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Archive for the ‘Population Health Management, Nutrition and Phytochemistry’ Category

Food Insecurity in Africa and GMOs

Reporter and Curator: Larry H. Bernstein, MD, FCAP 

Article ID #103: Food Insecurity in Africa and GMOs. Published on 1/13/2014

WordCloud Image Produced by Adam Tubman

 

This Report is a presentation from several articles since mid-2013 on the food shortage in Sub-Saharan Africa, where crop yields are among the lowest in the worlds.  In this series we have presented modiable  and epigenetic causes of CVD, among other topics, including diabetes, obesity, and exercise.  We have mentioned that while magnesium, fiber, a sufficient source of n-3 polyunsaturated fatty acids (from seafood or seaweed, or from flaxseed), and a functional methyl transporter as well as a source of methionine ( which requires a meat source, as B9 folate is plant sourced and does not fix the problem).  In this discussion we have both a voluntary and an involuntary course of living that leads to CVD and brain dysfunction, depending on where one lives, a “perfect storm”.

Part 1.  Tensions over Food Insecurity in Africa   Oct 8, 2013

Sharon Schmickle

Sub-Saharan Africa’s agricultural yields are among the lowest in the world, and nearly one-third of its people are malnourished. That much, tragically, is well established. Less clear are the reasons Africa’s farm output remains depressed despite hands-on work and billions of dollars invested by individuals, organizations and governments. News reports often explore specific aspects of the problem such as drought. This series takes the novel approach of looking at intertwined tensions underlying the many problems. Through stories told across the continent, Sharon Schmickle focus on several key themes:

  • Africa is caught in an ideological struggle over the nature and scope of agriculture with European—and, sometimes, American—organizations pitted against agribusiness and many agricultural scientists.
  • Institutions have failed African farmers. Public and private agencies often work at cross purposes, neglecting to follow through on crop-saving opportunities. Investments in research and agricultural extension have been inadequate.

Scientists have made impressive gains against the scourges that threaten crops. But they risk losing their breakthroughs against malnutrition, crop-destroying pests and drought if they overlook local tastes and customs.

The series, which also incorporates the work of local journalists, begins with an overview of Tanzania where government officials are divided in the global ideological standoff. Despite a government initiative called Kilimo Kwanza (Farmers First), many farmers lack access to the improved seeds and tissue cultures that could help them thwart yield-stealing diseases and pests. And many farmers are so locked into practices of the past that change comes hard if at all.

This narrative is not twisted to an anti-GMO slant, and could be viewed as a need for GMO harvests without the independence to develop them, and the struggle against a powerful industrial source that takes from an impoverished people.

Sharon Schmickle has been a journalist for MinnPost.com since 2007, and before that she worked for the Minneapolis Star Tribune where she reported from the paper’s Washington bureau…

http://pulitzercenter.org/sites/default/files/styles/responsive_cropped/public/09-16-13/1382/lunch_line_at_engaruka_primary_school_0.jpg

Roiling tensions underlie efforts to improve food security in Africa, often pulling at cross purposes on farmers, consumers and their countries.

Tanzania: Mixed Feelings on Genetically Modified Crops
Tanzania faces the question of whether food from GM crops will sell at markets like this one in Dar es Salaam. Image by Sharon Schmickle. Tanzania, 2013.

Part 2.  Nathanael Johnson lets the anti-GMO movement off the hook

By MICHAEL EISEN | Published: JAN 10, 2014

For the last six months, Nathanael Johnson has been writing about GMOs for the lefty environmental magazine Grist. The goal of his ultimately 26 part series was to try and bring some journalistic sanity to a topic that has gotten nasty in recent years. As Grist editor Scott Rosenberg is quoted on Dan Charles’ blog:
GMOs “were a unique problem for us,” says Rosenberg. On the one hand, most of Grist’s readers and supporters despise GMOs, seeing them as a tool of corporate agribusiness and chemical-dependent farming.

On the other hand, says Rosenberg, he’d been struck by the passion of people who defended this technology, especially scientists. It convinced him that the issue deserved a fresh look.

I’ve enjoyed reading the series. Johnson has investigated a wide range of issues related to GMOs with a generally empirical eye – trying to find data to help answer questions, while avoiding the polemicism that dominates discussions of the topic. Although I don’t think everything he has written is right, the series is a very useful starting point for people trying to wrap the heads around what can be a complex topic. He has clearly tried to delve deeply into every topic, and to not let dogma or propaganda from either side affect his conclusions.

Unfortunately, if the series has had an effect on what I presume is its target audience – the anti-GMO readers of Grist – it hasn’t shown up in online debates about GMOs. When I and others have pointed to Johnson’s series in response to outrageous statements from anti-GMO campaigners, he is dismissed as either a naive fool or just another Monsanto tool.

So I was surprised to read his concluding piece in the series, “What I learned from six months of GMO research: None of it matters“.

The most astonishing thing about the vicious public brawl over GMOs is that the stakes are so low.

His basic point is that a lot of hot air and political energy is spent trying to decide between two alternative futures that aren’t all that different.

In the GMO-free future, farming still looks pretty much the same. Without insect-resistant crops, farmers spray more broad-spectrum insecticides, which do some collateral damage to surrounding food webs. Without herbicide-resistant crops, farmers spray less glyphosate, which slows the spread of glyphosate-resistant weeds and perhaps leads to healthier soil biota. Farmers also till their fields more often, which kills soil biota, and releases a lot more greenhouse gases.

The banning of GMOs hasn’t led to a transformation of agriculture because GM seed was never a linchpin supporting the conventional food system: Farmers could always do fine without it. Eaters no longer worry about the small potential threat of GMO health hazards, but they are subject to new risks: GMOs were neither the first, nor have they been the last, agricultural innovation, and each of these technologies comes with its own potential hazards. Plant scientists will have increased their use of mutagenesis and epigenetic manipulation, perhaps. We no longer have biotech patents, but we still have traditional seed-breeding patents. Life goes on.

In the other alternate future, where the pro-GMO side wins, we see less insecticide, more herbicide, and less tillage. In this world, with regulations lifted, a surge of small business and garage-biotechnologists got to work on creative solutions for the problems of agriculture.

Genetic engineering is just one tool in the tinkerer’s belt. Newer tools are already available, and scientists continue to make breakthroughs with traditional breeding. So in this future, a few more genetically engineered plants and animals get their chance to compete. Some make the world a little better, while others cause unexpected problems. But the science has moved beyond basic genetic engineering, and most of the risks and benefits of progress are coming from other technologies. Life goes on.

In many ways he’s right. GMOs on the market today – and most of the ones planned – are about making agriculture more efficient and profitable for farmers and seed providers. This is not a trivial thing, but would global agriculture collapse without these GMOs? Of course not.

We rarely see transformative technologies coming. And remember that we are still in the very early days of genetic engineering of crops and animals. I suspect that you could go back and look at the early days of almost any new technology and convincingly downplay its transformative potential.

Most new technologies ultimately fail to deliver. But the proper stance to take is to say that we just don’t know. What we do know is that there are many pressing and complex problems facing the future of agriculture. And, given that there is no compelling reason not to allow GM techniques to proceed, why take this tool out of the hands of scientists?

People care about GMOs because they symbolize corporate control of the food system, or unsustainable agriculture, or the basic unhealthiness of our modern diet. On the other side, people care about GMOs because they symbolize the victory of human ingenuity over hunger and suffering, or the triumph of market forces, or the wonder of science.

What is most disturbing about the GMO debate – and why it matters – is that the anti-GMO movement at almost every turn rejects empiricism as a means of understanding the world and making decisions about it. GMO opponents have largely rejected Johnson and his series.

They do not appear to believe that the kind of questions that Johnson asks – “Does insect resistant corn reduce the amount of insecticide used on farms?” – can even be asked. They already know the answer, and are completely unmoved by evidence.

The world faces so many challenges now, and we can only solve them if we believe that the world can be understood by studying it, that we can think up and generate possible solutions to the challenges we face, and that we can make rational decisions about which ones to use or not to use.

– See more at: http://www.michaeleisen.org/blog/?p=1530#sthash.GVFidZev.dpuf

Part 3.  Africa: Context is Crucial to Seeing Challenge of Hunger

October 17, 2013 / Des Moines Register
http://pulitzercenter.org/sites/default/files/styles/slideshow/public/10-16-13/farmerprocessingmilkintobutter640.jpg

Women farmers are processing more of their milk. Image by Sharon Schmickle. Tanzania, 2013.

To understand food security in sub-Saharan Africa, context is crucial. Some 500 million small farms feed 80 percent of the people who live in regions that are perilously close to hunger.
Published Oct 17, 2013  SHARON SCHMICKLE

Iowans who take in this year’s World Food Prize Borlaug Dialogue in Des Moines can gain a wealth of expert perspectives on the important challenge of nourishing a growing world population during the next century.
Learning the full measure of the challenge, though, calls for reaching beyond the lectures and panel discussions — reaching into the local reasons it has been so difficult to achieve global food security.
Context is crucial in a world where some 500 million small farms feed 80 percent of the people who live in regions that are perilously close to hunger.
To visit farms in those regions is to learn why it has been so difficult to stand up to the moral challenge the late Norman Borlaug delivered time and again, insisting that access to adequate food is a basic human right.
It is to meet female farmers like Sharifa Said Nambanga, who struggles to feed five children with the rice she can grow on a small plot in Zanzibar. Women do a hefty share of the farm work around the world. Often, though, they are shut off from the extension services that should deliver improved seeds, fertilizer and the know-how to use agriculture’s modern methods. Feeling abandoned, they limp along as best they can on their own.
It is to meet pastoralists like Parmelo Ndiimu. He is a Maasai elder who watches helplessly while the trees he needs to feed his goats are cut to make charcoal for cooking in urban kitchens. “If we won’t be able to feed our goats, we will not be able to feed our children,” Ndiimu said. “And we will be gone.”
It is to meet Tanzanian farmers who work their small plots throughout a full growing season only to see weevils destroy half their bean harvest. They know firsthand the tension between farmers and the ever evolving pests that attack crops in the field and after harvest.
It is to see corn planted from family seed wither in the field, stalks barren and green leaves giving way to limp yellow strips. Theoretically, the simple remedy should be improved seeds. But nothing is simple in the process of getting those improved seeds to small-scale farmers, especially when the improvement involved genetic modification of the plants.
In his later years, Borlaug addressed context in sub-Saharan Africa, recognizing that along with improved seed, farmers also needed to knock down barriers in their marketing, storage and processing systems. He challenged African leaders to invest more in agriculture.
Within that framework, it is clear that millions of small-scale farmers — especially those in Africa — operate amid tensions that limit their opportunities to extract more food from the technology that has filled porridge bowls and bread baskets elsewhere.

Part 4. Betting on the Impact of Synthetic Biology In Healthcare – By Jenny Rooke

Jenny Rooke drives innovation in the life sciences field through investing and business building around brilliant scientists and engineers with novel technologies. Prior, Jenny held multiple executive roles at U.S. Genomics.

I am an ardent believer in the potential of synthetic biology – its technologies, methods, and talented practitioners – to transform human life on just about every dimension: What we eat, how we make things, the character of our environment and how we move through it, how we are born, and, eventually, how long we live.

My more circumspect investor side is forced to admit that the evidence base of practical (not to mention profitable) applications of synthetic biology remains, shall we say, a work in progress. The first wave of synthetic biology companies that focused on energy/biofuels has been largely disappointing commercially, despite some notable technical successes, due in part to challenges related to scale-up, feedstock economics, and distribution.

It seems reasonable to search for proof cases of synthetic biology’s utility in human health; after all, the vast majority of biotechnology’s impact to date (practically and financially) has been in healthcare, including the creation of entirely novel categories of therapeutics and molecular diagnostics.

To be fair, it’s early yet to expect too many synthetic biology success stories in medicine. Synthetic biology as a field is just over a decade old and if it takes on average a decade for a new drug to move from the lab to the market, well, the math is obvious. In addition, there remain a great deal of technical, clinical, and safety risk inherent to applying synthetic biology technologies to human health problems (consider the painful lessons from the analogous field of gene therapy). This helps explain the reluctance of incumbent healthcare companies and traditional healthcare investors to make big bets on synthetic biology until the technology’s practical utility is more proven.

In 2011 and 2012, the Bill & Melinda Gates Foundation put out a call for grant applications to “Apply Synthetic Biology to Global Health Challenges” under its Global Health division, which aims to harness advances in science and technology to save lives in developing countries. The foundation’s Grand Challenges Explorations, or GCE, program is an ideal mechanism for fostering applications of synthetic biology.

Synthetic biology will play a critical role in enabling novel, affordable healthcare solutions for developing countries. Image source: GrandChallenges.org

For more information on the Grand Challenges in Global Health program, including a brief description of each project and a discussion of observed themes, see the review article “Synthetic biology as a source of global health innovation” (Syst Synth Biol (2013) 7:67–72).

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Endothelial Dysfunction (release into the circulation of damaged endothelial cells) as A Risk Marker for Ischemia and MI

Reporter and Curator: Larry H Bernstein, MD, FCAP

Endothelial Dysfunction: An Early Cardiovascular Risk Marker in Asymptomatic Obese Individuals with Prediabete

AK Gupta, E Ravussin, DL Johannsen, AJ Stull,WT.Cefalu and WD Johnson at Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA Brit J Med & Med Res 2012; 2(3):413-423 [www.ScienceDomain.org]

provides an exceedingly interesting insight into the relationship between type 2 diabetes mellitus, obesity and risk for cardiovascular disease in patients who are asymptomatic prediabetics, defined as a fasting blood glucose between 1000 and 1240 mg/L, or a Hb A1c (may not accurate for African Americans) between 5.6 and 6.5.  They would be expected to show an abnormal 5-hr GTT.

Obesity is associated with the release from adipocytes of adiponectin, which it has been reported is countered by resistin.  We might also have the effect of the insulin secreting beta cell, that releases insulin without a relationship to an anabolic function, through IGF-1 related to feedback to the pituitary GH, which takes a dominant catabolic role. Thus, insulin resistance. This is an oversimplification, and far greater depth is found elsewhere.

This study is consistent with another study on  Metabolism Influences Cancer

Reuben Shaw, Ph.D., a geneticist and researcher at the Salk Institute: Metabolism Influences Cancer

Recent development on Human Stem Cell Therapies for comorbidity and Cardiovascular disease

Human Stem Cell Therapies: UCSD New Discovery addressing the Limiting Factor and Providing the Solution

http://pharmaceuticalintelligence.com/2014/01/06/human-stem-cell-therapies-ucsd-new-discovery-addressing-the-limiting-factor-and-providing-the-solution/

This study reported a potential early marker of myocardial infarction by the release into the circulation of damaged endothelial cells that are to be measured in patients suspected of severe ischemia in a clinical trial.  The question that I raised in my comment was whether this would have to be a special immunochemical assay of tagged cells, and if that were the case, would it be measured on an automated flow-based hemocytometer, which can differentiate several populations of cells – granulocytes, lymphocytes, red cells, platelets, immature granuloytes, BLASTS.  That would be a very practical extension of the technology for labs worldwide.

Abstract

Aims: To elucidate if endothelial dysfunction is an early CV risk marker in obese men and women with prediabetes.
Study Design: Cross-sectional study.

Place and Duration of Study: Clinical Research Unit, Pennington Biomedical Research Center, Baton Rouge, LA. United States.

Background: Overweight and obese status denotes an increasing adipose tissue burden which spills over into ectopic locations, including the visceral compartment, muscle and liver. Associated co-morbidities enhance cardiovascular (CV) risk. Endothelium which is the largest receptor-effector end-organ in our bodies, while responding to numerous physical and chemical stimuli maintains vascular homeostasis. Endothelial dysfunction (ED) is the initial perturbation, which precedes fatty streak known to initiate atherosclerosis: insidious process which often culminates as sudden catastrophic CV adverse event.

Methodology:  Asymptomatic men and women; [n=42] coming in after an overnight fast had demographic, anthropometric, clinical chemistry and

  • resting endothelial function (EF)
  • increased test finger peripheral arterial tone (PAT) relative to control;
    • expressed as relative hyperemia index (RHI)] assessments.

Results: Adults with desirable weight [n=12] and overweight [n=8] state, had normal fasting plasma glucose [Mean(SD)]: FPG [91.1(4.5), 94.8(5.8) mg/dL], insulin [INS, 2.3(4.4), 3.1(4.8) µU/ml], insulin sensitivity by homeostasis model assessment [HOMA-IR, 0.62(1.2), 0.80(1.2)] and desirable resting clinic blood pressure [SBP/DBP, 118(12)/74(5), 118(13)/76(8) mmHg].

Obese adults [n=22] had

  • prediabetes [FPG, 106.5(3.5) g/dL],
  • hyperinsulinemia [INS 18.0(5.2) µU/ml],
  • insulin resistance [HOMA-IR .59(2.3)],
  • prehypertension [PreHTN; SBP/DBP 127(13)/81(7) mmHg] and
  • endothelial dysfunction [ED;
  • reduced RHI 1.7(0.3) vs. 2.4(0.3); all p<0.05].

Age-adjusted RHI correlated with BMI [r=-0.53; p<0.001]; however,

    • BMI-adjusted RHI was not correlated with age [r=-0.01; p=0.89].

Conclusion: Endothelial dysfunction reflective of cardiometabolic changes in obese adults can be an early risk marker for catastrophic CV events.

Keywords: Fasting plasma glucose; healthy adults; reverse cholesterol transport pathway; insulin resistance; body weight; relative hyperemia index.

ABBREVIATIONS

ADA: American Diabetes association; BMI: body mass index; CVD: cardiovascular disease; CV: cardiovascular; DBP: diastolic blood pressure; ED: endothelial dysfunction; EF: resting endothelial function; FPG: fasting plasma glucose; HOMA-IR: homeostasis model assessment; INS: insulin; JNC 7: Joint National Commission 7; LDL-C/HDL-C: low density lipoprotein cholesterol to high density lipoprotein; NCEP ATP III: National Cholesterol Education Program Adult Treatment Panel III; PAT: peripheral arterial tone; PreDM: prediabetes; PreHTN: prehypertension; PBRC: Pennington Biomedical Research Center; RHI: relative hyperemia index; SBP: systolic blood pressure; Total-C/HDL-C: total cholesterol to high density lipoprotein cholestrol; TG/HDL-C: triglycerides to high density lipoprotein cholesterol; WC: waist circumference.

Introduction

Healthy adults with no chronic medical conditions, on no prescription medications (n=24) and with low cardiovascular risk, in a randomized-order, cross-over clinical trial, with a 2 week washout period, exhibitd improved endothelial function (measured with flow mediated dilatation) with a diet rich in antioxidants (Franzini et al., 2012). Healthy over weight and obese volunteers with normal glucose appear to attenuate flow mediated dilation after high
glycemic index carbohydrate meals (Suessenbacher et al., 2011). In matched (age, work place, physical activity, tobacco use, blood pressure, serum lipids and family history of premature coronary artery disease) male shift and no shift workers, peripheral endothelial function (peripheral arterial tone (PAT) index obtained with the EndoPAT technique) was impaired in shift workers, suggesting elevated cardiovascular risk (Lavi et al., 2009).

Endothelial function thus appears to be an exquisitely sensitive marker for a variety of populations, under various conditions. Although endothelial function has been evaluated in numerous disease conditions and perturbed with a variety of agents, there has, to our knowledge, not been a comparison of resting endothelial function in free living healthy lean, overweight and obese subjects. Using a noninvasive assessment for resting endothelial function (by measuring the peripheral arterial tone, Bonetti et al., 2004), we tested the hypothesis that fasting glucose escalation in otherwise asymptomatic obese men and women is functionally reflected as endothelial dysfunction.

Endothelial Function

Assessment of resting endothelial function was done with the participant in fasting state, after having avoided stimulants (caffeine, tobacco, alcohol, exercise) for 12 hours, at the same fixed clock hour (range 8-10 AM), using the EndoPAT 2000 device manufactured by ITAMAR Medical®. This assessment technique has been previously validated (Bonetti et al., 2004), has been used in numerous (>250) peer reviewed publications (Carty et al., 2012; Kuvin et al., 2003) and has been in routine use in our clinical core. Briefly: subjects coming
in from home, after an overnight fast and having avoided stimulants for 12-hours, were placed in a supine position for 20 minutes in a quiet room before the test. A patented single use finger sleeve was then placed on the index finger of each hand to continuously measure peripheral arterial tone. A blood pressure cuff applied to the upper arm of the non-dominant arm (test arm) was then used to occlude the brachial artery for 5 minutes. This was followed by a rapid release. The dominant arm without any manipulation served as the control. The
built in, validated software integrated the data gathered from the finger sleeves of the control (undisturbed) and the test arms (during the baseline, occlusion and release phases), thus providing the relative hyperemia index (RHI) for the test arm. This flow mediated dilatation induced change in the test arm, relative to the control arm, served as the measure for endothelial function (RHI).

The subjects with desirable and overweight body weight were significantly younger [36.7(19.1) and 27.4(3.9) years, respectively], than those who were obese [53.2(11.6) years]. We performed correlations between the measure for endothelial function (RHI) and confounding factors like BMI, age and gender. Age-adjusted RHI correlated with BMI [r=- 0.53, p<0.001]; however, BMI-adjusted RHI was not associated with age [r=-0.01, p=0.89]. Fig. 1 depicts panels for the regression line for RHI as a function of age, (and BMI, glucose
and HOMA-IR, respectively) superimposed on a scatter plot. No correlation was observed between endothelial function and age (r²=0.07), while endothelial function was highly correlated with body mass index, glucose and insulin sensitivity (r²=0.3).

DISCUSSION

Asymptomatic obese adults with prediabetes (when compared to asymptomatic desirable weight and overweight adults with normal glucose), exhibit above the upper limits for desirable fasting plasma total cholesterol (>200mg/dL) and triglycerides (>150 mg/dL), but due to a relatively lower HDL-C display higher cardiac risk ratios (Total-C/HDL-C; p=0.05 and TG/HDL-C; p=0.02). A lower HDL-C and the elevated cardiac risk ratios are early clinical indicators for an impaired reverse cholesterol transport (RCT) pathway, a process by which cholesterol from the periphery is transported to the liver (Tall, 1998). The RCT pathway has been shown to be a sensitive indicator of the net flux (deposition vs. removal) of cholesterol homeostasis at the endothelium (Gupta et al., 1993; Tall et al., 2000). It is at the endothelium that the first fatty streaks, which over time deteriorate into atherosclerosis, have been shown to develop (Rosenfeld et al., 2000).

Impaired endothelial dysfunction is the first step in the process of atherosclerosis, even before the development of the fatty streak (Davignon, 2004; Ross 1999). These healthy obese men and women with prediabetes, prehypertension and impaired reverse cholesterol transport pathway were assessed to have impaired resting endothelial function, which is consistent with latent early onset cardiovascular disease.

We have demonstrated a high prevalence of isolated prediabetes or prehypertension and co-existing prediabetes and prehypertension, among the otherwise healthy US adults (Gupta et al., 2011). We have also elucidated that asymptomatic obese adults with overly heightened systemic inflammation, tend to have prediabetes and prehypertension (Gupta et al., 2010a). These individuals by various conventional measures (larger waist circumference, exacerbated systemic inflammation, higher insulin resistance, elevated triglycerides, lower high-density lipoprotein cholesterol, above average cardiac risk ratios and a significant co-existence of two or three concomitant metabolic risk factors) appear to be on an accelerated pathway towards early adverse cardiovascular events (Gupta et al., 2010a, 2010b). With this study we provide a dynamic, non-invasive, functional correlate: significant resting endothelial dysfunction, as an early biomarker for pre-atherosclerosis in obese adults with prediabetes.

Increased organ ectopic adipose burden especially in the muscle and liver appears to drive clinically recognizable adverse cardio metabolic changes (Hamdy et al., 2006). Increased inflammation (local and systemic) along with enhanced insulin resistance (liver, muscle) manifests as dysglycemia, dyslipidemia, excess reactive oxygen species, hyper-coagulablility and loss of blood pressure control (Gastaldelli et al., 2010).

We demonstrate an early impairment in the reverse cholesterol transport pathway, indicating a net deposition versus removal of cholesterol at the endothelium. In asymptomatic obese men and women with predisease  conditions (prediabetes and prehypertension) when contrasted with ideal bodyweight or overweight adults with normoglycemia and normal blood pressure, resting endothelial dysfunction can be an early warning sign for future catastrophic cardiovascular adverse events.

© 2012 Gupta et al.; This is an Open Access article distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

REFERENCES on circulating Endothelial Progenitor Cells as Biomarkers for Cardiovascular Disease and their Angiogenesis Potential.

Asahara T, Murohara T, Sullivan A, et al. Isolation of putative progenitor endothelial cells for angiogenesis. Science 1997;275:964-967.

Takahashi T, Kalka C, Masuda H, et al. Ischemia- and cytokine-induced mobilization of bone marrow-derived endothelial progenitor cells for neovascularization. Nat Med 1999;5:434-438.

Kocher AA, Schuster MD, Szabolcs MJ, et al. Neovascularization of ischemic myocardium by human bone-marrow-derived angioblasts prevents cardiomyocyte apoptosis, reduces remodeling and improves cardiac function. Nat Med 2001;7:430-436.

Rauscher FM, Goldschmidt-Clermont PJ, Davis BH, et al. Aging, progenitor cell exhaustion, and atherosclerosis. Circulation 2003;108:457-463.

Hill JM, Zalos G, Halcox JPJ, et al. Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N Engl J Med 2003;348:593-600.

Vasa M, Fichtlscherer S, Adler K, et al. Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease. Circulation 2001;103:2885-2890

Laufs U, Werner N, Link A, et al. Physical training increases endothelial progenitor cells, inhibits neointima formation, and enhances angiogenesis. Circulation 2004;109:220-226.

Werner N, Kosiol S, Schiegl T, et al. Circulating endothelial progenitor cells and cardiovascular outcomes. N Engl J Med 2005;353:999-1007.

Aicher A, Heeschen C, Mildner-Rihm C, et al. Essential role of endothelial nitric oxide synthase for mobilization of stem and progenitor cells. Nat Med 2003;9:1370-1376.

Wollert KC, Meyer GP, Lotz J, et al. Intracoronary autologous bone-marrow cell transfer after myocardial infarction: the BOOST randomised controlled clinical trial. Lancet 2004;364:141-148.

Zhang H, Vakil V, Braunstein M, et al. Circulating endothelial progenitor cells in multiple myeloma: implications and significance. Blood 2005;105:3286-3294

Lyden D, Hattori K, Dias S, et al. Impaired recruitment of bone-marrow-derived endothelial and hematopoietic precursor cells blocks tumor angiogenesis and growth. Nat Med 2001;7:1194-1201.

Other related articles that were published in this Open Access Online Scientific Journal include the following:

Lev-Ari, A. 2/28/2013 The Heart: Vasculature Protection – A Concept-based Pharmacological Therapy including THYMOSIN

http://pharmaceuticalintelligence.com/2013/02/28/the-heart-vasculature-protection-a-concept-based-pharmacological-therapy-including-thymosin/

Lev-Ari, A. 2/27/2013 Arteriogenesis and Cardiac Repair: Two Biomaterials – Injectable Thymosin beta4 and Myocardial Matrix Hydrogel

http://pharmaceuticalintelligence.com/2013/02/27/arteriogenesis-and-cardiac-repair-two-biomaterials-injectable-thymosin-beta4-and-myocardial-matrix-hydrogel/

Lev-Ari, A. 11/13/2012 Peroxisome proliferator-activated receptor (PPAR-gamma) Receptors Activation: PPARγ transrepression for Angiogenesis in Cardiovascular Disease and PPARγ transactivation for Treatment of Diabetes

http://pharmaceuticalintelligence.com/2012/11/13/peroxisome-proliferator-activated-receptor-ppar-gamma-receptors-activation-pparγ-transrepression-for-angiogenesis-in-cardiovascular-disease-and-pparγ-transactivation-for-treatment-of-dia/

Lev-Ari, A. 8/29/2012 Positioning a Therapeutic Concept for Endogenous Augmentation of cEPCs — Therapeutic Indications for Macrovascular Disease: Coronary, Cerebrovascular and Peripheral

http://pharmaceuticalintelligence.com/2012/08/29/positioning-a-therapeutic-concept-for-endogenous-augmentation-of-cepcs-therapeutic-indications-for-macrovascular-disease-coronary-cerebrovascular-and-peripheral/ 

Lev-Ari, A. 8/28/2012 Cardiovascular Outcomes: Function of circulating Endothelial Progenitor Cells (cEPCs): Exploring Pharmaco-therapy targeted at Endogenous Augmentation of cEPCs

http://pharmaceuticalintelligence.com/2012/08/28/cardiovascular-outcomes-function-of-circulating-endothelial-progenitor-cells-cepcs-exploring-pharmaco-therapy-targeted-at-endogenous-augmentation-of-cepcs/

Lev-Ari, A. 8/27/2012 Endothelial Dysfunction, Diminished Availability of cEPCs, Increasing CVD Risk for Macrovascular Disease – Therapeutic Potential of cEPCs

http://pharmaceuticalintelligence.com/2012/08/27/endothelial-dysfunction-diminished-availability-of-cepcs-increasing-cvd-risk-for-macrovascular-disease-therapeutic-potential-of-cepcs/

Lev-Ari, A. 8/24/2012 Vascular Medicine and Biology: CLASSIFICATION OF FAST ACTING THERAPY FOR PATIENTS AT HIGH RISK FOR MACROVASCULAR EVENTS Macrovascular Disease – Therapeutic Potential of cEPCs

http://pharmaceuticalintelligence.com/2012/08/24/vascular-medicine-and-biology-classification-of-fast-acting-therapy-for-patients-at-high-risk-for-macrovascular-events-macrovascular-disease-therapeutic-potential-of-cepcs/

Lev-Ari, A. 7/19/2012 Cardiovascular Disease (CVD) and the Role of agent alternatives in endothelial Nitric Oxide Synthase (eNOS) Activation and Nitric Oxide Production

http://pharmaceuticalintelligence.com/2012/07/19/cardiovascular-disease-cvd-and-the-role-of-agent-alternatives-in-endothelial-nitric-oxide-synthase-enos-activation-and-nitric-oxide-production/

Lev-Ari, A. 4/30/2012 Resident-cell-based Therapy in Human Ischaemic Heart Disease: Evolution in the PROMISE of Thymosin beta4 for Cardiac Repair

http://pharmaceuticalintelligence.com/2012/04/30/93/

Lev-Ari, A. 7/2/2012 Macrovascular Disease – Therapeutic Potential of cEPCs: Reduction Methods for CV Risk

http://pharmaceuticalintelligence.com/2012/07/02/macrovascular-disease-therapeutic-potential-of-cepcs-reduction-methods-for-cv-risk/

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American Diet is LOW in four important Nutrients that have a direct bearing on Aging and the Brain

Reporter: Aviva Lev-Ari, PhD, RN

 

Four Nutrients That Will Help You Reach the Century Mark

The fact that you can manipulate your genes with happiness doesn’t mean you can completely disregard lifestyle choices, as that would be foolhardy. The basics are still important—diet, exercise, sleep, etc. Research suggests the modern American diet is increasingly low in four important nutrients that have a direct bearing on aging, and our brains are suffering for it. If you hope to one day become a healthy, happy centenarian, you must address the following:16

Vitamin D

DHA

Folate

Magnesium

Vitamin D

Vitamin D’s list of health benefits is amazingly long, including helping your brain combat the damage from free radicals, which helps prevent cognitive decline. The important factor when it comes to vitamin D is your serum level, which should be between 50-70 ng/ml year-round, and the only way to determine this is with a blood test.

Your skin produces vitamin D in response to ultraviolet light, so sun exposure or a safe tanning bed are the preferred methods of boosting your vitamin D. However, a D3 supplement can be used when necessary. Most adults need about 8,000 IUs of vitamin D3 per day to achieve serum levels of 40 ng/ml. If you take supplemental vitamin D3, you also need to make sure you’re getting enough vitamin K2, as these two nutrients work in tandem to ensure calcium is distributed into the proper areas in your body.

DHA (Docosahexaenoic Acid)

DHA is an omega-3 fat that plays a role in keeping your cell membranes healthy, flexible, and resistant to oxidative stress, which decreases inflammation. Chronic inflammation is a key factor in many degenerative diseases, including dementia. Low DHA is has been linked with depression, memory loss, and even elevated hostility, which reflect its importance to optimal brain function.

The American diet has far too many omega-6 fats and not enough omega-3 fats due to its heavy reliance on processed food. You can boost your DHA by eating more fish, such as salmon and sardines, but so much of the fish today is contaminated with mercury and other toxic compounds that I prefer to take a high quality omega-3 fat supplement such as krill oil.

Folate (Vitamin B9)

Folate helps prevent depression, seizure disorders, brain atrophy, and other neurological problems. Folate deficiencies correlate with impaired memory, slowed mental processing and overall cognitive decline, particularly in the elderly. Your body also needs folate to make red blood cells. Folate deficiency has been thought to lead to elevated homocysteine levels, which can be a major contributor to heart disease and Alzheimer’s. However, recent studies may have disproven that idea.17

People often confuse folate with folic acid, and it’s important to know the difference. Folate is the naturally-occurring form of the vitamin and contains all of the related isomers your body needs for optimal use. Folic acid is the synthetic form of the vitamin that is used in most supplements and in fortified foods.

It is always preferable to raise your folate levels by modifying your diet, as opposed to eating “enriched” foods or taking a multivitamin. Foods rich in folate include egg yolks, sunflower seeds, asparagus, avocados, broccoli, cauliflower, basil, parsley, and greens such as romaine, turnip, collards, and spinach.18 If you do think you need a supplement, make sure it lists “folate” on the label, rather than folic acid, as this suggests food sources were used.

Magnesium

Magnesium plays a role in your body’s detoxification processes and is therefore important for minimizing damage from environmental chemicals, heavy metals and other toxins. Even glutathione, considered by many to be your body’s most powerful antioxidant, requires magnesium in order to be synthesized. But this important mineral also helps your brain.

Magnesium acts as a buffer between neuron synapses, particularly those involved with cognitive functions (learning and memory). Magnesium “sits” on the receptor without activating it, in effect protecting the receptor from over-activation by other neurochemicals, especially glutamate. Glutamate is an “excitotoxin,” which can harm your brain if it accumulates, and magnesium helps prevent this. That’s why you often see magnesium advertised as a “calming” nutrient.

Good sources of magnesium are whole organic foods, especially dark green leafy vegetables, seaweed, dried pumpkin seeds, unsweetened cocoa, flaxseed, almond butter, and whey. If you choose to add a magnesium supplement, there are many forms so it can be a bit confusing. A newer type called magnesium threonate is particularly good due to its ability to penetrate cell membranes and cross your blood-brain barrier, which is important for preserving good cognitive function as you age.

SOURCE

http://articles.mercola.com/sites/articles/archive/2014/01/09/centenarians.aspx#!

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Preventive Medicine Philosophy: Excercise vs. Drug, IF More of the First THEN Less of the Second

Reporter and Curator: Aviva Lev-Ari, PhD, RN

How Centenarians Explain Their Longenity

What the Elders Themselves Have to Say

The majority of centenarians do not feel their chronological age; on average, they report feeling 20 years younger. They also tend to have positive attitudes, optimism, and a zest for life. Could it be that personality characteristics and worldviews play a more significant role than genetics, diet, or exercise?

One way to determine this is to ask centenarians questions about how they see the world, what they value, and to what they attribute their own longevity. What are their secrets to aging well? These individuals represent centuries of wisdom that should not be overlooked. So that’s what researchers are now doing—mining the minds of centenarians for nuggets of wisdom. Regardless of which interviews you read, this is where patterns really DO emerge. In interviews and surveys with centenarians, the following themes come up time and time again when asked to explain why they’ve lived so long:10

Keeping a positive attitude Eating good food
Exercising moderately (most report basic activities, like walking, biking, gardening, swimming, etc.) Clean living (not smoking or drinking excessively, etc.)
Living independently Family
“Good genes” Friends
Staying mentally active and always learning something new Faith/spirituality

 

VIEW VIDEO

http://articles.mercola.com/sites/articles/archive/2014/01/09/centenarians.aspx#!

By Dr. Mercola

One of the key health benefits of exercise is that it helps normalize your glucose, insulin, and leptin levels by optimizing insulin and leptin receptor sensitivity. This is perhaps the most important factor for optimizing your overall health and preventing chronic disease, and may explain why exercise is such a potent preventive medicine.

In fact, researchers recently suggested that exercise is “the best preventive drug” for many common ailments, from psychiatric disorders to heart disease, diabetes, and cancer.1 According to Jordan Metzl, a sports-medicine physician at New York City’s Hospital for Special Surgery and author of The Exercise Cure:

“Exercise is the best preventive drug we have, and everybody needs to take that medicine.”

And, as stated by Dr. Timothy Church,2 director of preventive medicine research at the Pennington Biomedical Research Center in Baton Rouge:

“Exercise strengthens the entire human machine — the heart, the brain, the blood vessels, the bones, the muscles. The most important thing you can do for your long-term health is lead an active life.”

Non-Exercise Movement Is Equally, if Not More, Important for Health

Unfortunately, many fail to get sufficient amounts of exercise. Worse yet, a majority of people may still endanger their health simply by sitting too much. Compelling evidence actually suggests that even if you exercise regularly,prolonged sitting is itself a risk factor for chronic disease and reduced lifespan…

Overall, federal data suggest only 21 percent of American adults meet the government recommendation to engage in two and half hours’ worth of aerobic and muscle-strengthening exercise each week, so there’s clearly a lot of room for improvement.  Ideally though, you’ll want to exercise regularly AND frequently interrupt your sitting in order to optimize your health and longevity. I’ll review the reasons for this below.

Exercise Benefits Found to Be EQUAL to Drugs for Heart Disease and Diabetes

A recent meta-review conducted by researchers at Harvard and Stanford3compared the effectiveness of exercise versus drug interventions on mortality outcomes for diabetes, coronary heart disease, heart failure, and stroke. After reviewing 305 randomized controlled trials, which included nearly 339,300 people, they found “no statistically detectable differences” between physical activity and medications for prediabetes and heart disease.

This is a potent reminder of the power of simple lifestyle changes, as well as the shortcomings of the drug paradigm!

Besides optimizing insulin/leptin receptor sensitivity, other beneficial biochemical changes also occur during exercise, including alterations in more than 20 different metabolites involved in fat burning and metabolism, among other things. As stated by Dr. Church, exercise indeed affects your entire body—from head to toe—in beneficial ways. This includes changes in your:

  • Muscles, which use glucose and ATP for contraction and movement. Tiny tears in your muscles make them grow bigger and stronger as they heal. Gaining more muscle through resistance exercises has many benefits, from losing excess fat to maintaining healthy bone mass and preventing age-related muscle loss as you age. The intensity of your resistance training can achieve a number of beneficial changes on the molecular, enzymatic, hormonal, and chemical level in your body.
  • Lungs. As your muscles call for more oxygen, your breathing rate increases. The higher your VO2 max—your maximum capacity of oxygen use—the fitter you are.
  • Heart. Your heart rate increases with physical activity to supply more oxygenated blood to your muscles. The fitter you are, the more efficiently your heart can do this, allowing you to work out longer and harder. Your blood pressure will also decrease as a result of new blood vessels forming.
  • Brain. The increased blood flow also benefits your brain, allowing it to almost immediately function better. Exercising regularly also promotes the growth of new brain cells, boosting your capacity for memory and learning. A number of neurotransmitters are also triggered, such as endorphins, serotonin, dopamine, glutamate, and GABA. Some of these are well-known for their role in mood control. Exercise, in fact, is one of the most effective prevention and treatment strategies for depression.
  • Joints and Bones.  Exercise can place as much as five or six times more than your body weight on them. Weight-bearing exercise is one of the most effective remedies against osteoporosis, as your bones are very porous and soft, and as you get older, your bones can easily become less dense and hence, more brittle — especially if you are inactive.

For Optimal Benefits, Make Sure You’re Exercising Correctly

I’ve often equated exercise to a drug from the perspective that they both need to be wisely prescribed in order to optimize your health. Simply doing random exercises for the sake of “exercising” will not achieve the benefits you seek. In fact it could cause serious injury, especially if you engage in strength training with poor form and no coaching. In terms of “dosage,” it’s important to note the changes in recommendations that have taken place over the past few years. While conventional aerobic exercise was long considered the “gold standard” of a good workout, research has refuted such notions.

Instead, high-intensity interval training (which requires but a fraction of the time compared to conventional cardio) has been shown to be FAR more efficient and effective, compared to longer, slower cardio workouts. In fact, exercises such as long distance running have been shown to be among the worst forms of exercise, in terms of health benefits.

The reason for this is quite simple. High intensity interval training (HIIT) mimics the movements of our hunter-gatherer ancestors, which included short bursts of high-intensity activities, but not long-distance running. This, researchers say, is what your body is hard-wired for. Basically, by exercising in short bursts, followed by periods of recovery, you recreate exactly what your body needs for optimum health. Twice-weekly sessions, which require no more than 20 minutes from start to finish, can help you:

  • Lower your body fat
  • Improve your muscle tone
  • Boost your energy and libido
  • Improve athletic speed and performance
  • Naturally increase your body’s production of human growth hormone (HGH)—a synergistic, foundational biochemical underpinning that promotes health and longevity. Conventional cardio will NOT boost your HGH level

The Importance of Non-Exercise Movement

Next, let’s address the issue of non-exercise movement. I also like to call this intermittent movement. This is the latest area of physical activity that’s gaining a lot of attention, and for good reason. Studies have repeatedly found strong correlations between prolonged sitting or inactivity and reduced life expectancy—even if you exercise regularly!

It appears that temporary vigorous exercise simply cannot compensate for the damage incurred by prolonged daily sitting. For example, a recent analysis4 of 18 studies, found that those who sat for the longest periods of time were twice as likely to have diabetes or heart disease, compared to those who sat the least. An earlier study5 that highlighted much of the recent evidence linking sitting with biomarkers of poor metabolic health, also found that total sitting time correlates with an increased risk of type 2 diabetes, heart disease, and other prevalent chronic health problems—even if you exercise regularly.

The answer, fortunately, is quite simple. You simply need to make sure you move your body more often. Simply standing upfrom a seated position has been found particularly effective at counteracting the ill effects of sitting. This is something I seek to do every 15 minutes while I am sitting. I set a timer to remind me. When the timer rings I get up and do some simple hamstring or chest stretches for a minute or two. I am testing a variety of different ones and hope to report on them later this year.

Earlier this year, I interviewed Dr. Joan Vernikos,6 former director of NASA’s Life Sciences Division and author of Sitting Kills, Moving Heals, on this topic. Her groundbreaking research reveals why standing up is such an effective remedy—it’s because when you stand up, your body acts against gravity. Sitting actually simulates a low-gravity type environment for your body, and your body deteriorates at a far more rapid pace in anti-gravity situations… Hence, the remedy is to continuously engage in physical movements, as this increases the forces of gravity on your body.

Simple everyday activities such as housecleaning, cooking, gardening, hanging clothes to dry, bending over to pick up a stray sock, reaching for an item on a high shelf, all fall within the spectrum of movements you would ideally engage in—more or less continuously—from morning until night. To learn more about this important aspect of health, please see this previousarticle.

Variety Is the Spice of Life and the Key to Optimal Health

In short, one of the keys to optimal health is to remain as active as you can, all day long. Whenever you have a chance to move and stretch your body in the course of going about your day—do it! That said, there’s no doubt that an ideal fitness regimen requires a little more effort. Fortunately, you can accomplish the bulk of it through high intensity exercises, which require a minimal time investment—as little as 20 minutes, two to three times a week. As a general rule, I recommend incorporating a wide variety of exercises, including the following:

    1. Stand Up Every 15 Minutes. While not intuitively obvious, emerging evidence clearly shows that even highly fit people who exceed the expert exercise recommendations are headed for premature death if they sit for long periods of time. My interview with NASA scientist Dr. Joan Vernikos goes into great detail why this is so, and what you can do about it.
    2. Interval (Anaerobic) Training: This is when you alternate short bursts of high-intensity exercise with gentle recovery periods.
    3. Strength Training: Rounding out your exercise program with a 1-set strength training routine will ensure that you’re really optimizing the possible health benefits of a regular exercise program. You can also “up” the intensity by slowing it down. For more information about using super slow weight training as a form of high intensity interval exercise, please see my interview with Dr. Doug McGuff.
    4. Core Exercises: Your body has 29 core muscles located mostly in your back, abdomen and pelvis. This group of muscles provides the foundation for movement throughout your entire body, and strengthening them can help protect and support your back, make your spine and body less prone to injury, and help you gain greater balance and stability.

Foundation Training, created by Dr. Eric Goodman, is an integral first step of a larger program he calls “Modern Moveology,” which consists of a catalog of exercises. Postural exercises such as those taught in Foundation Training are critical not just for properly supporting your frame during daily activities; they also retrain your body so you can safely perform high-intensity exercises without risking injury. Exercise programs like Pilates and yoga are also great for strengthening your core muscles, as are specific exercises you can learn from a personal trainer.

  1. Stretching: My favorite type of stretching is active isolated stretches. With Active Isolated Stretching, you hold each stretch for only two seconds, which works with your body’s natural physiological makeup to improve circulation and increase the elasticity of muscle joints. This technique also allows your body to repair itself and prepare for daily activity. You can also use devices like the Power Plate to help you stretch.

SOURCE

http://fitness.mercola.com/sites/fitness/archive/2014/01/10/exercise-preventive-drug.aspx

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Portion Control as a Strategy in Weight Management to lower the Risk for Cardiovascular Diseases

Reporter: Aviva Lev-Ari, PhD, RN

14 Ways to Cut Portions Without Feeling Hungry

» View Slide Show

14 ways to cut portions without feeling hungry

By Diana Kelly

Published December 31, 2013

  • PORTION_SIZE_640.jpg

To lose weight, you need to burn more calories than you consume, which inevitably means one thing: portion control. But you’re not necessarily doomed to a growling stomach until you reach your goal. “Portion control doesn’t mean you have to eat tiny portions of everything,” says Lisa Young, author of The Portion Teller Plan: The No-Diet Reality Guide to Eating, Cheating, and Losing Weight Permanently. “You don’t want to feel like you’re on a diet, but you have to eat fewer calories.”

Here are 14 easy ways to cut portions, trim calories, and lose fat without counting the minutes until your next meal.

Health.com: 16 Ways to Lose Weight Fast

Start with a glass of H2O

Drink 16 ounces (a big glass) of water before you eat, suggests Dawn Jackson Blatner, author of The Flexitarian Diet. Filling your belly with water will naturally make you less likely to overeat, she says. Plus, some symptoms of dehydration may actually be what’s causing your rumbling belly, so sipping some water before you eat may eliminate your “hunger” altogether.

Wear form-fitting clothes

We’re not suggesting you squeeze into pants that are too tight. However, wearing an outfit with a waistband or perhaps a jacket with buttons can serve as a tool to prompt you to slow down and assess how you feel during your meal, says Young. As your clothing begins to feel a little snugger, it may keep you from going back for seconds.

Add veggie fillers

Bulking up your meals with veggies is one easy way to cut calories while filling you up fast. Spinach, for example, can be used as a sandwich-topper or can add fiber and nutrients to pasta and stir-fries, says Blatner. Other ideas to eat more veggies: swap in mushrooms for half the ground meat in most recipes, make oatmeal more filling with diced apples, and use a whole-wheat pita in place of bread so you can stuff it with more veggies.

Health.com: 10 Ways Your Personality Affects Your Weight

Dine on dinnerware that helps you lose

The color of your plate may influence how much you eat, according to a 2012 Cornell University study. The researchers discovered that when a plate and the food on it had a low color-contrast (like pasta with Alfredo sauce on a white plate), people at a buffet served themselves 22 percent more than when there was a higher color-contrast (like pasta with red sauce on a white plate or pasta with Alfredo sauce on a red plate). The study conclusions suggest that if you want to eat less, select plates that have a color-contrast to the food you’re eating for dinner. Or if you want to eat more healthy foods, like a bigger salad, eat greens from a large green plate or bowl!

Make carbs the topper instead of the base

Rethink the way you use grains and starches. Take a breakfast parfait, for instance: instead of starting with a granola base, fill your cup with yogurt and then sprinkle just a tiny amount of granola on top for the crunch you crave. Making a stir-fry? Load up your plate with veggies and a serving of lean protein, then add a quarter cup of brown rice.

Set the scene for slower eating

Dim lights and listen to relaxing music to set the tone for a more leisurely meal, suggests Blatner. “Taking your time while eating increases enjoyment and decreases portions,” she says. Remember to chew slowly, put down your fork between bites, and sip water to make your meal last longer.

Health.com: 25 Ways to Cut 500 Calories a Day

Work for your food

Here’s another way to slow down your eating: munch on foods that require shelling, peeling, or individual unwrapping, suggests Blatner. Oranges, edamame, and pistachios in their shells are healthy options.

Don’t eat from the bag or box

When you sit down with a bag of chips, do you really know how many you’re eating? Researchers from Cornell University sought to answer this question in a study and found that people ate 50 percent more chips when they were given no visual cues as to how large a portion should be. So if you buy a bag of pretzels or tin of nuts that contains 10 servings, divide the contents of the container into 10 smaller baggies ahead of time.

Slurp your appetizer

Before you dive into your entrée, have some soup. Though it may seem counterintuitive to add more to your meal, research shows that starting a meal with soup may help you reduce your overall calorie intake. In a 2007 study, people who ate soup before their lunch entrée reduced their total calorie intake by 20 percent. Your best bet: a broth-based soup, preferably with veggies to help you feel full from the natural fiber, says Young. Here are a few healthy soup recipes to get you started.

Take a lap before serving yourself

In a Cornell University study published in PLoS One, researchers observed people at two separate breakfast buffet lines that featured the same seven items: cheesy eggs, potatoes, bacon, cinnamon rolls, low-fat granola, low-fat yogurt, and fruit. One line presented the foods from healthiest to least-healthy, while the other line had the order reversed. Regardless of which line they passed through, more than 75 percent of diners put the first food they saw on their plates; the first three foods they encountered in the buffet made up two-thirds of all the foods they added to their plate. So take a stroll around the buffet or dinner table before you serve yourself, suggests Young.

Drink from a tall glass

It’s okay to have a cocktail with your meal if that’s what you really want, but keep it to one glass and enjoy it slowly, suggests Young. To trick yourself into believing you’re having more, pour your drink into a tall, thin glass. A 2005 study published in the journal BMJ revealed that practiced bartenders who poured what they thought was a shot of alcohol (1.5 ounces) into a short, wide glass poured 20 percent more than when the glass was tall and thin. Add extra ice to your drink to make it look like even more!

Limit mealtime distractions

Turn off the TV and put your smartphone away while you eat. A recent review of studies found that people who watched television during meals tended to consume more than those who ate without any distractions. And for you office dwellers? Consider taking your lunch break away from your desk—in an American Journal of Clinical Nutrition study, people who played computer solitaire while having lunch felt less full at the end, and went on to eat more food later in the day than those who didn’t play the game.

Health.com: Lose 10 Inches in 10 Days

Use smaller serveware and dishes

Turns out that even food experts aren’t so savvy about eyeballing portion sizes. In a Cornell University study, 85 nutrition experts gathered for an ice cream social to celebrate the success of a colleague. They were randomly given either a small or large bowl, or a small serving scoop or large serving scoop. Then, the nutritionists were asked to complete a brief survey while the study researchers secretly weighed their bowls. Those given the larger bowls served themselves 31 percent more without realizing it, while those who used the larger scoop unknowingly served themselves 14.5 percent more. Moral of the story? Dish up your own food with a small utensil onto a small bowl or plate, and chances are you’ll eat less.

End your meal with a new kind of sweet treat

Many people have trained themselves to expect a sweet treat at the end of a meal, says Blatner. Swap in a new, healthier ritual after meals to signal that you’re done eating. She recommends brewing a flavorful decaf tea like peppermint, cinnamon, chocolate, or one of your favorite fruity varieties for low-or-no-calorie sweet-tooth satisfier.

This article originally appeared on Health.com.

http://www.health.com/health/gallery/thumbnails/0,,20769037,00.html

SOURCE

http://www.foxnews.com/health/2013/12/31/14-ways-to-cut-portions-without-feeling-hungry/

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Summary of Genomics and Medicine: Role in Cardiovascular Diseases

Summary of Genomics and Medicine: Role in Cardiovascular Diseases

Author: Larry H. Bernstein, MD, FCAP

The articles within Chapters and Subchapters you have just read have been organized into four interconnected parts.
  1. Genomics and Medicine
  2. Epigenetics – Modifyable Factors Causing CVD
  3. Determinants of CVD – Genetics, Heredity and Genomics Discoveries
  4. Individualized Medicine Guided by Genetics and Genomics Discoveries
The first part established the
  • rapidly evolving science of genomics
  • aided by analytical and computational tools for the identification of nucleotide substitutions, or combinations of them
that have a significant association with the development of
  • cardiovascular diseases,
  • hypercoagulable state,
  • atherosclerosis,
  • microvascular disease,
  • endothelial disruption, and
  • type-2DM, to name a few.
These may well be associated with increased risk for stroke and/or peripheral vascular disease in some cases,
  • essentially because the involvement of the circulation is systemic in nature.

Part 1

establishes an important connection between RNA and disease expression.  This development has led to
  • the necessity of a patient-centric approach to patient-care.
When I entered medical school, it was eight years after Watson and Crick proposed the double helix.  It was also
  • the height of a series of discoveries elucidating key metabolic pathways.
In the period since then there have been treatments for some of the important well established metabolic diseases of
  • carbohydrate,
  • protein, and
  • lipid metabolism,
such as –  glycogen storage disease, and some are immense challenges, such as
  • Tay Sachs, or
  • Transthyretin-Associated amyloidosis.
But we have crossed a line delineating classical Mendelian genetics to
  • multifactorial non-linear traits of great complexity and
involving combinatorial program analyses to resolve.
The Human Genome Project was completed in 2001, and it has opened the floodgates of genomic discovery.  This resulted in the identification of
genomic alterations in
  • cardiovascular disease,
  • cancer,
  • microbial,
  • plant,
  • prion, and
  • metabolic diseases.
This has also led to
  • the identification of genomic targets
  • that are either involved in transcription or
  • are involved with cellular control mechanisms for targeted pharmaceutical development.
In addition, there is great pressure on the science of laboratory analytics to
  • codevelop with new drugs,
  • biomarkers that are indicators of toxicity or
  • of drug effectiveness.
I have not mentioned the dark matter of the genome. It has been substantially reduced, and has been termed dark because
  • this portion of the genome is not identified in transcription of proteins.
However, it has become a lightning rod to ongoing genomic investigation because of
  • an essential role in the regulation of nuclear and cytoplasmic activities.
Changes in the three dimensional structure of these genes due to
  • changes in Van der Waal forces and internucleotide distances lead to
  • conformational changes that could have an effect on cell activity.

Part 2

is an exploration of epigenetics in cardiovascular diseases.  Epigenetics is
  • the post-genomic modification of genetic expression
  • by the substitution of nucleotides or by the attachment of carbohydrate residues, or
  • by alterations in the hydrophobic forces between sequences that weaken or strengthen their expression.
This could operate in a manner similar to the conformational changes just described.  These changes
  • may be modifiable, and they
  • may be highly influenced by environmental factors, such as
    1. smoking and environmental toxins,
    2. diet,
    3. physical activity, and
    4. neutraceuticals.
While neutraceuticals is a black box industry that evolved from
  • the extraction of ancient herbal remedies of agricultural derivation
    (which could be extended to digitalis and Foxglove; or to coumadin; and to penecillin, and to other drugs that are not neutraceuticals).

The best examples are the importance of

  • n-3 fatty acids, and
  • fiber
  • dietary sulfur (in the source of methionine), folic acid, vitamin B12
  • arginine combined with citrulline to drive eNOS
  • and of iodine, which can’t be understated.
In addition, meat consumption involves the intake of fat that contains

  • the proinflammatory n-6 fatty acid.

The importance of the ratio of n-3/n-6 fatty acids in diet is not seriously discussed when

  • we look at the association of fat intake and disease etiology.
Part 2 then leads into signaling pathways and proteomics. The signaling pathways are
  • critical to understanding the inflammatory process, just as
  • dietary factors tie in with a balance that is maintained by dietary intake,
    • possibly gut bacteria utilization of delivered substrate, and
    • proinflammatory factors in disaease.
These are being explored by microfluidic proteomic and metabolomic technologies that were inconceivable a half century ago.
This portion extended into the diagnosis of cardiovascular disease, and
  • elucidated the relationship between platelet-endothelial interaction in the formation of vascular plaque.
It explored protein, proteomic, and genomic markers
  1. for identifying and classifying types of disease pathobiology, and
  2. for following treatment measures.

Part 3

connected with genetics and genomic discoveries in cardiovascular diseases.

Part 4

is the tie between life style habits and disease etiology, going forward with
  • the pursuit of cardiovascular disease prevention.
The presentation of walking and running, and of bariatric surgery (type 2DM) are fine examples.
It further discussed gene therapy and congenital heart disease.  But the most interesting presentations are
  • in the pharmacogenomics for cardiovascular diseases, with
    1. volyage-gated calcium-channels, and
    2. ApoE in the statin response.

This volume is a splendid example representative of the entire collection on cardiovascular diseases.

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Introduction to Genomics and Epigenomics Roles in Cardiovascular Diseases

Introduction to Genomics and Epigenomics Roles in Cardiovascular Diseases

Author and Curator: Larry H Bernstein, MD, FCAP

This introduction is to a thorough evaluation of a rich source of research literature on the genomic influences, which may have variable strength in the biological causation of atherosclerosis, microvascular disease, plaque formation, not necessarily having expressing, except in a multivariable context that includes the environment, dietary factors, level of emotional stress, sleep habits, and the daily activities of living for affected individuals.  The potential of genomics is carried in the DNA, copied to RNA, and this is most well studied in the micro RNAs (miRNA).  The miRNA has been explored for the appearance in the circulation of specific miRNAs that might be associated with myocyte or endothelial cell injury, and they are also being used as targets for therapeutics by the creation of silencing RNAs (siRNA).  The extent to which there is evidence of success in these studies is limited, but is being translated from animal studies to human disease.  There is also a long history of the measurement of  circulating enzymes and isoenzymes (alanine amino transferase, creatine kinase, and lactate dehydrogenase, not to leave out the adenylate kinase species specific to myocardium), and more recently the release of troponins I and T, and the so far still not fully explored ischemia modified albumin, or of miRNAs for the diagnosis of myocardial infarction.

There is also a significant disagreement about the value of measuring high sensitivity C reactive protein (hs-CRP), which has always been a marker for systemic inflammatory disease, in both chronic rheumatic and infectious diseases having a broad range, so that procalcitonin has appeared to be better for that situation, and for early diagnosis of sepsis. The hs-CRP has been too easily ignored because of

1. the ubiquitous elevations in the population
2. the expressed concerns that one might not be inclined to treat a mild elevation without other risk factors, such as, LDL cholesterolemia, low HDL, absent diabetes or obesity.  Nevertheless, hs-CRP raises an reasonable argument for preventive measures, and perhaps the use of a statin.

There has been a substantial amount of work on the relationship of obesity to both type 2 diabetes mellitus (T2DM) and to coronary vascular disease and stroke.  Here we bring in the relationship of the vascular endothelium, adipose tissue secretion of adiponectin, and platelet activation.  A whole generation of antiplatelet drugs addresses the mechanism of platelet activation, adhession, and interaction with endothelium.   Very interesting work has appeared on RESISTIN, that could bear some fruit in the treatment of both obesity and T2DM.

It is important to keep in mind that epigenomic gene rearrangements or substitutions occur throughout life, and they may have an expression late in life.  Some of the known epigenetic events occur with some frequency, but the associations are extremely difficult to pin down, as well as the strength of the association.  In a population that is not diverse, epigenetic changes are passed on in the population in the period of childbearing age.  The establishment of an epigenetic change is diluted in a diverse population.  There have been a number of studies with different findings of association between cardiovascular disease and genetic mutations in the Han and also in the Uyger Chinese populations, which are distinctly different populations that is not part of this discussion.

This should be sufficient to elicit broad appeal in reading this volume on cardiovascular diseases, and perhaps the entire series.  Below is a diagram of this volume in the series.

PART 1 – Genomics and Medicine
Introduction to Genomics and Medicine (Vol 3)
Genomics and Medicine: The Physician’s View
Ribozymes and RNA Machines
Genomics and Medicine: Genomics to CVD Diagnoses
Establishing a Patient-Centric View of Genomic Data
VIDEO:  Implementing Biomarker Programs ­ P Ridker PART 2 – Epigenetics – Modifiable
Factors Causing CVD
Diseases Etiology
   Environmental Contributors
Implicated as Causing CVD
   Diet: Solids and Fluid Intake
and Nutraceuticals
   Physical Activity and
Prevention of CVD
   Psychological Stress and
Mental Health: Risk for CVD
   Correlation between
Cancer and CVD
PART 3  Determinants of CVD – Genetics, Heredity and Genomics Discoveries
Introduction
    Why cancer cells contain abnormal numbers of chromosomes (Aneuploidy)
     Functional Characterization of CV Genomics: Disease Case Studies @ 2013 ASHG
     Leading DIAGNOSES of CVD covered in Circulation: CV Genetics, 3/2010 – 3/2013
     Commentary on Biomarkers for Genetics and Genomics of CVD
PART 4 Individualized Medicine Guided by Genetics and Genomics Discoveries
    Preventive Medicine: Cardiovascular Diseases
    Walking and Running: Similar Risk Reductions for Hypertension, Hypercholesterolemia,
DM, and possibly CAD
http://pharmaceuticalintelligence.com/2013/04/04/walking-and-running-similar-risk-reductions-for-hypertension-hypercholesterolemia-dm-and-possibly-cad/
    Prevention of Type 2 Diabetes: Is Bariatric Surgery the Solution?
http://pharmaceuticalintelligence.com/2012/08/23/prevention-of-type-2-diabetes-is-bariatric-surgery-the-solution/
Gene-Therapy for CVD
Congenital Heart Disease/Defects
   Medical Etiologies: EBM – LEADING DIAGNOSES, Risks Pharmacogenomics for Cardio-
vascular Diseases
   Signaling Pathways     Response to Rosuvastatin in
Patients With Acute Myocardial Infarction:
Hepatic Metabolism and Transporter Gene
Variants Effect
http://pharmaceuticalintelligence.com/2014/
01/02/response-to-rosuvastatin-in-patients-
with-acute-myocardial-infarction-hepatic-
metabolism-and-transporter-gene-variants-effect/
   Proteomics and Metabolomics      Voltage-Gated Calcium Channel and Pharmaco-
genetic Association with Adverse Cardiovascular
Outcomes: Hypertension Treatment with Verapamil
SR (CCB) vs Atenolol (BB) or Trandolapril (ACE)
http://pharmaceuticalintelligence.com/2014/01/02/
voltage-gated-calcium-channel-and-pharmacogenetic-
association-with-adverse-cardiovascular-outcomes-
hypertension-treatment-with-verapamil-sr-ccb-vs-
atenolol-bb-or-trandolapril-ace/
      SNPs in apoE are found to influence statin response
significantly. Less frequent variants in
PCSK9 and smaller effect sizes in SNPs in HMGCR
http://pharmaceuticalintelligence.com/2014/01/02/snps-in-apoe-are-found-to-influence-statin-response-significantly-less-frequent-variants-in-pcsk9-and-smaller-effect-sizes-in-snps-in-hmgcr/

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The Cost to Value Conundrum in Cardiovascular Healthcare Provision

The Cost to Value Conundrum in Cardiovascular Healthcare Provision

Author: Larry H. Bernstein, MD, FCAP

Article ID #98: The Cost to Value Conundrum in Cardiovascular Healthcare Provision. Published on 1/1/2014

WordCloud Image Produced by Adam Tubman

I write this introduction to Volume 2 of the e-series on Cardiovascular Diseases, which curates the basic structure and physiology of the heart, the vasculature, and related structures, e.g., the kidney, with respect to:

1. Pathogenesis
2. Diagnosis
3. Treatment

Curation is an introductory portion to Volume Two, which is necessary to introduce the methodological design used to create the following articles. More needs not to be discussed about the methodology, which will become clear, if only that the content curated is changing based on success or failure of both diagnostic and treatment technology availability, as well as the systems needed to support the ongoing advances.  Curation requires:

  • meaningful selection,
  • enrichment, and
  • sharing combining sources and
  • creation of new synnthesis

Curators have to create a new perspective or idea on top of the existing media which supports the content in the original. The curator has to select from the myriad upon myriad options available, to re-share and critically view the work. A search can be overwhelming in size of the output, but the curator has to successfully pluck the best material straight out of that noise.

Part 1 is a highly important treatment that is not technological, but about the system now outdated to support our healthcare system, the most technolog-ically advanced in the world, with major problems in the availability of care related to economic disparities.  It is not about technology, per se, but about how we allocate healthcare resources, about individuals’ roles in a not full list of lifestyle maintenance options for self-care, and about the important advances emerging out of the Affordable Care Act (ACA), impacting enormously on Medicaid, which depends on state-level acceptance, on community hospital, ambulatory, and home-care or hospice restructuring, which includes the reduction of management overhead by the formation of regional healthcare alliances, the incorporation of physicians into hospital-based practices (with the hospital collecting and distributing the Part B reimbursement to the physician, with “performance-based” targets for privileges and payment – essential to the success of an Accountable Care Organization (AC)).  One problem that ACA has definitively address is the elimination of the exclusion of patients based on preconditions.  One problem that has been left unresolved is the continuing existence of private policies that meet financial capabilities of the contract to provide, but which provide little value to the “purchaser” of care.  This is a holdout that persists in for-profit managed care as an option.  A physician response to the new system of care, largely fostered by a refusal to accept Medicaid, is the formation of direct physician-patient contracted care without an intermediary.

In this respect, the problem is not simple, but is resolvable.  A proposal for improved economic stability has been prepared by Edward Ingram. A concern for American families and businesses is substantially addressed in a macroeconomic design concept, so that financial services like housing, government, and business finance, savings and pensions, boosting confidence at every level giving everyone a better chance of success in planning their personal savings and lifetime and business finances.

http://macro-economic-design.blogspot.com/p/book.html

Part 2 is a collection of scientific articles on the current advances in cardiac care by the best trained physicians the world has known, with mastery of the most advanced vascular instrumentation for medical or surgical interventions, the latest diagnostic ultrasound and imaging tools that are becoming outdated before the useful lifetime of the capital investment has been completed.  If we tie together Part 1 and Part 2, there is ample room for considering  clinical outcomes based on individual and organizational factors for best performance. This can really only be realized with considerable improvement in information infrastructure, which has miles to go.  Why should this be?  Because for generations of IT support systems, they are historically focused on billing and have made insignificant inroads into the front-end needs of the clinical staff.

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Multivitamins – Don’t help Extend Life or ward off Heart Disease and Improve state of Memory Loss

Reporter: Aviva Lev-Ari, PhD, RN

 

Experts: Don’t Waste Your Money on Multivitamins – Three studies find the supplements don’t help extend life or ward off heart disease and memory loss

http://www.nlm.nih.gov/medlineplus/news/fullstory_143473.html

Monday, December 16, 2013

HealthDay news image 

MONDAY, Dec. 16, 2013 (HealthDay News) — With three new studies finding that a daily multivitamin won’t help boost the average American’s health, the experts behind the research are urging people to abandon use of the supplements.

The studies found that popping a daily multivitamin didn’t ward off heart problems or memory loss, and wasn’t tied to a longer life span.

The studies, published in the Dec. 17 issue of the journal Annals of Internal Medicine, found that multivitamin and mineral supplements did not work any better than placebo pills.

Dietary supplements are a multibillion-dollar industry in the United States, and multivitamins account for nearly half of all vitamin sales, according to the U.S. Office of Dietary Supplements.

But a growing body of evidence suggests that multivitamins offer little or nothing in the way of health benefits, and some studies suggest that high doses of certain vitamins might cause harm.

As a result, the authors behind the new research said it’s time for most people to stop taking them.

“We believe that it’s clear that vitamins are not working,” said Dr. Eliseo Guallar, a professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health.

In a strongly worded editorial on the three studies, Guallar and his co-authors urged people to stop spending money on multivitamins.

Even a representatives of the vitamin industry asked people to temper their hopes about dietary supplements.

“We all need to manage our expectations about why we’re taking multivitamins,” Duffy MacKay, vice president of scientific and regulatory affairs for the Council for Responsible Nutrition, a trade group that represents supplement manufacturers, said in a prepared statement.

“Research shows that the two main reasons people take multivitamins are for overall health and wellness and to fill in nutrient gaps,” MacKay said. “Science still demonstrates that multivitamins work for those purposes, and that alone provides reason for people to take a multivitamin.”

However, Guallar said, it’s not clear that taking supplements to fill gaps in a less-than-perfect diet really translates into any kind of health boost.

“It would be great if all dietary problems could be solved with a pill,” he said. “Unfortunately, that’s not the case.”

For the first study, researchers randomly assigned almost 6,000 male doctors over the age of 65 to take either a daily Centrum Silver multivitamin or a look-alike placebo pill. Every few years, the researchers gave the men a battery of tests over the telephone to check their memories.

The men in the study were in pretty good health to begin with, and 84 percent said they faithfully took their pills each day.

After 12 years, there was no difference in memory problems between the two groups.

“No matter which way we broke it down, there was a null effect,” said study author Jacqueline O’Brien, a research associate at Brigham and Women’s Hospital in Boston. “Supplements are often marketed to have benefits for brain health and things like that, and this is a pretty clear takeaway message.”

The same study, however, had previously found that multivitamins might modestly reduce the risk of cancer and cataracts. Cancer risk was reduced by 8 percent, while the risk of cataracts dropped by 9 percent, compared to a placebo.

In the second study, researchers randomly assigned 1,700 heart attack survivors enrolled in a trial of therapy known as intravenous chelation to a daily regimen of high doses of vitamins and minerals or placebo pills.

Participants were asked to take six large pills a day, and researchers think many developed pill fatigue. Nearly half the participants in each part of the study stopped taking their medication before the end of the study. The average time people stuck with it was about two and a half years.

After an average of 55 months, there was no significant difference between the two groups in a composite measure that counted the number of deaths, second heart attacks, strokes, episodes of serious chest pain and procedures to open blocked arteries.

The third study, a research review, assessed the evidence from 27 studies on vitamin and mineral supplements that included more than 450,000 people. That study, conducted for the U.S. Preventive Services Task Force, found no evidence that supplements offer a benefit for heart disease or that they delay death from any cause. They found only a minimal benefit for cancer risk.

The results of the studies are so clear and consistent, the editorial writers said, that it’s time to stop wasting research money looking for evidence of a benefit.

“The probability of a meaningful effect is so small that it’s not worth doing study after study and spending research dollars on these questions,” Guallar said.

SOURCES: Eliseo Guallar, M.D., professor of epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore; Jacqueline O’Brien, Sc.D., research associate, Brigham and Women’s Hospital, Boston; Dec. 16, 2013, news release, Council for Responsible Nutrition, Washington, D.C.; Dec. 17, 2013, Annals of Internal Medicine

HealthDay
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SOURCES
http://www.nlm.nih.gov/medlineplus/news/fullstory_143473.html

http://consumer.healthday.com/cognitive-health-information-26/brain-health-news-80/experts-don-t-waste-your-money-on-multivitamins-683104.html

 

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