Podcasts about catecholamine

HIIT may be failing you for two big reasons. Spoiler alert, here they are: You aren't actually hormonally in a place you'll benefit. You are doing them outside a sweet spot that is optimal for results So I'll quickly address #1 and have a deeper discussion on #2 and what actually is happening during HIIT and why it has the potential to be so good, if you're ready! Your Glucose Metabolism to Know Why HIIT May Be Failing You The classic form of “all out” HIIT is the Wingate test. After about 3 to 5 minutes of warm-up the subject cycles for 30 seconds at maximum effort against a standardized resistance. Typically four to six Wingate tests are performed separated by 4 minutes of rest, for a total of 2 to 3 minutes of maximal exercise spread over 15 to 30 minutes. This “all out” cycle ergometer form of HIT is also referred to as sprint interval training (SIT). In intense exercise (>80% VO2max), unlike at lesser intensities, glucose is the exclusive muscle fuel. Catecholamine levels rise markedly, causing glucose production to rise seven- to eightfold while glucose utilization is only increased three- to fourfold. In people without diabetes there is a small blood glucose increase during intense exercise that increases further immediately at exhaustion and persists for up to 1 hour. Plasma insulin levels rise, correcting the glucose level and restoring muscle glycogen. This physiological response would be absent in type 1 diabetics. Your Aerobic Endurance to Know Why HIIT May Be Failing You HIIT is effective in improving aerobic endurance. In one study six “all out” SIT sessions over 2 weeks improved the mean cycle endurance time to fatigue while cycling at approximately 80% of pretraining VO2max by 100% (from 26 to 51 minutes). This required a total high-intensity exercise time of only 15 minutes with a total training time commitment of approximately 2.5 hours. In another study, a less intense version of HIIT (6–10 cycling bouts of 30 seconds each at 125% of the power at VO2max with 2 minutes recovery) produced a similar improvement in VO2max after 4 weeks of training, as was seen in the more intense SIT group (three to five “all out” 30-second cycling bouts with 4 minutes of recovery).  The less intense HIT required only half the intensity but double the repetitions of the SIT, and may be more practical for the nonathlete. After high-intensity exercise, insulin sensitivity is typically increased, meaning the body may require less insulin to utilize glucose effectively, which could lead to a slight rise in insulin levels during recovery as the body replenishes glycogen stores. The lower the conditioning level the more insulin is likely to be increased. The longer the activity level, the more insulin is likely to be secreted after exercise. If adequate recovery does not occur between intervals there may be a greater elevation in stress hormones. So either … keep the intensity high and the duration extremely short, or make this a longer session with up to 4 minutes between all-out bursts still with a total time of 20 minutes of interval rounds, adding warm up and cool down making it a 30 minute session. References: Adams OP. The impact of brief high-intensity exercise on blood glucose levels. Diabetes Metab Syndr Obes. 2013;6:113-122 https://doi.org/10.2147/DMSO.S29222 Erik A. Richter, Lykke Sylow, Mark Hargreaves; Interactions between insulin and exercise. Biochem J 12 November 2021; 478 (21): 3827–3846. doi: https://doi.org/10.1042/BCJ20210185 Resources: Flipping50 Membership:https://www.flippingfifty.com/cafe Sleep Yourself Skinny:https://www.flippingfifty.com/sleep-yourself-skinny Protein Products:https://www.flippingfifty.com/protein Other Episodes You Might Like: How to Exercise with High or Low Cortisol in Menopause:https://www.flippingfifty.com/getting-wrong-after-40 12 Strength Training Mistakes in Menopause Robbing Your Results:https://www.flippingfifty.com/12-strength-training-mistakes-in-menopause How to Exercise with High or Low Cortisol in Menopause:https://www.flippingfifty.com/high-or-low-cortisol-in-menopause

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.30.534970v1?rss=1 Authors: Li, L., Rana, A. N., Li, E. M., Feng, J., Li, Y., Bruchas, M. Abstract: Catecholamine signaling is thought to modulate cognition in an inverted-U relationship, but the mechanisms are unclear. We measured norepinephrine and dopamine release, postsynaptic calcium responses, and interactions between tonic and phasic firing modes under various stimuli and conditions. High tonic activity in vivo depleted catecholamine stores, desensitized postsynaptic responses, and decreased phasic transmission. Together this provides a clearer understanding of the inverted-U relationship, offering insights into psychiatric disorders and neurodegenerative diseases with impaired catecholamine signaling. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.26.534277v1?rss=1 Authors: Wilson, L. R., Plummer, N. W., Evsyukova, I. Y., Patino, D., Stewart, C. L., Smith, K. G., Fry, S. A., Deal, A. L., Kilonzo, V. W., Sciolino, N. R., Cushman, J. D., jensen, p. Abstract: Contextual fear learning is heavily dependent on the hippocampus. Despite evidence that catecholamines contribute to contextual encoding and memory retrieval, the precise temporal dynamics of their release in the hippocampus during behavior is unknown. In addition, new animal models are required to probe the effects of altered catecholamine synthesis on release dynamics and contextual learning. Utilizing GRABNE and GRABDA sensors, in vivo fiber photometry, and two new mouse models of altered locus coeruleus norepinephrine (LC-NE) synthesis, we investigate norepinephrine (NE) and dopamine (DA) release dynamics in dorsal hippocampal CA1 during contextual fear conditioning. We report that aversive foot-shock increases both NE and DA release in dorsal CA1, while freezing behavior associated with recall of fear memory is accompanied by decreased release. Partial loss of LC-NE synthesis reveals that NE release dynamics are modulated by sex. Moreover, we find that recall of recent fear memory is sensitive to both partial and complete loss of LC-NE synthesis throughout prenatal and postnatal development, similar to prior observations of mice with global loss of NE synthesis beginning postnatally. In contrast, remote recall is compromised only by complete loss of LC-NE synthesis beginning prenatally. Overall, these findings provide novel insights into the role of NE in contextual fear and the precise temporal dynamics of both NE and DA during freezing behavior, and highlight a complex relationship between genotype, sex, and NE signaling. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Did you take Flintstone Vitamins as a kid?Do you take vitamins now?-Do vitamins help?-What does Vitamin D do to help the brain?-If you're low on Vitamin D, what happens to your body?-Do you take Vitamin B12?  Pete gets a SHOT (yes, a needle) every month-What is Catecholamine do and should you be taking it? 

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.19.508617v1?rss=1 Authors: Yang, S. J., Del Bonis-O'Donnell, J. T., Giordani, F. A., Wang, J. W.-T., Lui, A., Piekarski, D., Irrinki, A., Schaffer, D., Landry, M. P. Abstract: Dopamine neuromodulation is a critical process that facilitates learning, motivation, and motor control. Disruption of these processes has been implicated in several neurological and psychiatric disorders including Huntington's Disease (HD). While several treatments for physical and psychiatric HD symptoms target dopaminergic neuromodulation, the mechanism by which dopaminergic dysfunction occurs during HD is unknown. This is partly due to limited capability to visualize dopamine dynamics at the spatiotemporal resolution of both neuromodulator release (ms) and dopaminergic boutons (m). Here we employ near-infrared fluorescent catecholamine nanosensors (nIRCats) to image dopamine release within the brain striatum of R6/2 Huntington's Disease Model (R6/2) mice. We find that stimulated dorsal striatal dopamine release decreases with progressive motor degeneration and that these decreases are primarily driven by a decrease in the number of dopamine hotspots combined with decreased release intensity and decreased release fidelity. Using nIRCat's high spatial resolution, we show that dopamine hotspots in late HD show increased ability to add new dopamine hotspots at high extracellular calcium concentrations and track individual dopamine hotspots over repeated stimulations and pharmacological wash to measure dopamine hotspots release fidelity. Compellingly, we demonstrate that antagonism of D2-autoreceptors using Sulpiride and direct blocking of Kv1.2 channels using 4-Aminopyradine (4-AP) increases the fidelity of dopamine hotspot activity in WT striatum but not in late HD striatum, indicating that D2-autoreceptor regulation of dopamine release through Kv1.2 channels is compromised in late HD. These findings, enabled by nIRCats, provide a more detailed look into how dopamine release is disrupted and dysregulated during Huntington's Disease to alter the coverage of dopamine modulation across the dorsal striatum. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.19.508617v1?rss=1 Authors: Yang, S. J., Del Bonis-O'Donnell, J. T., Giordani, F. A., Wang, J. W.-T., Lui, A., Piekarski, D., Irrinki, A., Schaffer, D., Landry, M. P. Abstract: Dopamine neuromodulation is a critical process that facilitates learning, motivation, and motor control. Disruption of these processes has been implicated in several neurological and psychiatric disorders including Huntington's Disease (HD). While several treatments for physical and psychiatric HD symptoms target dopaminergic neuromodulation, the mechanism by which dopaminergic dysfunction occurs during HD is unknown. This is partly due to limited capability to visualize dopamine dynamics at the spatiotemporal resolution of both neuromodulator release (ms) and dopaminergic boutons (m). Here we employ near-infrared fluorescent catecholamine nanosensors (nIRCats) to image dopamine release within the brain striatum of R6/2 Huntington's Disease Model (R6/2) mice. We find that stimulated dorsal striatal dopamine release decreases with progressive motor degeneration and that these decreases are primarily driven by a decrease in the number of dopamine hotspots combined with decreased release intensity and decreased release fidelity. Using nIRCat's high spatial resolution, we show that dopamine hotspots in late HD show increased ability to add new dopamine hotspots at high extracellular calcium concentrations and track individual dopamine hotspots over repeated stimulations and pharmacological wash to measure dopamine hotspots release fidelity. Compellingly, we demonstrate that antagonism of D2-autoreceptors using Sulpiride and direct blocking of Kv1.2 channels using 4-Aminopyradine (4-AP) increases the fidelity of dopamine hotspot activity in WT striatum but not in late HD striatum, indicating that D2-autoreceptor regulation of dopamine release through Kv1.2 channels is compromised in late HD. These findings, enabled by nIRCats, provide a more detailed look into how dopamine release is disrupted and dysregulated during Huntington's Disease to alter the coverage of dopamine modulation across the dorsal striatum. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

GuestsDr. Gretchen Sacha, PharmD, BCCCPCleveland ClinicDr. Patrick M. Wieruszewski, PharmD, BCCCPMayo ClinicHostDr. Carolyn M. Bell, PharmD, BCCCPMedical University of South Carolina

Catecholamine is used in patients with septic shock to augment hemodynamics and achieve goal mean arterial pressure. Ludwig H. Lin, MD, is joined by Gretchen L. Sacha BCCCP, PharmD, to discuss this retrospective observational study to evaluate the associations of catecholamine dose, lactate concentration, and timing from shock onset at vasopressin initiation with in-hospital mortality. (Sacha G, et al. Crit Care Med. 2022;50:614-623). Dr. Sacha is a critical care clinical specialist at Cleveland Clinic in Cleveland, Ohio. This podcast is sponsored by Sound Physicians.

In this podcast, Dr. Scott Sharkey, senior consulting cardiologist with Minneapolis Heart Institute, provides a discussion on cardiomyopathy and more specifically Takotsubo syndrome. Enjoy the podcast! Objectives:     Upon completion of this podcast, participants should be able to: Describe how Takotsubo cardiomyopathy was discovered. Differentiate the diagnostic criteria for Takotsubo cardiomyopathy from other cardiology related conditions. Identify treatment options for Takotsubo cardiomyopathy. CME credit is only offered to Ridgeview Providers & Allied Health Staff for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks.  You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org. Click on the following link for your CME credit: CME Evaluation: "Achin' Breaking Hearts: Takotsubo Syndrome w/Dr. Scott Sharkey" (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.)  DISCLOSURE ANNOUNCEMENT  The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview Medical Center & Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws.  It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented. Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event. SHOW NOTES: CHAPTER 1: Cardiomyopathy. According to Dr. Sharkey, it is a general term for cardiac muscle disease, often times of unknown cause. Usually it refers to a dilated, poorly, contracting heart. Though it's also been called stress cardiomyopathy, Takotsubo does not behave like most cardiomyopathies. It's a microcirculatory disease, causing a stunned myocardium similar to an acute myocardial infarction, but with non-obstructive epicardial coronary arteries. Dr. Sharkey and his colleagues first noticed this phenomenon in patients with myocardial infarction that showed deep T wave inversions on EKG, and initial ECHOs with ejection fractions of 25-30%. Weeks later, these injuries would resolve, findings they attributed to a stunned myocardium. This phenomenon was then seen in a patient with a TBI, who again had a deep T wave inversion, and a large left ventricular regional wall motion abnormality with normal coronary arteries. The regional wall motion abnormality, again, resolved. These findings were noted in 20 similar cases that were then published in 1998. Though to note, this same syndrome was also present in the Japanese literature at this time. Later, it was noted patients were developing these symptoms not just from severe illness or trauma, but also from deeply emotional situations. This led to a write-up in Circulation in 2005, which received the 'Paper of the Year' award. From the early days to now, Dr. Sharkey went from seeing three to four patients per year with Takotsubo, to present day, one to two patients per week. The Minneapolis Heart Institute Foundation has done, and continues to do robust research on Takotsubo, noting that there is a subset of vulnerable patients that actually have recurrences of Takotsubo., They have also been able to study specific triggers for Takotsubo, like drug use, pheochromocytoma and critical illness in general. CHAPTER 2: Triggers for Takotsubo. As mentioned before, drug use, pheochromocytoma or critical illness are causes, but really any physical illness as well as any emotional stress are triggers for this syndrome. Death of a spouse is a good example of an emotional trigger, though as exemplified in the discussion, it can be any emotional situation. Teasing out the patient's history and the specific precipitation event is an art form. The autonomic nervous system is implicated here. Catecholamine levels are very elevated in these patients, as opposed to lower levels seen in acute MI patients. Pheochromocytoma and accidental overdose of epinephrine will cause this as well. The pathophysiology of the event is still being researched. It's postulated that this is all caused by vasospasms of the circulation or direct myocardial injury due to the catecholamine excess. It's presumed that effects occur on micro-circulatory level, and any disruption in blood flow is brief, less than 15-20 minutes, enough to raise serum troponins and cause wall motion abnormality. The involvement is circumferential, so the ECG findings are more diffuse. EKG changes include ST segment elevation in about 40% of patients. Otherwise T wave inversion is often seen, but is a later development. ST depression is not generally seen in Takotsubo, and would instead indicate a coronary artery occlusion. Echo findings show a classic, distinctive finding: poor contractility or akineses from the mid-heart to the apex, while the base of the heart is hypercontractile. Also called apical ballooning, the apex can be seen ballooning outward on echocardiograms. This is what is reminiscent of a Japanese clay pot, octopus trap, aka Takotsubo. And yes, the name is most certainly credited to the Japanese. CHAPTER 3: When a patient presents with an acute cardiac event that looks like Takotsubo, the patients still must undergo coronary angiogram to exclude a coronary occlusion. Cardiac echo and cardiac MRI are used to help diagnose this disease. Beta blockers and ACE inhibitors are used early on in treatment, but Dr. Sharkey suspects that patients would probably recover without them. The reality is, most of these patients get better. The myocardium, in the setting to Takotsubo, should recover. A process that usually takes one to two weeks. Anti-platelets do not play a role here, but anticoagulants are often given until the myocardium has recovered to prevent a small risk of left ventricular thrombus. Left ventricular outflow tract obstruction is a complicating factor in Takotsubo. Many of these patients are middle aged to older women, and have basal septal hypertrophy. This exacerbates, the outflow obstruction, which causes hypotension and shock in Takotsubo, 15-20% of the time. The left ventricular outflow obstruction should resolve with the resolution of Takotsubo. As mentioned, Takotsubo can have a recurrent phenomenon, and remarkably, these patients all recover their heart function. Curiously, the precipitating cause for these patients tends to be emotional. Though used in the initial treatment, beta blockers are not prescribed long-term for Takotsubo patients. In fact, Dr. Sharkey found that 30% of patients with a Takotsubo event were already on beta blockers, and 80% of those who have had recurrent Takotsubo were already on beta blockers and ACE inhibitors. CHAPTER 4: Patient presentation: Patients can present with chest discomfort and/or shortness of breath, much like an acute MI patient. They can also present with an acute concern of another nature. Dr. Sharkey gave the example of a patient presenting with a pasteurella multocida infection causing an airway obstruction. The patient's ongoing hypotension led to further work up and diagnosis of Takotsubo. Takotsubo patients can also be discovered during inpatient stays when incidental ECG wave form changes, troponin elevation, tachycardia, and/or hypotension are noted. About 10% of Takotsubo patient's develop cardiogenic shock. Most survive their ICU stay, even if advanced treatment, like intra-aortic balloon pumps or ECMO are required. For the critically ill, where beta blocker use is contraindicated in the light hypotension, Dr. Sharkey preferred choice of vasopressin followed by phenylephrine. Fortunately, patients recover from Takotsubo. However, malignant arrhythmias and cardiac arrest can happen. Patients are counseled to present to emergency care if their symptoms ever return. Thank-you for listening.

Adaptation to stress-such as the fear response obtains dopaminergic input to striatum and prefrontal cortex and is thought to signal unexpected events and facilitate a shift in attention to promote new learning within the contralateral primary somatosensory cortex (SI) which has been associated with the agentic categories of both the quality and quantity of thought event ontology. This process works in conjunction with the bilateral secondary somatosensory cortex (SII) process involved in executive decision making. Where stimulated, the primary sensory motor-neuronal process is integrated with novel extra-dimensional learning . Recall that this fear stress response can lose functional valency upon immune-regulating, senescent secretory phenotypes. In the aging brain, where CRF axon terminals are widely distributed, (including within catecholamine and serotonin nuclei) there are widespread cortical projections into the medial prefrontal cortex; linking executive functional responses to adverse stimuli. Dr. Daniel J. Guerra Authentic Biochemistry Published 20 Jan 2021 Refs Neuroimage. 2008 May 1;40(4):1765-71. Biol Psychiatry. 2009 Sep 15; 66(6): 586–593. --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

Thank you for joining us for our 2nd Cabral HouseCall of the weekend! I’m looking forward to sharing with you some of our community’s questions that have come in over the past few weeks… Let’s get started!    Jen: Hi Dr. Cabral,i am interested in your thoughts on a good chatecolamine support supplement? I've considered Procite I have experienced fatigue, apathy, lack of focus, poor memory, decreased libido, and exhaustive depression. Would love to know your thoughts and what you would recommend.Thank you so much! Cheryl: Hi Dr. Cabral, my husband (53 yrs old) has had rheumatoid arthritis for nearly 25 years and has also had sjogrens syndrome for many years. He has recently been diagnosed with COPD even though he has never smoked or even been around second hand smoke. His doctors are baffled. Could the COPD be related to the RA and/or sjogrens? Is it possible to reverse the symptoms of the COPD? Hoping to have him start working on the RA etc asap. Thank you for all you do!! Leslie: Dear Dr. Cabral, I have been on your 21 day detox and I am just finishing and going on to do the fatlossity program. The reasons are varied.. a lot of general toxicity complaints and I am experiencing a lot of relief from the detox and plan to do the quarterly detoxes in the future. Perhaps even a 14 day detox after 8 or 12 weeks of Fatlossity. I have one question. The thing that is difficult to get away from here is chlorine in the water. We live on a spring water system, which has many benefits, but it must be treated as it has been tested to have e-coli. My partner puts chlorine bleach in it every 12 weeks or so.Since we have lived here.. I have seen my face get puffy and a lot of sagging and aging happening very rapidly. I have always been a low starch eater and eat lots of greens and vegetables and no processed foods.. but still suffering toxicity. Thankful for the detox, seeing lots of benefits, but just concerned about the water we bath in, cook with and drink. Lisa: Hi Dr. Cabral! Hope you and your family are staying safe and healthy! Thank you so much for still doing your podcast during this pandemic. I truly appreciate it! My question is in regards to my son who has PANS. It appears that "killing" anything in his body just flares him up so bad. Dispite doing the child's protocol numerous times, adding liver support, adrenal supports, DNS and other wonderful supplements from you, I'm struggling to get my son back to baseline.Our local doctor suggest I try Sovereign Silver with him. I get conflicting information in regards to silver. Some say they would never give it to their child (especially one with poor genetics) because you can't detox the silver.I know you use it in your mold protocol. I imagine that if you use it in your protocols, then it is safe. Why is there conflicting information about Silver?Thank you so much, Long time listener- Lisa Ella: Hi Dr. Cabral! Thank you so much for all you do, you’ve given so many people hope again. I’ll try to keep this short. I’m a 44 year old woman. I did the big 5 last year late spring. Started the modified CBO protocol last September, because of a lot of summer travel. Cut out gluten, dairy and eggs since then. I started to develop pain on the right side of my abdomen/waist area. I had an ultrasound that showed nothing, then I had a cat scan that showed some benign cysts on my liver, but showed nothing that could be the cause of the pain (insurance only paid for testing of upper abdomen even though I experienced pain in the lower abdomen too. It seems like the pain travels and sometimes my right lower back hurts, sometimes my right waist area, sometimes it seems to come from my gut, sometimes it’s near my ribcage, sometimes some of the above combined . My doctor has no idea what it could be and taking more tests is out of the question right now since we hardly have an income now because of the corona virus. I know you always say that there’s always someone out there going through the same thing as you. Have you ever heard of anything like this? I’m afraid to work out, because I don’t want to make it worse. I’m afraid to go to my doctor, because of the corona virus. I don’t want to go from doctor to doctor in these scary times. Also my tongue still has this coating on it and I still have nail ridges and hair loss (genetic), a lot of waking up at night. I still do the daily foundational protocol level 1 at the moment. I’m doing the immune boosting protocol on top of it. Thank you so much for your time and for listening! You’re the best!   Thank you for tuning into this weekend’s Cabral HouseCalls and be sure to check back tomorrow for our Mindset & Motivation Monday show to get your week started off right! - - - Show Notes & Resources:  http://StephenCabral.com/1570 - - - Dr. Cabral's New Book, The Rain Barrel Effect https://amzn.to/2H0W7Ge - - - Join the Community & Get Your Questions Answered: http://CabralSupportGroup.com - - -   Dr. Cabral’s Most Popular Supplements: > “The Dr. Cabral Daily Protocol” (This is what Dr. Cabral does every day!) - - - > Dr. Cabral Detox  (The fastest way to get well, lose weight, and feel great!) - - - > Daily Nutritional Support Shake  (#1 “All-in-One recommendation in my practice) - - - > Daily Fruit & Vegetables Blend  (22 organic fruit & vegetables “greens powder”) - - - > CBD Oil  (Full-spectrum, 3rd part-tested & organically grown) - - - > Candida/Bacterial Overgrowth, Leaky Gut, Parasite & Speciality Supplement Packages - - - > See All Supplements: https://equilibriumnutrition.com/collections/supplements  - - -   Dr. Cabral’s Most Popular At-Home Lab Tests: > Hair Tissue Mineral Analysis (Test for mineral imbalances & heavy metal toxicity) - - - > Organic Acids Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Thyroid + Adrenal + Hormone Test  (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Adrenal + Hormone Test (Run your adrenal & hormone levels) - - - > Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Omega-3 Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - > Stool Test (Use this test to uncover any bacterial, h. 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Catecholamine Metabolism

What is SCAPE? For this podcast, we're discussing the acute pulmonary edema presentation. This patient is hypertensive (SBP >140mmHg), severely dyspneic, with diffuse rales and clearly anxious. The "no-shitter, drowning-before-your-very-eyes" type of pulmonary edema.  This is the SCAPE patient. SCAPE = Sympathetic Crashing Acute Pulmonary Edema. Patho Quick Hits The core causative factor in the SCAPE patient is an acute increase in left ventricular filling pressure. There are a myriad of causes for a sudden increase in LV pressure, but the end result is a redistribution of fluid into the lungs. 1) Acute increase in LV filling pressure. 2) Fluid redistribution into the lungs and alveolar space. 3) Hypoxia ensues. 4) Catecholamine production and increase in SVR. 5) Activation of the RAAS. It's important to remember that the majority of these patients are not volume overloaded. This is a fluid distribution problem due to increased LV pressure. As the RV continues to pump fluid into the pulmonary circulation, the LV cannot move that fluid forward because of the increased afterload. This creates a pressure gradient that transmits that pressure back into the pulmonary capillaries. 5 Major Causes of SCAPE - Exacerbation of chronic LV failure - Acute myocardial ischemia or infarction involving 25% or more of the myocardial mass - Severe systemic hypertension - Left sided valvular disorders - Acute tachydysrhythmias and bradysrhythmias Treatment In the out of hospital realm, the core treatments are Non Invasive Positive Pressure Ventilation (NIPPV) via CPAP or BiPAP, coupled with nitroglycerine as a first-line medication. For the "regular guy" toolbox, the treatment pathway looks a little like this: 1) Treating the underlying cause if evident. 2) NIPPV 3) NTG 4) More NTG 5) More NTG 6) More NTG  Do not delay NIPPV to see if other therapies (like a NRB) will work first. In the awake patient maintaining their own airway presenting with SCAPE, have a low threshold to apply your NIPPV mode of choice. These patients need PEEP: they generally have an oxygenation problem, and not a ventilation problem. To that point, most prehospital disposable CPAP systems do not deliver 100% FiO2. The O_two and Pulmodyne O2-MAX systems we generally use are either fixed FiO2 or provide a titration of FiO2 based on oxygen flow. The O_two system will provide between 59% and 77% FiO2 at oxygen flow rates between 8L/min and 25 L/min respectively. The Pulmodyne O2-MAX system provides 30% FiO2 regardless of PEEP, or with an additional adapter may provide 30%, 60%, or 90% FiO2 independent of the set PEEP. Nitrogylcerin If sublingual NTG is all you have, give it. Often, too. Lifting up the CPAP mask for 20 seconds is highly unlikely to cause clinically relevant harm. If you have the option of IV NTG, that should be your go-to. Standard dosing strategies for IV NTG of 5-40mcg/min are likely ineffective, and there is literature to support higher dosing strategies. Consider that we bolus 400mcg of SL NTG, and that the bioequivalence of SL NTG is comparable to around an IV NTG dose of 60-80mcg/min, so rapid titration of IV NTG even up to 100mcg/min is not entirely unreasonable and largely supported by current literature. Bibliography Dec, G. W. (2007). Management of Acute Decompensated Heart Failure. Current Problems in Cardiology, 32(6), 321–366. https://doi.org/10.1016/j.cpcardiol.2007.02.002 Mosesso, V. N. J., Dunford, J., Blackwell, T., & Griswell, J. K. (2003). Prehospital therapy for acute congestive heart failure: state of the art. Prehospital Emergency Care : Official Journal of the National Association of EMS Physicians and the National Association of State EMS Directors, 7(1), 13–23. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=reference&D=med4&NEWS=N&AN=12540139 Aguilar, S., Lee, J., Castillo, E., Lam, B., Choy, J., Patel, E., … Serra, J. (2013). Assessment of the addition of prehospital continuous positive airway pressure (CPAP) to an urban emergency medical services (EMS) system in persons with severe respiratory distress. The Journal of Emergency Medicine, 45(2), 210–9. https://doi.org/10.1016/j.jemermed.2013.01.044 Levy, P., Compton, S., Welch, R., Delgado, G., Jennett, A., Penugonda, N., … Zalenski, R. (2007). Treatment of Severe Decompensated Heart Failure With High-Dose Intravenous Nitroglycerin: A Feasibility and Outcome Analysis. Annals of Emergency Medicine, 50(2), 144–152. https://doi.org/10.1016/j.annemergmed.2007.02.022 Mebazaa, A., Gheorghiade, M., Piña, I. L., Harjola, V.-P., Hollenberg, S. M., Follath, F., … Filippatos, G. (2008). Practical recommendations for prehospital and early in-hospital management of patients presenting with acute heart failure syndromes. Critical Care Medicine, 36(Suppl), S129–S139. https://doi.org/10.1097/01.CCM.0000296274.51933.4C Agrawal, N., Kumar, A., Aggarwal, P., & Jamshed, N. (2016). Sympathetic crashing acute pulmonary edema. Indian Journal of Critical Care Medicine, 20(12), 719. https://doi.org/10.4103/0972-5229.195710 Mattu, A., Martinez, J. P., & Kelly, B. S. (2005). Modern management of cardiogenic pulmonary edema. Emergency Medicine Clinics of North America. https://doi.org/10.1016/j.emc.2005.07.005 Scott Weingart. EMCrit Podcast 1 – Sympathetic Crashing Acute Pulmonary Edema (SCAPE). EMCrit Blog. Published on April 25, 2009. Accessed on September 11th 2018. Available at [https://emcrit.org/emcrit/scape/ ].

  Join Dan (@drusyniak) &howard (@heshiegreshie) as they palaver with Dr. Geoff Isbister (@geoff_isbister) about the poison playground that is Australia. Snakes, spiders and quetiapine, oh my! Learn what color of snake to look out for (hint: all of them), learn how Australians do research (on themselves), and why generally leaving your house down under is a terrible idea. So be like an Aussie, have no fear and turn up the volume. Delicious Links Join Dr. Isbister at The University of Newcastle Australia clinical toxicology research group The amazing, and bizarre, discovery of Irukandji Syndrome A great overview of neurotoxic marine poisoning And what discussion of Australia would be complete without a discussion of spider bites. And another. . . More than dermal problems. Catecholamine-induced cardiomyopathy resulting from life-threatening funnel-web spider envenoming. “A pints a pound the whole world round”. As it is with intentional overdoses.Quetiapine Poisoning - A Case Series Potentially practice changing, practical approach to a commonly misinterpreted value. Drug induced QT prolongation: the measurement and assessment of the QT interval in clinical practice Hungry? Not sure what to do with that little yellow and brown jar? Hugh Jackman Shows Jimmy How to Really Eat Vegemite The official Twitter account of Vegemite Before trying anything, learn about the pioneers who did it first. Who Goes First? The Story of Self-Experimentation in Medicine by Lawrence K. Altman How a prank phone call to Tobias Drundridge sparked an international controversy. Well, it's true. Apparently, the dingo really did eat (kill) the baby. ReBOA Official Translation Australian: Strewth, I got into a bingle after chucking a u-e on my way to the bottle o. Coppas and ambos came, blood everywhere. Took me to the A&E, it was chockablock. Non-bogan / English: Oh no. I was in a car accident, when I was on my way to the liquor establishment. I was performing a U-turn. The police and the paramedics arrived, there was blood all around. I was taken to the ER and it was full. Australian: G'day ya bastards! Howaaaare youse, awrite? Out in the whoop whoop, if trauma strikes, you're in the sticks kilometers away from bugger all. With a massive injury, you'd be stuffed if you used outdated technology like the MAST snake. Its pretty flaky mate and is all cracking the shits. Non-bogan / English: Hello friends. How are you? Good? In the Outback, if trauma strikes, you're in the remote countryside, quite isolated. With massive trauma, you'd be in trouble if you used outdated technology like the MAST (military anti shock trouser) snake. It's pretty unreliable and quite frustrating. Australian: But thanks to your ‘ol cobbers at Witness Protection Products Straya, we have a better way. ReBOA - Resuscitative Extra-Vascular BOA constrictor. She's a bloody ripper. It's got a swish design, unlike other devices that have heads like a dropped pie and frankly, I reckon they've got a few ‘roos loose in the top paddock. But with ReBOA, she'll be right mate. Non-bogan / English: But thanks to your friends at Witness Protection Products Australia, we have a better way. ReBOA. Resuscitative Extravascular BOA constrictor. It's great. It's got a nice design, unlike other unattractive devices that I don't consider sensible. But with ReBOA, it's going to be fine. Australian: When you're flat out like a lizard drinking and need to make sure patients, who are like dog's breakfast, get a fair suck of the sauce bottle, you don't want to carry on like a pork chop. ReBOA is an absolute piece of piss. Just take the snake and apply right above the budgie smugglers and let nature do her work. No complications. Just continuous, unremitting abdominal pressure. Is that good or what? Bloody oath!! And its a fair dinkum mate. Non-bogan / English: When you're very busy and need to make good decisions for patients that are a mess, you don't want to be dramatic. The ReBOA is super easy. Just take the snake and apply right above the undies and let nature do her work. No complications. Just continuous, unremitting abdominal pressure. Is that good? The answer is an enthusiastic yes. Honestly. Australian: In Straya, everything's out to kill ya, so get the toughest gear around. Don't be a drongo. REBOA - it's Aussie for resuscitation. Non-bogan / English: In Australia, everything's deadly, so get the best tool for the job. Don't be a fool. ReBOA - it's Australian for resuscitation. Special Thanks We just want to take a moment to thank you, our listeners, for one year of toxicology fun. This is the last episode of our first season, and we're thrilled to have you along with us for the ride. As a bit of housekeeping, we're going to be discontinuing the @dantastictox Twitter handle, and focus our social media efforts on the larger endeavor at The Tox & The Hound. As always, we are looking for feedback - comments, questions, suggestions, recipes, etc. Let us know. Reach us at @toxandhound. We want to hear from you! Thank you to our house band Pretty Simple Duo (@prettysimpleduo), Josh Shelov (@shelovj) and Witness Protection Products, Australia. Interested in #FOAMtox? Like this podcast? Join us over on The Tox and The Hound. It's like a podcast, but for your eyes. Listen on iTunes or Spotify! Earholes happy? Rate and review! Show the love! Koala by Holger Link Down Under by lurii78

Prof. Rudi Wiesner talks with Dr Julie Ann Lough about his recently published research: Catecholamine metabolism induces mitochondrial DNA deletions and leads to severe adrenal degeneration during ageing

Commentary by Dr. Valentin Fuster

Pheochromocytomas are tumors of the adrenal gland that secrete catecholamine. Closely related tumors called extraadrenal paragangliomas can arise at extraadrenal sites. Catecholamine secretion from these tumors causes headache, perspiration, palpitations and hypertension. If not recognized and treated, pheochromocytoma and extraadrenal paraganglioma can lead to arrhythmias, myocardial infarction, stroke and death.

Conditions are described for controlled plasma membrane permeabilization of rat pheochromocytoma cells (PC12) and cultured bovine adrenal chromaffin cells by Streptolysin O (SLO). The transmembrane pores created by SLO invoke rapid efflux of intracellular 86Rb+ and ATP, and also permit passive diffusion of proteins, including immunoglobulins, into the cells. SLO-permeabilized PC12 cells release [3H]dopamine in response to micromolar concentrations of free Ca2+. Permeabilized adrenal chromaffin cells present a similar exocytotic response to Ca2+ in the presence of Mg2+/ ATP. Permeabilized PC12 cells accumulate antibodies against synaptophysin and calmodulin, but neither antibody reduces the Ca2+-dependent secretory response. Reduced tetanus toxin, although ineffective when applied to intact chromaffin cells, inhibits Ca2+-induced exocytosis by both types of permeabilized cells studied. Omission of dithiothreitol, toxin inactivation by boiling, or preincubation with neutralizing antibodies abolishes the inhibitory effect. The data indicate that plasma membrane permeabilization by Streptolysin O is a useful tool to probe and define cellular components that are involved in the final steps of exocytosis.

The glyoxylic-acid-induced fluorescence technique was applied to demonstrate patterns of catecholaminergic innervation within the auditory brainstem of echolocating bats and the house mouse. In the cochlear nucleus of the rufous horseshoe bat (Rhinolophus rouxi) and the mustache bat (Pteronotus parnelli), species-specific catecholaminergic innervation patterns are found that contrast with the relatively homogeneous innervation in the rodent. In both bats the subnuclei of the cochlear nucleus receive a differentially dense supply of catecholaminergic fibers, and within the subnuclei, the catecholamine innervation densities can be correlated with the tonotopic frequency representation. The areas devoted to the high-frequency echolocation calls are less densely innervated than those regions which are responsive to lower frequencies. Apart from this common scheme, there are noteworthy distinctions between the two bats which correlate with specialized cytoarchitectural features of the cochlear nucleus. The marginal cell group, located medially to the anteroventral cochlear nucleus of Pteronotus, receives the densest supply of catecholaminergic fibers of all auditory nuclei. This plexus is formed by a morphologically distinct population of catecholaminergic fibers.

Two possible cellular pathways of catecholamines from the chromaffin vesicles of PC 12 cells to the surrounding medium are explored in this study. The direct one circumventing the cytoplasm can be activated in a-toxin-permeabilized cells with micromolar levels of free Ca2+. Catecholamine metabolites formed in the cytoplasm (i.e., 3,4-dihydroxyphenylacetic acid and 3,4-dihydroxyphenylethanol) are neither formed nor released from the cells under these conditions. However, when vesicular catecholamines were discharged into the cytoplasm by addition of the ionophore nigericin, such metabolites are formed and released into the medium independent of Ca2+. Both types of experiments provide direct evidence for the operation of Ca2+-induced exocytosis of dopamine and noradrenaline in permeabilized PC12 cells. The Ca2+ dependence of dopamine or noradrenaline release, as measured by the determination of the endogenous catecholamines using the high-performance liquid chromatography technique, exhibits two different phases. One is already activated below 1 pM free Ca2+ and plateaus at 1-5 pM free Ca2+, while a second occurs in the presence of larger amounts of free Ca2+ (10-100 pM). Ca2+-induced catecholamine release from the permeabilized cells can be modulated in different ways: It is enhanced by the phorbol ester 12-0-tetradecanoylphorbol 13-acetate and the diacylglycerol 1 -oleyl-2-acetylglycerol provided Mg*+/ATP is present, and it is inhibited by guanosine 5’-0-(3-thiotriphosphate). The latter effect is abolished by pretreatment of the cells with pertussis toxin but not by cholera toxin. Thus, it appears that Ca2+-induced exocytosis can be modulated via the protein kinase C system, as well as via GTP binding proteins.