Podcasts about friedewald

Back in January, Verboten was featured on the feed for the popular show Escape This Podcast, and that exposure was amazing, so we want to be able to pay it forward and spotlight an excellent podcast that we think you'll love! Tangents is like if pub trivia met a Choose Your Own Adventure book; it's one of the most innovative game formats for trivia we've ever seen, and Russ's personality and voice are a welcome guide through each topsy-turvy episode. Enjoy this episode, featuring Verboten host Jay Borsom, recorded and released in December 2023, and follow the feed for more! Tangents on Spotify ----more---- Editing's expensive and listening to ads sucks! Help us hire an editor by supporting us on Patreon, where you can now hear episodes of Verboten completely ad-free! All patrons get to add an "amenity" to the isolation booth as well moving forward! Connect with us on Facebook, Instagram, and Bluesky! To contact the show directly, email us at VerbotenPod@gmail.com! Think you have the best words? Apply to appear on the show at https://ptepodcasts.com/appearance-request/! Please consider leaving the show a 5 star rating and review. See you next week! ©2024, Verboten. Proud member of the PTE Network.

Northwestern Medicine Chief of Breast Imaging in the Department of Radiology Dr. Sarah Friedewald joins Rob Johnson and Jane Clauss on the Big 89 to discuss the importance of early detection, the appropriate age for a first mammogram, and how to ease your mammogram anxiety. See omnystudio.com/listener for privacy information.

In this episode, the Creativity Department is joined by Susan Martin and Melissaa Friedwald of the Bower Center in Bedford, Virginia to discuss how art educators can build relationships with local arts and cultural organizations. Melissa goes into how having a local arts center gives her students the opportunity to discover a community outside of the art room and real-world experience. Melissa and Susan walk us through the process of how they collaborated on the LOVEworks project for the Bedford welcome center – including how they planned the project with students, allocated materials, how the students infused their own artistic style, and how they incorporated student participation from multiple schools. Listen in to hear more! 

Bei dem Parteitag der Hessen SPD in Friedewald erklärte Nanca Faeser noch einmal ihre Pläne. Und wir berichten über die Pläne des Frankfurter Ex-OB Peter Feldmann: Er will aus der SPD austreten.

- Bewährungsstrafe nach Bombenfund in Friedewald.

Throwback Trivia Takedown takes trivia back to the glory days from the late 20th century to the early 2000's. Two challengers go head to head in a duel of the decades where the one with the most nostalgic knowledge of pop culture comes out victorious. Do you know your nostalgia? bfopnetwork.com

Dr. Sarah Friedewald of the American College of Radiology discusses the importance of yearly mammograms. 

- Rekord: eine halbe Million Menschen beim Lullusfest in Bad Hersfeld. - Zwei KFZ-Diebstähle in Kassel-Niederzwehren in einer Nacht: Polizei nimmt mutmaßlichen Autodieb am Steuer von gestohlenem Wagen fest.

- Clevere Jungs retten Rentner Ehepaar im osthessischen Friedewald. - Gudensberg: Zwei Scherverletzte bei Fackelentzündung.

- Lkw in Brand geraten: A4 bei Friedewald stundenlang gesperrt. - Endlich raus: Weideauftrieb des Antoniushofs Fulda.

- Tödlicher Unfall auf der A4 bei Friedewald. - Neues Gehege für Wildkatzen im Wildtierpark Edersee.

By Blanca Mallak. I will discuss the matter of technology and privacy. Now as many people know technology is all around us. Even a generation has grown to be too dependent on it. I will elaborate on the impacts the internet has on young adults' relationships with parents and the fact that our personal information can be seen without our permission. Not only will I give information over this but I will also help the listener recognize the fact that people choose to ignore the situation because of the benefits we get from technology. Works Cited “Privacy and Technology.” SafeHome.org, 20 Aug. 2021, https://www.safehome.org/resources/privacy-and-technology/. Alexander, John. “How Technology Is Killing Privacy.” ScholarWorks@GVSU, https://scholarworks.gvsu.edu/honorsprojects/397/. Mesch, Gustavo S. “Technology and Youth.” New Directions for Youth Development, vol. 2012, no. 135, 2012, pp. 97–105., doi:10.1002/yd.20032. Friedewald, Michael, and Ronald Pohoryles. “Technology and Privacy.” Innovation: The European Journal of Social Sciences, vol. 26, no. 1/2, 2013.

- Kasseler Märchenwald im Schwarzbuch des Steuerzahlerbundes.

- Landgericht Fulda: Mutter vom Missbrauchsvorwurf freigesprochen - Weltkriegsbombe in Friedewald ist entschärft -

We've got a GREAT match this week on Blitz. Listen in as Russ Friedewald, Samantha Ross, and Will Boylan go head to head to head. Next week, we'll have the Wave 24 championship!

- Effektive Jugendkriminalitätsbekämpfung: Eröffnung "Haus des Jugendrechts" in Kassel. - Auszeichnung für das Kasseler Theaterstübchen für das beste Programm deutschlandweit.

In dieser Episode von FotoFemme erzähle ich euch etwas über die geschichtlichen Hintergründe der Fotografie. Es geht um die weiblichen Vertreterinnen ab der Entstehung der ersten Fotografie bis nach dem zweiten Weltkrieg. Es werden drei Beispiele für weibliche Pionier*innen der Fotografie erläutert und neben ihren Arbeiten, die persönlichen Lebenshintergründe von mir kommentiert. Namen und Empfehlungen für diese Episode - Fotografinnen: Sarah Anne Bright, Julia Margaret Cameron, Dora Kallmus (Madame d`Ora) Namen der Magnum Photo Gründungsmitglieder: Maria Eisner, Rita Vandivert Bücher: "Meisterinnen des Lichts" von Friedewald, Boris & "Frauen sehen Frauen" von Schirmer/Mosel München Titelbild: © Madame D'Ora (Dora Kallmus) Quelle des Titelbilds: https://www.vogue.de/mode/artikel/madame-dora, Vogue Deutschland

Seth Martin, MD, discusses his research on the direct method of estimating low-density lipoprotein cholesterol and how to better use this method in practice.

Dr Carolyn Lam:                Welcome to Circulation On the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr Carolyn Lam, associate editor from the National Heart Center and Duke National University of Singapore.                                                 In this day and age of endovascular treatment for acute ischemic stroke, does time to treatment really matter? Well, we will be discussing results of the MR CLEAN Registry from real-world clinical practice, coming right up after these summaries.                                                 The first original paper this week describes the first mouse model of progerin-induced atherosclerosis acceleration. Progerin is an aberrant protein that accumulates with age, causes a rare genetic disease known as Hutchinson-Gilford Progeria Syndrome. Patients with Progeria Syndrome have ubiquitous progerin expression and exhibit accelerated aging and atherosclerosis, dying in their early teens mainly from myocardial infarction or stroke. The mechanisms underlying progerin-induced atherosclerosis remain unexplored, in part due to the lack of appropriate animal models. First author Dr Hamczyk, corresponding author Dr Andrews, and colleagues from CNIC in Madrid performed an elegant series of experiments and generated not only the first mouse model of progerin-induced acceleration of atherosclerosis, but also provided the first direct evidence that progerin expression restricted to vascular smooth muscle cells but not to macrophages was sufficient to induce premature atherosclerosis and death. Progerin-induced loss of vascular smooth muscle cells caused atherosclerotic plaque destabilization that led to myocardial infarction. Ubiquitous and vascular smooth muscle cell specific progerin expression increased LDL retention in aortic media, likely accelerating atherosclerosis.                                                 The next original paper implicates dysregulation of mitochondrial dynamics as a therapeutic target in human and experimental pulmonary arterial hypertension. Now, mitotic fission is increased in pulmonary arterial hypertension. The fission mediator, dynamin-related protein 1, or Drp1, must complex with adaptor proteins to cause fission. In the current paper from co-first authors Dr Chen and Dasgupta, corresponding author Dr Archer from Queens University in Ontario Canada, and colleagues, the authors examined the role of two recently discovered but poorly understood Drp1 adaptor proteins known as mitochondrial dynamics protein of 49 and 51 kilodalton. They found pathological elevation of these mitochondrial dynamic proteins in pulmonary artery smooth muscle cells and endothelial cells in both human and experimental pulmonary arterial hypertension that accelerated mitotic fission and supported rapid cell proliferation. Mitochondrial dynamics protein's expression was epigenetically upregulated by a decreased expression of microRNA-34a-3p. Circulatory microRNA-34a-3p expression was decreased in both patients with pulmonary arterial hypertension and preclinical models, silencing the mitochondrial dynamics proteins or augmenting microRNA-34a-3p regressed experimental pulmonary arterial hypertension, thus, proving to be potential new therapeutic targets for pulmonary arterial hypertension.                                                 Dyslipidemia guidelines currently recommend that non-HDL cholesterol and apolipoprotein B, or apoB, are secondary targets to the primary target of LDL cholesterol. However, how frequently does non-HDL cholesterol guideline targets change management, and what is the utility of apoB targets after meeting LDL and non-HDL targets?                                                 Well, answers are provided in the next paper from first author Dr Sathiyakumar, corresponding author Dr Martin, and colleagues from Johns Hopkins University School of Medicine. These authors analyzed more than 2,500 adults in the US National Health and Nutrition Examination Survey, as well as more than 126,000 patients from the Very Large Database of Lipids Study with apoB. They identified all individuals as well as those with high-risk clinical features, including coronary disease, diabetes, and metabolic syndrome who met the very high and high-risk guidelines targets of LDL cholesterol of less than 70 and less than 100 mg/dL, respectively, and this was measured using either the Friedewald estimation or a novel, more accurate method. They found that after using the more accurate method of estimating LDL cholesterol, guidelines suggested non-HDL targets could alter management in only 1 to 2% of individuals, including those with coronary disease and other high risk clinical features.                                                 However, using the Friedewald estimated LDL cholesterol gave a much higher percentage. Among all individuals with both LDL cholesterol less than 100 and non-HDL cholesterol less than 130 mg/dL, only 0-0.4% had an apoB above or equal to 100 mg/dL. Thus, the utility of current non-HDL targets appears to be contingent on the accuracy of LDL cholesterol estimation. When using a novel, more accurate estimation method to assess LDL cholesterol, the non-HDL cholesterol is infrequently above current guidelines' suggested targets after the LDL target is met. Current guidelines suggest that apoB targets also provide only modest utility after cholesterol targets are met. These findings were robust to high-risk clinical features, sex, fasting status, and presence of lipid-lowering therapies.                                                 The final paper tells us that HIV infection increases the risk of developing peripheral artery disease. Dr Beckman from Vanderbilt University Medical Center and colleagues studied almost 92,000 participants in the Veterans Aging Cohort Study from 2003-2014 over a median follow-up of nine years. They excluded participants with known prior peripheral artery disease or prevalent cardiovascular disease. They found that infection with HIV was associated with a 19% increased risk of incident peripheral artery disease beyond that explained by traditional atherosclerotic risk factors. Once peripheral artery disease had developed, HIV infection increased the risk of mortality compared to uninfected patients. Whereas for those with sustained CD4 cell counts above 500, there was no excess risk of incident peripheral artery disease events compared to uninfected people. Furthermore, worsening HIV infection as measured by CD4 cell count and HIV viral load was associated with increased incident peripheral artery disease and mortality. In summary, HIV infection increased the risk of developing peripheral artery disease and mortality. The findings also suggest that aggressive antiretroviral therapy to reduce viral load and increase CD4 cell counts may reduce the risk of developing peripheral artery disease. Furthermore, clinicians should solicit clinical complaints and physical signs consistent with peripheral artery disease to facilitate the diagnosis of peripheral artery disease in patients with HIV and ensure the addition of guideline-based anti-atherosclerotic therapies in these patients.                                                 Well, that wraps it up for our summaries. Now for our feature discussion.                                                 When it comes to acute ischemic stroke treatment, we've learned from trials of intravenous thrombolytics that time is brain. But what about the situation with endovascular treatment of strokes? Also, what's the situation like in the real world? Well, today's featured paper really provides precious data telling us about time-to-endovascular treatment and outcomes in acute ischemic stroke. I am so delighted to have with us the first and corresponding author of the MR CLEAN Registry, Dr Maxim Mulder from Erasmus University Medical Center, as well as our editorialist, Dr Micheal Hill, from University of Calgary, and our associate editor, Dr Graeme Hankey, from University of Western Australia, all here to discuss this hugely important topic.                                                 Maxim, could we start with you? So, MR CLEAN Registry means there was a MR CLEAN trial. Could you tell us a little bit more about your paper? Dr Maxim Mulder:           Sure, well to start with, I think it's important to make sure all the people know the difference between the MR CLEAN trial and the registry since of course the trial was to show whether the intra-arterial treatment is effective when it comes to acute ischemic stroke treatments and then, of course, for people treated within six hours. When the MR CLEAN trial finished we continued in the Netherlands with all the participating centers from the trial to gather all the data from everybody who is treating in the whole country with the intra-arterial treatment, but they're not anymore in the light of the trial but in the clinical practice. We've had a lot of trials, but we don't have a lot of clinical practice date yet of the intra-arterial treatment, so that's where it all started.                                                 So, what we found is we consider our data, so with the least possible selections or the only selection was basically to treat within six and a half hours and have patients that had a proven large vessel occlusion that were treated in the Netherlands and of course as we also know from when intravenous therapy was introduced that what happens in clinical trials doesn't necessarily happen when a new treatment is introduced into clinical practice. There are less strict criteria for patients to get treated, and you know everybody, of course, there is a lot of debate about which patients should be treated. In clinical trials it is very strictly coordinated, but in clinical practice there's a lot more room to have an interpretation and also treat a different population. So, we also see that our population is somewhat older and has more comorbidities than in all the trials. Also what we found, of course, our most important finding was that when compared to all the trials or the large trials combined together in the Emberson analysis about time that when we look at the influence or the association of time with functional outcome of intra-arterial treatment that this association is clearly stronger than we found in the previous, the trial data.                                                 So, I think that's a very important finding. Also, for everybody who's now treating this patient in clinical practice. Dr Carolyn Lam:                Exactly. I mean this is really stunning results. If I could paraphrase from your paper, every hour delay in time from stroke onset to the start of endovascular treatment resulted in a 5.3% decreased probability of functional independence and a 2.2% increase in mortality. This is stunning. Thank you, thank you for publishing these results with us in Circulation. I would like to ask Michael, I love the point you made in the editorial that time of stroke onset is really quite a difficult thing to determine. Could you tell us your thoughts about that, Michael? Dr Micheal Hill:                  I mean, it's something like 15-20% of the time stroke is unwitnessed, either because stroke occurs in sleep and the patient is discovered with their stroke symptoms on awakening. Or the patient is simply alone and has their stroke unwitnessed by any bystander. Even in so-called witness stroke, there are probably significant errors in determining the exact time of stroke onset because it's an emergency, and everybody's flustered and time anchors are not necessarily well known. And, so, I think it's an important point that the actual measurement of time is challenging, yet it's still an easier clinical tool for us to use in gauging the extent or evolution of stroke. That's the most important thing to point out here is that this population effect that Max has observed in the MR CLEAN registry is certainly concordant with clinical trial data.                                                 I certainly think it's correct, and, as you pointed out in your comments, dramatic, but a really important issue is that for the individual patient, there's quite a lot of variance in the evolution of stroke. So, whereas, on a population basis, it's absolutely true that the average time from estimated time of stroke onset to treatment initiation is absolutely critical; in some patients, the individual might be still a good candidate for treatment even in late time windows, and some patients, even after a couple hours, the damage is already extensive, and they may not be good candidates for treatment. It still requires individual decision making, and it still leaves a lot of room for clinical judgment largely based on imaging. Dr Carolyn Lam:                True, and I think you've really succinctly put that solid take-home message in the title really, which is acute ischemic stroke biology really demands fast treatment. I think that's the one thing that we'd really like clinicians to come away with. You agree? Dr Micheal Hill:                  Absolutely. Especially, I think, the advantage of looking at whole populations and large, I mean this is a large registry, the MR CLEAN registry, and the group should be congratulated because it's clearly the biggest registry in the world right now of available data, and it's only getting larger week by week as they carry on with their work. You know the whole Netherlands group, the MR CLEAN group, are a fantastic group, but absolutely right, on a population basis, we absolutely have to get our systems in place so that on average we're treating patients incredibly fast. On an individual basis, the clinicians and the teams treating an individual patient still need to make judgments about that patient's eligibility for treatment. It's easy when the times are fast, so if you're an hour and a half from onset, nearly everybody's gonna be a good candidate for treatment, but as time elapses you need to make judgements on the basis of imaging. Dr Carolyn Lam:                Well put. You know, Graeme, you're over there in Australia. What are your take-home messages about how generalizable these findings are to places outside perhaps of the Netherlands? Dr Graeme Hankey:        I think you're asking about the external validity. I think the internal validity is certainly there. As Michael said, this is the largest registry that we have that's been published data on this before. It's certainly novel, and we're very confident that the results are valid, although this is an observational study and not a randomized trial. The association between time and outcome seems to be independent of the major patient factors that may influence time to endovascular therapy. For example, younger people who are less frail and they're alert and they're mobile can get to treatment earlier. So, you might say, well of course they're gonna have a better outcome. But these factors were adjusted for. And, of course, there are procedural factors that could influence the association between time and outcome, but we're very confident in the results and the novelty of them in supporting and building on the randomized trial data.                                                 We're also very confident in the registry and the nature of the population. The results are likely to be generalizable beyond the Netherlands population where this was conducted in routine clinical practice, certainly across Caucasian populations that are similar and with similar stroke interventional and assessment protocols, and I would hope to see this sort of study validated externally in other populations. But, also, as Michael said, I think this study not just highlights the importance of time as a factor and its implications for systems of care and recognizing people with disabling stroke and ensuring they’re assisted urgently to the appropriate imaging but also to acknowledge that time isn't the only factor. And as Michael has alluded to, our brain tissue has different collateral circulations and different probable genetic factors and metabolic factors. So, someone with a stroke at one hour, it might be all over for them. Whereas, another person with a stroke at 24 hours ago, they might have salvageable tissue.                                                 So, although, generally time is an important prognosticator as we've learned here, there are probably other factors that need to be considered and accounted for. But this certainly takes us a step forward, and, in answer to your question, I think we have confidence in its generalizability. Dr Carolyn Lam:                Thank you Graeme. Maxim, in line with that, are there any next steps you plan? Dr Maxim Mulder:           In light of the most recent trials, the DAWN and DEFUSE 3 trial about 6 to 25-hour, 24-hour window, I think that both of the trials are very exciting, and they shine a new light into a new set of patients that are still able to offer a great benefit intra-arterial treatment. In my opinion, the most important thing, especially in those two trials, those are highly selective patients, especially selected on all the extra imaging parameters, and I guess that there's a whole larger population that could still benefit in this time window and that's also one of the things we're currently studying in one of our new trials in the Netherlands in the MR CLEAN-LATE trial, and that is randomizing patients who are having a large vascular occlusion 6 to 24 hours, and the only extra criteria they should meet is they should have at least a little bit of collateral circulation on the ischemic brain side. Dr Carolyn Lam:                Michael and Graeme, what do you think are the priorities for next steps in research. Dr Micheal Hill:                  I guess overall in the field, I don't think there's any doubt that faster treatment is better. What we need to do across the world is make sure that everybody's receiving it on a system-wide basis. Right? I think there needs to be a lot of more careful work done on getting systems of care in place to make sure that patients are getting the treatment they can get. We have very many weaknesses. Some are related to lack of accreditation. Some are related to the resources required to get people treated quickly. Some are related to continuing resistance in some specialties to even giving intravenous thrombolytic drugs. So, I think faster treatment in general for acute stroke is a theme; it's not just limited to endovascular treatment. It's treatment for patients for intravenous thrombolysis. It's also actually true for TIA and minor stroke. We've had recent data on fast antiplatelet therapy, so, it's not an emergency in the same way in terms of minutes, but it's still a general theme of acute stroke care.                                                 We need to be like the Ferraris and the Formula One, right? And get ourselves moving. That's a big challenge for people. Right? It's a big stress on systems. But, I think there are other examples in medicine. We've seen this evolution in acute coronary care, and we've seen the evolution in acute trauma care. In many ways, the next things that need to really continue to happen are publications like this and getting the message out that people need to start changing their mind. The biggest thing that I find when I talk to people or talk at meetings or talk to administrators is that they say, "Well, we can't do this many CTs that fast. We can't respond that fast." And the answer is actually that you can't change the biology of the disease, so if you decide you wanna treat stroke patients, you better figure out how to change your systems. It's a question of will here rather than trying to bend the disease to the system. Dr Carolyn Lam:                Wonderfully put. Can't change the biology so we better change the systems. How about you, Graeme? Any last words? Dr Graeme Hankey:        Just to concur with Michael’s comments there and Max's underlying theme that time is very important. And as Michael alludes to, it's not just acute ischemic stroke due to large vascular disease, it's also acute intracerebral hemorrhage. We're learning now really if we're gonna have an effect in the bleeding brain probably we have to do that within the first three hours and maybe not be waiting so late. And as Michael alludes to, someone with a minor ischemic stroke who's had a hot volcano gone off in their neck, as you know, ruptured atherosclerotic plaque, it's like those volcanoes in Hawaii, they're gonna keep going off again. And the risk is 5% in the next two days and 10% in the next week. So, a TIA and a mild ischemic stroke, it is a medical emergency to find the cause and to get it treated, and that's why the synopsis of this message from Max's study is that people, if they do avail themselves of acute assessment early, even if they don't have a large vessel occlusion causing an ischemic stroke, they may actually have their intracerebral hemorrhage treated quickly or, more evidence based at the moment, their TIA or mild ischemic stroke have the cause ascertained and treated emergently and reduce that early risk of recurrence should they survive. Dr Carolyn Lam:                Excellent points. Thank you so much, gentlemen. This has been an amazing podcast.                                                 Thank you so much for joining us today. Don't forget to tune in again next week, listeners.  

Interview with Seth Martin, MD, MHS, author of Comparison of Low-density Lipoprotein Cholesterol Assessment by Martin/Hopkins Estimation, Friedewald Estimation, and Preparative Ultracentrifugation: Insights From the FOURIER Trial, and Neil J. Stone, MD, author of Measuring Low-Density Lipoprotein Cholesterol: When Is More Accurate Better?

Dave Feldman is a software engineer who discovered for himself the benefits of a ketogenic diet in April 2015, experiencing what he describes as “seven blissful months” - until getting some labs back that included a 300+ total cholesterol.  He learned he was a “hyper-responder,” which inspired him to learn all he could about cholesterol and the lipid system. For the last 2.5 years he’s been using self-experimentation methods to meticulously adjust dietary macronutrient ratios in order to manipulate his blood chemistry.  He’s found out that the lipid system is actually quite easy to change, and does so in surprising ways related to diet. Dave is here today with Dr. Tommy Wood to share his discoveries about all things cholesterol: LDL, HDL, VLDL, lean-mass hyper-responders, and what you need to know to evaluate your own labs.  Dave is an active speaker and blogger, and his N=1 experiments are detailed on his blog at cholesterolcode.com. Here’s the outline of this interview with Dave Feldman: [00:00:19] Video from Low Carb Breckenridge 2017: Dave Feldman: The Dynamic Influence of a High Fat Diet on Cholesterol Variability. [00:00:47] Dave’s background. [00:01:17] Cholesterol doubled, hyper-responder. [00:01:54] Distributed object networks. [00:02:46] Changing fat intake to manipulate cholesterol levels. [00:03:01] Cholesterol Drop Protocol. [00:05:27] Reverse engineering cellular energy. [00:06:20] Lipoprotein. [00:09:37] Very low-density lipoprotein (VLDL), triglycerides. [00:10:00] Metabolic syndrome, insulin resistance. [00:10:29] Intermediate density lipoprotein (IDL). [00:14:35] Hydrolysis of fatty acids. [00:17:11] 3-day average, LDL-C, LDL-P. [00:19:05] Nuclear magnetic resonance spectroscopy (NMR), Friedewald equation. [00:21:00] Direct vs Calculated LDL-C. [00:23:25] Non-low carbers. [00:24:15] Carb swapping. [00:27:16] Vegans. [00:28:07] Sex hormones. [00:29:35] Metabolic flexibility. [00:29:59] Lean mass hyper-responders. [00:34:59] Hypothyroidism, T3, testosterone, creatinine. [00:37:08] Dave’s interview with Ken Sikaris on Low Carb Conversations podcast. [00:37:34] All-cause mortality. [00:38:15] Study: Fulks, Michael, Robert L. Stout, and Vera F. Dolan. "Association of cholesterol, LDL, HDL, cholesterol/HDL and triglyceride with all-cause mortality in life insurance applicants." J Insur Med 41.4 (2009): 244-53. [00:40:00] APOC2, C-reactive protein. [00:44:44] 99% of the LDL particle lifespan. [00:45:59] Atherosclerosis. [00:46:31] Lipopolysaccharides (endotoxin). [00:50:23] Cyrex Array 2 - Intestinal Antigenic Permeability Screen. [00:52:15] Study: Varbo, Anette, Jacob J. Freiberg, and Børge G. Nordestgaard. "Extreme nonfasting remnant cholesterol vs extreme LDL cholesterol as contributors to cardiovascular disease and all-cause mortality in 90000 individuals from the general population." Clinical chemistry 61.3 (2015): 533-543. [00:51:38] Peter Attia, Thomas Dayspring. [00:53:23] Remnant cholesterol. [00:59:44] Cholesterolcode.com. [01:00:38] Low Carb Breckenridge, Low Carb Cruise, Ketocon, Ketofest, @DaveKeto.

Dr. Carolyn Lam:               Welcome to Circulation on the Run, your weekly podcast summary and backstage pass to the journal and its editors. I'm Dr. Carolyn Lam, associate editor from the National Heart Center and Duke-National University of Singapore. Our feature paper today focuses on LDL cholesterol results from non-fasting samples and a personalized novel method of LDL cholesterol estimation that you will surely want to know about. So stay tuned, coming up right after these summaries.                                                 The first paper provides new evidence that RUNX1, a gene intensively studied in the cancer and blood research fields, has a critical role in cardiomyocytes following myocardial infarction. Co-first authors, Dr. McCarroll and He, corresponding author Doctor Loughrey and colleagues from University of Glasgow generated a novel tamoxifen-inducible cardiomyocyte-specific RUNX1-deficient mouse and showed that RUNX1-deficient mice were protected against adverse cardiac remodeling post-MI, maintaining ventricular wall thickness and contractile function. Furthermore, these mice lacked eccentric hypertrophy and their cardiomyocytes exhibited markedly improved calcium handling.                                                 At the mechanistic level, these effects were achieved through increased phosphorylation of phospholamban by PKA and relief of sarcoplasmic reticulum calcium pump inhibition. Thus, these data identified RUNX1 as a novel therapeutic target with translational potential to counteract the effects adverse cardiac remodeling post-MI.                                                 The next paper invites us to consider that some our resource-intensive quality improvement initiatives may not be fulfilling their intended goals or even justify their costs. In this paper by first author, Dr. Kutty, corresponding author, Dr. Chan and colleagues from St. Luke's Mid America Heart Institute, the authors evaluated the association between the implementation of pediatric medical emergency teams and the risk-adjusted mortality at the hospital level.                                                 To do this, they looked within the pediatric health information system for freestanding pediatric hospitals and calculated the annual risk-adjusted mortality rates for sites between 2000 and 2015. A random slopes interrupted time series analysis was then used to examine whether implementation of a medical emergency team was associated with lower than expected mortality rates based on the pre-implementation trends. The authors found that before medical emergency team implementation, hospital mortality rates were decreasing by 6% annually across all hospitals. After medical emergency team implementation, the hospital mortality continued to decrease by 6% annually with no deepening of the mortality slope as compared with the pre-implementation trend for the overall cohort or when analyzed separately within each of the study hospitals. Five years after implementation across study sites, there was no difference between predicted and actually mortality rates.                                                 Thus, in summary, the implementation of medical emergency teams in a large sample of pediatric hospitals in the US was not associated with a reduction in hospital mortality beyond the existing pre-implementation trends. This study's null findings on hospital mortality suggests that either medical emergency teams have no effect on mortality or are being poorly implemented in the real world. These issues are discussed in an accompanying editorial by Joshua Koch and Sandeep Das from UT Southwestern.                                                 The next study tells us that carotid stent fractures are not associated with adverse events. First and corresponding author, Dr. Weinberg from Massachusetts General Hospital and his colleagues reported the stent fracture rate and its association with instant re-stenosis and adverse outcomes in the Asymptomatic Carotid Trial 1, which was a prospective multi-center trial of standard surgical risk patients with severe asymptomatic carotid artery stenosis randomized to carotid artery stenting or carotid endarterectomy. Stent fracture occurred in only 5.4% of patients and there was no association between stent fracture and in-stent re-stenosis or with the primary endpoint, which was a composite of death, stroke or myocardial infarction during the 30 days after the procedure or ipsilateral stroke during the 365 days after the procedure.                                                 These findings suggest that routine surveillance for carotid stent fracture may be unnecessary and, if a fracture is identified in an asymptomatic patient, intervention may rarely be required.                                                 Heart rhythm disorder management procedures are increasingly being performed and the next paper tells us important information on mortality and cerebrovascular events following such procedures.                                                 Co-first authors Lee and Ling, corresponding authors Dr. Mulpuru and colleagues from Mayo Clinic in Phoenix, Arizona, performed a retrospective cohort study of all patients undergoing heart rhythm disorder management procedures between 2000 and 2016 at the Mayo Clinic from all three campuses in Rochester, Phoenix and Jacksonville. Among almost 49,000 patients undergoing a total of above 62,000 procedures, the overall mortality and cerebrovascular event rate was 0.36% and 0.12%, respectively. Lead extraction procedures had the highest overall mortality of 0.21% and the highest cerebrovascular event rates at 0.62%. However, most of the deaths and cerebrovascular events occurred after device implantation procedures due to the sheer volume of device implantation procedures, which represented 48% of all the procedures performed.                                                 The most common cause of death directly related to these procedures was cardiac tamponade, being responsible for 40% of all directly related deaths. This highlights the importance of development of protocols for quick identification and management of cardiac tamponade, even in procedures typically believed to be of lower risk such as device implantation.                                                 And that wraps it up for our summaries this week. Now, for our feature discussion.                                                 Lipid testing plays a major role in our day-to-day management of our cardiovascular patients and fasting samples have long been the standard for assessing LDL cholesterol and triglycerides since fasting is believed to reduce the triglyceride variability and allow for a more accurate derivation of the commonly used Friedewald calculated LDL cholesterol. Well, I think that's an assumption we have taken for granted, I mean, since 1972 when the Friedewald calculation was first proposed, but in this day and age, several clinical guidelines from Europe, Canada and the US have now recommended non-fasting lipid testing for routine clinical evaluations and it's time to re-evaluate perhaps the Friedewald LDL or other methods for determining LDL.                                                 Today's feature paper addresses this issue spot-on and we're thrilled to have with us the corresponding author of a very important paper and he is Dr. Seth Martin from the Johns Hopkins Ciccarone Center for Prevention of Cardiovascular Disease and we also have with us Dr. Anand Rohatgi, associate editor from UT Southwestern. Welcome, gentlemen. Dr. Anand Rohatgi:          Thank you, Carolyn. Dr. Seth Martin:                Thank you. Dr. Carolyn Lam:               Seth, that was a super-long lead up from me, but I just find your paper so intriguing. Could you please paint the background of the idea behind your paper today and the rationale for questioning the Friedewald equation? Dr. Seth Martin:                Yeah, my pleasure. This was the first paper to look at directly fasting versus non-fasting using our new algorithm. To give a little background on the algorithm, we had recognized that the Friedewald equation, which had been the standard for decades as you mentioned, would really become problematic in the setting of low LDL concentrations. In fact, Dr. Friedewald himself and his co-authors said that in their original publication in 1972 because what's subtracted out is the LDL cholesterol and it's not a particularly accurate estimate by their equation, but at the time, it was viewed as acceptable because the concentrations of LDL weren't all that low.                                                 Now, in the modern era, things are different. We treat the lower LDL. We're lucky to have new drugs that allow us to achieve low LDL levels and meanwhile we have many more patients with obesity and diabetes, leading to higher triglyceride levels, so this all means that that estimated component of the equation becomes a bigger part of the equation and that's what spurred us on to say, "Well, cane we estimate that better?" And we were very lucky to have access to a huge data set that had over a million patients and had directly measured VLDL cholesterol as well as triglycerides, so that allowed us to really more specifically address this estimated component of the equation.                                                 To just give the brief details on what the equation does, is we take the original Friedewald equation from what I view is a one-size-fits-all approach where we divide triglycerides by 5 in milligrams per deciliter and now we just match the patient based on their lipid profile using the same data as the Friedewald equation with the more personalized factors, so taking it from one size fits all to a more precision or personalized fit and it's one of 180 different factors that the patient may get matched with and what we've found is that this type of approach is more flexible, so it's going ... as patients triglyceride levels go up in the setting of low LDL and as they go into non-fasting states, this type of approach can adapt to that better and provide a more reliable, accurate estimate of LDL cholesterol. Dr. Carolyn Lam:               That is so cool. It really is. It just makes so much sense in this day and age of proceeding towards personalized medicine, to make sure we apply equations that are personalized, so your paper essentially shows that applying this new equation works better than the traditional equation, particularly in the non-fasting states, right? And for states of low LDL cholesterol or perhaps high triglycerides. Would that be a good summary? Dr. Seth Martin:                Yeah, that's a great summary and this paper ... I'm really lucky. It was led by one of the fantastic Osler medical residents, Vasanth Sathiyakumar, who is going to be a future star in cardiology, I believe, and he did a great job leading our paper, which shows that in the non-fasting state, what happens is triglyceride levels are higher and this means that the Friedewald equation becomes less accurate and I think this has been a little bit overlooked in recent trends where there's been a big push to do more non-fasting lipid profiles, which really is great for patients, more convenient and it makes a lot of sense, but we have to be also, in an era of precision medicine, getting precise data and if we're going to be making clinical decisions based on LDL concentration, we want to make sure we have good information there and what our paper shows is that there should be some level of caution when using non-fasting Friedewald LDL at low levels, but our new algorithm does provide a more robust estimate in that setting. Dr. Carolyn Lam:               Anand, this is begging for the question, "What do you think are going to be the practical implications of this very important paper?" Dr. Anand Rohatgi:          I think the clinical implications are huge and I think that's why we were so excited when we received this, that sort of the potential impact was there. I can tell you personally my clinic is in the afternoon and so it's a struggle to try to get patients to get fasting lipid levels and often they can't do it when they're coming to see me and so the importance of non-fasting lipid levels is clear and what Seth's group has done is showed that we can actually accurately estimate the LDL levels. A lot of people struggle with trying to still calculate the non-HDL levels and, as Seth pointed out, oftentimes when you're non-fasting, the triglyceride levels are higher and the calculated LDL from Friedewald is artificially low, so it's very hard to combine the convenience of just looking at the lipid levels and having sort of a confidence in the actual calculated LDL, so in this case clinicians can have their patients get their lipid levels at any time and with this algorithm that's already being used by major laboratory services will have relatively high confidence that the LDL that they see is very accurate and then they can make a decision based off of that and they can counsel in real time based off of that, so it really changes the ability to engage with patients at any time and is not restrictive.                                                 I can tell you many patients sometimes won't even get their lipid levels for weeks just because they can't arrange for it to be done on a fasting state and so this really liberates patients and it really enhances the doctor-patient relationship, I think. Dr. Carolyn Lam:               I agree, Anand. I like that word that you used, "liberate" the patient. Honestly, I think some of my patients cheat a little too and they don't really fast as they should before their fasting lipids and this is going to be incredibly helpful.                                                 I have a couple of questions for you, though, Seth. In terms of understanding the limitations of what you may have tested in the current study, we all know that with triglycerides in the super-high level of more than 400, for example, the Friedewald equation breaks down. Did you test this with the new equation because I think you excluded this group as well in the current study, did you not? Dr. Seth Martin:                That's correct, yes. Traditionally, the Friedewald equation has excluded folks from calculation who have triglyceride levels, as you said, of 400 milligrams per deciliter or more and the reason for that is that's the setting where chylomicrons are more likely to be present and therefore we're trying to estimate VLDL cholesterol and it wouldn't make sense to do that if there's a lot of triglycerides and chylomicrons.                                                 That being said, we did look at this previously and found that in that setting our equation works quite a bit better than Friedewald, but it's still inaccurate I would say about a third of the time due to the presence of chylomicrons, so it's an area where we should certainly be more cautious in estimating LDL cholesterol if the triglycerides are that high, but honestly in that setting, often the clinical priority is going to revolve around triglyceride lowering and the LDL may not be the most immediate priority for clinical treatment. Dr. Carolyn Lam:               And then just another question, recognizing that our podcast is heard throughout the world, in this day and age of precision medicine, how about accounting for potential ethnic differences, possibly? Did you account for differences in race, gender perhaps in these equations? Dr. Seth Martin:                What we found is that this really is a lipid-dependent phenomenon in terms of the ratio of triglycerides to VLDL in estimating LDL. We previously looked at age and sex and found that they contributed very, very little information to actually explaining this ratio and so I think that it is something that's likely going to be preserved across different demographic groups. I can say to our listeners in places ... in Asia that the equation has been validated over there and so there's some reassurance that even around the world and other places like Brazil, that it is holding up, so I think that largely this is going to be dependent on someone's lipid profile and it is quite simple in that regard, that we don't have to likely worry about too much differences between men, women, older, younger or different ethnicities. Dr. Anand Rohatgi:          I have a question for Seth. As we mentioned, this is an international audience and guidelines do differ on their emphasis on lipid targets now as everyone is aware, some still emphasizing them and others, like the American guidelines, de-emphasizing targets, so Seth, the question i had for you is based off of your work. Where do you see that fitting in with how the different guidelines and societies are trying to emphasize or de-emphasize lipid targets. Dr. Seth Martin:                The amazing thing is we're all ... really have access to the same data. We've worked together throughout the globe to generate clinical trial evidence that guides us as well as all sorts of other type of evidence to guide us in clinical practice, so just on a very broad conceptual level, my hope is that over time with the great exchange of information around the world that we're going to converge more on consensus recommendations and then, of course, there may be needs to adapt those recommendations to different cultures and that can be taken into account, so I'm hoping there'll be a push towards more consensus and as we get our updated American guidelines, it's looking like this upcoming year, I hope that we come into even more harmony with the rest of the world.                                                 I think for a long time we've had this LDL goal in many different guidelines as less than 70, so that's part of the reason our work has focused on that level. The European guidelines have a target level for high-risk patients of less than 70 for LDL and I think what we saw in the recent consensus document on non-statins from the American College of Cardiology was a push to be thinking at that level when the LDL is 70 or above as a time to have a clinician and patient discussion about whether we should be intensifying therapy, so I guess would say the guidelines in my view, and Anand I would be curious of your view, are more alike than different, but I hope they become even more in harmony because really we're all basing our decisions on the same evidence base and I think it can be a bit confusing when we have disparate recommendations.                                                 The same can be said for the issue of recommendations for fasting versus non-fasting guidelines, which have not been harmonized either, but Anand I'd be curious to your thoughts as well on this topic. Dr. Anand Rohatgi:          I would agree with you. I think they're more alike than different. It's just what may be the high level sort of things have come out to the lay public and others, but I agree with you. If you really read them, they're emphasizing risk reduction by the therapies and by controlling the risk factors, in particular the lipid levels, so I think that's where your work is really important and insightful and I think will be incorporated in all of the respective guideline revisions. Dr. Carolyn Lam:               I completely agree and we're so proud to be publishing your excellent work in circulation. Thank you, Seth. Thank you, Anand.                                                 Thank you, listeners, for joining us today. Don't forget to tune again next week.  

Dr. Vilmos Fux LIVE auf der Paleo Convention Berlin Dr. Vux wird auf der PaleoCon 2016 einen Vortrag über Vitamin D halten! Was: Paleo Convention 2016 Wann: 6. & 7. August 2016 Wo: Berlin, Germany - Postbahnhof Berlin Tickets: Eventbrite (hier klicken) In Folge #061 Das Video der aktuellen Folge direkt auf Youtube öffnen Kurze Zusammenfassung Ist Cholesterin alleine ein wichtiger, relevanter Parameter für deine Gesundheit, oder worauf kommt es wirklich an? LDL Cholesterin wird (meist) nur berechnet und nicht gemessen. Die Friedewald-Formel ist für alle eher ungenau, die unter 100 mg/dl Triglyzeride hbane (also sich Low Carb ernähren) sowie für extrem hohe TG Werte (in Österreich wird der berechnete Wert bei der Versicherung SVA ab 250 TG nicht mehr herangenommen) Julia's LDL Cholesterin Rechner Einen langen ausführlichen Artikel zu Gesundheits Parametern hat Julia in ihrem Blog geschrieben (hier klicken). Dazu gibt es auch Julia's englischen Vortrag von der Health Unplugged 2015, London, den du hier auf YouTube findest. Bücher Die Klinik der Glutenintoleranz im Erwachsenenalter: eine retrospektive Studie und neue Erkenntnisse - Dr. Vilmos Fux Weitere Folgen Folge #042: Dr. Jeffry Gerber Denverdietdotor und Ivor Cummins The Fat Emporer Artikel Cholesterin und LCHF: Das solltest du wissen Wem nützt die Angst vor Cholesterin - Gastartikel von Robert Schönauer Alte Menschen mit niedrigem Cholesterin sterben früher Warum du die meisten Pflanzenöle meiden solltest Webseiten JULIAS BLOG PAWELS BLOG

Aggressive strategies to lower Low Density Lipoprotein cholesterol in circulation are recommended for prevention of cardiovascular events. Most often laboratories report LDL-cholesterol based on an equation using measured values of total cholesterol, HDL - cholesterol and triglycerides, the so called Friedewald calculation named after the first author who published that work in Clinical Chemistry back in 1972.

Interview with Sarah M. Friedewald, MD, author of Breast Cancer Screening Using Tomosynthesis in Combination With Digital Mammography

AIR DATE: February 16, 2012 at 7PM ETFEATURED EXPERT: FEATURED TOPIC: “All Things Lipids (Cholesterol 101)” Episode 6 of “Ask The Low-Carb Experts” features the topic “All Things Lipids (Cholesterol 101)” with blogger and doctoral candidate in Nutritional Sciences at the University of Connecticut  where he will be graduating this Spring. He is the creator and maintainer of Cholesterol-and-Health.Com and is the author of two blogs, The Daily Lipid at Cholesterol-and-Health.Com and Mother Nature Obeyed at WestonAPrice.org. He is also a frequent contributor to Wise Traditions, the quarterly journal of the Weston A. Price Foundation. Chris is the author of five publications in peer-reviewed journals, including a letter to the editor of the Journal of the American College of Cardiology criticizing the conclusions of a widely publicized study about the effect of saturated fat on blood vessel function, and letter to the editor of the American Heart Journal arguing that the effect of cholesterol ester transfer protein inhibitors on vitamin E metabolism should be studied before these drugs are deemed safe for preventing heart disease, a hypothesis published in Medical Hypotheses about the molecular mechanism of vitamin D toxicity and the involvement of vitamins A and K in this mechanism, a pilot study in humans suggesting that vitamin E protects against some of the negative effects of sugar consumption published in the Journal of Nutritional Biochemistry, and a review published in Nutrition Reviews about the potential for green tea to prevent or treat nonalcoholic fatty liver diseases. Chris Masterjohn has thoroughly studied the impact of cholesterol on your health and the answers he has discovered might just surprise you. If you have questions about cholesterol, HDL, LDL, triglycerides and more then this is the podcast for you. Here are some of the questions Chris addressed in this podcast: DARREL ASKS:My cholesterol has been high for quite a while. I was previously on Lipitor which made me feel pretty bad (old and feeble even though I’m neither) so I quit. This week my doctor got back my blood work and noticed my number was high (295) and insisted I go back on Lipitor. He said I was a ‘heart attack brewing’. I don’t want to and need some ammunition. Point me in the right direction. MARK ASKS:I have a senior lady that her doctor has recommended her to take statins for a while. She doesn’t want to go on them, and her doctor just ran an Lp(a) test and hers was at 80. I seem to recall that statins don’t really affect Lp(a) and it’s mostly genetic. I’m not sure of her triglyceride/HDL ratio at this time, but should she be worried? Seems that Lp(a) is only an issue if you have heart disease or a lot of inflammation. JOHN ASKS: http://diabetes.diabetesjournals.org/content/early/2011/05/18/db11-0085 Question: Is MGmin LDL the silver bullet of atherosclerosis? I’ve read suggestions that small, dense LDL is the killer, but I see studies suggesting that large, fluffy LDL can also be atherogenic. JAMIE ASKS:In some countries (like Australia) you cannot get your cholesterol measured down to “small dense” and “large fluffy”. They only measure the basics, Triglycerides, HDL, LDL and Total cholesterol. From these numbers, is there a good ratio to indicate good health versus poor health? SHARON ASKS:My husband has high cholesterol which is made worse by another necessary medication he takes. Triglycerides were over 700; he is taking very high doses of statins, bring it to 600; We started Paleo (no sugars; no grains; full-fat dairy and meats) and blood results after two weeks showed them at 199. Is this possible to have such a dramatic change so quickly from this diet? If followup blood work shows continued improvement, what is the number that would get his doctor to take him off of the statins? SAM ASKS:I’m a 42-year-old male with little to no family history of heart disease. My latest VAP results include: Tot LDL-Chol Direct 167 H mg/dLTot. HDL-Cholesterol Dir. 52 mg/dLTot. VLDL-Cholesterol Dir. 23 mg/dLSum Total Cholesterol 241 H mg/dLTriglycerides-Direct 75 mg/dLTot. NonHDL Chol(LDL+VLDL) 189 H mg/dLTotal apoB100 – calc. 118 H mg/dLLP(a) Cholesterol 4.0 mg/dLIDL Cholesterol 23 H mg/dLReal LDL-Cholesterol 140 H mg/dLSum Total LDL-C 167 H mg/dLREAL-LDL Size Pattern A ARemnant Lipoprot(IDL+VLDL3) 37 H mg/dL My doctor insists I take a statin such as Lipitor. I say I may not need it. Which one of us is right? Also, is it possible that statins inhibit the formation of arterial plaque over time? PAUL ASKS:What are your thoughts on all the alarmism surrounding glycation and fructation? KAREN ASKS:I’m about to have blood work done to be underwritten for term life insurance. I’m concerned that my cholesterol levels may have elevated because I’ve only been LC’ing for about 9 months. If it comes back bad, do you have any advice for how to explain what’s going on to help mitigate the consequences? LEO ASKS:It’s been almost 2 years since going low carb. Before that time I was taking fenofibrate for almost 8 years because of very high trig (700 -380) and low HDL (37) because of eating SAD. Now my trig is 100 – 75, HDL is 57 and still improving without taking meds. I read that eating saturated fat and red wine will help increase HDL. At my last doctor visit he suggested in begin statins because my total cholesterol was 250 and my LDL was 148 and to see a cardiologist. I asked that he do the test for determining large and small LDL particles to which he replayed he was not qualified to request that test! I also mentioned to him that the LDL level is really a fictitious number gathered by the Friedewald equation. Would you suggest I see a cardiologist and check further? Would it be a good idea to request a CAC score, Lp(a) and test for density particles of LDL? WILLY ASKS:How are you? My question is what is Lp(a)’s role in heart disease and should we really even track it. As I recall Dr. Kurt Harris from the panu blog has what is considered a high level yet has a very low calcium score. While some on Dr. Davis heart scan blog have levels lower than his and suffer from high calcium scores or other cardiovascular issues. If we should be concerned with this lipid what is the best way to lower it? Niacin? Saturated Fats? Low Carb? I wonder if Lp(a) is just the new kid on the block for Big Pharma trying to keep the lipid hypothesis alive. VALERIE ASKS:Chris, In your most recent interview with Chris Kresser you indicate that a TC:HDL ratio of 4 might be cause for concern and should be evaluated. My husband and I just got our results back, our ratios are 4.3 and 4.6. We can rule out recovering from obesity and fatty liver disease. What do you advise we do if anything? Get retested to establish our averages? Without going into too much detail, we have been following a WAPF/Paleo diet for 4 years, we are healthy and fit, I am 47, my husband is 40. Next, I have in my notes a TC range of 180-250 as found in traditional cultures. Can you also provide a range for HDL and LDL? And last, what foods, herbs, supplements, and food preparation techniques would you advise to support a healthy LDL receptor uptake process? KYLE ASKS:There seems to be a growing interest in the blogosphere with the work of Dr. Ray Peat. A major tenet of Peat’s philosophy revolves around the toxicity of virtually any dose of polyunsaturated fats (PUFA)–both n3 and n6. Given your past work on EFAs and PUFAs in general, I’d love to hear your thoughts on Dr. Peat’s stance. LUKE ASKS:What is the relation of lipid volume in the blood and speed of blood flow in the arteries and the body in general? (e.g, the documentary “Supersize Me” made a big deal about animal fat causing slower measured blood flow) ELLEN ASKS:I believe higher cholesterol levels are healthier and protective against many illnesses. If my normal total cholesterol is around 205, and I make a diet change that has the effect of dropping my total cholesterol to 165, am I compromising the protective aspect of cholesterol? LDL is also lower at 92 and HDL has stayed about the same (55). Trigs are at 92. CRP is .75 and HbA1c is 5.5. MACKAY ASKS:Patient just came back with very high cholesterol, but sub markers were phenomenal. HDL 99Triglycerides 66HSCRP .4 Positive for celiac, although eats very little wheat. Total cholesterol 450. What could cause this? EDWARD ASKS:Regarding lab measurements…lipid panels: Cholesterol measurement – what is actually being measured in standard lipid profiles, and what is being estimated? Is LDL calculated based on your TG measurement? DEANNA ASKS:My stepdad has high cholesterol (mostly high Triglycerides) and has for many years—I have attached his lab report from last May—his numbers were better. Total cholesterol 252Triglycerides 534HDL 33Testosterone 235Free testosterone 8.9 He takes: 160mg Fenofibrate, Benicar, Lovaza, DHEA, Niacin, and just started taking Red Yeast Rice. My mother thought he was on a statin—but Fenofibrate and Lovaza aren’t statins are they? Are they just as bad? Haven’t heard much discussion on these meds. Filed Under: , ,