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Summary of Translational Medicine – e-Series A: Cardiovascular Diseases, Volume Four – Part 1

Posted in Academic Publishing, Acute Myocardial Infarction, Advanced Drug Manufacturing Technology, Alzheimer's Disease, Atherogenic Processes & Pathology, Autologous Cell Therapy, Automated Cell Processing, Bio Instrumentation in Experimental Life Sciences Research, Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, Bone Disease and Musculoskeletal Disease, Bone marrow derived cells, Ca2+ triggered activation, Ca2+ triggered activation, Cachexia, Calcium Signaling, Calmodulin, Calmodulin Kinase and Contraction, Cardiac & Vascular Repair Tools Subsegment, Cardiac and Cardiovascular Surgical Procedures, Cardiac muscle regeneration, Cardiomyopathy, Cardiovascular Pharmacogenomics, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Chemical Genetics, Chronic Thromboembolic Pulmonary Hypertension (CTEPH) and Pulmonary Arterial Hypertension (PAH), Circulating Progenitor Cells, Coagulation Therapy and Internal Bleeding, Competition in regenerative stem cell science, Computational Biology/Systems and Bioinformatics, Curation, Cytoskeleton, Diabetes Mellitus, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Drug Delivery Platform Technology, Drug Toxicity, Electrophysiology, Endothelial cells, Epigenetics and Cardiovascular Risks, Etiology, Evolutionary cognition, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Genomic Expression, Health Economics and Outcomes Research, Human Immune System in Health and in Disease, International Global Work in Pharmaceutical, Interviews with Scientific Leaders, Medical and Population Genetics, Medical Device Therapies for Altzheimer’s Disease, Medical Devices R&D Investment, Medical Imaging Technology, Image Processing/Computing, MRI, CT, Nuclear Medicine, Ultra Sound, Metabolomics, Molecular Genetics & Pharmaceutical, Myocardial metabolism, Myocardial ischemia, myocardial perfusion, Myocardial adenine nucleotide metabolism, Na-K transport, Na-K-ATPase, Neurohumoral Transmission, Nitric Oxide in Health and Disease, Nutrition, Nutritional Supplements: Atherogenesis, lipid metabolism, Origins of Cardiovascular Disease, Oxidative phosphorylation, Personalized and Precision Medicine & Genomic Research, Pharmaceutical Analytics, Pharmacologic toxicities, Pharmacotherapy of Cardiovascular Disease, Phosphorylation, PKC, Population Health Management, Genetics & Pharmaceutical, Population Health Management, Nutrition and Phytochemistry, Proteomics, Regenerative Biology and Medicine, S-nitrosylation, Signaling, Skeletal muscle regeneration, Statistical Methods for Research Evaluation, Stem Cells for Regenerative Medicine, Stents & Tools, Synaptic vesicle, Systemic Inflammatory Response Related Disorders, Technology Advance Assessment of, Translational Effectiveness, Translational Science, Ubiquitinylation, Water Transporters, tagged bioengineering, Cardiovascular Disorders, computational biology, Coronary artery disease, DNA Sequencing, functional proteomics, gene expression, gene silencing, genetic engineering, Heart Failure, Human Genome Project, Hypertension, MicroRNA, mtRNA, myocardial infarction, nitric oxide, Nitric oxide synthase, Personalized medicine, protein modifications, Proteomics, reverse engineering, RNA, signaling pathways, Stem cell, synbiology on April 28, 2014| Leave a Comment »

Summary of Translational Medicine – e-Series A: Cardiovascular Diseases, Volume Four – Part 1

Author and Curator: Larry H Bernstein, MD, FCAP

and

Curator: Aviva Lev-Ari, PhD, RN

Article ID #135: Summary of Translational Medicine – e-Series A: Cardiovascular Diseases, Volume Four – Part 1. Published on 4/28/2014

WordCloud Image Produced by Adam Tubman

 

Part 1 of Volume 4 in the e-series A: Cardiovascular Diseases and Translational Medicine, provides a foundation for grasping a rapidly developing surging scientific endeavor that is transcending laboratory hypothesis testing and providing guidelines to:

• Target genomes and multiple nucleotide sequences involved in either coding or in regulation that might have an impact on complex diseases, not necessarily genetic in nature.
• Target signaling pathways that are demonstrably maladjusted, activated or suppressed in many common and complex diseases, or in their progression.
• Enable a reduction in failure due to toxicities in the later stages of clinical drug trials as a result of this science-based understanding.
• Enable a reduction in complications from the improvement of machanical devices that have already had an impact on the practice of interventional procedures in cardiology, cardiac surgery, and radiological imaging, as well as improving laboratory diagnostics at the molecular level.
• Enable the discovery of new drugs in the continuing emergence of drug resistance.
• Enable the construction of critical pathways and better guidelines for patient management based on population outcomes data, that will be critically dependent on computational methods and large data-bases.

What has been presented can be essentially viewed in the following Table:

 

Summary Table for TM – Part 1

 

 

 

There are some developments that deserve additional development:

1. The importance of mitochondrial function in the activity state of the mitochondria in cellular work (combustion) is understood, and impairments of function are identified in diseases of muscle, cardiac contraction, nerve conduction, ion transport, water balance, and the cytoskeleton – beyond the disordered metabolism in cancer.  A more detailed explanation of the energetics that was elucidated based on the electron transport chain might also be in order.

2. The processes that are enabling a more full application of technology to a host of problems in the environment we live in and in disease modification is growing rapidly, and will change the face of medicine and its allied health sciences.

 

Electron Transport and Bioenergetics

Deferred for metabolomics topic

Synthetic Biology

Introduction to Synthetic Biology and Metabolic Engineering

Kristala L. J. Prather: Part-1    <iBiology > iBioSeminars > Biophysics & Chemical Biology >

http://www.ibiology.org Lecturers generously donate their time to prepare these lectures. The project is funded by NSF and NIGMS, and is supported by the ASCB and HHMI.
Dr. Prather explains that synthetic biology involves applying engineering principles to biological systems to build “biological machines”.

http://synthetic_biology/Introduction_to_Synthetic_Biology_and_Metabolic_Engineering/Kristala_ L.J._Prather/E2/iBiology.htm#/sthash.71kZ0ofr.dpuf

Dr. Prather has received numerous awards both for her innovative research and for excellence in teaching.  Learn more about how Kris became a scientist at

http://science360.gov/obj/video/753bb4fa-aafb-4315-848e-51066ed9799a/finding-way-kristala-l-jones-prather-phd 

Prather 1: Synthetic Biology and Metabolic Engineering  2/6/14IntroductionLecture Overview In the first part of her lecture, Dr. Prather explains that synthetic biology involves applying engineering principles to biological systems to build “biological machines”. The key material in building these machines is synthetic DNA. Synthetic DNA can be added in different combinations to biological hosts, such as bacteria, turning them into chemical factories that can produce small molecules of choice. In Part 2, Prather describes how her lab used design principles to engineer E. coli that produce glucaric acid from glucose. Glucaric acid is not naturally produced in bacteria, so Prather and her colleagues “bioprospected” enzymes from other organisms and expressed them in E. coli to build the needed enzymatic pathway. Prather walks us through the many steps of optimizing the timing, localization and levels of enzyme expression to produce the greatest yield. Speaker Bio: Kristala Jones Prather received her S.B. degree from the Massachusetts Institute of Technology and her PhD at the University of California, Berkeley both in chemical engineering. Upon graduation, Prather joined the Merck Research Labs for 4 years before returning to academia. Prather is now an Associate Professor of Chemical Engineering at MIT and an investigator with the multi-university Synthetic Biology Engineering Reseach Center (SynBERC). Her lab designs and constructs novel synthetic pathways in microorganisms converting them into tiny factories for the production of small molecules. Dr. Prather has received numerous awards both for her innovative research and for excellence in teaching.

VIEW VIDEOS

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=0

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=12

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=74

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=129

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=168

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk

 

David Bartel: micro-RNAs

 

I. Introduction to microRNAs

https://www.youtube.com/watch?feature=player_embedded&v=dupzE66J8u4#t=0

– See more at: http://www.ibiology.org/ibioseminars/genetics-gene-regulation/david-bartel-part-1.html#sthash.nGGr1tIt.dpuf

II. Regulatory Effects of Mammalian microRNAs

https://www.youtube.com/watch?feature=player_embedded&v=TcZK_A_wcWQ#t=0

https://www.youtube.com/watch?feature=player_embedded&v=TcZK_A_wcWQ

Calcium Cycling in Synthetic and Contractile Phasic or Tonic Vascular Smooth Muscle Cells

in INTECH
Current Basic and Pathological Approaches to
the Function of Muscle Cells and Tissues – From Molecules to HumansLarissa Lipskaia, Isabelle Limon, Regis Bobe and Roger Hajjar
Additional information is available at the end of the chapter
http://dx.doi.org/10.5772/48240

1. Introduction
Calcium ions (Ca ) are present in low concentrations in the cytosol (~100 nM) and in high concentrations (in mM range) in both the extracellular medium and intracellular stores (mainly sarco/endo/plasmic reticulum, SR). This differential allows the calcium ion messenger that carries information
as diverse as contraction, metabolism, apoptosis, proliferation and/or hypertrophic growth. The mechanisms responsible for generating a Ca signal greatly differ from one cell type to another.

In the different types of vascular smooth muscle cells (VSMC), enormous variations do exist with regard to the mechanisms responsible for generating Ca signal. In each VSMC phenotype (synthetic/proliferating and contractile [1], tonic or phasic), the Ca signaling system is adapted to its particular function and is due to the specific patterns of expression and regulation of Ca.
For instance, in contractile VSMCs, the initiation of contractile events is driven by mem- brane depolarization; and the principal entry-point for extracellular Ca is the voltage-operated L-type calcium channel (LTCC). In contrast, in synthetic/proliferating VSMCs, the principal way-in for extracellular Ca is the store-operated calcium (SOC) channel.
Whatever the cell type, the calcium signal consists of  limited elevations of cytosolic free calcium ions in time and space. The calcium pump, sarco/endoplasmic reticulum Ca ATPase (SERCA), has a critical role in determining the frequency of SR Ca release by upload into the sarcoplasmic
sensitivity of  SR calcium channels, Ryanodin Receptor, RyR and Inositol tri-Phosphate Receptor, IP3R.
Synthetic VSMCs have a fibroblast appearance, proliferate readily, and synthesize increased levels of various extracellular matrix components, particularly fibronectin, collagen types I and III, and tropoelastin [1].
Contractile VSMCs have a muscle-like or spindle-shaped appearance and well-developed contractile apparatus resulting from the expression and intracellular accumulation of thick and thin muscle filaments [1].

Schematic representation of Calcium Cycling in Contractile and Proliferating VSMCs

 

Figure 1. Schematic representation of Calcium Cycling in Contractile and Proliferating VSMCs.

Left panel: schematic representation of calcium cycling in quiescent /contractile VSMCs. Contractile re-sponse is initiated by extracellular Ca influx due to activation of Receptor Operated Ca (through phosphoinositol-coupled receptor) or to activation of L-Type Calcium channels (through an increase in luminal pressure). Small increase of cytosolic due IP3 binding to IP3R (puff) or RyR activation by LTCC or ROC-dependent Ca influx leads to large SR Ca IP3R or RyR clusters (“Ca -induced Ca SR calcium pumps (both SERCA2a and SERCA2b are expressed in quiescent VSMCs), maintaining high concentration of cytosolic Ca and setting the sensitivity of RyR or IP3R for the next spike.
Contraction of VSMCs occurs during oscillatory Ca transient.
Middle panel: schematic representa tion of atherosclerotic vessel wall. Contractile VSMC are located in the media layer, synthetic VSMC are located in sub-endothelial intima.
Right panel: schematic representation of calcium cycling in quiescent /contractile VSMCs. Agonist binding to phosphoinositol-coupled receptor leads to the activation of IP3R resulting in large increase in cytosolic Ca calcium pumps (only SERCA2b, having low turnover and low affinity to Ca depletion leads to translocation of SR Ca sensor STIM1 towards PM, resulting in extracellular Ca influx though opening of Store Operated Channel (CRAC). Resulted steady state Ca transient is critical for activation of proliferation-related transcription factors ‘NFAT).
Abbreviations: PLC – phospholipase C; PM – plasma membrane; PP2B – Ca /calmodulin-activated protein phosphatase 2B (calcineurin); ROC- receptor activated channel; IP3 – inositol-1,4,5-trisphosphate, IP3R – inositol-1,4,5- trisphosphate receptor; RyR – ryanodine receptor; NFAT – nuclear factor of activated T-lymphocytes; VSMC – vascular smooth muscle cells; SERCA – sarco(endo)plasmic reticulum Ca sarcoplasmic reticulum.

 

Time for New DNA Synthesis and Sequencing Cost Curves

By Rob Carlson

I’ll start with the productivity plot, as this one isn’t new. For a discussion of the substantial performance increase in sequencing compared to Moore’s Law, as well as the difficulty of finding this data, please see this post. If nothing else, keep two features of the plot in mind: 1) the consistency of the pace of Moore’s Law and 2) the inconsistency and pace of sequencing productivity. Illumina appears to be the primary driver, and beneficiary, of improvements in productivity at the moment, especially if you are looking at share prices. It looks like the recently announced NextSeq and Hiseq instruments will provide substantially higher productivities (hand waving, I would say the next datum will come in another order of magnitude higher), but I think I need a bit more data before officially putting another point on the plot.

 

cost-of-oligo-and-gene-synthesis

Illumina’s instruments are now responsible for such a high percentage of sequencing output that the company is effectively setting prices for the entire industry. Illumina is being pushed by competition to increase performance, but this does not necessarily translate into lower prices. It doesn’t behoove Illumina to drop prices at this point, and we won’t see any substantial decrease until a serious competitor shows up and starts threatening Illumina’s market share. The absence of real competition is the primary reason sequencing prices have flattened out over the last couple of data points.

Note that the oligo prices above are for column-based synthesis, and that oligos synthesized on arrays are much less expensive. However, array synthesis comes with the usual caveat that the quality is generally lower, unless you are getting your DNA from Agilent, which probably means you are getting your dsDNA from Gen9.

Note also that the distinction between the price of oligos and the price of double-stranded sDNA is becoming less useful. Whether you are ordering from Life/Thermo or from your local academic facility, the cost of producing oligos is now, in most cases, independent of their length. That’s because the cost of capital (including rent, insurance, labor, etc) is now more significant than the cost of goods. Consequently, the price reflects the cost of capital rather than the cost of goods. Moreover, the cost of the columns, reagents, and shipping tubes is certainly more than the cost of the atoms in the sDNA you are ostensibly paying for. Once you get into longer oligos (substantially larger than 50-mers) this relationship breaks down and the sDNA is more expensive. But, at this point in time, most people aren’t going to use longer oligos to assemble genes unless they have a tricky job that doesn’t work using short oligos.

Looking forward, I suspect oligos aren’t going to get much cheaper unless someone sorts out how to either 1) replace the requisite human labor and thereby reduce the cost of capital, or 2) finally replace the phosphoramidite chemistry that the industry relies upon.

IDT’s gBlocks come at prices that are constant across quite substantial ranges in length. Moreover, part of the decrease in price for these products is embedded in the fact that you are buying smaller chunks of DNA that you then must assemble and integrate into your organism of choice.

Someone who has purchased and assembled an absolutely enormous amount of sDNA over the last decade, suggested that if prices fell by another order of magnitude, he could switch completely to outsourced assembly. This is a potentially interesting “tipping point”. However, what this person really needs is sDNA integrated in a particular way into a particular genome operating in a particular host. The integration and testing of the new genome in the host organism is where most of the cost is. Given the wide variety of emerging applications, and the growing array of hosts/chassis, it isn’t clear that any given technology or firm will be able to provide arbitrary synthetic sequences incorporated into arbitrary hosts.

 TrackBack URL: http://www.synthesis.cc/cgi-bin/mt/mt-t.cgi/397

 

Startup to Strengthen Synthetic Biology and Regenerative Medicine Industries with Cutting Edge Cell Products

28 Nov 2013 | PR Web

Dr. Jon Rowley and Dr. Uplaksh Kumar, Co-Founders of RoosterBio, Inc., a newly formed biotech startup located in Frederick, are paving the way for even more innovation in the rapidly growing fields of Synthetic Biology and Regenerative Medicine. Synthetic Biology combines engineering principles with basic science to build biological products, including regenerative medicines and cellular therapies. Regenerative medicine is a broad definition for innovative medical therapies that will enable the body to repair, replace, restore and regenerate damaged or diseased cells, tissues and organs. Regenerative therapies that are in clinical trials today may enable repair of damaged heart muscle following heart attack, replacement of skin for burn victims, restoration of movement after spinal cord injury, regeneration of pancreatic tissue for insulin production in diabetics and provide new treatments for Parkinson’s and Alzheimer’s diseases, to name just a few applications.

While the potential of the field is promising, the pace of development has been slow. One main reason for this is that the living cells required for these therapies are cost-prohibitive and not supplied at volumes that support many research and product development efforts. RoosterBio will manufacture large quantities of standardized primary cells at high quality and low cost, which will quicken the pace of scientific discovery and translation to the clinic. “Our goal is to accelerate the development of products that incorporate living cells by providing abundant, affordable and high quality materials to researchers that are developing and commercializing these regenerative technologies” says Dr. Rowley

 

Life at the Speed of Light

http://kcpw.org/?powerpress_pinw=92027-podcast

NHMU Lecture featuring – J. Craig Venter, Ph.D.
Founder, Chairman, and CEO – J. Craig Venter Institute; Co-Founder and CEO, Synthetic Genomics Inc.

J. Craig Venter, Ph.D., is Founder, Chairman, and CEO of the J. Craig Venter Institute (JVCI), a not-for-profit, research organization dedicated to human, microbial, plant, synthetic and environmental research. He is also Co-Founder and CEO of Synthetic Genomics Inc. (SGI), a privately-held company dedicated to commercializing genomic-driven solutions to address global needs.

In 1998, Dr. Venter founded Celera Genomics to sequence the human genome using new tools and techniques he and his team developed.  This research culminated with the February 2001 publication of the human genome in the journal, Science. Dr. Venter and his team at JVCI continue to blaze new trails in genomics.  They have sequenced and a created a bacterial cell constructed with synthetic DNA,  putting humankind at the threshold of a new phase of biological research.  Whereas, we could  previously read the genetic code (sequencing genomes), we can now write the genetic code for designing new species.

The science of synthetic genomics will have a profound impact on society, including new methods for chemical and energy production, human health and medical advances, clean water, and new food and nutritional products. One of the most prolific scientists of the 21st century for his numerous pioneering advances in genomics,  he  guides us through this emerging field, detailing its origins, current challenges, and the potential positive advances.

His work on synthetic biology truly embodies the theme of “pushing the boundaries of life.”  Essentially, Venter is seeking to “write the software of life” to create microbes designed by humans rather than only through evolution. The potential benefits and risks of this new technology are enormous. It also requires us to examine, both scientifically and philosophically, the question of “What is life?”

J Craig Venter wants to digitize DNA and transmit the signal to teleport organisms

http://pharmaceuticalintelligence.com/2013/11/01/j-craig-venter-wants-to-digitize-dna-and-transmit-the-signal-to-teleport-organisms/

2013 Genomics: The Era Beyond the Sequencing of the Human Genome: Francis Collins, Craig Venter, Eric Lander, et al.

http://pharmaceuticalintelligence.com/2013/02/11/2013-genomics-the-era-beyond-the-sequencing-human-genome-francis-collins-craig-venter-eric-lander-et-al/

Human Longevity Inc (HLI) – $70M in Financing of Venter’s New Integrative Omics and Clinical Bioinformatics

http://pharmaceuticalintelligence.com/2014/03/05/human-longevity-inc-hli-70m-in-financing-of-venters-new-integrative-omics-and-clinical-bioinformatics/

 

 

Where Will the Century of Biology Lead Us?

By Randall Mayes

A technology trend analyst offers an overview of synthetic biology, its potential applications, obstacles to its development, and prospects for public approval.

• In addition to boosting the economy, synthetic biology projects currently in development could have profound implications for the future of manufacturing, sustainability, and medicine.
• Before society can fully reap the benefits of synthetic biology, however, the field requires development and faces a series of hurdles in the process. Do researchers have the scientific know-how and technical capabilities to develop the field?

Biology + Engineering = Synthetic Biology

Bioengineers aim to build synthetic biological systems using compatible standardized parts that behave predictably. Bioengineers synthesize DNA parts—oligonucleotides composed of 50–100 base pairs—which make specialized components that ultimately make a biological system. As biology becomes a true engineering discipline, bioengineers will create genomes using mass-produced modular units similar to the microelectronics and computer industries.

Currently, bioengineering projects cost millions of dollars and take years to develop products. For synthetic biology to become a Schumpeterian revolution, smaller companies will need to be able to afford to use bioengineering concepts for industrial applications. This will require standardized and automated processes.

A major challenge to developing synthetic biology is the complexity of biological systems. When bioengineers assemble synthetic parts, they must prevent cross talk between signals in other biological pathways. Until researchers better understand these undesired interactions that nature has already worked out, applications such as gene therapy will have unwanted side effects. Scientists do not fully understand the effects of environmental and developmental interaction on gene expression. Currently, bioengineers must repeatedly use trial and error to create predictable systems.

Similar to physics, synthetic biology requires the ability to model systems and quantify relationships between variables in biological systems at the molecular level.

The second major challenge to ensuring the success of synthetic biology is the development of enabling technologies. With genomes having billions of nucleotides, this requires fast, powerful, and cost-efficient computers. Moore’s law, named for Intel co-founder Gordon Moore, posits that computing power progresses at a predictable rate and that the number of components in integrated circuits doubles each year until its limits are reached. Since Moore’s prediction, computer power has increased at an exponential rate while pricing has declined.

DNA sequencers and synthesizers are necessary to identify genes and make synthetic DNA sequences. Bioengineer Robert Carlson calculated that the capabilities of DNA sequencers and synthesizers have followed a pattern similar to computing. This pattern, referred to as the Carlson Curve, projects that scientists are approaching the ability to sequence a human genome for $1,000, perhaps in 2020. Carlson calculated that the costs of reading and writing new genes and genomes are falling by a factor of two every 18–24 months. (see recent Carlson comment on requirement to read and write for a variety of limiting  conditions).

Startup to Strengthen Synthetic Biology and Regenerative Medicine Industries with Cutting Edge Cell Products

http://pharmaceuticalintelligence.com/2013/11/28/startup-to-strengthen-synthetic-biology-and-regenerative-medicine-industries-with-cutting-edge-cell-products/

Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

http://pharmaceuticalintelligence.com/2013/05/17/synthetic-biology-on-advanced-genome-interpretation-for-gene-variants-and-pathways-what-is-the-genetic-base-of-atherosclerosis-and-loss-of-arterial-elasticity-with-aging/

Synthesizing Synthetic Biology: PLOS Collections

http://pharmaceuticalintelligence.com/2012/08/17/synthesizing-synthetic-biology-plos-collections/

Capturing ten-color ultrasharp images of synthetic DNA structures resembling numerals 0 to 9

http://pharmaceuticalintelligence.com/2014/02/05/capturing-ten-color-ultrasharp-images-of-synthetic-dna-structures-resembling-numerals-0-to-9/

Silencing Cancers with Synthetic siRNAs

http://pharmaceuticalintelligence.com/2013/12/09/silencing-cancers-with-synthetic-sirnas/

Genomics Now—and Beyond the Bubble

Futurists have touted the twenty-first century as the century of biology based primarily on the promise of genomics. Medical researchers aim to use variations within genes as biomarkers for diseases, personalized treatments, and drug responses. Currently, we are experiencing a genomics bubble, but with advances in understanding biological complexity and the development of enabling technologies, synthetic biology is reviving optimism in many fields, particularly medicine.

BY MICHAEL BROOKS    17 APR, 2014     http://www.newstatesman.com/

Michael Brooks holds a PhD in quantum physics. He writes a weekly science column for the New Statesman, and his most recent book is The Secret Anarchy of Science.

The basic idea is that we take an organism – a bacterium, say – and re-engineer its genome so that it does something different. You might, for instance, make it ingest carbon dioxide from the atmosphere, process it and excrete crude oil.

That project is still under construction, but others, such as using synthesised DNA for data storage, have already been achieved. As evolution has proved, DNA is an extraordinarily stable medium that can preserve information for millions of years. In 2012, the Harvard geneticist George Church proved its potential by taking a book he had written, encoding it in a synthesised strand of DNA, and then making DNA sequencing machines read it back to him.

When we first started achieving such things it was costly and time-consuming and demanded extraordinary resources, such as those available to the millionaire biologist Craig Venter. Venter’s team spent most of the past two decades and tens of millions of dollars creating the first artificial organism, nicknamed “Synthia”. Using computer programs and robots that process the necessary chemicals, the team rebuilt the genome of the bacterium Mycoplasma mycoides from scratch. They also inserted a few watermarks and puzzles into the DNA sequence, partly as an identifying measure for safety’s sake, but mostly as a publicity stunt.

What they didn’t do was redesign the genome to do anything interesting. When the synthetic genome was inserted into an eviscerated bacterial cell, the new organism behaved exactly the same as its natural counterpart. Nevertheless, that Synthia, as Venter put it at the press conference to announce the research in 2010, was “the first self-replicating species we’ve had on the planet whose parent is a computer” made it a standout achievement.

Today, however, we have entered another era in synthetic biology and Venter faces stiff competition. The Steve Jobs to Venter’s Bill Gates is Jef Boeke, who researches yeast genetics at New York University.

Boeke wanted to redesign the yeast genome so that he could strip out various parts to see what they did. Because it took a private company a year to complete just a small part of the task, at a cost of $50,000, he realised he should go open-source. By teaching an undergraduate course on how to build a genome and teaming up with institutions all over the world, he has assembled a skilled workforce that, tinkering together, has made a synthetic chromosome for baker’s yeast.

 

Stepping into DIYbio and Synthetic Biology at ScienceHack

Posted April 22, 2014 by Heather McGaw and Kyrie Vala-Webb

We got a crash course on genetics and protein pathways, and then set out to design and build our own pathways using both the “Genomikon: Violacein Factory” kit and Synbiota platform. With Synbiota’s software, we dragged and dropped the enzymes to create the sequence that we were then going to build out. After a process of sketching ideas, mocking up pathways, and writing hypotheses, we were ready to start building!

The night stretched long, and at midnight we were forced to vacate the school. Not quite finished, we loaded our delicate bacteria, incubator, and boxes of gloves onto the bus and headed back to complete our bacterial transformation in one of our hotel rooms. Jammed in between the beds and the mini-fridge, we heat-shocked our bacteria in the hotel ice bucket. It was a surreal moment.

While waiting for our bacteria, we held an “unconference” where we explored bioethics, security and risk related to synthetic biology, 3D printing on Mars, patterns in juggling (with live demonstration!), and even did a Google Hangout with Rob Carlson. Every few hours, we would excitedly check in on our bacteria, looking for bacterial colonies and the purple hue characteristic of violacein.

Most impressive was the wildly successful and seamless integration of a diverse set of people: in a matter of hours, we were transformed from individual experts and practitioners in assorted fields into cohesive and passionate teams of DIY biologists and science hackers. The ability of everyone to connect and learn was a powerful experience, and over the course of just one weekend we were able to challenge each other and grow.

Returning to work on Monday, we were hungry for more. We wanted to find a way to bring the excitement and energy from the weekend into the studio and into the projects we’re working on. It struck us that there are strong parallels between design and DIYbio, and we knew there was an opportunity to bring some of the scientific approaches and curiosity into our studio.

 

 

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Requiem for Palliative Cardiology: The Voice of Dr. Esselstyn on Plant-Based Nutrition

Posted in Atherogenic Processes & Pathology, Frontiers in Cardiology and Cardiovascular Disorders, Health Economics and Outcomes Research, HTN, Human Immune System in Health and in Disease, Nutrition, Nutritional Supplements: Atherogenesis, lipid metabolism, Origins of Cardiovascular Disease, Personalized and Precision Medicine & Genomic Research, Population Health Management, Nutrition and Phytochemistry on February 2, 2014| 3 Comments »

Requiem for Palliative Cardiology: The Voice of Dr. Esselstyn on Plant-Based Nutrition

Reporter: Aviva Lev-Ari, PhD, RN

 

SELECTED ARTICLES BY DR. ESSELSTYN

Articles on the Arrest and Reversal Study: Is the Present Therapy for Coronary Artery Disease the Radical Mastectomyof the Twenty-First Century? A Strategy to Arrest and Reverse Coronary Artery Disease: A 5 -Year Longitudinal Study of a Single Physician’s Practice Esselstyn CB Jr. et al: The Journal of Family Practice 1995 December; 41(6): 560-68 Updating a 12 -Year Experience With Arrest and Reversal Therapy for Coronary Heart Disease (An Overdue Requiem for Palliative Cardiology) Esselstyn CB Jr. The Am J of Cardiology 1999 August 1; 84:339-341 Resolving the Coronary Artery Disease Epidemic through Plant-Based Nutrition (with photos of disease reversal) Esselstyn CB Jr: Preventive Cardiology 2001;4: 171-177 Patient Profiles In Cholesterol Lowering, Moderation Kills Esselstyn CB Jr. Cleve Clinic J of Med 2000 August; 67 (8): 560-564 Selected Articles: Beyond Surgery Presidential Address Esselstyn CB Jr. Surgery Dec 1991; 110(6): 923-27 More Than Coronary Artery Disease  Esselstyn CB Jr. : The Am J of Cardiology 1998 November 26; 82 (10B):5T-9T Changing the Treatment Paradigm for Coronary Artery Disease Esselstyn CB Jr.: The Am J of Cardiology 1998 November 26; 82(10B): 1T-4T Reflections and News: How to Keep David Letterman (and yourself) Off the Operating Table A Revolution to Restore America’s Health Huffington Post Interview with Dr. Esselstyn The Collapse of Cardiology: A Time to Rejoice? Olympic Reflections 50 Years Later Plant-based Nutrition News and Results Sample Recipes Video: Becoming Heart Attack Proof (62 minute presentation) For more video presentations, visit the MEDIA PAGE

SOURCE

http://www.heartattackproof.com/articles.htm

EXCERPT from
PREVENT AND REVERSE HEART DISEASE 

by Caldwell B. Esselstyn, Jr., MD

Chapter One
Eating to Live

I believe that coronary artery disease is preventable, and that even after it is underway, its progress can be stopped, its insidious effects reversed. I believe, and my work over the past twenty years has demonstrated, that all this can be accomplished without expensive mechanical intervention and with minimal use of drugs. The key lies in nutrition—specifically, in abandoning the toxic American diet and maintaining cholesterol levels well below those historically recommended by health policy experts.

The bottom line of the nutritional program I recommend is that it contains not a single item of any food known to cause or promote the development of vascular disease. I often ask patients to compare their coronary artery disease to a house fire. Your house is on fire because eating the wrong foods has given you heart disease. You are spraying gasoline on the fire by continuing to eat the very same foods that caused the disease in the first place.

I don’t want my patients to pour a single thimbleful of gasoline on the fire. Stopping the gasoline puts out the fire. Reforming the way you eat will end the heart disease.

Here are the rules of my program in their simplest form:

• You may not eat anything with a mother or a face (no meat, poultry, or fish).

• You cannot eat dairy products.

• You must not consume oil of any kind—not a drop. (Yes, you devotees of the Mediterranean Diet, that includes olive oil, as I’ll explain in Chapter 10.)

• Generally, you cannot eat nuts or avocados.

You can eat a wonderful variety of delicious, nutrient-dense foods:

• All vegetables except avocado. Leafy green vegetables, root vegetables, veggies that are red, green, purple, orange, and yellowand everything in between

• All legumes—beans, peas, and lentils of all varieties.

• All whole grains and products, such as bread and pasta, that are made from them—as long as they do not contain added fats.

• All fruits.

It works. In the first continuous twelve-year study of the effects of nutrition in severely ill patients, which I will describe in this book, those who complied with my program achieved total arrest of clinical progression and significant selective reversal of coronary artery disease. In fully compliant patients, we have seen angina disappear in a few weeks and abnormal stress test results return to normal.

SOURCE

http://www.heartattackproof.com/excerpt.htm

Q&A with Caldwell B. Esselstyn, Jr., MD

Caldwell B. Esselstyn, Jr., MD, F.A.C.S.

Please note: If your question is about finding a doctor in your area who supports a plant-based diet, please see this link: How to Find a Plant-Based Doctor.

1. How is your approach to treating heart disease unique?

My program is a nutrition-based therapy that has been scientifically-proven to reverse heart disease. There is no other treatment plan backed by a study as long as the one I conducted, or a study that has produced such dramatic, visible results. Coronary angiograms (X-Rays) of the patients in my study show an actual reversal of the disease. To experience these benefits, my patients must stick to my plant-based diet program strictly, but the effects are more than worth the effort. For those that are very sick, it is the most effective treatment option–far less dangerous and more effective than invasive surgical procedures such as stents and bypass (except in acute emergencies), and much more effective than drugs alone. Traditional cardiology has relied on technology to ease the symptoms of heart disease, but has not addressed its causes. My approach is not another stop-gap solution, it prevents heart disease from occurring in those who don’t yet have the disease, and it heals the body and reverses the disease when symptoms are present.

Best of all, over time the benefits endure and continue to improve. I am always excited when I see arrest and reversal in patient after patient and their joy and relief when they are free of the disease that was destroying them.

2. What would you say to someone considering a stent or other surgical procedure or drug therapy, to treat their heart disease?

All heart patients who are not absolute emergencies should first have an aggressive opportunity at non surgical medical therapy. This is not just my opinion but that of expert cardiolgists from Boston, Hartford, Houston, Stanford, San Diego, Seattle and Cleveland. The difference in my case is that I advocate an aggressive plant based nutrition program to arrest and reverse the disease and to avoid all surgery. Drugs alone do not prevent heart attacks and stop symptoms of heart disease.

3. How do you encourage your patients to stay on the diet?

There is no question it is hard at first. And it is hardest eating out at friends’ houses. However, I am always impressed how well my patients do once they experience the relief of chest pain, weight loss, and the improved feeling of well being they have eating a plant-based diet. Then the motivation comes from within. It also helps that within 8-12 weeks of starting the program the fat receptor in the brain down regulates and they lose the craving for fat. And as they start feeling better and better, they know that they are the ones– not their physician or their surgeon–that have control over the disease. It is a powerful feeling!

4. Why does the diet eliminate oil entirely?

NO OIL! Not even olive oil, which goes against a lot of other advice out there about so-called good fats. The reality is that oils are extremely low in terms of nutritive value. They contain no fiber, no minerals and are 100% fat calories. And above all they contain saturated fat which immediately injures the endothelial lining of the arteries when eaten. It doesn’t matter whether it’s olive oil, corn oil, coconut il or any other kind , avoid ALL oil. This is so important I have detailed oil in Chapter 10.

5. Can you actually enjoy food on the program?

We LOVE our food. Our children and grandchildren love our food and the patients love the food. Everyone loves the food once they give it a try. It is all a matter of attitude–and you do need a positive attitude to get started and to understand that this new way of eating is the best thing you can do for your body. Then, the body will help you adjust. You actually begin to lose your physiologically-based craving for fat. Once that occurs, you can fully appreciate the natural taste of plant foods–the colorful tastes and textures are difficult to surpass.

6. Why should I change? My health is excellent.

No one escapes in the end–eventually the traditional western diet guarantees some form of disease in all of us. While it may not be heart disease at the moment, eventually it will be or hypertension, diabetes, stroke,obesity, gall stones, diverticulitis, rheumatoid arthritis, lupus, multiple sclerosis, or a greater likelihood of breast, prostate, colon, ovarian and uterine cancers. Even erectile dysfunction and dementia. The world famous Framingham Heart Study now approaching its 60th year looked at 1,000 people at age 50 who had normal blood pressure. They looked at the same group at age 70, and 90% now had high blood pressure. But there is something that you can do now to stop the cascading events that occur in the body and lead to disease. You can change your diet and begin safeguarding your health for the future.

More Commonly Asked Questions

Protein – Where do I get my protein / What protein drink is best? 
Extra protein powder and shakes are truly unnecessary and have the potential for harm if they contain animal protein. The protein available in a diet of whole grains, legumes and beans, and red, yellow and green vegetables is adequate to nourish even professional champion athletes such as the iron man, professional football, mixed marshal arts, track and field,

Calcium – Where do I get calcium?
Calcium supplementation is unnecessary. There is more than adequate calcium in a plant- based diet of whole grains, legumes and grains and especially the green leafy vegetables.

Vitamins – What Vitamins should I take?
Take Vitamin B-12. If eating copious amounts of leafy green vegetables, a multi vitamin is unnecessary. Have blood tested for Vitamin D level and supplement as appropriate to maintain blood level in the normal range.

Fish Oil – Should I take fish oil?
Fish oil is not essential. Fish get their omega 3 from plants. It is difficult to be deficient in Omega 3 if eating 1-2 tablespoons of flax seed meal or chia seeds and green leafy vegetables at several meals. There is also research that suggests that those on plant based nutrition become highly efficient in their own manufacture of omega 3. Patients on fish oil are also at increased risk for bleeding.

Flax Seed Oil/ Flax Seed Meal – What about flax seed oil?
Flax seed meal is well tolerated and supplies a bonus of omega 3 using 1 or 2 tablespoons on cereal daily. Avoid flax seed oil.

Olive oil, canola oil, coconut oil, Sunflower oil, soybean oil, peanut oil, any oil –
Which oil is best?
Avoid oils. They injure the endothelium, the innermost lining of the artery, and that injury is the gateway to vascular disease. All oil is also empty calories.

Lotions with oil – Is it all right to use lotions with oil on my skin?
It is fine to use lotions with oil on your skin.

Omega 3 – How do I get my Omega 3’s?
Omega 3’s are essential fatty acids supplied in adequate amounts in people consuming plant based nutrition with plenty of green leafy vegetables. However 1-2 tablespoons of flax seed meal or chia seeds daily is perfectly accepted.

Family history – I have a bad family history? Does it matter?
Our data indicates even those with strong family history when eating plant based are protected from vascular disease. Family history loads the gun but lifestyle pulls the trigger.

Nuts – What about nuts? I hear so many different opinions.
My preference is no nuts for heart disease patients. That also eliminates peanuts and peanut butter even though peanuts are officially a legume. For those with established heart disease to add more saturated fat that is in nuts is inappropriate. For people with no heart disease who want to eat nuts and avocado and are able to achieve a cholesterol of 150 and LDL of 80 or under without cholesterol lowering drugs, some nuts and avocado are acceptable. No nuts for heart disease patients, includes peanuts and peanut butter, even though peanuts are officially a legume. Chestnuts are the one nut, very low in fat, it is ok to eat.

Seeds (sunflower, pumpkin, sesame, etc.) Are seeds ok to eat?
1 -2 tablespoons of ground flax seeds or chia seeds daily for omega 3 are appropriate for everyone to eat including heart patients if they wish. Some seeds baked in bread or crackers is acceptable. Just don’t eat handfuls.

Coconut water – Is it all right to drink coconut water?
Coconut water is 8% saturated fat (If the fat is less than .5 per serving it does not have to be listed on the label) and about 50% sugar. So save your money and don’t use it.

Prostate cancer- Does plant based eating help prostate cancer?
Prostate cancer is greatly lessoned by plant- based nutrition as best exemplified by the 1958 report confirming by autopsy 18 deaths in the entire nation of Japan.

Egg whites, fat free milk, yogurt – So What is wrong with egg whites, fat free yogurt, skim milk?
Egg whites, fat free milk and yogurt are ALL animal protein, and animal protein injures the lining of the arteries. Do not eat.

Cholesterol Number fluctuation – Why do my cholesterol numbers fluctuate? 
Fluctuation of cholesterol is normal. It is nice to have it fluctuating in a range that would indicate you are unlikely to have cardio vascular problems.

Losing weight – What can I do to stop losing too much weight?
If you are losing too much weight, EAT MORE calories. Increase portion size. Eat snacks. Eat more whole grains and beans.

Tired, no energy – Why am I tired and have no energy since eating plant-based? 
If you feel tired and lacking in energy, be sure you are eating enough calories. Also exercise because you need to use energy to make energy. Depression also contributes to lack of energy. But first of all eat more.

Not losing weight – Why haven’t I lost weight/ Why have I stopped losing weight?
If not losing enough weight, eliminate flour products like bread, pasta and bagels. Instead, eat whole grains like rice, quinoa, barley and farro, etc. Reduce portion size. Increase leafy green vegetables and exercise.

Triglycerides- Why did my triglycerides go up?
If your triglycerides are high, cut back on simple carbohydrates, which would include alcohol, wine, beer, white flour products, sugars including dried fruit, honey maple syrup, molasses, rich desserts, fruit juice or an excess of fruit,

HDL- My doctor is so concerned because my HDL has gone down
It is not uncommon for HDL to fall when consuming plant based nutrition. Do not be alarmed. The capacity of HDL to do its job has been shown recently by scientific research that there is no relationship between the capacity of the HDL molecule to function optimally and its blood level. Recent research has confirmed that the HDL molecule can be injured and weakened when one is ingesting a pro inflammatory western diet and conversely it appears despite a lower than normal level to be optimized by anti inflammatory plant based-nutrition.

LDL – Where should my LDL be?
LDL is the bad cholesterol. The closer it can be to 80-85, the better. However, if one is unable to take statin drugs and eating plant-based nutrition, and the LDL won’t go lower than 95-105, it would appear that they will still be fine. The lesson we learned from the Tarahumara Indians, who never have cardiovascular disease, is that the most key protective element is not so much the pure LDL number as is knowing that nothing ever is eaten which is a building block of vascular disease or can injure endothelium.

Statins – Should I take statins or not?
Statins are not the reason that cultures such as the Tarhumara and the Papua Highlanders do not have cardiovascular disease. Statins appear to have minimal if any benefit in primary prevention but are of some help in slowing disease progression for those who already have an established diagnosis of cardiovascular disease. Clearly some of our most profound successes in arresting and reversing disease were with patients who either refused or were incapable of taking statins. Nothing is as powerful for the prevention of cardiovascular disease as plant based nutrition.

Coumadin – Can I eat leafy greens when I am on Coumadin?
Coumadin (Warfarin) is an anti clotting drug shown to have significant benefit in protecting people with atrial fibrillation from having a stroke. Can patients on Coumadin eat all the green leafy vegetables with vitamin k, which may shorten their clotting time? The answer most emphatically is YES! Merely inform the physician who is monitoring the Coumadin and clotting time that you are regularly going to be eating copious amounts of healthy green leafy vegetables. He/she will appropriately adjust the Coumadin dose.

Juicing- Is it all right to juice?
Do not juice. You lose all the fiber and its benefits.

Fruit juice – What about fruit juice?
Drinking fruit juice is like pouring the sugar bowl down your throat. It is fine to eat the whole fruit. Do not drink the juice.

Smoothies – How about smoothies? I love them! 
Avoid smoothies. The fiber is so finely pureed that its helpful properties are potentially compromised. The sugar is separated from the fiber of the fruit, bypasses salivary digestion and results in a surge of glucose. The accompanying fructose contributes to inflammation, hypertension and endothelial injury.

A Fib- Will plant nutrition work for A Fib?
While A Fib is largely independent of nutrition, and is a heart rhythm abnormality, there are some subset of cases which are presumably related to less than optimal heart circulation. While it would be totally inappropriate for me to suggest plant – based nutrition would cure atrial fibrillation, the many ancillary benefits would indicate plant based nutrition would be of value.

Calcium score- Is a calcium score helpful?
With cardiac CT you get a big hit of radiation. If you have been eating the typical American diet, you already have heart disease as autopsy studies have shown.

SOURCE

http://www.heartattackproof.com/qanda.htm

Caldwell B. Esselstyn, Jr Speaking Schedule 2014

Engine 2 “Farms 2 Forks” Immersions – A chance to spend two days with Dr. Esselstyn Join Dr. Esselstyn, his wife Ann, his son Rip, and his daughter Jane at the Engine 2/Forks Over Knives’/”Farms 2 Forks” weekend retreats!  For three days, you can learn the medical, nutritional, psychological, and practical tools that you and your family can turn into a lifetime of good health and enjoyable food.   Joining the Esselstyn’s at events will be nutrition expert, Michael Greger MD, and Dr. Doug Lisle, food psychologist and author of “The Pleasure Trap”.  Special guest speakers will include Dr. Neal Barnard, Dr. John McDougall, and T. Colin Campbell. For more information or to register, visit the event website at www.farms2forks.com. Wednesday, February 5, 2014 Columbia Presbyterian Grand Rounds Myrna Daniels Auditorium, 1st floor Vivian & Seymour Milstein Family Heart Center 173 Fort Washington Ave New York City 12:00pm-1:00pm Open to the public Tuesday, February 11, 2014 Essy Cooper Clinic Dallas, Texas 4:00-5:00 for details contact Christine Dicken at 972-560-2667 Tuesday, February 18, 2014 E&A Twinsberg Library Twinsberg, Ohio 7:00 pm Friday, February 21- Sunday, 23, 2014 E&A McDougal Advanced Study Weekend Santa Rosa, California 800-941-7111 for details February 28th — March 2nd, 2014 E&A Engine 2 Phoenix Retreat Hyatt Regency Phoenix 122 North Second Street Phoenix, AZ 85004 Engine 2 and Forks Over Knives are kicking off the 2014 series in beautiful, sunny Phoenix, and are sure the warm, inviting February weather will bring people from across the country for a weekend of inspiration and change in the desert. We will be gathering at the Hyatt Regency, right in the middle of cosmopolitan downtown Phoenix, with easy access to the airport and everything that the city has to offer. With the Esselstyn family leading the way, we will tackle a myriad of topics designed to increase your plant-based knowledge, and send you home overflowing with information for yourself, your loved ones, your coworkers, and anyone else you encounter! For details: www.engine2diet.com Tuesday, March 11, 2014 Essy Cleveland Clinic Cleveland, Ohio Lerner NA5-08 12:00-1:00 Wednesday, March 19, 2014 Essy Cleveland Clinic Pediatric Grand Rounds A 11 800 conference room 4:00 pm Thursday, March 27, 2014 Essy Drury University Springfield, Missouri Health Care Forum Details:417-880-5001 Friday, April, 18, 2014 Essy Mayo Clinic Rochester, Minnesota 7:30 -8:30 am April 25th — April 27th, E&A Engine 2 Retreat Portland 2014 Hilton Portland & Executive Tower 921 Sixth Avenue Portland, OR 97204 If you haven’t been to Portland, Oregon, you are really missing out. Wait, here’s your chance! Engine 2 and Forks Over Knives are thrilled to bring an Engine 2 Retreat weekend to one of the most beautiful, green, and spectacular cities is America. We are setting up shop right smack in the middle of downtown Portland, which lies in the shadow of the majestic and awe-inspiring Mount Hood. Our location is an easy walking distance from all of the coffee shops, eclectic stores, and vibrant culture that this most “European” of American cities has to offer. For details: www.engine2diet.com Saturday, May 3, 2014 Essy Iowa Osteopathic Association DeMoine, Iowa Embassy Suite Hotel 9:00 Thursday, May, 15- Sunday, May 17 E&A Gold Symposium Boulder, Colorado Details: 303-625-2098 Sunday, May 18- Thursday May 22 E&A Engine 2 Retreat Sedona Sedona Hotel 3500 E. Bill Gray Road Sedona, AZ 86336 Rip Esselstyn invites you to join Engine 2 and Whole Foods Market team members in Sedona, Arizona in 2014 for a weeklong immersion intensive retreat, scheduled for May 17th — 23rd at the Sedona Mago Retreat Center. Featuring the all-star cast from our sold-out Engine 2 Retreat Weekends, this 7-day/6-night life-changing week will give you an in-depth medical & nutritional education about why & how to adopt a plant-strong lifestyle. In addition, the curriculum delves deeply into the psychological and practical methods & practices for successfully implementing sustainable lifestyle changes, with multiple lectures and breakout sessions led by esteemed doctor Caldwell B. Esselstyn, famed nutritionist Michael Greger, and renowned psychologist Doug Lisle. For details: www.engine2diet.com June 27th – 29th, 2014 E&A Engine 2 Retreat Chicago Double Tree Chicago – Oak Brook 1909 Spring Rd Oak Brook, IL 60523 Engine 2 and Forks Over Knives are thrilled to return to the Windy City for another wonderful inspiring and motivating plant-strong Engine 2 Retreat. We can’t get enough of the warm & welcoming midwestern hospitality, and we enjoy returning here each year. This year we’ll be just west of downtown Chicago in the wonderful suburb of Oak Brook, IL. With Rip as your host, we will tackle a myriad of topics designed to increase your plant-based knowledge. More For details: engine2diet.com August 16th – 17th, 2014 The Ultimate Weekend Experience: Plant-Stock E&A Engine 2 Retreat Claverack Esselstyn Family Farm 56 Willowdale Farms Claverack, NY 12513 On the Esselstyn family’s idyllic 400-acre farm in the beautiful Catskills, “Plant-Stock” brings you the ultimate plant-strong experience. We have lined up a rockstar roster to motivate and inspire you to take back your health. The weekend will feature all the plant-strong heavyweights, including Dr. Caldwell B. Esselstyn, Jr., T. Colin Campbell, Michael Moss, and many more special guests to be announced throughout the coming year. A rousing success last year, the event created a whole network of plant-strong ambassadors. We hope you will join us, take this information home with you, and put it into practice with your family, friends, and community! Be the change. For details: engine2diet.com Sunday, September 8 E&A Aspen Valley Hospital Cardiac Rehab opening Aspen, Colorado 1:00-4:00 Friday, September 12 – Sunday September 14, 2014 E&A Engine 2 Immersion Austin, Texas Details:engine2.com Thursday, September 18 – Saturday September 20 Essy Plant Based National Health Conference San Diego, California October 12th – 18th, 2014 E&A E2 Weeklong Immersion Intensive: Sedona, Arizona Sedona Hotel 3500 E. Bill Gray Road Sedona, AZ 86336 Rip Esselstyn invites you to join Engine 2 and Whole Foods Market team members in Sedona, Arizona in 2014 for a weeklong immersion intensive retreat, scheduled for October 12th – 18th at the Sedona Mago Retreat Center. Featuring the all-star cast from our sold-out Engine 2 Retreat Weekends, this 7-day/6-night life-changing week will give you an in-depth medical & nutritional education about why & how to adopt a plant-strong lifestyle. In addition, the curriculum delves deeply into the psychological and practical methods & practices for successfully implementing sustainable lifestyle changes, with multiple lectures and breakout sessions led by esteemed doctor Caldwell B. Esselstyn, Jr.famed nutritionist Michael Greger, and renowned psychologist Doug Lisle. For details: engine2diet.com Wednesday, October 23 – Sunday, October 26 E&A Lithuania  SOURCE http://www.heartattackproof.com/speaking_dates.htm

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Voices from the Cleveland Clinic: On the New Lipid Guidelines and On the ACC/AHA Risk Calculator

Posted in Atherogenic Processes & Pathology, Cardiovascular Pharmacogenomics, Chemical Biology and its relations to Metabolic Disease, Frontiers in Cardiology and Cardiovascular Disorders, Health Economics and Outcomes Research, HTN, Interviews with Scientific Leaders, Medical and Population Genetics, Nutritional Supplements: Atherogenesis, lipid metabolism, Origins of Cardiovascular Disease, Pharmacotherapy of Cardiovascular Disease, Population Health Management, Nutrition and Phytochemistry, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Systemic Inflammatory Response Related Disorders on January 21, 2014| Leave a Comment »

Voice from the Cleveland Clinic: On the New Lipid Guidelines and On the ACC/AHA Risk Calculator

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #107: Voices from the Cleveland Clinic: On the New Lipid Guidelines and On the ACC/AHA Risk Calculator. Published on 1/21/2014

WordCloud Image Produced by Adam Tubman

This article covers the following related topics:

I. Voices from Cleveland Clinic: Love ‘Em or Leave ‘Em: Experts on Both Sides Debate the New Lipid Guidelines

http://www.medscape.com/viewarticle/819288?nlid=45683_2562&src=wnl_edit_medp_card&uac=93761AJ&spon=2

II.  JAMA Weighs In on CVD Guidance, Statins in Primary Prevention

http://www.medscape.com/viewarticle/814960

III.  How Good Is the New ACC/AHA Risk Calculator?

http://www.medscape.com/viewarticle/814579

IV.  New Cholesterol Guidelines Abandon LDL Targets

http://www.medscape.com/viewarticle/814152

V. New CV Risk-Assessment Guidance Counts Stroke With CHD Risk

http://www.medscape.com/viewarticle/814206

VI.  NIH Says ATP 4, JNC 8 Guidance Out ‘in a Matter of Months’ (With a Twist)

http://www.medscape.com/viewarticle/806563

VII.  New European Hypertension Guidelines Released: Goal Is Less Than 140 mm Hg for All

http://www.medscape.com/viewarticle/806367

VIII.  New guidelines on primary stroke prevention from AHA/ASA

http://www.medscape.com/viewarticle/790766

IX.  New ACC/AHA/NHLBI Guidance on Lifestyle for CVD Prevention

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X. New Obesity Guidelines: Authoritative ‘Roadmap’ to Treatment

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XI.  USPSTF Updates Adult Obesity-Overweight Screening Guidelines

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Voices from the Cleveland Clinic: On the New Lipid Guidelines and On the ACC/AHA Risk Calculator

Love ‘Em or Leave ‘Em: Experts on Both Sides Debate the New Lipid Guidelines

Michael O’Riordan

January 20, 2014

DALLAS, TX and WASHINGTON, DC — It has been two months since the new clinical guidelines for the treatment of cholesterol were published^[1], and feedback is starting to slowly emerge as clinicians begin incorporating the recommendations into clinical practice.

The American College of Cardiology (ACC) and American Heart Association (AHA) guidelines, which were developed in conjunction with the National Heart, Lung, and Blood Institute (NHLBI), were a radical departure from previous iterations, most notably in their abandonment of LDL-cholesterol targets. In the past, clinicians were advised to treat patients with cardiovascular disease to less than 100 mg/dL or the optional goal of less than 70 mg/dL.

As reported by heartwire  at the time, the expert panel stated there was simply no evidence from randomized, controlled clinical trials to support treatment to a specific target. As a result, the new guidelines make no recommendations for specific LDL-cholesterol or non-HDL targets for the primary and secondary prevention of atherosclerotic cardiovascular disease.

Dr Stanley Hazen

For one clinician, Dr Stanley Hazen (Cleveland Clinic, OH), the strict adherence to only clinical-trial data is a limitation and not a strength of the new guidelines.

“First, it ignores a wealth of information on the pathophysiology of the disease process. Second, it presumes that the reason trials are designed is to answer guideline questions,” he told heartwire . “They aren’t. Trials are designed by pharmaceutical companies trying to get claims issued on their drugs. More important, the absence of randomized clinical-trial data does not justify inaction if LDL cholesterol remains elevated.”

Accelerating Vascular Age

In his commentary published January 8, 2014 in the Cleveland Clinic Journal of Medicine, Hazen, along with first author Dr Chad Raymond (Cleveland Clinic, OH), lay out their concerns with the clinical guidelines and highlight some of the shortcoming with the new recommendations^[2].

For Hazen, there are multiple reasons that physicians should continue to treat to specific LDL-cholesterol targets, the first and foremost being that patients are different and no single treatment fits such a large and heterogeneous patient population at risk for cardiovascular disease and stroke. The guidelines simply call for a moderate- or high-dose statin in high-risk patients depending on the clinical scenario and no subsequent assessment of LDL cholesterol.

“In the very highest-risk patients, the ones with extraordinarily high levels of cholesterol, those who get maximally tolerated statins, if there is still a substantial LDL-cholesterol burden, they are going to have substantial residual risk,” he said. “The preponderance of data in aggregate shows that there is higher residual risk proportionate to the LDL level that’s remaining. The new guidelines completely ignore the pathophysiology of the disease process—a disease that takes decades to develop.”

The clinical guidelines are unique among documents past in that the emphasis is strictly on statin therapy rather than LDL-cholesterol-lowering medications more generally. In individuals with atherosclerotic cardiovascular disease, high-intensity statin therapy—such as rosuvastatin (Crestor, AstraZeneca) 20 to 40 mg or atorvastatin 40 to 80 mg—should be used to achieve at least a 50% reduction in LDL cholesterol unless otherwise contraindicated or when statin-associated adverse events are present. In that case, doctors should use a moderate-intensity statin. Similarly, for those with LDL-cholesterol levels >190 mg/dL, a high-intensity statin should be used with the goal of achieving at least a 50% reduction in LDL-cholesterol levels.

For Hazen, the new clinical guidelines “turn back the clock on cardiovascular disease prevention” and have the potential to both overtreat older low-risk patients and undertreat those who are young yet are at higher lifetime risk.

For example, he cites a 25-year-old man who presents because his 45-year-old father just died from a heart attack. He has a fasting total cholesterol level of 310 mg/dL, HDL cholesterol of 50 mg/dL, triglyceride level of 400 mg/dL, and LDL cholesterol of 180 mg/dL. Even with the strong family history of premature coronary disease, because of his young age, the current guidelines do not suggest treatment because they do not apply to those less than 40 years old. However, even if his age were 40, his calculated 10-year risk would be <7.5% based on a new and controversial risk calculator published alongside the guidelines.

“I can’t imagine there is a lipidology expert or cardiologist out there who would think that this patient does not deserve aggressive preventive efforts and intervention,” said Hazen. “It is lifetime risk and lifetime exposure to higher LDL cholesterol that contributes to the disease process. Ignoring that scientific fact in a document whose focus is on treating cholesterol to prevent cardiovascular disease is simply illogical.”

A Massive Paradigm Shift

Speaking with heartwire , Dr James de Lemos (University of Texas Southwestern Medical Center, Dallas) suspects there remains some hesitancy on the part of practicing primary-care physicians to adopt the guidelines, mainly because they are a “massive paradigm shift that dramatically changes the approach to disease.” He said while there are always early adopters, there have been some questions as to which major journals and cardiology organizations would line up behind them (and nearly all have, with the exception of the American Association of Clinical Endocrinologists ).

For cardiologists, on the other hand, the shift to focus on four specific types of patients is not so dramatic, because these are patients they routinely see in clinical practice. For de Lemos, it is reasonable to focus on at-risk patients and treat according to that level of risk. He still incorporates measuring LDL-cholesterol levels, however, noting that the measurement can provide some reassurance or concern depending on the threshold achieved with treatment, dietary changes, and exercise.

Dr Mariel Jessup

To heartwire , Dr Mariel Jessup (University of Pennsylvania, Philadelphia), the president of the AHA, said that immediately following their publication many of her colleagues began implementing the guidelines and using the new calculator for risk assessment. In doing so, they identified patients on statins who did not require the lipid-lowering drugs as well as patients who weren’t on them but should be.

“In the first week, we were all coming to terms with what contributes to risk,” said Jessup. She added that she hasn’t heard a great deal of criticism about the guidelines and believes most physicians are getting on board with the new changes.

She noted that a member of the Penn faculty recently delivered medical grand rounds on the new lipid guidelines and while it was mostly positive, one criticism that arose was the emphasis on randomized, controlled clinical-trial data. Jessup said that even though the new guidelines focus on clinical-trial data, this does not negate findings from observational or epidemiological studies.

Dr Roger Blumenthal

Dr Roger Blumenthal (Johns Hopkins Ciccarone Preventive Cardiology Center, Baltimore, MD), on the other hand, predicts a return to LDL treatment goals in the not-so-distant future.

“I think the guidelines will revert back to the way they were once we get a positive study showing that adding another agent to a statin reduces risk,” Blumenthal said. He predicts positive results with anacetrapib (Merck, Whitehouse Station, NJ), the novel cholesteryl ester transfer protein (CETP) inhibitor, or one of the investigational proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, when given on top of statins. “When that happens, the new randomized controlled trial data would support going lower than what would be achieved with giving just 40 mg or 80 mg of atorvastatin.”

In very selected patients, Blumenthal still aggressively targets to low LDL levels, even if this requires adding a second agent. For example, in patients treated with a statin, LDL cholesterol might be reduced to 80 mg or so, but triglyceride levels remain high or HDL cholesterol is low. He notes that the ACCORD study with fenofibrate was borderline nonsignificant in patients with low HDL cholesterol and high triglyceride levels. Beyond fibrates, he notes there have been angiographic studies published in support of the “lower-is-better” hypothesis.

Jessup said that most physicians understand why the LDL targets were eliminated, but many institutions used the thresholds as a performance measure. Penn Health, for example, used the number of patients treated to the old LDL-cholesterol targets as an internal marker of performance for physicians in internal medicine and general practice. “As you struggle to come up with an easily defined target that you can use to talk about quality in a large practice, and not just among cardiologists, that’s one less target you can use,” said Jessup.

Concerns Among Clinicians as Well

Dr Rita Redberg

Dr Rita Redberg (University of California, San Francisco) also has significantconcerns about the new guidelines, albeit for entirely different reasons. An outspoken critic when the guidelines were presented, her views have not changed, telling heartwire that she is already looking forward to the next version of the cholesterol guidelines. When they were first published and presented, Redberg, along with Dr John Abramson (Harvard Medical School, Boston, MA), argued that statins were beneficial for individuals with heart disease but do not reduce the risk of death in individuals with a 10-year risk of cardiovascular disease of less than 20%.

“I have not been implementing these guidelines because I don’t think they’re in the best interests of my patients, and I really do look forward to the revisions,” she said. “I’m all for looking at risk, and I’m all for targeting prevention strategies on the basis of risk, so I think this is a strong point of the new guidelines. However, that is really undermined by the risk calculator, in which anybody over age 65 basically needs to be on a statin. I don’t think the data support this.”

The new cholesterol guidelines weathered a rough roll-out their first week when Drs Paul Ridker and Nancy Cook (Brigham and Women’s Hospital, Boston, MA) calculated the 10-year risk of cardiovascular events in three large-scale primary prevention cohorts—the Women’s Health Study(WHS), the Physicians’ Health Study (PHS), and the Women’s Health Initiative Observational Study (WHI-OS)—and found the new algorithm overestimated the risk by 75% to 150%.

Dr James de Lemos

To de Lemos, the controversial aspect of the new guidelines remains in the primary-prevention population. For those without cardiovascular disease but who have LDL-cholesterol levels ranging from 70 mg/dL to 189 mg/dL and a 10-year risk of cardiovascular disease >7.5%, physicians can initiate treatment with a statin. Given the controversy surrounding the risk calculator, there have been suggestions that people who don’t need statins will receive treatment.

“It doesn’t mean the concept is flawed,” de Lemos told heartwire , “but it just might not be ready to implement widely.” As a result, he suspects that physicians might be keeping the risk calculator at arm’s length until it is studied and debated further. As for his own use, de Lemos said he doesn’t calculate 10-year risk in every patient, even though he is fairly aggressive with initiating statin therapy, and that his decisions are more intuitive and empirical, something which he doesn’t see changing.

Jessup said the risk calculator, as well as the clinical guidelines, will be updated as new information emerges. While she was not able to speak to specifics, Jessup is aware of researchers testing the predictive strength of the risk calculator in different cohorts to see how well it performs. In general, she said the calculator performs reasonably well.

Some Docs Finding the Calculator Helpful

Dr Sekar Kathiresan

Dr Sekar Kathiresan (Brigham and Women’s Hospital, Boston, MA), who runs a primary-prevention clinic, does use the new clinical guidelines and the new risk calculator to inform his decisions about whether or not to start patients with a moderate- or high-dose statin. He said Ridker and Cook raise a valid scientific point in terms of how well it is calibrated, but this should be put in perspective, given that physicians for the past 20 years or so have used the Framingham Risk Score, a score derived from a few thousand white individuals from one town in the US. The new risk equation increases the population sampled, includes different ethnicities, and is derived from more than one geographic area.

“Is the pooled-cohort equation perfect?” he asked. “No, it won’t be perfect, because it’s an attempt to estimate risk on a sample of 25 000 people.”

Blumenthal made similar comments, telling heartwire that the risk calculator is a better way to estimate risk in women and African Americans, for example. Given that the risk calculator might overestimate risk, he expands his definition of intermediate risk to include patients with a 5% to 15% 10-year risk of cardiovascular disease. In doing so, even if the risk calculator overestimates by a factor of two, they have some wiggle room in discussing care with the patient.

In addition, Blumenthal said the guidelines emphasize a discussion with the patient about care in those with a 10-year risk exceeding 7.5%, just as would be done with an intermediate-risk patient. The discussion can lead to further refinement of risk by taking family history into account or by performing a computed tomography (CT) scan to assess coronary artery calcium (CAC).

To Kathiresan, moving away from LDL-cholesterol targets will require some time before they become readily accepted, mainly because physicians have gotten used to the targets. For the most part, though, he views the changes to the guidelines as more of a “tweak.”

“I don’t find them as radical as some people do,” Kathiresan told heartwire . “I actually think the major thing that was accomplished was taking the focus away from using medications to change lab tests and to now focus on medication proven to reduce the risk of disease. This is a huge plus for the new guidelines.”

In cardiology, the evidence base is very rich, with many trials and millions of dollars spent to evaluate whether specific medicines work to reduce disease risk in specific clinical situations, he added. This is the evidence that should be used to inform clinical practice. For this reason, he entirely agrees with the new focus on statins and not simply lipid-lowering agents.

“There is an incredible amount of inappropriate use of both niacin and fibrates in the US, all based on the fact that they change lab tests,” said Kathiresan. “The clinical-trial evidence for those two medicines is disappointingly poor.”

Hazen is a coinventor on pending and issued patents held by the Cleveland Clinic relating to cardiovascular diagnostics and therapeutics. He is a paid consultant to the Cleveland Heart Lab, Esperion, Liposciences, Merck, Pfizer, and Procter & Gamble. He has received research funds from Abbott, Astra Zeneca, Cleveland Heart Lab, Esperion, Liposciences, Procter & Gamble, and Takeda. In addition, he is entitled to royalty payments for inventions/discoveries related to cardiovascular diagnostics and therapeutics from Abbott Laboratories, Cleveland Heart Lab, Esperion, Frantz Biomarkers, and Liposciences . 

de Lemos acknowledges grant support from Roche Diagnostics and Abbott Diagnostics and has consulted for Diadexus. 

Kathiresan reports serving as a consultant to Merck, Pfizer, Celera, and Alnylam.

Jessup, Blumenthal, and Redberg report no conflicts of interest.

REFERENCES

1. Stone NJ, Robinson J, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association. J Am Coll Cardiol 2013. Article. Circulation 2013. Article.
2. Raymond C, Cho L, Rocco M, Hazen SL. New cholesterol guidelines: Worth the wait? Cleve Clin J Med 2014; DOI: 10.3949/ccjm.81a.13161. Article

SOURCE

http://www.medscape.com/viewarticle/819288#1

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Pathophysiological Effects of Diabetes on Ischemic-Cardiovascular Disease and on Chronic Obstructive Pulmonary Disease (COPD)

Posted in Atherogenic Processes & Pathology, Best evidence, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, Cardiovascular Research, Curation, Curation methodology, Diabetes Mellitus, Discovery process, Evidence-based decision-making, Evolutionary cognition, Experimental validation, Explanatory, Frontiers in Cardiology and Cardiovascular Disorders, Health Economics and Outcomes Research, Human Immune System in Health and in Disease, Indigent Nutrition, Innovation in Immunology Diagnostics, International Global Work in Pharmaceutical, Interviews with Scientific Leaders, Medicare and Medicaid, Metabolomics, Nephrology, Neurohumoral Transmission, Nitric Oxide in Health and Disease, Nutrition, Nutritional Supplements: Atherogenesis, lipid metabolism, Origins of Cardiovascular Disease, Pharmacotherapy of Cardiovascular Disease, Population Health Management, Genetics & Pharmaceutical, Population Health Management, Nutrition and Phytochemistry, Proteomics, Systemic Inflammatory Response Related Disorders, Theoretic convergence, Translational Effectiveness, Translational Research, Translational Science, Uninsured and Underinsured, tagged AMI, Arterial stiffness, comorbidities - type 2 DM, COPD, coronary vascular disease, Diabetes management, Diabetes mellitus type 2, hs-CPR, Nutrition and Metabolism Disorders, Nutritional Supplements, prediabetes, proinflammatory, statins, waist circumference on January 15, 2014| Leave a Comment »

Pathophysiological Effects of Diabetes on Ischemic-Cardiovascular Disease and on Chronic Obstructive Pulmonary Disease (COPD)

Curator:  Larry H. Bernstein, MD, FCAP

Article ID #106: Pathophysiological Effects of Diabetes on Ischemic-Cardiovascular Disease and on Chronic Obstructive Pulmonary Disease (COPD). Published 1/15/2014

WordCloud Image Produced by Adam Tubman

This is a multipart article that develops the pathological effects of type-2 diabetes in the progression of a systemic inflammatory disease with a development of neuropathy, and fully developing into cardiovascular disease.  It also identifies a systemic relationship to the development of chronic obstructive pulmonary disease (COPD).

The more we learn about diabetes, we learn about its generalized systemic effects.

This article has the following SIX Parts:

Part 1. Role of Autonomic Cardiovascular Neuropathy in Pathogenesis of ischemic heart disease in patients with diabetes mellitus

Part 2. A Longitudinal Cohort Study of the Cardiovascular Experience of Individuals at High Risk for Diabetes

Part 3.  Clinical significance of cardiovascular dysmetabolic syndrome

Part 4.   Waist circumference a good indicator of future risk for type 2 diabetes and cardiovascular disease

Part 5.   How to use C-reactive protein in acute coronary care

Part 6.  Chronic obstructive pulmonary disease and glucose metabolism: a bitter sweet symphony

INTRODUCTION

Type 2 diabetes mellitus is a common chronic disease which develops insidiously over time, and is associated with obesity, nutritional imbalance (high fructose beverages, high starch and processed foods, carbohydrate excess intake, and an imbalance of proinflammatory to anti-inflammatory polyunsaturated  fatty acids), which makes it an acquired and manageable disease.  The long term effects of T2DM is played out on cardiovascular disease and stroke-risk, obstructive sleep apnea, progressive renal insufficiency, development of neuropathy, congestive heart failure and chronic obstructive pulmonary disease, all of which are occuring related to an systemic inflammatory condition that proceeds for some time prior to the identification of overt diabetes.
A detailed story of a significant part of these associations continues in the SIX Part series.

Part 1. Role of Autonomic Cardiovascular Neuropathy in Pathogenesis of ischemic heart disease in patients with diabetes mellitus

This article is an abstract only of a related publication of the pathogenesis of autonomic neuropathy in diabetics leading to ischemic heart disease.

Subjects: Medicine (General), Medicine, Medicine (General),
Health Sciences Authors: Popović-Pejičić Snježana, Todorović-Đilas Ljiljana, Pantelinac Pavle
Publisher: Društvo lekara Vojvodine Srpskog lekarskog društva
Publication: Medicinski Pregled 2006; 59(3-4): Pp 118-123 (2006) ISSN(s): 0025-8105  Added to DOAJ: 2010-11-11
http://dx.doi.org/10.2298/MPNS0604118P  http://www.doiserbia.nb.rs/img/doi/0025-8105/2006/0025-81050604118P.pdf

Keywords: diabetes mellitus, autonomic nervous system diseases, heart diseases, myocardial ischemia, comorbidity

Introduction.

Diabetes is strongly associated with macrovascular complications, among which

• ischemic heart disease is the major cause of mortality.

Autonomic neuropathy increases the risk of complications, which calls for an early diagnosis. The aim of this study was to determine

• both presence and extent of cardiac autonomic neuropathy,

in regard to the type of diabetes mellitus, as well as

• its correlation with coronary disease and
• major cardiovascular risk factors.

Material and methods. We have examined 90 subjects, classified into three groups, with 30 patients each: those with type 1 diabetes, type 2 diabetes and control group of healthy subjects. All patients underwent

• cardiovascular tests (Valsalva maneuver, deep breathing test, response to standing, blood pressure response to standing sustained, handgrip test),
• electrocardiogram,
• treadmill exercise test and
• filled out a questionnaire referring to major cardiovascular risk factors: smoking, obesity, hypertension, and dyslipidemia.

Results. Our results showed that cardiovascular autonomic neuropathy was

• more frequent in type 2 diabetes,
• manifesting as autonomic neuropathy.

In patients with autonomic neuropathy, regardless of the type of diabetes,

• the treadmill test was positive, i.e. strongly correlating with coronary disease.

In regard to coronary disease risk factors,

• the most frequent correlation was found for obesity and hypertension.

Discussion

Cardiovascular autonomic neuropathy is considered to be the principal cause of arteriosclerosis and coronary disease. Our results showed that the occurrence of cardiovascular autonomic neuropathy increases the risk of coronary disease due to dysfunction of autonomic nervous system.

Conclusions

Cardiovascular autonomic neuropathy is a common complication of diabetes that significantly correlates with coronary disease. Early diagnosis of cardiovascular autonomic neuropathy points to increased cardiovascular risk, providing a basis for preventive and therapeutic measures.

Part 2. A Longitudinal Cohort Study of the Cardiovascular Experience of Individuals at High Risk for Diabetes

This second part is a description of a longitudinal cohort study of individuals at high-risk for diabetes.  Unlike the SSA study, the study is not focused on protein-energy malnutrition.

Protocol for ADDITION-PRO: a longitudinal cohort study of the cardiovascular experience of individuals at high risk for diabetes recruited from Danish primary care

Subjects: Public aspects of medicine, Medicine, Public Health, Health Sciences
Authors: Johansen NB, Hansen Anne-Louise S, Jensen TM, Philipsen A, Rasmussen SS, Jørgensen ME, Simmons RK, Lauritzen T, Sandbæk A, Witte DR
Publisher: BioMed Central    Date of publication: 2012 Dec Published in: BMC Public Health 2012; 12(1): 1078    ISSN(s): 1471-2458   Added to DOAJ: 2013-03-12 http://dx.doi.org/10.1186/1471-2458-12-1078       http://www.biomedcentral.com/1471-2458/12/1078

Keywords: Diabetes, Cardiovascular disease, Primary care, Complications, Microvascular, Impaired fasting glucose, Impaired glucose intolerance, Aortic stiffness, Physical activity, Body composition

Background

Screening programmes for type 2 diabetes inevitably find more individuals at high risk for diabetes than people with undiagnosed prevalent disease. While well established guidelines for the treatment of diabetes exist, less is known about treatment or prevention strategies for individuals found at high risk following screening. In order to make better use of the opportunities for primary prevention of diabetes and its complications among this high risk group, it is important to

• quantify diabetes progression rates and to examine
• the development of early markers of cardiovascular disease and
• microvascular diabetic complications.

We also require a better understanding of the

• mechanisms that underlie and drive early changes in cardiometabolic physiology.

The ADDITION-PRO study was designed to address these issues among individuals at different levels of diabetes risk recruited from Danish primary care.

Methods/Design

ADDITION-PRO is a population-based, longitudinal cohort study of individuals at high risk for diabetes. 16,136 eligible individuals were identified at high risk following participation in a stepwise screening programme in Danish general practice between 2001 and 2006.

• All individuals with impaired glucose regulation at screening,
• those who developed diabetes following screening, and
• a random sub-sample of those at lower levels of diabetes risk

were invited to attend a follow-up health assessment in 2009–2011 (n = 4,188), of whom 2,082 (50%) attended. The health assessment included

• detailed measurement of anthropometry,
• body composition,
• biochemistry,
• physical activity and
• cardiovascular risk factors including aortic stiffness and central blood pressure.

All ADDITION-PRO participants are being followed for incident cardiovascular disease and death.

Discussion

The ADDITION-PRO study is designed to increase

• understanding of cardiovascular risk and
• its underlying mechanisms among individuals at high risk of diabetes.

Key features of this study include

• (i) a carefully characterised cohort at different levels of diabetes risk;
• (ii) detailed measurement of cardiovascular and metabolic risk factors;
• (iii) objective measurement of physical activity behaviour; and
• (iv) long-term follow-up of hard clinical outcomes including mortality and cardiovascular disease.

Results will inform policy recommendations concerning cardiovascular risk reduction and treatment among individuals at high risk for diabetes. The detailed phenotyping of this cohort will also allow a number of research questions concerning early changes in cardiometabolic physiology to be addressed.

Part 3.  Clinical significance of cardiovascular dysmetabolic syndrome

This study also addresses the issue of diabetes insulin resistance leading to cardiovascular dysmetabolic syndrome.

Subjects: Diseases of the circulatory (Cardiovascular) system,
Specialties of internal medicine, Internal medicine, Medicine, Cardiovascular, Medicine (General), Health Sciences
Authors: Deedwania Prakash C Publisher: BioMed Central            Date of publication: 2002 Jan
Published in: Trials 2002; 3: 1(2)   ISSN(s): 1468-6708  Added to DOAJ: 2004-06-03
http://dx.doi.org/10.1186/1468-6708-3-2   http://cvm.controlled-trials.com/content/3/1/2

Keywords: cardiovascular dysmetabolic syndrome, coronary heart disease, diabetes mellitus, hyperinsulinemia, insulin resistance

Although diabetes mellitus is predominantly a metabolic disorder,

• recent data suggest that it is as much a vascular disorder.
• Cardiovascular complications are the leading cause
  • of death and disability in patients with diabetes mellitus.

A number of recent reports have emphasized that

• many patients already have atherosclerosis in progression
• at the time they are diagnosed with clinical evidence of diabetes mellitus.

The increased risk of atherosclerosis and cardiovascular complications in diabetic patients is related to

• the frequently associated dyslipidemia, hypertension, hyperglycemia, hyperinsulinemia, and endothelial dysfunction.

The evolving knowledge regarding the variety of

• metabolic,
• hormonal, and
• hemodynamic abnormalities in patients with diabetes mellitus

has led to efforts designed for early identification of individuals at risk of subsequent disease. It has been suggested that

• insulin resistance, the key abnormality in type II diabetes,
• often precedes clinical features of diabetes by 5–6 years.

Careful attention to the criteria described for the cardiovascular dysmetabolic syndrome

• should help identify those at risk at an early stage.

The application of nonpharmacologic as well as newer emerging pharmacologic therapies can have beneficial effects

• in individuals with cardiovascular dysmetabolic syndrome and/or diabetes mellitus
• by improving insulin sensitivity and related abnormalities.

Early identification and implementation of appropriate therapeutic strategies would be necessary

• to contain the emerging new epidemic of cardiovascular disease related to diabetes.

Part 4.   Waist circumference a good indicator of future risk for type 2 diabetes and cardiovascular disease

Subjects: Public aspects of medicine, Medicine, Public Health, Health Sciences
Authors: Siren Reijo, Eriksson Johan G, Vanhanen Hannu
Publisher: BioMed Central      Date of publication: 2012 Aug
Published in: BMC Public Health 2012; 12: 1(631)    ISSN(s): 1471-2458   Added to DOAJ: 2013-03-12
http://dx.doi.org/10.1186/1471-2458-12-631    http://www.biomedcentral.com/1471-2458/12/631

Keywords: Waist circumference, Type 2 diabetes, Cardiovascular disease, Middle-aged men

Background

Abdominal obesity is a more important risk factor than overall obesity in

• predicting the development of type 2 diabetes and cardiovascular disease.

From a preventive and public health point of view it is crucial that

• risk factors are identified at an early stage,
• in order to change and modify behaviour and lifestyle in high risk individuals.

Methods

Data from a community based study was used to assess

• the risk for type 2 diabetes,
• cardiovascular disease and
• prevalence of metabolic syndrome in middle-aged men.

In order to identify those with increased risk for type 2 diabetes and/or cardiovascular disease

• sensitivity and specificity analysis were performed, including
• calculation of positive and negative predictive values, and
• corresponding 95% CI for eleven different cut-off points,
  • with 1 cm intervals (92 to 102 cm), for waist circumference.

Results

A waist circumference ≥94 cm in middle-aged men,

• identified those with increased risk for type 2 diabetes
• and/or for cardiovascular disease

with a sensitivity of 84.4% (95% CI 76.4% to 90.0%), and a specificity of 78.2% (95% CI 68.4% to 85.5%). The positive predictive value was 82.9% (95% CI 74.8% to 88.8%), and negative predictive value 80.0% (95% CI 70.3% to 87.1%), respectively .

Conclusions

Measurement of waist circumference in middle-aged men

• is a reliable test to identify individuals at increased risk for type 2 diabetes and cardiovascular disease.

This measurement should be used more frequently in daily practice in primary care

• in order to identify individuals at risk and when planning health counselling and interventions.

Part 5.  How to use C-reactive protein in acute coronary care

Luigi M. Biasucci, Wolfgang Koenig, Johannes Mair, Christian Mueller, Mario Plebani, Bertil Lindahl, Nader Rifai,Per Venge,Christian Hamm, and the Study Group on Biomarkers in Cardiology of the Acute Cardiovascular Care Association of the European Society of Cardiology
Department of Cardiology B, Aarhus University Hospital, Tage Hansens Gade2, Aarhus DK-8000,Denmark; Germany, U.K., U.S., Italy
European Heart Journal Advance Access published Nov 7, 2013.  Current Opinion.  http://dx.doi.org/10.1093/eurheartj/eht435

Introduction

 C-reactive protein (CRP) is an acute phase protein and an established marker for detection, risk stratification, and monitoring of infections, and inflammatory and necrotic processes.. Because C-reactive protein is sensitive but not specific, its values must be nterpreted  in the clinical context. Inpatients with acute myocardial infarction (AMI), CRP increases within 4–6h of symptoms, peaks 2–4 days later,and returns to baseline after 7–10 days.

CRP has gained interest recently as a marker for risk stratification in acute coronary syndrome (ACS) when measured by high-sensitivity CRP assays. These assays have greater analytical sensitivity and reliably measure CRP concentrations within the reference range with low imprecision (5–10%). Because of evidence that atherosclerosis is an inflammatory disease, high-sensitivity CRP can be used as a biomarker of risk
in primary prevention and in patients with known cardiovascular disease. The aim of this review is to evaluate the use of CRP in patients with acute coronary disease.

The in-vitro stability of high-sensitivity C-reactive protein is excellent. Specific blood sampling conditions aren’t necessary.  However, retesting may be necessary with some assays if there is marked lipaemia.  Baseline and subsequent measures are in good for agreement for risk stratification despite biological variability of 30–60%.

The upper reference limit is method-dependent but usually 8mg/L for standard assays. The distribution of high-sensitivity CRP concentrations is skewed in both genders with a 50th percentile of_1.5mg/L (excluding women on hormone replacement therapy). Race differences have been reported. Most studies have reported no relationship with age,  but to circadian and seasonal variation. CRP concentrations are increased by smoking, obesity, and hormone replacement therapy and reduced by exercise, moderate alcohol drinking, and statin use. Correction for these factors is essential in reference range studies. CRP assays are not standardized. We recommend  the use of third-generation high-sensitivity CRP assays that combine features of standard and high-sensitivity CRP assays.  Required assay precision should be < 10% in the range of 3 and 10 mg/L.

Biochemical and analytical issues

Critical clinical concepts

(1) CRP concentrations are reported in mg/L
(2) CRP test results are method-dependent

•  classification of patients into risk categories is usually comparable

(3) Third generation CRP assay are recommended
(4) No specific patient preparation before blood sampling is necessary
(5) The in-vitro stability of CRP is high

This is only a portion of the published concensus document. What is relevant to this discussion is that the hs-CRP is an extremely valuable marker for inflammatory disease.  It is not ordered often enough because of the broad range of values that we have become accustomed to for years, and it is elevated in rheumatologic conditions, but even then, it is widely used in pediatrics because children may present with rapidly emergent sepsis with very minimal sympoms.
The hs-CRP has opened a window to subliminal inflammatory disease that is diabetes, with accompanied arteriolar endothelial inflammation.

Part 6.  Chronic obstructive pulmonary disease and glucose metabolism: a bitter sweet symphony

Subjects: Diseases of the circulatory (Cardiovascular) system,
Specialties of internal medicine, Internal medicine, Medicine, Cardiovascular, Medicine (General), Health Sciences
Authors: Mirrakhimov Aibek E
Publisher: BioMed Central      Date of publication: Oct 2012   ISSN(s): 1475-2840
Published in: Cardiovascular Diabetology 2012; 11(1):132   Added to DOAJ: 2013-03-12
http://dx.doi.org/10.1186/1475-2840-11-132      http://www.cardiab.com/content/11/1/132

Keywords: COPD, Dysglycemia, Insulin resistance, Obesity, Metabolic syndrome, Diabetes mellitus endothelial dysfunction, Vasculopathy

Chronic obstructive pulmonary disease, metabolic syndrome and diabetes mellitus

• are common and underdiagnosed medical conditions.

It was predicted that chronic obstructive pulmonary disease

• will be the third leading cause of death worldwide by 2020.

The healthcare burden of this disease is even greater

• if we consider the significant impact of chronic obstructive pulmonary disease on
  • the cardiovascular morbidity and mortality.

Chronic obstructive pulmonary disease

• may be considered as a novel risk factor for new onset type 2 diabetes mellitus via

multiple pathophysiological alterations such as:

1. inflammation and oxidative stress,
2. insulin resistance,
3. weight gain and
4. alterations in metabolism of adipokines.

On the other hand, diabetes may act as an independent factor,

• negatively affecting pulmonary structure and function.

Diabetes is associated with an increased risk of

1. pulmonary infections,
2. disease exacerbations and
3. worsened COPD outcomes.

On the top of that, coexistent OSA

• may increase the risk for type 2 DM in some individuals.

The current scientific data necessitate a greater outlook on chronic obstructive pulmonary disease and

• chronic obstructive pulmonary disease may be viewed as a risk factor for
• the new onset type 2 diabetes mellitus.

Conversely, both types of diabetes mellitus should be viewed as

• strong contributing factors for the development of obstructive lung disease.

Such approach can potentially improve the outcomes and medical control for both conditions,

• and, thus, decrease the healthcare burden of these major medical problems.

CONCLUSIONS

This discussion  presents a spectrum of cardiovascular risk associated with type 2 diabetes mellitus, with high risk for CVD, stroke, endothelial dysfunction, and an association with obesity, measured by waist circumference, and an underlying proinflammatory state that can be measured by CRP.

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