fast as possible, preferably most in parallel to one another. And if any steps are unnecessary, they're bypassed altogether. Dr. Negar Asdaghi:         Despite all these modifications to date, time from conventional imaging to angiosuite arrival remains both the longest and the most variable interval in the intra-hospital workflow prior to endovascular therapy. So, it's not surprising that many recent studies have evaluated whether the current model of hospital arrival, then transfer to the scanner for imaging, then transfer to the angiosuite for endovascular therapy, can be replaced by a simpler model where, based on clinical assessment, a patient with high likelihood of having a target vessel occlusion can directly be transferred to the angiosuite, where fast stroke imaging, including CT, CT angiogram, and CT perfusion, are completed on the angiotable using the flat panel imaging technology. Dr. Negar Asdaghi:         If the patient is then found to be eligible to receive reperfusion therapies, including intravenous thrombolytics, they can receive the treatments and then proceed to endovascular thrombectomy without any further delays. So, in this issue of the journal, in the study titled "Direct to Angiosuite Versus Conventional Imaging in Suspected Large Vessel Occlusion," Dr. Raul Nogueira from Department of Neurology at Emory University and colleagues performed a systematic review and meta-analysis of published articles on this topic. So, they included seven articles for this analysis after pulling over 4000 articles using the common search engines for this meta-analysis. These articles included two single-centered European randomized controlled trials, one conducted in Germany, and the other one conducted in Spain, and five observational studies for a total of 1971 patients. The primary outcome was the odds of achieving favorable neurological recovery as defined by a modified Rankin Scale of zero to two at 90 days. Dr. Negar Asdaghi:         Now, a few things to note: All studies reported door-to-puncture times, but not all reported door-to-reperfusion times or rate of successful reperfusion, and we know that these metrics are important in predicting the odds of safety and efficacy outcomes of endovascular therapy. And also it's important to note that not all details of the safety and efficacy outcome measures were reported in all of those seven studies. So, with that, here are the main findings of the meta-analysis. First off, amongst patients who were directly transferred to the angiosuite across these seven studies, the overall rate of false activation was 28%, meaning that after imaging assessment, 28% of those who were directly taken to the angiotable were not found to have a target occlusion, and as such, there was no need to further proceed to endovascular thrombectomy. And this is a practical finding of this meta-analysis as we deal with resource allocation and concerns of potentially overwhelming the neurointerventional teams. Dr. Negar Asdaghi:         Now, moving on to the next finding of the study, the direct angio approach significantly reduced door-to-puncture times by a median of 30 minutes, and door-to-reperfusion times, when these metrics were available, by a median of 33 minutes as compared to the conventional imaging approach. So, bypassing conventional CT does translate into faster time metrics. These were, of course, expected findings of this meta-analysis, but nonetheless, important to quantify. But these faster time metrics did not improve the endovascular procedural outcomes, meaning that the direct to angio approach did not increase the odds of achieving a TICI 2b or better reperfusion, which is how successful reperfusion is defined, or the odds of achieving full reperfusion, meaning modified TICI 2c or greater reperfusion. Dr. Negar Asdaghi:         So, it's great to get to the angiosuite fast, but that does not impact the procedural outcomes of endovascular therapy. Despite the above, the faster approach resulted in a significantly better functional independence outcome as measured by mRS Scale at 90 days, again emphasizing how important time is when it comes to endovascular outcomes. Now, the authors also performed a number of subgroup analysis in this meta-analysis, which I'd like to highlight some of them. We know that the impact of time on endovascular outcomes is more robust in the early time window. So, not surprisingly, when restricting the primary outcomes to those presenting within six hours from symptom onset, the favorable effect of direct to angio approach persisted in the early time window as well. Dr. Negar Asdaghi:         Another important subgroup analysis was when restricting data to those patients who were transferred from a primary hospital to an endovascularly-capable center, the direct angio method didn't really have a significant impact on improving the primary outcome. Why is that? Let me repeat. So, when they restricted the analysis to those patients who were transferred from one hospital to an endovascularly-capable center, they did not find the same significant positive impact on endovascular outcomes in the direct to angio approach. I think the way we can explain this from a pathophysiological standpoint is that transferred patients are more likely to be slow progressors and, therefore, less likely to be impacted by delays in the workflow process as compared to the fast progressors. Dr. Negar Asdaghi:         Take-home message: We've got to be fast in the fast progressors, and it's safe to assume that those who are within the first six hours after presentation are more likely to be fast progressors, and these workflow modifications are, therefore, much more robust and much more impactful in patients who present early on after their symptoms onset. And finally, in terms of safety outcomes, there were no significant differences in the rate of symptomatic intracerebral hemorrhage rate or the 90-day mortality rates either for the whole study population or when the analysis was restricted to those treated in the early time window. Dr. Negar Asdaghi:         So, in summary, what we learned from this large meta-analysis is that as compared to the current conventional imaging model, the direct transfer to angio model is not only plausible and unlikely to overwhelm the interventional teams, as only less than 30% of patients in a direct method were not eligible for endovascular thrombectomy, but also this method is safe and results in significant improvements in workflow time metrics and functional outcomes. So, as the saying goes, select faster, select less, and treat more will likely be the future of endovascular therapy, particularly in the early time window. Dr. Negar Asdaghi:         We know that oral anticoagulants reduce the risk of ischemic events in patients with atrial fibrillation. Nonvitamin K antagonist oral anticoagulants, or NOACs, also known as direct oral anticoagulants, or DOACs, are currently the standard of care for treatment of patients with non-valvular atrial fibrillation. Now, we have to keep in mind that although NOACs reduce the risk of ischemic stroke and systemic embolism in atrial fibrillation, they don't completely abolish the risk. So, they're not curative treatments for AFib, and patients can still experience embolic events despite appropriate treatment with these agents. In a meta-analysis of randomized trials, the residual risk of ischemic events in patients treated with NOACs was estimated at 1.4% per year, but this number is a lot lower than what is reported by real-life observational studies. Dr. Negar Asdaghi:         In the large multicenter RENO study, which was published in this journal in 2019, we learned that in the setting of atrial fibrillation treated with a NOAC, a number of factors, including atrial enlargement, dyslipidemia, scoring high on the CHA2DS2-VASc score, and the use of low dose of NOACs, especially off-label low dose use of these medications, are significantly associated with increased risk of recurrent ischemic events despite treatment. But there's still a number of important questions that we routinely encounter in practice, most important of which is how to manage these patients with these so-called breakthrough ischemic events moving forward? Do we switch them to a different NOAC or go back to a vitamin K antagonist? Should we add an antiplatelet treatment to the regimen? And importantly, how do we counsel these patients and their families on their future risk of recurrent ischemic or hemorrhagic events? Dr. Negar Asdaghi:         So, in the current issue of the journal, the RENO investigators, led by Dr. Maurizio Paciaroni and Valeria Caso, set out to answer some of these important questions as part of the RENO-EXTEND study, which basically followed the patients in the RENO cohort for at least 12 months, evaluating them for either recurrent ischemic or hemorrhagic events, whether occurring intra or extracranially. So, a bit about this cohort. The RENO study was a multicenter observational cohort across 43 centers in Europe and the United States, including consecutive patients with atrial fibrillation who presented to the hospital with an acute ischemic stroke despite being on a NOAC therapy. Patients were enrolled in the study only if they were compliant with their NOAC treatment and they had not missed their treatment for any reasons for greater than 24 hours prior to their index event. Dr. Negar Asdaghi:         The patients were followed in the cohort and the choice of whether or not to start and timing, very importantly, for resumption of anticoagulation therapies were left to the discretion of the treating physicians. For the current paper, they analyzed 1240 patients. After the index event, 39.5%, so close to 40%, had their NOACs changed to another NOAC, mostly to a different class of NOAC. 42.5% continued with the same NOAC at the same dose. 6.7% continued with the same NOAC, but the dose was increased, and a small percentage were shifted to warfarin, that was only 4.7% of the patients. And 6.6% were shifted to low molecular weight heparin or were never prescribed oral anticoagulations after that index event for a variety of reasons, such as earlier ischemic recurrence, early hemorrhagic transformation, or early death or severe index stroke. And the overall median follow up in the study was 15 months. Dr. Negar Asdaghi:         So, with that, here are the main study findings. The annual rate of the primary outcome of recurrent ischemic or hemorrhagic events, again, a reminder that these could have been intra or extracranial events, was 13.4%. The majority of these events were ischemic stroke, followed by major extracranial bleeding, then intracranial bleeding and systemic embolism. We have to note that this overall primary outcome rate is a lot higher than what was observed as part of the randomized trials of NOACs, as we noted earlier, which is an important finding of these real-life studies. Now, with regards to the factors predicting the primary outcome, having a higher CHA2DS2-VASc score and persistent hypertension were both predictive of recurrent ischemic events, whether ischemic stroke or systemic embolism. Next, the predictive factors for hemorrhagic events, either intracranial or major extracranial bleeding, included age, for each year increase in age, the odds increased by 1.1; history of major bleeding in the past; and, very importantly, a scenario that not uncommonly happens in routine practice, which is the addition of antiplatelet to a NOAC after the so-called NOAC failure. Dr. Negar Asdaghi:         And finally, it turns out that changing that failed NOAC to a different agent didn't really seem to make a difference at all. As we mentioned earlier, close to 40% of patients were changed from one NOAC to another agent after the index ischemic event, and when they looked at the primary outcome, there was no difference in the rate of combined ischemic and hemorrhagic events, or the ischemic events alone, or bleeding outcomes alone, amongst patients who changed their NOAC to a different agent as compared to those who did not. The authors performed a number of subanalyses to see whether a particular strategy, for example, a switch from a particular class of NOACs to another class, or change in dosage, or NOAC to warfarin change, may be more or less beneficial in reducing the primary outcome, and there was really no difference between any of these strategies with the exception of one group. Dr. Negar Asdaghi:         It turns out that the cumulative risk of ischemic and hemorrhagic events were a lot higher in those 6.6% of patients in whom NOAC treatment was changed to low molecular weight heparin injection. But I think one should consider this observation as hypothesis generating. First off, it was just a very small percentage of patients in this study that actually did go through this switch. And also we should note that in practice, we reserve a switch to low molecular weight heparin injection in only special cases. Some examples would be patients in whom there's a consideration of a hypercoagulable state, whether cancer related or not. But regardless, I think what we learned from this finding is that the patients in whom low molecular weight heparin injection is considered after a NOAC or an anticoagulant failure are likely very high risk patients for recurrent thromboembolic and hemorrhagic events. Dr. Negar Asdaghi:         So, in summary, we learned a number of important lessons from RENO-EXTEND study. Number one, patients with atrial fibrillation presenting with a breakthrough ischemic stroke, despite treatment with NOAC, represent a high-risk group of patients who continue to be at a substantial risk for recurrent events, mostly ischemic, but also hemorrhagic. And this substantial risk was actually over 10% in the current study. Number two, we also learned that various strategies of changing the dose or class of anticoagulants don't seem to have much, if any, benefit in reducing the recurrent event outcomes. And finally, the addition of antiplatelet to oral anticoagulant therapies in this situation is not a good idea. This strategy gets us more in trouble and can increase the risk of bleeding and confers practically no benefits. Finally, these are the types of patients in whom we may have to consider other treatment options, such as left atrial appendage closure, and I'm sure we'll hear more on this in the future. Dr. Negar Asdaghi:         Having an abnormal lipid profile has long been recognized as a risk factor for development of vascular disorders, particularly leading to atherosclerosis, but this association varies for the different components of the lipid panel and is most robust for elevated low density lipoprotein cholesterol levels, or LDL, causing various vascular disorders. Amongst patients with ischemic stroke and TIA, randomized trials have also shown that lowering LDL can reduce the risk of major cardiovascular events, including the risk of ischemic stroke, but the connection between elevated triglyceride levels and the risk of recurrent ischemic stroke is less clear. Moving from lipids to sugar, the presence of uncontrolled diabetes increases the risk of stroke by two to five folds, depending on the patient population studied and coexistence of other risk factors. In contrast, impaired glucose tolerance, which is an intermediate metabolic state between normal glucose tolerance and diabetes, has also been found to be associated with an increased risk of stroke in patients with coronary artery disease, but this association is less clear amongst patients with ischemic stroke. Dr. Negar Asdaghi:         In clinical practice, fasting blood glucose and lipid profiles are routinely measured post-stroke, but we put a greater emphasis on the elevated LDL and hemoglobin A1C levels, and, in general, pay less attention, if any, to other metabolic derangements, including the impaired glucose tolerance state or even abnormal triglyceride levels. So, the question is, what is the impact of these metabolic derangements on the risk of stroke recurrence amongst patients presenting with ischemic stroke? In the current issue of the journal, in the study titled "A Combined Oral Triglyceride and Glucose Tolerance Test After Acute Ischemic Stroke to Predict Recurrent Vascular Events: The Berlin 'Cream&Sugar' Study," we learn about these important associations. Joining me now is the first author of this paper, Dr. Alexander Nave. Dr. Nave is a neurologist and clinician scientist at Charité University Hospital in Berlin. He leads a junior research group as part of the Center of Stroke Research in Berlin and has a special interest in stroke rehabilitation and cardioembolic risk factors of stroke. Good morning, Alex, from Miami. Good afternoon to you in Berlin. Thank you for joining us. Welcome to our podcast. Dr. Alexander Nave:       Hi, thank you very much. I'm very happy to be with you. Dr. Negar Asdaghi:         All right. Let's go over the background of what we knew on the association between elevated triglyceride levels and the risk of recurrent stroke. Dr. Alexander Nave:       Sure. So, as you pointed out earlier, diabetes and hypercholesterolemia are well established risk factors for first and recurrent ischemic stroke. However, for triglyceride levels, this association is less well understood and somewhat inconclusive. So, prior large epidemiological studies of the healthy population from the U.S. and from Denmark have shown an independent association of triglyceride levels in the risk of vascular events, including ischemic stroke. This association was actually stronger for non-fasting triglycerides levels compared to fasting triglycerides levels. In the ischemic stroke population, however, there were only a few investigations with conflicting results. So, the SPARCL trial, for example, which was a large secondary prevention stroke trial with more than 3000 stroke patients, showed that triglyceride levels were associated with major cardiovascular events, but not with recurrent ischemic stroke. So, therefore, we designed the Berlin “Cream&Sugar” study to investigate the association of postprandial triglyceride levels following an oral triglyceride tolerance test with recurrent vascular risk. Dr. Negar Asdaghi:         So, let me just summarize. From SPARCL, actually, we knew that an increased level of triglycerides were associated with increased risk of development of cardiovascular events, so things such as coronary artery events and so on, but not an increased risk of stroke. And that's where you come in with the new study, the Berlin “Cream&Sugar” study. Now, before we talk about the study, can you tell us a little bit about the tests that were done, the oral triglyceride and glucose tolerance tests? Dr. Alexander Nave:       Absolutely. So, both tests eventually help us to evaluate the glucose and lipid metabolism of a patient. So, the OGTT, the oral glucose tolerance test, as most of the listeners probably know, is a test that helps us to assess the ability of the patient to metabolize glucose after receiving a drink with a standard dose of 75 grams of glucose. The blood glucose levels after one hour and two hours then help us to diagnose diabetes or pre-diabetic state of the patient. So, we're not only evaluating the fasting state, but we can also quantify the body's response to a glucose challenge. And as an equivalent, the OTTT, the oral triglyceride tolerance test, will test the ability of a patient to metabolize triglycerides after oral ingestion of a lipid challenge, which is usually a certain amount of fat. However, this test is less well studied and without any standardized diagnostic criteria so far. And in contrast to the OGTT, the OTTT has not been tested in the stroke population so far. Dr. Negar Asdaghi:         So, we're not just looking at those metrics of fasting sugar or fasting lipids and triglycerides specifically, we're looking at the patient's ability to metabolize glucose or triglyceride levels. So, now, with that understanding, can you tell us a little bit about the methodology of the study? Dr. Alexander Nave:       Yes, of course. So the Berlin “Cream&Sugar” study was a prospective observational study recruiting acute stroke patients between 2009 and 2017 at the Charité University Hospital in Berlin. And we included first-ever ischemic stroke patients within three days to seven days after onset of stroke, and all patients received a sequential OTTT OGTT. So, all recruited patients received fasting blood sampling in the morning before taking the OTTT with 250 cc of cream, which corresponds to 30% of fat intake. So, all patients without known diabetes mellitus additionally had the OGTT with 75 grams of glucose starting three hours after the OTTT. Dr. Alexander Nave:       And all patients received consecutive blood tests at three hours, four hours, and five hours after start of the OTTT to determine the course of glucose and triglyceride levels in the blood. And after one year, we performed follow up of all patients. The primary outcome was recurrent fatal or non-fatal ischemic stroke, and secondary outcome was a composite endpoint of recurrent vascular events, including ischemic stroke, TIA, myocardial infarction, and coronary revascularization, as well as cardiovascular death. And we compared patients with high versus low fasting and nonfasting triglyceride and glucose levels, respectively, using Cox regression analysis. Dr. Negar Asdaghi:         Okay. 250 cc of cream and 75 grams of sugar right after a stroke. Was it challenging to recruit patients? Dr. Alexander Nave:       Yes, that was a task. And we did experience some difficulties during the course of the study. It was not easy to ask a patient to drink a glass of cream during the first week after suffering from a stroke, obviously. In fact, a substantial number of patients eventually did not participate or did not complete the OTTT. However, in our study, we showed that performing a sequential OGTT OTTT within seven days after stroke was feasible. Approximately 10% of patients reported only minor adverse events such as nausea, diarrhea, and bloating. But with regards to the study population, overall, we enrolled 755 patients, 523 have completed the challenge and entered follow up. So, considering the fact that we had some difficulties in recruitment, was not surprising that we predominantly ended up with minor ischemic stroke patients, considering that we did not include patients with dysphagia or patients that were not able to give informed consent in the early phase after stroke. The median NIHSS was one with an interquartile range of zero to three. And, as I mentioned previously, this was because patients with impaired swallowing could not be included into the study. Dr. Negar Asdaghi:         Okay. So, 750 patients within a week after their stroke, majority of them, as you mentioned, had mild ischemic events, were enrolled, and then they underwent sequential OTTT and OGTT tests. And then they were followed for a year for the primary outcomes. Now I think we're ready to hear the primary results. Dr. Alexander Nave:       Sure. So, overall, 54 patients, 10% of the total population, reached a study endpoint within one year follow up. 31 patients experienced recurrent ischemic stroke within one year. So, when we compared the highest quartiles of triglyceride levels to the lowest quartiles, neither fasting nor postprandial triglyceride levels were associated with recurrent stroke. Similarly, fasting triglyceride levels were not associated with major cardiovascular events one year after stroke. Surprisingly though, higher postprandial triglycerides, measured at five hours after OTTT, were significantly associated with a lower risk for recurrent vascular events. The hazard ratio was 0.42, and the confidence interval 0.18 to 0.95. So, regarding glucose levels, on the other hand, we found no associations between glucose levels and recurrent vascular risk at all. Dr. Negar Asdaghi:         Interesting. So, before I ask you what your takeaway is from all of this, the first question is the 10% rate of primary outcome. Were you at all surprised by this? This seems quite high for the recurrent rate of vascular events after the first year after ischemic stroke and TIA. Dr. Alexander Nave:       Well, actually, when the “Cream&Sugar” study was designed, we expected the recurrent event rate to be even higher, approximately 10% of recurrent stroke events within one year and not 10% recurrent vascular events as a composite outcome. But as we know from previous registries, such as the TIA registry, the recurrent risk of vascular events after TIA and minor stroke is much lower now. So, I think with the reported 7% of recurrent stroke events, we're actually quite in line with the reports of the TIA registry, considering the fact also that we had no TIA patients enrolled in our study and had quite a high proportion of patients with large artery atherosclerosis as well as atrial fibrillation. Dr. Negar Asdaghi:         So, thank you. This is a grim reminder that ischemic stroke patients remain at high risk of having recurrent vascular events. Alex, what should be our top two takeaway messages from your study? Dr. Alexander Nave:       So, first, I think a sequential OTTT OGTT probably does not contribute a lot to future vascular risk stratification in ischemic stroke patients. So, I think all patients and carers can be relieved. There's no need to implement an OTTT into routine clinical care. However, based on our results, I think further studies are necessary and needed to better understand the importance of glucose and lipid metabolism in patients after acute ischemic stroke. And eventually we might figure out some nice information how we can improve risk prediction. Dr. Negar Asdaghi:         So, it's good to know that we don't have to ask patients to drink a lot of cream after stroke. Can you tell us a little bit about the future of the Berlin “Cream&Sugar” study group? What are the next steps for the authors and the study group? Dr. Alexander Nave:       Absolutely. Well, since there's no urgent need to start another large study soon, I think it would be reasonable to get our data and merge it with datas from other groups who also investigated the role of an OTTT in cardiovascular risk cohorts, also to increase power and detect some other signals. And we want to have a more detailed look at the variability of triglycerides and glucose levels following sequential OTTT OGTT. So, not only go into the absolute levels that you can measure at certain time points, but also how much these parameters fluctuate over time. Dr. Negar Asdaghi:         To Alexander Nave, it's been a pleasure interviewing you on the podcast today. We look forward to covering more of your work in the future. Dr. Alexander Nave:       Thank you very much. It was a pleasure to talk to you. Dr. Negar Asdaghi:         And this concludes our podcast for the August 2022 issue of Stroke. Please be sure to check out this month's table of contents for the full list of publications, including three topical reviews, from “Strategies for Maintaining Brain Health: The Role of Stroke Risk Factors Unique to Elderly Women” to “Ethical Considerations in Surgical Decompression for Stroke.” These articles summarize a large body of evidence, which I encourage you to review. And before we end our August podcast, I'd like to take a moment to recognize the incredible dedication and hard work of our medical students and fellows, especially the young doctors who are just starting their training this year. Dr. Negar Asdaghi:         And if you happen to be one of those young doctors who is listening to our podcast in one of those sleepless on-call nights, I want to recount the story of Dr. Carl David Anderson, who won the Nobel Prize in physics for his discovery of the first particle of antimatter known as positron on August 2, 1932. A positron is actually the identical twin of the well-known negative electron, and its discovery in the 1930s truly changed our understanding of the origin of the universe, and it's practically impacted all aspects of science, not to mention it's impacted medicine and medical imaging. But the moral of the story lies in the fact that on August 2, when Anderson announced his discovery, he was a post-doctoral fellow himself, hadn't even graduated yet. So, if you are such a trainee, I hope you know that your hard work, combined with that incredible scientific inquisition, has the potential to change our understanding of the universe. And what better way to do this? You guessed it, than staying alert with Stroke Alert. Dr. Negar Asdaghi:         This program is copyright of the American Heart Association, 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit AHAjournals.org.

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Dieser Podcast entstand durch die freundliche Unterstützung vom DDH-M Show Notes Erwähnte Podcasts / Blogs 242 – DDH-M – Ernährung bei Diabetes und Herz-Kreislauf-Erkrankungen 244 – DDH-M – Ernährung bei Diabetes Typ 2 und Nicht-Alkoholischer-Fettleber 246 – DDH-M – Ernährung bei diabetisch bedingter Nierenerkrankung https://www.ddh-m.de https://menschen-mit-diabetes.de/ https://menschen-mit-diabetes.de/ratgeber https://menschen-mit-diabetes.de/service/downloads https://www.ernaehrungsinstitut-miersch.de Kontaktdaten https://www.iu.de/hochschule/lehrende/miersch-claudia/ www.schwangerschaftsdiabetes.net www.ernaehrungsinstitut-miersch.de ** Danke für´s Zuhören **   Besuche mich auch auf Instagram: @Zuckerjunkies   *** NEU FB-Gruppe: https://Zuckerjunkies.com/facebook   ** kostenloses eBook über Fett-Protein-Einheiten – ** ►► https://zuckerjunkies.com/produkte/  

On this episode, Faraz Khan asks the chief medical officer of WebMD, Dr John White, about the shocking cases of diabetes and what can be done to reverse or manage this dangerous disease. [Sponsor Message: If you would like to grow thicker, fuller and healthier hair naturally without any drugs or chemicals, then make sure to check out https://fullyvital.com] Here are some of the topics we discuss: 1. Dr John Whyte background 2. Why does WebMD exist? 3. Why is there such a shocking increase in diabetes and pre-diabetes 4. Lets get definitions out of the way: what is prediabetes and what is considered diabetes? Also touch on type 1 and type 2 diabetes. 5. Diagnosis methods. Fasted blood test vs. HbA1 vs. OGTT. Explain the difference to the audience and which one is more accurate? 6. Do your genes play a role in diabetes? 7. Let's get into exactly how in the body people get pre-diabetes and type 2 diabetes; What is the internal mechanism in your organs and cells of how you go from a normal person to diabetic? 8. What are the complications of diabetes? It looks like a lot of organs and systems can be affected by diabetes, what are some of the big ones for the audience? 9. Can we reverse pre-diabetes and type 2 diabetes 10.  How can people monitor their status to see if they are approaching the danger zone? Is a fasted blood test once or twice a year enough, or should people be monitoring it more closely with continuous glucose monitors or other methods? 11. Can we truly cure pre-diabetes and diabetes? What does it take? 12. Let's talk food choices. please expand on how people's food choices can have such a big impact on diabetes. 14. Do supplements such apple cider vinegar, cinnamon, berberine, bitter melon, fenugreek work? 15. Where do the pharma dugs fit into the model like metformin? 16. What is a good exercise protocol to stave off or manage diabetes effectively? 17. Where can people find you online? Get the full show notes for this episode on https://antiaginghacks.net

Having spent the majority of my pregnancy in lockdown (106 days to be exact), I've had lots of time to think about how the journey has been for me so far. Pregnancy can be incredibly daunting and isolating, let alone adding PCOS into the mix! Obviously the first trimester is nerve wracking but the second trimester can feel like just as much of a rollercoaster.You're getting used to your body changing quite drastically, most people actually know you're pregnant, you're figuring out what exercise looks like for you, you're hoping you're out of the woods with nausea and food aversions, you're realising you're getting closer to actually meeting your baby, you've got the dreaded pregnancy glucose challenge to face, you've got more energy but you're not feeling too massive and slow just yet. Phew — there's a lot that happens in the second trimester. It's getting real real now!Loads of you who are pregnant with PCOS, have been before and plan to be in the future absolutely loved my first trimester episode. So I'm giving the people what they want of course and releasing my second trimester learnings ASAP!I'm giving you all the juicy details on all things second trimester of being pregnant with PCOS. Everything from what's gotten better for me since first trimester and what I'm still struggling with, to what exercise you're actually okay to do in pregnancy, to still dealing with constipation in the second trimester, to food aversions and their changes in this stage as well as iron levels in PCOS pregnancy, pelvic floor WOFs (I found I was a bit of an overachiever in this area!), sweet cravings, gestational diabetes testing and much more.This episode is for you if:You're currently pregnant or are trying to conceiveYou are trying to navigate the changes happening in your body at the momentBeing pregnant with PCOS, you're quite worried about doing the gestational diabetes glucose testYour PCOS symptoms are changing (maybe even getting better) during your pregnancyYou want to know if pregnancy can ‘undo' PCOS symptomsYou don't know what types of exercise are actually okay in pregnancyYou want to know more about how you should feel after exercising while pregnantIron levels are an issue for you (either low or high iron)You want to know what the heck a pelvic floor WOF is and why it's importantYou're still dealing with constipation and some food aversionsYou want to hear other people's experiences of being pregnant with PCOSSome things we cover in this episode:What's gotten better for me since first trimester and what I'm still struggling withDealing with that sweet tooth while being pregnant with PCOSThe dreaded OGTT for gestational diabetes riskPCOS symptoms changing in pregnancySpending my entire second trimester in strict lockdown and how I copedKeeping active and what that looks like in PCOS pregnancyStruggling with focusing on workKeeping watch of my iron levelsResources and References:Caitlin Day: The Vagina PhysioUnity Studios7 question quiz: What does a ‘vagina physio' do?My Book: Getting Pregnant with PCOSLinks to our programs:The PCOS ProtocolEggducated

Sabina, Musikerin und Mutter von drei Kindern hat durch Carnivore zahlreiche Erkrankungen heilen können. Depressionen, Suizidversuche, epileptische Anfälle (Sekundenabsenzen), Rheuma, Endometriose, Ganzkörperschmerzen, Akne. Sabina kann inzwischen sehr gut erkennen, welche Lebensmittel bei ihr welche Symptome verursachen.Rind, das nicht grasgefüttert ist, erzeugt bei ihr Rheuma. Wenn, dann geht ohnehin nur das Fleisch von Wiederkäuern bei ihr, also kein Schweinefleisch oder Geflügel.Übelkeit bei Kokosnuss, Rheuma bei Schokolade und Kaffee, Milchprodukte führen zu Entzündungen im Magen-Darm-Bereich, Schüttelfrost und Ganzkörperschmerzen. Eiklar führt zu Übelkeit, Fisch auch zu Rheuma, wenn er aus Aquakultur stammt, Früchte führen zu Blähungen, zumindest rohe Früchte, auch zu Epilepsie durch die Kohlenhydrate, Durchblutungsstörungen in den Beinen, Wassereinlagerungen, Grüner Salat führt zu Rheuma wegen der Oxalate, deshalb wurde das Rheuma während der ketogenen Phase auch nicht besser. Nachtschattengewächse führen auch zu Rheuma, Nüsse führen zu Entzündungen. Sabina ist zu Carnivore über das Ausschlussverfahren gekommen. Das heißt, sie hat Stück für Stück mehr und mehr Lebensmittel weggelassen, die ihr nicht gut taten und so kam sie zunächst zu Low Carb. In der zweiten Schwangerschaft hat sie den Glucose-Toleranztest nicht bestanden. Sie litt also vermutlich unter Schwangerschaftsdiabetes. Sie hatte dann ein schwer übergewichtiges Baby. Deshalb wechselte sie in der dritten Schwangerschaft zu Keto und so langsam zu Carnivore. Laktations Ketoazidosis nach der dritten Schwangerschaft. Sie vermutet, dass das durch zu viel Milchabgabe bei zu wenig Nährstoffaufnahme kam. Es wurde also zu schnell Fett abgebaut, so dass eine Laktations Ketoazidose entstand. Die Symptome waren auch rapider Gewichtsverlust, Übelkeit, häufiges Urinieren, kein Durst, schneller Atem wegen Sauerstoffmangel, schwindendes Bewusstsein, Schwäche. Nun stillt sie immer noch, aber ergänzt ihre Ernährung täglich mit etwas Honig und Apfelmus, um nicht mehr in so eine starke Ketose zu gelangen, wie damals. Sie bemerkt auch, dass sie mehr Milch zur Verfügung hat, wenn sie diese Kohlenhydrate konsumiert.Jetzt durch Carnivore ist ihre Akne weg, die Augensäcke, die Darmkrämpfe sind weg, die Depressionen und auch Ekzeme und Endometriose sind komplett weg. Epileptische Anfälle ebenso, die Ganzkörperschmerzen und der Blähbauch, Haarausfall ist auch weg. Schwächeanfälle entstehen durch zu wenige Mahlzeiten. Regelmäßige Halsschmerzen sowie die Hämorrhiden sind auch weg. Hornhaut kommt ebenfalls nicht mehr. Zahnfleischprobleme ebenfalls weg, Entzündungen am Bein, Konzentrationsschwierigkeiten und Müdigkeit. Die Sonnenverträglichkeit ist wesentlich verbessert, Stimmungsschwankungen sind ebenfalls weg. Schweiß ist geruchlos. Bei zu vielen Trockenfrüchten riecht ihr Schweiß anschließend wieder.Hört rein in die unheimliche interessante Episode mit Sabina! Ihr findet Sabina auf Instagram unter @sabinastucki.Ihr findet uns auf Instagram unter:@fleischzeitpodcast, @fastencoachdave, @carnitarierinAndreas Website, wo ihr auch Das Handbuch der Carnivoren Ernährung erwerben sowie den Link zum Coaching finden könnt: www.carnitarier.deZur Salzmische von Dave oder zu seinen Coaching beim Fasten oder bei Carnivore kontaktiert ihr ihn unter dave@salzmische.de oder unter der Telefonnummer +49 1515 9454596.Haftungsausschluss:Alle Inhalte im Podcast werden von uns mit größter Sorgfalt recherchiert und publiziert. Dennoch übernehmen wir keine Haftung für die Richtigkeit, Vollständigkeit oder Aktualität der Informationen. Sie stellen unsere persönliche subjektive Meinung dar und ersetzen auch keine medizinische Diagnose oder ärztliche Beratung. Dasselbe gilt für unsere Gäste. Konsultieren Sie bei Fragen oder Beschwerden immer Ihren behandelnden Arzt.

Benjamin Bikman, PhD is an internationally renowned scientist and pathophysiology professor at Brigham Young University in Provo, Utah. Currently, his professional focus is to better understand the origins and consequences of metabolic disorders, including obesity and diabetes, with a particular emphasis on the role of insulin. He frequently publishes his research in peer-reviewed journals and presents at international science and public meetings. ​On this podcast, Ben talks with NBT Scientific Director Megan Hall about insulin resistance: what causes it, how it develops in the body, and the downstream effects of this all-too-common condition. Ben discusses the role of insulin as a regulator of human metabolism and its relevance in the development of most chronic diseases. He also offers a simple and effective prescription for optimal metabolic health and healthy ageing.  Here's the outline of this interview with Benjamin Bikman: [00:00:00] Ben's previous (2017) appearance on the NBT Podcast: Ketones, Insulin and the Physiology of Fat Cells. [00:00:42] Ben's background and his study of metabolism. [00:02:27] Ben's lab at BYU. [00:03:05] Insulin resistance, defined. [00:05:19] Causes of insulin resistance. [00:06:15] Problems with measuring insulin resistance. [00:10:24] Effects of diet, inflammation and stress on creating insulin resistance. [00:14:18] How insulin resistance develops in the body. [00:20:31] Fat hypertrophy vs hyperplasia. [00:22:24] The Athlete's Paradox. [00:24:22] Insulin resistance at the level of the brain; Alzheimer's as Type 3 Diabetes. [00:28:25] Brain fog; Stephen Cunnane, PhD., Research Center on Aging, Universite de Sherbrooke. [00:28:53] Young women with PCOS exhibit brain hypometabolism and insulin resistance; Study: Castellano, Christian-Alexandre, et al. "Regional brain glucose hypometabolism in young women with polycystic ovary syndrome: possible link to mild insulin resistance." PLoS One 10.12 (2015): e0144116. [00:29:41] Pathological vs physiological insulin resistance. [00:33:14] Just 50g of carbohydrate the night before improves outcomes on oral glucose tolerance test (OGTT); Study: Klein, Klara R., et al. "Carbohydrate intake prior to oral glucose tolerance testing." Journal of the Endocrine Society 5.5 (2021): bvab049. [00:38:20] Problems with the focus on calories in nutrition research. [00:43:09] Video: Dr. Benjamin Bikman - 'Insulin vs. Glucagon: The relevance of dietary protein'. [00:46:55] Book: Why We Get Sick: The Hidden Epidemic at the Root of Most Chronic Disease and How to Fight It. [00:51:22] Study: Walton, Chase M., et al. "Ketones Elicit Distinct Alterations in Adipose Mitochondrial Bioenergetics." International Journal of Molecular Sciences 21.17 (2020): 6255. [00:51:52] Untreated diabetes and metabolic rate; A Study of Metabolism in Severe Diabetes, by Francis G. Benedict and Elliott P. Joslin. [00:52:26] Insulin significantly reduces energy expenditure; Study: Nair, K. S., D. Halliday, and J. S. Garrow. "Increased energy expenditure in poorly controlled type 1 (insulin-dependent) diabetic patients." Diabetologia 27.1 (1984): 13-16. [00:54:42] Ketogenic diet and lifespan; Megan's study: Roberts, Megan N., et al. "A ketogenic diet extends longevity and healthspan in adult mice." Cell metabolism 26.3 (2017): 539-546. [00:55:56] Effects of β-Hydroxybutyrate on skeletal muscle mitochondria; Study: Parker, Brian A., et al. "β-Hydroxybutyrate elicits favorable mitochondrial changes in skeletal muscle." International journal of molecular sciences 19.8 (2018): 2247. [00:56:42] Effects of ketones on β-cell function; Study: Gropp, Jarom, et al. "β-Hydroxybutyrate improves β-cell mitochondrial function and survival." Journal of Insulin Resistance 2.1 (2017): 1-8. [00:58:44] Paper out of UC Davis: Zhou, Zeyu, et al. "A ketogenic diet impacts markers of mitochondrial mass in a tissue specific manner in aged mice." Aging (Albany NY) 13.6 (2021): 7914. [01:00:04] Ketone concentrations during a 36-hour fast; Study: Deru, Landon S., et al. "The Effects of Exercise on Beta-Hydroxybutyrate Concentrations over a 36-h Fast: A Randomized Crossover Study." Medicine and Science in Sports and Exercise (2021). [01:02:27] Prescription for optimal metabolic health and healthy ageing. [01:03:15] 4 pillars: control carbs, prioritize protein, don't fear fat, fast. [01:05:19] Where to find Ben: Instagram, HLTH Code meal replacement shake.

For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page

We're testing the home Insulin Survey by Imaware. I unbox & do my first sticks. And guess what my glucose challenge will be - a 20 oz Cherry Coke.For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page

Carla ist Coachin für Frauen mit Insulinresistenz. Sie klärt auf ihrem Blog www.lifesugar.de über alle Anzeichen von Insulinresistenz auf. Des Weiteren zeigt sie Wege und Handlungsmöglichkeiten auf, die einem aus dem Teufelskreis der Insulinresistenz heraushelfen können, auch was die psychische Komponente angeht.Carla selbst musste eine lange Odyssee durchmachen, bis sie endlich die Diagnose Insulinresistenz erhielt. Wie sie mit Keto und einem deutlich höheren Anteil tierischer Produkte in ihrer Ernährung ihre Gesundheit wiedererlangen konnte, erfahrt ihr in diesem Podcast. Ihr findet uns auf Instagram unter:@fleischzeitpodcast@fastencoachdave@carnitarierinAndreas Website:www.carnitarier.deHaftungsausschluss:Alle Inhalte im Podcast werden von uns mit größter Sorgfalt recherchiert und publiziert. Dennoch übernehmen wir keine Haftung für die Richtigkeit, Vollständigkeit oder Aktualität der Informationen. Sie stellen unsere persönliche subjektive Meinung dar und ersetzen auch keine medizinische Diagnose oder ärztliche Beratung. Dasselbe gilt für unsere Gäste. Konsultieren Sie bei Fragen oder Beschwerden immer Ihren behandelnden Arzt.

Inflammation panel (CRP, MPO, MACR, Lp-PLA2), OGTT (oral glucose tolerance test), and Kraft insulin survey—these are definitive tests to check whether you got insulin resistance and/or cardiovascular inflammation. If you want them done but don't know how where to get them, we have a new program for lab screening plus free webinars.For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page

The FDA released a statement about reports of metformin that's sold in the US containing NDMA (a carcinogen). This is in light of metformin sold outside the US having low levels of NDMA. The detected levels, though, are "within the range that is naturally occurring in some foods and in water."  FDA still recommends (and I agree with them) the continued use of metformin as prescribed while their investigation is ongoing. (In this live session, I'll also cover questions about CGM, CIMT, statins, gut biome, and insulin resistance.)For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources:  ·PrevMed's website·PrevMed's YouTube channel·PrevMed's Facebook page

Join Steph Lowe, AKA  'The Natural Nutritionist" for an eye-opening episode which reveals diet + lifestyle factors that can affect your OGTT results  + the diagnosis + management of Gestational Diabetes. A great episode to marry up with our prior episode on Gestational Diabetes with Diabetes Educator Emily Fitz - episode 46.You can find Steph over on instagram: _stephlowe_ @thenaturalnutritionist, on her podcast - "Health, Happiness + Human Kind, or her website - thenaturalnutritionist.com.au

To watch this episode, please visit Rachel’s YouTube channel. Listeners can find Dr. Gabrielle Lyon at her website https://drgabriellelyon.com, and on Instagram @drgabriellelyon Dr. Gabrielle Lyon is a Washington University fellowship-trained physician in Nutritional Science and Geriatrics and is board certified in Family Medicine and Osteopathic Manipulation. Her specialty in muscle-centric medicine™ has led her to be featured on “The Doctors”, with published articles in Muscle and Fitness, Women’s Health, Men’s Health, and Harper’s Bazaar. The application of her expertise ranges from brain and thyroid health to lean body mass support and longevity. In her private practice, Dr. Lyon leverages evidence-based medicine and cutting-edge science to restore metabolism, balance hormones, and optimize body composition with the end goal of helping others discover lifelong vitality. In this episode, we talk about prioritizing protein, the differences between protein sources and examples of how they are not created equal, how the time you eat affects your circadian rhythm, if keto is safe during pregnancy and more! "If you are protein forward and you anchor your plate in protein, you're going to have a better ability to satiate yourself, you're much less likely to binge eat or overeat, and you're much more likely to have a favorable metabolic effect." Dr. Gabrielle Lyon Top Takeaways: Recommended amount of daily protein intake per individual Differences between protein sources such as meats, whey, collagen, etc. Benefits of creatine as you age Dr. Lyon’s recommendations on how to find quality supplements Today’s Questions: What is muscle-centric medicine? Can you talk about the main reasons why having/building muscle is so important for overall health? Importance of protein and ideal intake? Why is all protein not created equal? Is it possible to build muscle over the age of 50? If so, what should be the main factors to focus on? Can you discuss the research on higher protein (specifically leucine) when breaking a fast? Why is leucine so important? Does it matter when we eat food (breakfast/lunch/dinner)? Are there ‘good or bad’ foods to eat together? Safety of low-carb/keto diets in pregnancy and effect of OGTT at 28 weeks? What’s a typical day of eating look like for you? What if any supplements would you recommend to include in your kind of every day? Show Notes: [0:00] Welcome back to MetFlex and Chill! Rachel introduces Dr. Gabrielle Lyon to the listeners [0:30] Dr. Gabrielle Lyon gives listeners brief background of how she got to her passion [1:00] Dr. Donald layman [1:30] Question: What is muscle-centric medicine? [3:30] Question: Can you talk about the main reasons why having/building muscle is so important for overall health? [6:00] Question: Importance of protein and ideal intake? [7:30] High Quality Protein: Amino acids, Isoleucine, Beilein, Leucine [9:00] Question: Why is all protein not created equal? [13:30] Bioavailability [14:30] Is it possible to build muscle over the age of 50? If so, what should be the main factors to focus on? [15:00] Physiological phenomenon called: anabolic resistance [20:00] Question: Can you discuss the research on higher protein (specifically leucine) when breaking a fast? [22:00] Question: Why is leucine so important? [24:00] Question: Does it matter when we eat food? (breakfast/lunch/dinner)? Are there ‘good or bad’ foods to eat together? [29:00] Question: Safety of low-carb/keto diets in pregnancy and effect of OGTT at 28 weeks? [31:00] Question: What’s a typical day of eating look like for you? [34:30] Question: What if any supplements would you recommend to include in your kind of every day? [36:00] Question: Is there anything you’ve changed your mind about in the last year? And why? [38:00] If you want to see more of Dr. Gabrielle’s content check her out on Instagram @drgabriellelyon on youtube at Dr. Gabrielle Lyon [40:06] End --- Join the FREE MetFLex Life Course: www.metflexandchill.com Rachel Gregory (@rachelgregory.cns) is a Board-Certified Nutrition Specialist, Strength and Conditioning Specialist, and Author of the best-selling book, 21-Day Ketogenic Diet Weight Loss Challenge. She received her Master’s Degree in Nutrition & Exercise Physiology from James Madison University and Bachelor’s Degree in Sports Medicine from the University of Miami. Rachel helps her clients transform their lives by starting with the physical (body), realizing the power of the mental (mindset), and ultimately gaining massive confidence that bleeds into every aspect of their lives (family, relationships, work, etc.).

The vast majority of heart attack and stroke is not caused by full-blown diabetes but prediabetes. In this podcast, let's cover some quick facts about prediabetes, the types of tests, and how to manage such conditions. Prediabetes or type 2 diabetes? Why hemoglobin A1c test is not reliable; Oral glucose tolerance test (OGTT) vs. fasting blood sugar (FBS);The optimum insulin numbers; How to manage prediabetes/diabetes;How diet (e.g. low-carb, carnivore) affects your glucose metabolism.For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources: PrevMed's prediabetes articlePrevMed's websitePrevMed's YouTube channelPrevMed's Facebook page

John Lorscheider was a frequent contributor and moderator of our forum and YouTube channel. He was also a PrevMed patient. Like most of us, John's family and personal history include significant cardiovascular risk. In this podcast, listen:a bit about John's background;about John's inflammation and carotid IMT test results;how OGTT and insulin survey helped John discovered that he was borderline diabetic;how John used calcium scan to track his plaque growth/regression;about the several changes John implemented (medications, supplements, diet, exercises) to successfully lower his calcium score by 59% within 16 months.For more information, contact us at 859-721-1414 or myhealth@prevmedheartrisk.com. Also, check out the following resources: PrevMed's websitePrevMed's YouTube channelPrevMed's Facebook page

As a follow up to AMA #14 where Peter explained his framework for analyzing labs, this “Ask Me Anything” (AMA) episode focuses on a number of real-world case studies exploring metabolic dysregulation, low testosterone, menopause, hypothyroidism, elevated uric acid, and more. From the examples discussed, you can follow along how our clinical team goes about interpreting diagnostic measures and applying relevant research findings. Once again, Bob Kaplan, Peter’s head of research, will be asking the questions. If you’re a subscriber, you can now listen to this full episode on your private RSS feed or on our website at the AMA #15 show notes page. We discuss: Should you stop taking supplements before getting a lab test? [2:45]; Family history—Questions to ask and what to look for [5:30]; The purpose of an oral glucose tolerance test (OGTT) [12:15]; Case study—Insufficient muscle mass for proper glucose disposal [17:15]; Why hemoglobin A1c is a relatively unhelpful metric [24:00]; Case study—Exceeding carbohydrate tolerance [26:30]; Case study—Metabolic dysfunction and a framework for metabolic health [33:30]; Peter’s ideal tracking of metabolic health for all his patients [43:30]; Contrasting presentations of hypogonadism—Low free testosterone [45:00]; How sleep, exercise, and alcohol affect testosterone levels? [56:20]; Case study—Surprisingly fast onset of menopause [59:25]; Case study—Hypothyroidism and high cholesterol [1:07:00]; Case study—Elevated uric acid and hypertension [1:10:55]; and More. Learn more: https://peterattiamd.com/ Show notes page for this episode: https://peterattiamd.com/ama15 Subscribe to receive exclusive subscriber-only content: https://peterattiamd.com/subscribe/ Sign up to receive Peter's email newsletter: https://peterattiamd.com/newsletter/ Connect with Peter on Facebook | Twitter | Instagram.

In the Covid-19 world, those individuals, especially older males, with comorbidities, like hypertension and diabetes, are at increased risk to complications, if this SARS 2 disease is contracted.The journal Cell Metabolism reported in June of 2018 that early time restricted feeding (eTRE)–between 8 am and 2 pm–increases insulin sensitivity and lowers blood pressure–even in the absence of weight loss, in prediabetic men.Intermittent fasting (IF), which alternates periods of eating and fasting, has been speculated to improve cardiometabolic health more than conventional dieting. Yet, most of the IF evidence, to date, in humans has suggested that the benefits accrue mostly from weight loss.The study authors, from the Pennington Biomedical Research Center in Baton Rouge, Columbia State University, the American Diabetes Association, and the University of Alabama, state that there was a, “need to determine whether the benefits of interventions, such as IF, are mediated only through weight loss or through mechanisms that are independent of weight loss.”These investigators used a “proof-of-concept trial”—using a form of IF called time-restricted feeding (TRF)—to determine whether IF had benefits independent of weight loss.TRF, note the Pennington team, “is a type of IF that extends the daily fasting period between dinner and breakfast the following morning, and, unlike most forms of IF, it can be practiced either with or without reducing calorie intake and losing weight.”TRF is limiting daily food intake to a window of ten hours or less—with fasting the remaining 14 hours, over a 24-hour period. The typical American eats over a 12-hour window (8am to 8 pm on average).The researcher's study period spanned five weeks, in which a group of prediabetic men adopted an (eTRF) schedule—over a six-hour period–versus a second control group of male prediabetics, who adhered to a twelve-hour eating window.The participants consumed only food provided by study staff, were fed enough food to maintain their weight, and ate all meals, while being monitored by study staff.From a metabolic, medical standpoint, glucose tolerance, postprandial (after a meal) insulin, and insulin sensitivity, as measured using a 3-hr oral glucose tolerance test (OGTT) were assessed, while the secondary endpoints were cardiovascular risk factors and markers of inflammation and oxidative stress.It was determined that, “5 weeks of (eTRF) improved insulin levels, insulin sensitivity, beta cell responsiveness, blood pressure, and oxidative stress levels in men with prediabetes—even though food intake was matched to the control arm and no weight loss occurred.”Before you embark on such an eating schedule, be sure to check with your primary care physician to see how such a plan might impact your health profile.

We get a lot of questions from our clients about postprandial fatigue. Never heard of it? Well you’ve certainly familiar with the term “food coma” - and perhaps with the experience of being in one. What causes this phenomenon and why does it affect some people more than others? Is it normal to need a nap after lunch?  On this podcast I’m joined by NBT Scientific Director Megan Hall to talk about postprandial fatigue - the sleepiness, difficulty focusing, and even dizziness or nausea that strikes after consuming a meal. Megan talks about some of the biological processes behind the need for a post-meal snooze, and when to suspect a deeper pathology. She also offers practical tips to help you resolve your own postprandial fatigue. Thank you everyone who so generously supports this podcast on Patreon - without your support, we wouldn’t be able to keep this podcast independent and free of ads. So thank you. And just a reminder - as a Patreon supporter - not only do you have our eternal gratitude, but also... You get some awesome gifts - including 20-35% discounts on all supplements we recommend when working with clients, which saves many of our supporters $50-$100 a month over what they were previously paying on Amazon. So by supporting the podcast, they’re actually spending LESS money each month. In addition to that, you can also get access to our Office Hours, where Megan answers questions twice a week. You can submit all your own questions, as well as listen to all the replays, covering everything from krill oil to mitochondrial support. We’ve worked really hard to make sure that the bonuses you get are actually way more valuable than what you pay whatever level you choose to support us at. So if you’d like to support the podcast and get access to the discounts and Office Hours, just head over to NBT.link and sign up there. Here’s the outline of this interview with Megan Hall: [00:04:25] Common symptoms of postprandial fatigue. [00:05:46] Reactive hypoglycemia; Study: Johnson, Debra D., Kay E. Dorr, and Wendell M. Swenson. "Reactive hypoglycemia." JAMA 243.11 (1980): 1151-1155.  [00:06:35] Diagnosing reactive hypoglycemia; Study: CHALEW, STUART, et al. "Diagnosis of reactive hypoglycemia: pitfalls in the use of the oral glucose tolerance test." Southern Medical Journal 79.3 (1986): 285-287. [00:09:00] Symptoms and causes of hypoglycemia. [00:09:37] Increased insulin sensitivity; Studies: 1. Brun, J. F., et al. "Increased insulin sensitivity and basal insulin effectiveness in postprandial reactive hypoglycaemia." Acta Diabetologica 33.1 (1996): 1-6; 2. Vexiau, P., B. Legoff, and G. Cathelineau. "Insulin and cortisol secretion during OGTT in patients with reactive hypoglycaemia with or without clinical symptoms." Hormone and metabolic research 15.09 (1983): 419-421. [00:09:47] Hypocortisolism; Studies: 1. Meyer, Gesine, et al. "Nocturnal hypoglycemia identified by a continuous glucose monitoring system in patients with primary adrenal insufficiency (Addison's disease)." Diabetes Technology & Therapeutics 14.5 (2012): 386-388; 2. Christiansen, Jens Juel, et al. "Effects of cortisol on carbohydrate, lipid, and protein metabolism: studies of acute cortisol withdrawal in adrenocortical failure." The Journal of Clinical Endocrinology & Metabolism 92.9 (2007): 3553-3559. [00:10:05] Hypothyroidism; Studies: 1. Kalra, Sanjay, Ambika Gopalakrishnan Unnikrishnan, and Rakesh Sahay. "The hypoglycemic side of hypothyroidism." Indian Journal of Endocrinology and Metabolism 18.1 (2014): 1; 2. Yadav, Tek Chand, et al. "Recurrent hypoglycemia: An unusual finding of hypothyroidism." Thyroid Research and Practice 14.3 (2017): 127. [00:10:53] What to do about hypoglycemia. [00:13:09] Accelerated gastric emptying. [00:16:20] Reactive hypoglycemia after exercise. [00:18:51] Postprandial hyperglycemia; Study: Gerich, John E. "Clinical significance, pathogenesis, and management of postprandial hyperglycemia." Archives of internal medicine 163.11 (2003): 1306-1316. [00:20:38] Problems associated with hyperglycemia; Studies: 1. Ceriello, Antonio, et al. "Meal-induced oxidative stress and low-density lipoprotein oxidation in diabetes: the possible role of hyperglycemia." Metabolism 48.12 (1999): 1503-1508; 2. Ceriello, Antonio, et al. "Meal-generated oxidative stress in type 2 diabetic patients." Diabetes care 21.9 (1998): 1529-1533; 3. Cavalot, F. "Do data in the literature indicate that glycaemic variability is a clinical problem? Glycaemic variability and vascular complications of diabetes." Diabetes, Obesity and Metabolism 15.s2 (2013): 3-8; 4. Ceriello, Antonio, et al. "Evidence for an independent and cumulative effect of postprandial hypertriglyceridemia and hyperglycemia on endothelial dysfunction and oxidative stress generation: effects of short-and long-term simvastatin treatment." Circulation 106.10 (2002): 1211-1218; 5. Tibaldi, Joseph. "Importance of postprandial glucose levels as a target for glycemic control in type 2 diabetes." Southern medical journal 102.1 (2009): 60-66. [00:21:24] Insulin resistance. [00:21:39] Video: PAH 2016 - A systems analysis approach to insulin resistance, with Dr. Tommy Wood. [00:23:02] What to do: Look at diet; 1. Krebs, Jeremy D., et al. "Improvements in glucose metabolism and insulin sensitivity with a low-carbohydrate diet in obese patients with type 2 diabetes." Journal of the American College of Nutrition 32.1 (2013): 11-17; 2. Lin, Po-Ju, and Katarina T. Borer. "Third exposure to a reduced carbohydrate meal lowers evening postprandial insulin and GIP responses and HOMA-IR estimate of insulin resistance." PloS one 11.10 (2016): e0165378; 3. MacDonald, Ian A. "A review of recent evidence relating to sugars, insulin resistance and diabetes." European journal of nutrition 55.2 (2016): 17-23; 4. Bradley, Una, et al. "Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial." Diabetes 58.12 (2009): 2741-2748. [00:28:46] Mediterranean diet; Study: Guasch-Ferré, Marta, et al. "Dietary polyphenols, Mediterranean diet, prediabetes, and type 2 diabetes: a narrative review of the evidence." Oxidative Medicine and Cellular Longevity 2017 (2017). [00:29:56] Endotoxemia and insulin resistance 1. Moreira, AP Boroni, and R. de Cássia Gonçalves Alfenas. "The influence of endotoxemia on the molecular mechanisms of insulin resistance." Nutrición hospitalaria 27.2 (2012): 382-390; 2. Cani, Patrice D., et al. "Metabolic endotoxemia initiates obesity and insulin resistance." Diabetes 56.7 (2007): 1761-1772. [00:30:24] Megan's outline for this podcast.  [00:31:19] When fatigue after a meal might be normal. [00:33:08] Article: Why a pandemic flu shot caused narcolepsy. [00:33:49] Both high fat and high carb meals can cause sleepiness; Study: Wells, Anita S., et al. "Effects of meals on objective and subjective measures of daytime sleepiness." Journal of applied physiology 84.2 (1998): 507-515. [00:33:56] Intestinal stimulation can cause sleepiness; Kukorelli, Tibor, and Gábor Juhász. "Electroencephalographic synchronization induced by stimulation of small intestine and splanchnic nerve in cats." Electroencephalography and clinical neurophysiology 41.5 (1976): 491-500. [00:34:20] Sleepiness after eating vs. just chewing; Study: MJ Harnish, SR Greenleaf, WC Orr, “A comparison of feeding to cephalic stimulation on postprandial sleepiness.” Physiology & behavior 64.1 (1998):93-96. [00:34:38] Cholecystokinin (CCK) may affect the alert centers in the brain; Study: Wells, Anita S., et al. "Influences of fat and carbohydrate on postprandial sleepiness, mood, and hormones." Physiology & behavior 61.5 (1997): 679-686. [00:37:13] Thermogenesis; Study: Zammit, Gary K., et al. "Postprandial sleep and thermogenesis in normal men." Physiology & behavior 52.2 (1992): 251-259. [00:37:40] Summary: How to fix the problem. [00:38:43] Nutrisense for continuous glucose monitoring (CGM). [00:46:29] Timing your walk with glucose peak; Study: Reynolds, Andrew N., and Bernard J. Venn. "The timing of activity after eating affects the glycaemic response of healthy adults: a randomised controlled trial." nutrients 10.11 (2018): 1743. [00:51:01] Support NBT on Patreon to access the forum.  

Arseny Chernov is the founder of Food Buddy an endurance nutrition coaching company and has a diploma of nutrition science as well as being an ironman athlete and tech professional.Engage with Foodbuddy on https://instagram.com/foodbuddy or https://fb.me/foodbuddyMentioned the following:• Estimated Energy Requirement Calculator: http://bit.ly/foodbuddy-eer• Conrad P. Earnest, Jeff Rothschild, Christopher R. Harnish & Alireza Naderi (2019) Metabolic adaptations to endurance training and nutrition strategies influencing performance, Research in Sports Medicine, 27:2, 134-146, DOI: https://doi.org/10.1080/15438627.2018.1544134• Rothschild JA, Bishop DJ, Effects of Dietary Supplements on Adaptations to Endurance Training, Sports Med. 2019 Sep 17, DOI: https://doi.org/10.1007/s40279-019-01185-8• Supplement for 100+ km/week joints running load: http://bit.ly/foodbuddy-geladrink• Inspiring Book: Throwing Rocks at the Google Bus https://amzn.to/34fuqUs• Inspiring Book: iGen: Why Today's Super-Connected Kids Are Growing Up Less Rebellious https://amzn.to/2JC1n5v• Inspiring Book: 80/20 Running: Run Stronger and Race Faster by Training Slower https://amzn.to/2NtNLKJ• Best sub-100$ thing: coaching by Merle Talviste, https://www.swimsmoothsingapore.com/squad• Best sub-100$ thing: Injini 2.0 Toe-socks https://amzn.to/2L4FyuY , Drymax socks: https://amzn.to/2QjXAiKTell us about your background in nutrition and history in endurance sports. What came first?Went from ~110 kg 80 kg myself. 10h 39min in Ironman Cairns (140.6), 29h 18min in PYT166 100-miler with 8000 meters elevation. Got a lab coat - did a Specialist Diploma in Nutrition Science at NYP Singapore, on top of my Master Degree in technology. I launched my own app for iOS called FoodBuddy, sunsetting it now unfortunately.My wife Lily's fully recovered from the neck disc tear through nutrition and well-being planned. Now runs duathlons.Foodbuddy is all about coaching 1x1, enterprise workshops (most impactful format), also present in Regional Committees (RC-s) in Singapore as I'm a People's Association Trainer.Standard Chartered Singapore Marathon 2018 official nutrition coach, run workshops, Facebook live-s.My mentors: Andre Blumberg, Matt Fitzgerald. Coached in “kampung spirit” of Integrated Riding Racing Team (IRRT) - takes a village to ride fast! Kudos to Merle Talviste (Swim Smooth coaching Singapore)Tell us about your philosophy on nutritionNutritional choices (what to take) is NOT diet (sum of intake). Let's get terms right. Most important aspect is Hunger vs. Appetite. Figure your Estimated Energy Requirement: http://bit.ly/foodbuddy-eer Set yourself up for the reality around you. Then get bored! How I pre-select to fight appetite. Recipes. Patterns.VICE uploaded “Mac & Cheese for 17 years” - “I've tried celery. I threw that shit out instantly” - https://www.youtube.com/watch?v=v1TWvXwgKr0 .Crazy case of some nervosa, definitely not anorexia nervosa though.Anyways, it's ABCD - no single right answer! Nutritional Needs Assessment uncovers it:● Anthropometric (i.e. BMI %%-s, fat loss progress, )● Biochemical (nutrient deficiencies, cholesterol level, OGTT for Diabetes)● Clinical (skin state, etc.)● Dietary (ecological / social status, certain food restrictions due to religion, food log, habits)As to athletes… aspiring vs. amateur, let's be real.● Eliud Kipchoge - Maurten hydrogel 2018, 2019. By the way there's a study that it's not really working as it's supposed to?.. Well, it works for Eliud anyways.● Chris Froome - haribo gummy candies in Giro D'Italia 2018 while losing 1 kg over 5 days.So did Peter Sagan.For us, ex-hunters with 10,000-s of years of experience, - everything edible is great in moderation.There are lots of diets that endurance athletes follow from Vegan, to Paleo to HCLF to Full Keto. What do you believe is the ideal diet for endurance sportsSuccessful event is a factor of preparation, mental health, in-race nutrition, luck (i.e. weather). Successful result is equivalent to “high performance”. High performance usually means lower mass.There's a new movie about vegan diet that throws in a bunch of claims by the way:● “Roman gladiators didn't eat meat” - that's an anecdote from archaeologist, Andrew Curry, in Archaelogoly Magazine 2008: Karl Grossschmidt of Medical University of Vienna, Vienna (MedUni Vienna). Gladiators, it seems, were fat. Consuming a lot of simple carbohydrates, such as barley, and legumes, like beans, was designed for survival in the arena. Packing in the carbs also packed on the pounds. "Gladiators needed subcutaneous fat," Grossschmidt explains. "A fat cushion protects you from cut wounds and shields nerves and blood vessels in a fight." Not only would a lean gladiator have been dead meat, he would have made for a bad show. Surface wounds "look more spectacular," says Grossschmidt. "If I get wounded but just in the fatty layer, I can fight on," he adds. "It doesn't hurt much, and it looks great for the spectators."● Claim “on par”. Plants could be an extremely good source of protein if all 9 essential amino acids + Nitrogen containing amino acids, but to say that it is on par with animal protein in terms of minerals like iron, vitamins like creatine, and synthesis availability (which are incredibly important for high performing athletes) is an outright BS.For vegetarians, it is important to know that Protein Quality = Amino Acid Composition + Digestibility (soy is best, up to 90% where 100% is meat)Beef is less than egg whiteI eat eggs and drink milk = top PQ food :-) therefore, are you ovo-lacto-vegetarian :-)Complementary: legumes + grains (different amino-acids).Biological Value = (nitrogen retained, g / nitrogen absorbed, g) * 100Higher = better matchLower = lower matchFAT content in meat is higher, yes. There are two types of fat absorption: for saturated fat it's through lymphatic system (chylomicrons, leading to LDL) and through intestine walls then venes and to liver (for unsat / polyunsat). Former flies past the adipose tissue reserves through lymphatic system, resulting in subcutaneous fat refills uncontrolled. Latter is controllable but again, there are two vehicles that can be determined using biochemical blood test -- High Density Lipoproteins (HDL) GOOD lipoprotein -- very small size, Low Density Lipoprotein (LDL) BAD as can potentially clog the arterias.LCHFRothschild JA, Bishop DJ, Effects of Dietary Supplements on Adaptations to Endurance Training, Sports Med. 2019 Sep 17, DOI: https://doi.org/10.1007/s40279-019-01185-8 (shout out, he's in New Zealand doing his PhD)Over the past 20 years, research suggested that strategically reducing carbohydrate (CHO) availability during an athlete's training can modify the metabolic responses in lieu of simply maintaining a high CHO diet. Several methods have been explored to manipulate CHO availability and include: Low-carb, high-fat (LCHF) diets, performing two-a-day training without glycogen restoration between sessions, and a “sleep-low” approachArguments in favor of trying to increase fat-burning capacity focus around the ability to utilize the large stores of endogenous lipids found even in very lean athletes, while preserving the relatively limited supply of muscle and liver glycogen. Yet despite this theoretical advantage, measurable performance improvements from deliberately increasing fat burning capacity have been elusive.Each of these methods can confer beneficial metabolic adaptations for the endurance athlete including increases in mitochondrial enzyme activity, mitochondrial content, and rates of fat oxidation, yet data showing a direct performance benefit is still unclear.Do you believe in strict macros or simply calories in calories outThey all converge to one another, if you do it right. Estimated Energy Requirements (EER) is key here, and think about 7 days sliding windos.Another way to think about food is through the portions count of a particular quality. Kind of Matt Fidzgerald's approach. Know your EER + tweak PAL. Think last 7 days window. Control thirst-induced hunger. Eat breakfast like a pro.How do you believe the diet differs for each endurance sportEverywhere it's Gravity. Gravity is mass. Mass also non-linear to skin area, there's a formula to that. Thus the more mass - the more heat-induced stress from energy production, but not proportionally enough evaporation. Fat % reduction vs. temperature range vs. VO2max. Same stuff.What is your philosophy on nutrition during raceDepends on the race. Drink by thirst, do not fall below, do Protein.What is your philosophy on nutrition in recoverySleep. Compensation vs. recovery. DOMS. Antioxidants. Orange, Lime, Strawberries. Guava.Protein ratio to Carbohydrates. 30% of EER means ~0.8g/kg/day . Increase with intensity. Don't compensate!I do collagen peptides for 100+ km weeksHow do you feel about fasting as a method for endurance athletes.Time restricted eating and longer term fastsExercise more! Ride up grades, don't buy upgrades!What about alcohol? Red wine good / bad? Volume?7 cal/g, balance with life.Do you recommend protein shakes?Depends on training volume, but the the NuZest is great.What about supplements? Vitamins, minerals, fish oils? Do you recommend and how do you suggest people review which supplements they should get. I've done DNAFit which showed a genetic lack of B6 and B12Do the Clinical blood test and talk to doctor. Sleep.I do collagen peptides for 100+ km weeksDrinking during endurance sports? Hypernatremia is a big risk. Do you suggest taking on salt during exercise.Comrades Marathon study by Tim Noakes, author of “Waterlogged”. Water follows electrolytes, salt inhibits the water. Same in inter-cellular and intracellular. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2564296/Are there any ‘superfoods' which you recommend, Apple cider vinegar, Flak seeds, Chia seeds, nuts.Train more!Chia is great brekkie, keeps the Latin American economy going as side-effect ;-)“PROTEIN DIGESTIBILITY OF CHIA SEED Salvia hispanica L” -- digged through faeces to find out.CHIA SEE contains 18% of protein content, a level markedly greater than other nutritional grains such as wheat (14%), corn (14%), rice (8.5%), oats (15.3%) and barley (9.2%) -- grind in to flour or buy as powder.Fiber content. And it's cool :-) But, low protein digestibility according to FAO/OMS (42) standards. 79.80%Raw seed only 34% It looks like grinding would help protein digestion of raw seed. This treatment improve digestibility that could happen due to the fact that grinding divide and expose all seed component allowing enzymes actions. Finally, soybean flour shows an intermediate digestibility score, which is in concordance with previously a report.BEETROOTConrad P. Earnest, Jeff Rothschild, Christopher R. Harnish & Alireza Naderi (2019) Metabolic adaptations to endurance training and nutrition strategies influencing performance, Research in Sports Medicine, 27:2, 134-146, DOI: https://doi.org/10.1080/15438627.2018.1544134The limited evidence suggests there may be small but favourable effects of endurance training with nitrate supplementation, which are possibly related to changes in muscle fibre type. Beetroot juice may be more effective than nitrate salts, though the eficiency of supplementation can be affected by inter-individual variability [97] and environmental conditions [98]. All studies to date have used high-intensity training protocols, as dietary nitrate is particularly effective at augmenting physiological responses in type II fibresSugar, is it really the enemy?Yes. Dopamine! Not good :-(Meat, is it really the enemy?Often high fat in meat, plug cooking with oil... But again, it's vs. choices, vs. tastes, vs… Well, for protein - nothing beats egg whites. You choose!Around your endurance athlete CV. How many IronMan have you run. What was your best performance?PB 10:39 in Cairns 140.629:18 in PYT166Have you ever DNFd? What's your favourite DNF and why? What did you learn?NopeWhat makes you emotionalMusic, good movies. Watched “Big” with Tom Hanks recently, what a great movie. Endorphins from meditative trail running.Most inspirational bookiGen by Jean Twenge / Crucial Conversations by Al Switzler / Throwing Rocks at Google Bus Douglas Rushkoff / 80/20 Running by M.FitzgeraldFavourite podcastsUnfortunately I'm the audiobooks kind of guy at best :-( Will do more Endurance Asia!Favourite endurance tech appsStrava of Alan Bradley :-) RAAM Solo, now RedBul TransSiberian... and being Friends on Facebook with Jag Lanante and Andre Blumberg.Best kit you've bought under $100• Best sub-100$ thing: coaching by Merle Talviste, https://www.swimsmoothsingapore.com/squad• Best sub-100$ thing: Injini 2.0 Toesocks https://amzn.to/2L4FyuY , Drymax socks: https://amzn.to/2QjXAiKProudest moment personal / physical / professionalMy daughter. My wife's recovery from neck disc tear.Closing remarks advice anyone thinking of coming up with or doing a challenge, whether it be a expedition adventure race, ironman, ultra marathon or Everest..Set goals, look backwards, imagine, visualize, and think backwards how to get there. Always neg-split. Always set interim achievable goals!Engage and reach out on Social media :-)

Der Gestationsdiabetes (GDM) ist definiert, als eine erstmals in der Schwangerschaft aufgetretene mittels Nüchternblutzucker oder mit einem standardisierten 75g oralen Glukosetoleranztest (oGTT) diagnostizierte Glukosetoleranzstörung. Der GDM gehört zu den häufigsten Schwangerschaftskomplikationen in Deutschland. Mitbedingt durch bessere Screeninguntersuchungen und strengere Diagnosekriterien, hat seine Inzidenz in den letzten Jahren stetig zugenommen. Da aktuelle Studien zeigen, dass bereits gering erhöhte Blutzuckerwerte in der Schwangerschaft mit einer Zunahme sowohl an maternalen als auch an kindlichen Komplikationen einhergehen, wurden die Diagnosekriterien modifiziert und im Jahr 2011 in einer neuen Leitlinie publiziert. Erstmals existiert nun eine gute Evidenzbasis zur Diagnose und Therapie des GDM. Ziel dieser Arbeit war es, in einer retrospektiven Analyse die Effektivität der aktuellen Therapie des Gestationsdiabetes anhand der Behandlungsergebnisse am Diabeteszentrum der LMU München, zu erfassen. Die Ergebnisse wurden mit den Daten aktueller internationaler Studien (ACHOIS, MFMU, HAPO) verglichen. Die Studie umfasste 297 Gestationsdiabetikerinnen (GDM-Kollektiv), die im Zeitraum vom 01.01.2008 bis 30.06.2011 im Diabeteszentrum der Medizinischen Klinik Innenstadt der LMU München betreut wurden. Davon entbanden 167 Patientinnen (LMU-Kollektiv) ihre Kinder in der Klinik für Gynäkologie und Geburtshilfe der LMU München. Von diesen konnten zusätzliche perinatale Daten erhoben werden. Als Vergleichskollektiv (n = 8773) wurden alle Frauen erfasst, die im selben Zeitraum ebenfalls an der Klinik für Gynäkologie und Geburtshilfe der LMU München entbanden. Der Vergleich der Baseline-Charakteristika der Frauen mit GDM und des Vergleichskollektivs bestätigte vor allem den präkonzeptionellen BMI als Risikofaktor für GDM. Diagnostik und Therapiebeginn erfolgte bei den Patientinnen mit Insulintherapie signifikant früher, als bei den Frauen mit rein diätetischer Therapie. Die Patientinnen im Insulin-Kollektiv wiesen signifikant höhere Nüchtern- und 1-h Werte im 75-g oGTT auf. Nach den alten Diagnosekriterien wären 55,5 % der Patientinnen im LMU-Kollektiv nicht als GDM diagnostiziert worden. Mitbedingt durch die neuen Kriterien kam es zu einem Anstieg der Inzidenz um 50%. Die Rate an mütterlichen und kindlichen Komplikationen war insgesamt gering. Im GDM-Kollektiv fand sich trotz Therapie ein höherer LGA-Anteil (Geburtsgewicht > 90. Perzentile) als im Vergleichskollektiv (14,5% vs. 5,3%), welcher höher lag, als in aktuell publizierten Interventionsstudien. Die Raten von SGA (Geburtsgewicht < 10. Perzentile), primärer und sekundärer Sectio caesarea waren im GDM-Kollektiv nicht erhöht. Um zu klären, weshalb es trotz strenger Therapievorgaben zu einer erhöhten LGA-Rate nach GDM kommen konnte, erfolgte eine Unterteilung des GDM-Kollektivs nach dem Geburtsgewicht (≤ 90. vs. > 90. Perzentile). Als einziger signifikanter Unterschied zeigte sich der Zeitpunkt der Diagnosestellung des GDM. Entsprechend lag der LGA-Anteil bei Diagnosestellung ≤ 28. SSW mit 5,6% auf dem Niveau des Vergleichskollektivs. Die an unserem Zentrum praktizierte, nach den Leitlinien der DDG orientierte GDM-Therapie, bewirkte eine sehr niedrige mütterliche und kindliche Komplikationsrate. Bei rechtzeitiger Diagnosestellung lag die LGA-Rate auf dem Niveau des Vergleichskollektivs und ist mit den Ergebnissen aktueller Interventionsstudien durchaus vergleichbar. Unsere Daten unterstreichen noch einmal die Bedeutung eines generellen GDM-Screenings bei allen Frauen. Parallel zur Therapie des GDM sollte in enger Zusammenarbeit mit den betreuenden Gynäkologen eine sonografische Kontrolle des fetalen Wachstums erfolgen um Therapieanpassungen entsprechend der Entwicklung des Kindes durchführen zu können.

Aufgrund der steigenden Lebenserwartung von Patienten mit cystischer Fibrose (CF) nimmt die Prävalenz einer gestörte Glukosetoleranz (IGT) und eines CF-assoziierten Diabetes mellitus (CFRD)kontinuierlich zu. In der vorliegenden Arbeit wurde die Prävalenz von Glukosestoffwechselstörungen und deren Einfluss auf den klinischen Status in einer nicht vorselektionierten Gruppe von erwachsenen CF Patienten (n=34) im Vergleich zu neu-diagnostizierten Patienten mit Typ 2 Diabetes (n=9) und gesunden Kontrollpersonen (n=10) mittels oGTT untersucht. Desweiteren wurde durch Messung von Insulin, intaktem Proinsulin, intaktem GLP1 und der Bestimmung verschiedener Indices für die ß-Zellfunktion und die Insulinresistenz mögliche pathophysiologische Mechanismen in verschiedenen Stadien der Glukosetoleranzstörung untersucht. Bei den CF Patienten (Alter 30,2±8 Jahre, BMI 20,9 ±2,5 kg/m2) zeigten 50% der Patienten eine gestörten Glukosetoleranz (12% IFG, 23% IGT, 15% neu diagnostizierter CFRD). Im oGTT war der maximale Insulinpeak und die totale Insulinsekretionskapazität nicht unterschiedlich in den CF-Gruppen (AUCinsulin0-120min NGT: 3296±547 μU/ml, IFG: 3694±809 μU/ml, IGT: 3337±535 μU/ml, CFRD: 2387±318 μU/ml) und den Kontrollpersonen(3704±335 μU/ml). Bei CF-Patienten war ähnlich wie bei DM2 Patienten eine verminderte erste Phase der Insulinsekretion und eine zeitliche Verschiebung des Insulinpeaks nachweisbar, die mit der Verschlechterung der Glukosetoleranz assoziiert war (Stumvoll-FPIR NGT:450±291; IFG:252±203; IGT:309±254; CFRD:18±41; Kontrollen:950±388). Die Insulinsekretion korrelierte invers mit dem Glukoseprofil, so dass bei IFG und IGT hohe postprandiale Glukosespiegel innerhalb der ersten 60 Minuten und ein Blutzuckerabfall nach 120-180 min zu beobachten waren. Die Proinsulinspiegel und die GLP-1 Spiegel im oGTT waren nicht unterschiedlich im Vergleich zu den gesunden Kontrollen. Im Gegensatz zu den DM2 Patienten konnte bei CF Patienten keine deutliche Insulinresistenz festgestellt werden. Bei den CF Patienten war eine Verschlechterung der Lungenfunktion und des Ernährungszustandes mit zunehmender Glukoseintoleranz zu sehen. Hohe maximale Glukosespiegel(rs=-0,50, p=0,002), der Insulinogenic Index (rs = 0,36, p

During an oral glucose tolerance test (OGTT) glucose and insulin levels were measured in 26 patients with prolactin-producing pituitary tumours without growth hormone excess. Basal glucose and insulin levels did not differ from the values of an age-matched control group. After glucose load the hyperprolactinaemic patients showed a decrease in glucose tolerance and a hyperinsulinaemia. Bromocriptine (CB 154), which suppressed PRL, improved glucose tolerance and decreased insulin towards normal in a second OGTT. — Human PRL or CB 154 had no significant influence on insulin release due to glucose in the perfused rat pancreas. — These findings suggest a diabetogenic effect of PRL. CB 154 might be a useful drug in improving glucose utilization in hormone-active pituitary tumours.