The epidemiology of cardiovascular disease in type 2 diabetes mellitus,natural medicine for high blood sugar,type 1 diabetes disability tax credit us - Plans On 2016

An estimated 382 million people worldwide have diabetes, according to a new report from the International Diabetes Federation. People who have Type 1 diabetes do not produce insulin, a hormone the body needs to convert sugar and starches into energy.
People with Type 2 diabetes have developed a resistance to the insulin their body produces. Gestational diabetes occurs during pregnancy and can increase both the mother and baby's chances of developing Type 2 diabetes later in life. The Middle East and North Africa currently have the highest rates of adult diabetes prevalence compared to other world regions, according to the report, but Africa will see the greatest increase in cases over the next two decades. In addition to those that already have diabetes, IDF estimates 316 million people have IGT, or impaired glucose tolerance - also known as prediabetes.
Diabetes is spreading because junky processed foods full of sugars, simple carbohydrates and artificial ingredients are saturating the markets. There is no worry at least getting diabetes as there is one herb called Cat's Whiskers herb which can effectively reduce the blood sugar level to normal level.
MANANA COMENZAMOS LAS DENUNCIAS INTERNACIONALES EN TODOS LOS PAISES POR EL USO DE TECNOLOGIAS INVASIVAS.
COMENZAMOS EN VENEZUELA CON POLITICOS E HIJOS CON LOS QUE HEMOS TRATADO DE CONVERSAR PARA QUE SUS PADRES DEJAN DE REALIZAR ESTOS CRIMENES.
As a parent of two kids with Type 1 diabetes, I greatly appreciate how the author of this article clarified the difference between Type 1 and Type 2 diabetes. Also note how the article mentions that ONLY 5% of diabetics in America have Type 1, which is an auto-immune disease with no cure. I am also diabatic patient but you must becareful from junks,sugar and must exercise regularly.
Education is vital when it comes to diabetes, and it is highly encouraged to become an expert in your own right. Actually my cousin sister is also suffering by diabetes and i know how much it will take prevention.
CNN welcomes a lively and courteous discussion as long as you follow the Rules of Conduct set forth in our Terms of Service. DrSanjayGupta: For the first time in history, the CDC is recommending pregnant women not travel to an American neighborhood.
DrSanjayGupta: Florida officials confirm 1st cases of Zika transmission by mosquitoes in US.
Get a behind-the-scenes look at the latest stories from CNN Chief Medical Correspondent, Dr. The International Diabetes Federation (IDF) -- the umbrella organization for 200 diabetes associations in more than 160 countries -- just released its 2013 Diabetes Atlas. If you've been following the trend in diabetes, it will not surprise you to know diabetes continues to rise, unabated, around the world.
Type 2 diabetes, which many consider an epidemic currently, is increasing worldwide predominantly due to poor diet, sedentary lifestyle and the fact that we are living longer. Leonor Guariguata, IDF biostatistician and coordinator for the Diabetes Atlas, told me via email something shocking.
Already, diabetes extracts a high cost in health care dollars, economies' financial stability, lost productivity, and it destroys lives and families. Sir Michael Hirst, IDF President, told me via email that research shows one in 10 of the world's population will have diabetes by 2035.
Diabetes imposes unacceptably high human, social and economic costs on countries at all income levels (p.
Why are we willing to further erode our nation's economic progress with a stunning "ignore now, pay overwhelmingly later" game? The refrain in public health is that, "People will make the healthy choice when the healthy choice is the easy choice." Guariguata agrees.
If diabetes is in your family, make sure everyone gets a fasting blood sugar test and see whether you have diabetes or Stage 1, pre-diabetes.
Science, Technology and Medicine open access publisher.Publish, read and share novel research.
Anemia of Chronic Kidney Disease in Diabetic Patients: Pathophysiologic Insights and Implications of Recent Clinical TrialsVictoria Forte1, Miriam Kim1, George Steuber1, Salma Asad 1 and Samy I. KDOQI Clinical Practice Guideline and clinical practice recommendations for anemia in chronic kidney disease.
Nevertheless this may be an option occasionally for cats that are very difficult inject insulin.
Tagged with: Diabetes Natural Cure diabetes natural treatment remedy for type 2 diabetes Reverse diabetes. Zinc monomethionine is a water soluble readily what are the symptoms of borderline diabetes bioavailable organic form of the essential trace element zinc. Oil dosage 600 mg dha epa daily Is food for canine diabetes Sweaty Palms A Sign Of Diabetes natural growth factors.
I would recommend these as a quick option over fast food or other frozen meal options for my diabetic patients.
Significant determinants of diabetes are age, body-mass index (BMI), waist-hip ratio, low physical activity, and family history of diabetes. Indians develop diabetes at a younger age and  those younger than 45 years accounts for 36% of all diabetics in India.13  Longer duration of diabetes leads to greater complications and this could threaten the national economy.
CVD risk is primarily due to elevated lipids and blood pressure (much more than elevated blood sugar). The latest data (2012) shows a prevalence of diabetes in excess of 25% in most states as shown in the figure 108.
Disclaimer : Please note that the content on CADI Research Foundation attempts to define practices that meet the needs of most patients in most circumstances.
The IDF expects that number to rise to 592 million by 2035, when one in every 10 people will have the disease. In fact, she says the estimates are conservative, and that diabetes may be a much bigger problem than we think. Type 1 diabetes used to be called juvenile onset diabetes because it is usually diagnosed in adolescence. Most people who develop Type 2 diabetes are adults, although experts worry about the increasing number of young people being diagnosed. Micronesia, Saudi Arabia, Kuwait and Qatar also reported higher-than-average prevalence rates. Approximately 80% of the people living with diabetes are in low- and middle-income countries. Urban centers in Africa are showing higher prevalence rates than cities in Europe, Guariguata said, and many cases go undiagnosed and untreated because of a lack of awareness in these countries. These drugs are sold to the most over-nourished populations and it is over-nourishment that causes diabetes. This has been proven for more than 10-20 yrs and yet sadly 99.9% of the westerners still think that herbs can cure cancers and diabetes are nonsense.
My sisters friend has been averaging 15k for months now and she works about 20 hours a week.
One thing is for sure, type 2 diabetes will continue to spike as long as Psychotropic Medications are prescribed.
Sanjay Gupta, Senior Medical Correspondent Elizabeth Cohen and the CNN Medical Unit producers. That despite being a non-communicable disease, where there are changes in risk factors and environments, diabetes will spread from one community to the other, essentially acting like a communicable disease. 14) of diabetes deaths are in people under 60 years old, handicapping Africa's ability for development.
In every respect -- human, financial, societal -- the burden of diabetes is, and is becoming, crippling.
Put pressure on your policy makers to vote for health, and create a healthier lifestyle for yourself and your family. Hoylaerts1[1] Center for Molecular and Vascular Biology, Belgium[2] Occupational & Environmental Medicine, Unit of lung toxicology University of Leuven, Belgium1. Once you are aware of the earliest warning signs of diabetes you can diabetes uk scotland jobs take charge of your health and avoid the debilitating consequence of this lifelong disease. Once you are aware of the earliest warning signs of diabetes you can take charge of your health and avoid the debilitating consequence of this lifelong disease. Insulin produces satiety inject it into the brain and people eat less: diabetes drugs without weight gain mody diabetes undiagnosed diabetic retinopathy labor Recurrent severe hypoglycemia. A new study published this week in the journal Diabetologia shows a correlation between the incidence of Type 1 diabetes and vitamin D3 serum levels. Platinum Guests learn about diabetes diet kenya diabetes and obesity as Scripps Florida Researchers tackle a global Sunday school and youth groups First diabetes pop quiz Presbyterian The general story was great and unique. Over the past 30 years, the prevalence of diabetes has increased to 12-18% in urban India and 3-6% in rural India with significant regional variations.1, 3, 4 5, 6 These rates in India are 50-80% higher than China (10%). The driving forces behind the epidemic are urbanization (30%) and economic development with resultant increase in GDP, sedentary lifestyle, western diet, and fast food diet on a background of genetic susceptibility.
Unfortunately, management of blood pressure and cholesterol remains dismally poor among diabetics in India (see Diabetes Control).
High prevalence of diabetes and cardiovascular risk factors associated with urbanization in India.
Methods for establishing a surveillance system for cardiovascular diseases in Indian industrial populations. Prevalence of risk factors for coronary atherosclerosis in a cross-sectional population of Andhra Pradesh. High prevalence of diabetes and impaired glucose tolerance in India: National Urban Diabetes Survey. Age- and sex-specific prevalence of diabetes and impaired glucose regulation in 11 Asian cohorts. Peroxisome proliferator-activated receptor-gamma co-activator-1alpha (PGC-1alpha) gene polymorphisms and their relationship to Type 2 diabetes in Asian Indians. Role of genetic polymorphism peroxisome proliferator-activated receptor-gamma2 Pro12Ala on ethnic susceptibility to diabetes in South-Asian and Caucasian subjects: Evidence for heterogeneity. Mortality rates due to diabetes in a selected urban south Indian population–the Chennai Urban Population Study [CUPS--16]. However, everyone is unique, and the extent to which the information applies specifically to you should be a key point of discussion between you and your cardiologist or health care provider.
A large part of this is due to the growing obesity problem; while all types of diabetes are on the rise, the number of people with Type 2 diabetes is expected to double in less than 25 years. You agree that anything you post may be used, along with your name and profile picture, in accordance with our Privacy Policy and the license you have granted pursuant to our Terms of Service.
They'll share news and views on health and medical trends - info that will help you take better care of yourself and the people you love.
Like the child and his brother in Africa who walk four hours in no shoes once a week to get insulin from the one clinic.
IntroductionNumerous epidemiological studies report consistent associations between exposure to urban air pollution and cardio-respiratory morbidity and mortality.


I replaced the chicken with dough the carrots with marinara parsnips with mozzarella and potatoes with pepperoni. It is estimated that 1 in 4 people (without diabetes) have a genetic predisposition (which means they are born more likely to develop it) for insulin resistance. It’s when the blood glucose level (blood sugar level) of the mother goes too high during pregnancy. I honestly do consider myself something of a genius just glutinous rice and diabetes based off IQ tests administered to me in grade school but lets face it.
The two major forms of diabetes are type 1 previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes and type 2 previously clled best foods for diabetics with kidney disease diabetes dogs treatment cost I diabetes drug names was getting burned out on the orange flavor Is Sweaty Palms A Sign Of Diabetes and decided to try this.
The ultimate judgment regarding your care must be made by you and your healthcare provider together, in light of circumstances specific to you as a patient. Or the young wife in India who has sold all the family possessions to buy her husband medicine and nurse him. One of the important discoveries of these epidemiological studies during the last decade was that the increased mortality associated with enhanced air pollution exposure was not due only to pulmonary diseases, but mainly to cardiovascular diseases.
Type 1 diabetes, also called insulin-dependent diabetes or juvenile-onset diabetes, involves lack of insulin and is relatively uncommon.
Or my neighbor's Type 2 diabetes that has caused her health to fail dramatically so for days she doesn't leave the apartment. Or coaching???” But it does seem to me that this wait is appropriate to the severity of your condition.
Optimal glycemic control in type 1 diabetes mellits (T1DM) requires Is Sweaty Palms A Sign Of Diabetes Intensive Insulin Therapy. Browne, et al.The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin. Mc Farlane, Mitigating the cardiovascular risk of anemia in patients with type 2 diabetes and CKD: Does darbepoetin help? This seems rather radical but if you are in poor health and suspect your diet miht be the cause the possibility of food allergy or intolerance is worth considering.
Because you will need to take insulin every day you will learn how to give yourself this shot.
Type 2 diabetes generally manifests after age 40 and therefore has the obsolete name of adult onset-type diabetes. Poellinger, Hyperglycemia regulates hypoxia-inducible factor-1 alpha protein stability and function.
Poor blood flow compromises the body’s ability to heal open wounds (often called ulcers) and fight infection. As I said, I did the research spending hours and days discovering that what the doctors were really telling me, and probably what they're telling you, had nothing to do with trying to cure my high glucose levels or even teach me how to NATURALLY bring them under control. Mc Farlane, Cardiovascular disease associated with anemia in diabetic patients with chronic kidney disease. Massy, Emerging biomarkers for evaluating cardiovascular risk in the chronic kidney disease patient: how do new pieces fit into the uremic puzzle? The focus in the initial epidemiological research was directed towards the association between both short-term and long-term exposure to air pollution and arterial cardiovascular effects, such as myocardial infarction. These landmark studies, in the beginning of the 90's, were quickly followed by experimental studies in humans and in rodents, to unravel the underlying pathophysiological mechanisms. The number of publications in this field increased exponentially, so that by the beginning of 2011, a search through PubMed using the MeSH terms 'air pollution' and 'cardiovascular disease' retrieved almost 1300 hits.Ambient environmental air pollutants include gaseous (carbon monoxide, nitrogen oxides, sulfur dioxide, ozone) and particulate components.
Although exposure to some gaseous components has been linked to cardiovascular events, the larger body of evidence points towards the deleterious effects of the particulates in air pollution. Therefore, this chapter will focus mainly on the cardiovascular morbidity induced by PM exposure.Active cigarette smoking has been established as a major independent cause of cardiovascular disease (HHS 2004). The inhaled dose of fine particles from ambient air pollution, as from secondhand cigarette smoke, is extremely small compared with that from active cigarette smoking. Accordingly, the estimated relative risks from active smoking, even at relatively light smoking levels, are substantially larger than the risks from ambient air pollution or secondhand smoke. However, the risks induced by these latter 2 types of exposure are higher than would be expected from a simple linear extrapolation based on the amount of inhaled PM from active smoking (Pope et al. The role of air pollution exposure as a risk factor for arterial events now being beyond discussion, a few years ago, epidemiologists started investigating a possible association with venous thrombotic events. To understand the pathophysiological mechanisms underlying the observed link between air pollution and cardiovascular morbidity, one should take into account the complex interplay of prohemostatic and antihemostatic mechanisms, with different protagonists for the arterial and the venous vasculature. The human cardiovascular system consists of a functional vascular network for blood distribution, subdivided in a systemic and pulmonary circulatory system. The systemic circulation transports oxygenated blood through the arteries from the left heart to the organs and returns oxygen-depleted blood through the veins to the lungs.
The pulmonary circulation subsequently transports the oxygen-depleted blood from the heart to the lungs, where it is oxygenated and returned to the heart.Vascular integrity throughout the vascular tree is maintained by the vessel wall itself, as well as by a complex hemostatic mechanism involving blood platelets and coagulation factors. The critical need to rapidly form a stable, localized clot in response to vascular injury (='hemostasis') must be balanced with the need to maintain blood flow within the vessels.
Different antihemostatic mechanisms prevent clot formation under resting physiological conditions, and limit clot growth to the site of vascular injury.
When prohemostatic tendencies proceed beyond the physiological need to maintain vascular integrity, a pathological thrombus may form, obstructing the normal blood flow (='thrombosis').
In the arterial system, thrombus formation induces oxygen-deprivation (ischemia) of the downstream tissues, such as myocardial infarction and cerebral ischemia. The formation of an arterial thrombus largely depends on the activation of blood platelets, and is most often triggered by the rupture of an atherosclerotic plaque. Indeed, the chronic localized deposition of lipids into the arterial vessel wall (atherosclerosis) leads to the formation of plaques that can rupture when unstable, hereby exposing their procoagulant contents to the circulation (Ross 1999). Hence, while often being asymptomatic in itself over many years, atherosclerosis formation may cumulate into an acute burst of symptomatic arterial thrombus formation.
In the venous system, thrombus formation results from a decrease in blood flow, in conjunction with a hypercoagulable state and endothelial dysfunction (Virchow's triad), and most often affects the deep veins of the legs (deep vein thrombosis, DVT).
Particle triggered pathophysiological mechanismsInhaled particles deposit in various segments of the human respiratory tract. While the larger PM10 particles impact to a large extent in the nasopharyngeal and tracheal region, the smaller PM2.5 particles penetrate deeper into the bronchi and bronchioli, whereas the UFP reach the alveolar regions. 1999)) have shown that, by reducing the heart rate variability, PM may increase the risk for cardiac arrhytmias and sudden death. In addition, elevations in air pollution have been associated with ST-segment depression (Pekkanen et al. The exact underlying mechanisms remain to be elucidated, but stimulation of irritant receptors in the airways and subsequent reflex activation of the nervous system as well as direct effects of pollutants on cardiac ion channels have been suggested (Brook et al.
2004b).A second mechanism of action comprises the translocation of inhaled particles into the systemic circulation. Direct effects may occur via UFP that readily cross the pulmonary epithelial barrier, along with soluble constituents released from the larger particles (e.g.
Systemic translocation of particles was demonstrated in experimental animal models (Nemmar et al. Although evidence of systemic translocation from human studies is less clear, with both positive (Nemmar et al.
2006) findings, it is likely that this pathway also exists in humans, given the deep penetration of UFP into the alveoli and the close apposition of the alveolar wall and the capillary network.
Radioactivity in the systemic circulation was already detected 1 minute after the inhalation of radioactively labelled carbon particles in humans, with peak radioactivity levels between 10 and 20 minutes (Nemmar et al. However, this fraction increased to 4.7% following pretreatment of the lungs with lipopolysaccharides, suggesting a role for pulmonary inflammation in enhancing the extrapulmonary translocation of particles (Chen et al.
Different translocation mechanisms, ranging from endocytosis by alveolar type I and endothelial cells, over phagocytosis by macrophages to passage through widened tight junctions are recognized and depend on the particle surface chemistry (Oberdorster, Oberdorster and Oberdorster 2005).
However, a detailed description of the different pathways is beyond the scope of this article. Once UFP have translocated to the blood circulation, they can be distributed throughout the body, and interact with the vascular endothelium or circulating cells, such as blood platelets and leukocytes.Inhaled PM executes its deleterious effects also via a third, more chronic mechanism, namely pulmonary inflammation and oxidative stress. Exposure to PM induces a proinflammatory response in human lungs (Ghio, Kim and Devlin 2000), consistent with observations in in vivo animal models (Nemmar et al.
The presence of soluble transition metals in PM enhances the inflammatory responses via increased oxidative stress (Jiang et al. The PM-induced pulmonary inflammation is followed by the release of inflammatory cytokines, such as interleukin (IL)-1?, IL-6 and granulocyte macrophage colony-stimulating factor (van Eeden et al.
2001) in the circulation, resulting in the release of bone-marrow derived neutrophils and monocytes (Tan et al. The generation of a systemic inflammatory response, mostly demonstrated by increases in C-reactive protein (CRP) (Peters et al. Upon PM exposure, IL-6 translocates from the lung into the systemic circulation (Kido et al.
Elevated concentrations of IL-6 are associated with an increased risk of cardiovascular events (Ridker et al. Knock-out mice that lacked IL-6 were protected against the prothrombotic effects of PM exposure (Mutlu et al.
Increasing evidence points to an extensive cross-talk between inflammation and hemostasis, whereby inflammation leads to activation of blood platelets and of coagulation, and activated blood platelets and coagulation factors also considerably contribute to the inflammatory action (Levi and van der Poll 2010).In the following paragraphs, the deleterious effects of PM exposure on arterial and venous parameters will be discussed. By virtue of their respective protagonist roles, blood platelet activation will mainly be discussed in the paragraph on arterial events, while coagulation activation will mainly be discussed in the paragraph on venous events.
Formally, arterial thrombosis, the basis for myocardial infarction, is the result of vessel wall injury and formation of a platelet-rich thrombus. Venous thrombosis, the basis for VTE (venous thromboembolism) results from coagulation activation and formation of a fibrin-rich thrombus. It should be noted, however, that both blood platelet and coagulation activation intervene in arterial and venous thrombosis, and that both systems highly interact with each other (Prandoni 2009). Air pollution and arterial eventsOver the last 2 decades, a vast number of epidemiological studies (reviewed in (Maitre et al.
2006)) have provided convincing evidence to conclude that chronic exposure to PM enhances atherosclerosis and that acute exposure increases the risk of atherosclerotic plaque rupture, triggering arterial thrombosis, myocardial infarction and cardiovascular mortality. Relative risk levels for cardiovascular disease may differ between different studies, due to differences in study design. Short-term effects have been most often studied in time-series and case-crossover studies, while long-term effects have been studied in case-control and cohort studies.
Relative risk levels are generally lower in time series studies than in other epidemiological designs.
Nevertheless, the associations between cardiovascular disease and PM exposure are consistent, whatever the type of method used (Maitre et al. An association with mortality was also found for traffic-related air pollution and several traffic exposure variables, although relative risks were small (Beelen et al. The effects of long-term PM exposure on cardiovascular mortality have been shown elegantly by the demonstration of a parallelism between air quality improvement and reduction in cardiovascular events on a population-based level (Laden et al. A potential benefit in general mortality can be expected within 2 years after the reduction of PM exposure (Schwartz et al.
Considering a large body of evidence, a recent updated version of the American Heart Association scientific statement on 'Air Pollution and Cardiovascular Disease' (Brook et al.


Chronic PM exposure and atherosclerosisWhat etiological agent can explain the link between chronic air pollution exposure and cardiovascular mortality? Distance from the residence to a major road correlated with the degree of coronary artery calcification, a measure for atherosclerosis (Hoffmann et al.
Another study in 5172 adults investigated 20-year PM exposure and found an association, although weaker than in the previous studies, with carotid intima media thickness, but not with other measures of atherosclerosis i.e. A recent study demonstrates that long-term PM exposure is not only related to the degree, but also to a faster progression rate of atherosclerosis (Kunzli et al. 2010).Along with this epidemiological evidence, experimental research also established a link between exposure to PM and the development of atherosclerosis.
Repeated exposure to PM10 in rabbits was associated with both systemic inflammation and the progression of the atherosclerotic process, the extent of which correlated with the extent of PM10 phagocytosed by alveolar macrophages (Suwa et al. 2008).Atherosclerosis is now considered an inflammatory disease with low density lipoprotein (LDL) cholesterol accumulation in the arteries as the primary risk factor (Ross 1999). However, up to 50% of the patients who develop atherosclerosis do not have high cholesterol (Braunwald 1997). Therefore, it is the relationship between the accumulated lipids and other harmful components of inflammation in the arterial vessel wall that is of concern. LDL infiltration of the arterial vessel wall is followed by oxidative modification to oxidized LDL (ox-LDL) in the subendothelial space and chemotaxis of monocytes. These monocytes differentiate into macrophages and the subsequent phagocytosis of ox-LDL leads to the formation of foam cells and the release of inflammatory mediators, inducing a vicious cycle of inflammation. Further stages include smooth muscle cell proliferation, formation of a fibrous cap with necrotic core and calcification (Ross 1999).
Thickening of the vessel wall and obliteration of the vascular lumen induces downstream ischemia of the tissues. PM exposure can induce atherosclerosis via different pathways: systemically translocated UFP or their chemical constituents induce activation of proatherogenic molecular pathways in endothelial cells, by oxidative stress. Inflammatory mediators released from the lungs may promote chemotaxis of monocytes into the vessel wall.
PM induces high-density lipoprotein (HDL) dysfunction with loss of its anti-inflammatory properties (Araujo and Nel 2009).Oxidative transformation of LDL into ox-LDL is a key step in the initiation and progression of atherosclerosis (Stocker and Keaney 2004), and circulating levels of ox-LDL are therefore an early marker, and a risk factor for the disease (Wallenfeldt et al.
The correlation between PM exposure and circulating levels of ox-LDL on an individual level was shown by Jacobs et al., demonstrating a dose-dependent association between this parameter and the carbon load of airway macrophages, a personal marker for chronic exposure to fossil fuel derived ultrafine particles (Jacobs et al. 2011).It has been previously shown that particles can induce oxidative stress both in vitro (Jimenez et al. 2009), experimental studies suggest that the smaller particles are more pathogenic, as a result of their greater propensity to induce systemic prooxidant and proinflammatory effects (Araujo et al.
Indeed, ambient UFP trigger the induction of the antioxidant gene heme oxygenase 1 (HO-1) to a higher degree than ambient PM2.5 or coarse particles, both in vitro (Li et al. The high number of UFP, in conjunction with a large surface-to-mass ratio increases the bioavailability of the pro-oxidant chemicals (polycyclic aromatic hydrocarbons, transition metals etc.) present on the UFP's surface. The number of chemicals that are displayed on the surface of particles increases exponentially as the size shrinks below 100 nm (Oberdorster et al. Acute PM exposure and arterial thrombosisNot only chronic, but also short-term PM exposure has been linked to cardiovascular mortality: Both the American NMMAPS (National Morbidity, Mortality, and Air Pollution Study (Dominici et al.
2003)) and the European APHEA2 (Air Pollution and Health: A European Approach (Katsouyanni et al. 2003)) studies (approximately 50 million and 43 million persons included respectively) demonstrated small increases in cardiovascular mortality with increasing PM exposure. In an attempt to evaluate the coherence of studies across continents, the APHENA (A Combined European and North American Approach) analyzed data of these 2 aforementioned studies and Canadian studies (Samoli et al. An extensive review of studies investigating a link between short-term PM exposure and cardiovascular mortality is provided in (Brook et al. 2001a) demonstrated an increased risk of myocardial infarction in association with elevated concentrations of fine PM2.5, both in the previous 2-hours period and the day before the onset. 2007).Although the magnitude of the risk on myocardial infarction induced by short-term PM exposure is rather small on a personal level, it is of major importance on a population level, by virtue of the large number of people exposed. Taking into account both risk magnitude and risk prevalence by measurement of the population attributable fraction (PAF), Nawrot et al. 2011).Epidemiological studies suggest an association between short-term increases in PM exposure and atherosclerotic plaque rupture, causing arterial thrombosis and myocardial infarction. In contrast to the growing number of mechanistic studies investigating the role of chronic PM exposure on atherogenesis, the precise mechanisms explaining the role of short-term PM exposure in acute plaque rupture largely remain to be elucidated.
However, several epidemiological and mechanistic studies demonstrated that, in parallel to atherosclerotic plaque rupture, direct or indirect activation of circulating blood platelets by PM contributes to the arterial thrombosis risk.
Indeed, the extent to which a growing thrombus occludes the vascular lumen may in part depend on platelet hyperactivity.Under physiological circumstances, the high blood pressure generated on the arterial side of the circulation requires a powerful, almost instantaneous prohemostatic response in order to minimize blood loss from sites of vascular injury. Upon damage of the endothelial cell layer covering the luminal side of blood vessels, circulating blood platelets adhere to the exposed subendothelial matrix through the binding of the glycoprotein (GP) Ib-IX-V receptor to exposed von Willebrand factor (vWF).
Blood platelet adhesion is further enhanced by the binding of different GP receptors to other subendothelial matrix proteins, such as collagen and fibrin(ogen). Upon adhesion and activation of the blood platelets by various agonists, vWF and fibrinogen molecules cross-link different platelets, resulting in blood platelet aggregation and the formation of an initial platelet plug which covers the site of endothelial lesion. The simultaneous activation of the coagulation cascade leads to the formation of a network of insoluble fibrin strands that further stabilize the initial platelet plug. Air pollution exposure can induce an inappropriate activation of blood platelets beyond the physiological need to restore vessel damage, resulting in arterial thrombosis (Fig. 2008).Short-term, but not long-term PM exposure was found to enhance platelet function, as measured ex vivo by a shortening of the closure time of the Platelet Function Analyzer (PFA-100, Siemens Healthcare Diagnostics), in patients with diabetes (Jacobs et al.
Platelet function was not correlated with leukocyte counts, suggesting that short-term PM exposure may have effects on platelet function independently of systemic inflammation, as was also shown in experimental animal models (Nemmar et al.
Ambient PM10 levels have also been associated with augmented platelet aggregation 24 to 96 hours after exposure in healthy adults, in the absence of increased CRP or fibrinogen (Rudez et al. In patients with coronary heart disease, mean concentrations over 24 hours of ambient UFP, but not PM2.5 or PM10 were positively associated with the levels of soluble CD40 ligand, a marker for platelet activation.
However, different pathophysiological mechanisms seem to be responsible for the observed prothrombotic risk at different time points. Pretreatment of hamsters with a histamine H1-receptor antagonist, an anti-inflammatory drug, abolished pulmonary inflammation at all time points and reduced DEP-induced thrombosis at 6 and 24 hours post-instillation, indicating a crucial role for inflammation in thrombogenicity at these time points. Likewise, the administration of other anti-inflammatory drugs, such as dexamethasone and selective inhibitors of basophils, macrophages and neutrophils, also significantly reduced the PM-induced prothrombogenicity at 24 hours (Nemmar et al.
2005).In contrast, pretreatment with the histamine H1-receptor antagonist did not reduce thrombosis as soon as 1 hour after DEP exposure (Nemmar et al. In agreement with these results, 1 hour after intratracheal instillation, well-defined positively charged ultrafine (60 nm) polystyrene particles significantly enhanced platelet-rich thrombus formation, while 400 nm particles, incapable of systemic translocation, did not affect thrombus formation, despite similar increases in neutrophils, lactate dehydrogenase and histamine levels in the bronchoalveolar lavage fluid (Nemmar et al.
Pulmonary instillation of carbon nanotubes elevated platelet-leukocyte conjugates at 6 hours and increased the peripheral thrombotic potential at 24 hours after exposure.
P-selectin is found in storage Weibel-Palade bodies of endothelial cells and in ?-granules of platelets, from where it can be expressed on the outer membrane upon activation. Surface expression of P-selectin initiates capture and rolling of circulating leukocytes over stimulated endothelium (Theilmeier et al. Increased levels of platelet-leukocyte conjugates have been demonstrated in Indian women who used biomass as cooking fuel, producing higher levels of PM, as compared to women cooking with a cleaner fuel (liquefied petroleum gas) (Ray et al.
Taken together, these studies suggest that the release of pulmonary cell-derived mediators (eg. P-selectin) after several hours, along with the more rapid activation of circulating platelets by direct contact with UFP may mediate peripheral prothrombotic effects.4. EpidemiologyIn addition to the well-recognized PM-related adverse effects on the arterial vascular system, recent epidemiological evidence also suggests an association between exposure to PM and venous thromboembolism (VTE). The observed exposure-response relationship was approximately linear over the observed PM10 range, so that PM10 at the higher concentrations within the international limits can still increase the risk of DVT, as compared to the lowest concentration measured. These authors found, in the same study subjects, that living near major traffic roads was also associated with an increased risk of DVT, even after controlling for the community-level PM pollution (Baccarelli et al. Very recently, exposure to PM has also been associated with hospital admission for VTE in Chile. Regardless of the treatment category, no evidence was found of an association between short- or long-term (up to 1 year) PM exposure and VTE (Shih et al. A prospective study in 13,134 middle-aged persons, including men and women, also provided evidence against an association between VTE and long-term air pollution exposure, as assessed by residential distance to a major road (Kan et al. PathophysiologyAt lower rates of shear found in the venous circulation, the contribution of blood platelets to clot formation is of lesser importance than in the arterial circulation, leaving a protagonist role for the coagulation cascade in venous hemostasis.
Activation of the coagulation cascade is initiated by activation of coagulation factor VII (FVII) by binding to tissue factor (TF), expressed on subendothelial cells such as fibroblasts and vascular smooth muscle cells.
The complex of TF and activated FVII (FVIIa) initiates a cascade of subsequent coagulation factor activations, resulting in the generation of thrombin. Thrombin (FII) is a key enzyme, converting fibrinogen monomers to fibrin polymers that clot into a fibrin plug, and amplifying the coagulation cascade through activation of FV, FVIII and FXI.The mechanisms underlying the observed increase in venous thrombosis in association with exposure to air pollution remain largely unknown, and published results with regard to markers of secondary hemostasis activation are conflicting.
Although some epidemiological and controlled exposure studies demonstrated an association between PM exposure and shortening of the prothrombin time (PT) or increased levels of fibrinogen and vWF, others failed to demonstrate positive associations with these or other markers of coagulation, in humans (Table 1). In fact, disappointingly few studies reported on PM-induced coagulatory changes that could form the basis for the observed link between air pollution and DVT. How can this conundrum of PM-induced DVT in the absence of a procoagulant phenotype be explained?One explanation for the lack of positive associations between PM exposure and measurement of parameters of coagulation might be found in the short observation time frame that was used in most studies. While short-term PM exposure enhances blood platelet activation, a more chronically sustained exposure appears to be necessary to induce significant changes in the coagulatory cascade.
This hypothesis is corroborated by epidemiological findings in which the risk for DVT was only associated with the mean PM concentration over a one year period, and not with any shorter time-point (Baccarelli et al. This was confirmed by animal studies in which short- term exposure of healthy mice to intratracheally instilled DEP or UPM enhanced arterial, but not venous thrombosis (Emmerechts et al. Likewise, exposure of rats to concentrated PM from New York City air did not alter levels of fibrinogen, FVII or thrombin-antithrombin complexes (TAT) (Nadziejko et al. 2002).Significant increases in the level of fibrinogen, or decreases in the levels of the anticoagulant proteins activated protein C or tissue factor pathway inhibitor (TFPI) upon short-term PM exposure have been observed in rodents, but at doses of 100 ?g or higher per mouse (Cozzi et al. One study stands out among other studies on procoagulant changes and PM exposure: Mutlu et al. The reason for the discrepancy between this and other studies being unclear, this study is of value since it demonstrated the absence of a PM-induced prothrombotic phenotype in interleukin-6 (IL-6) knock-out mice, recognizing a major role of inflammatory factors in the induction of procoagulant changes following PM exposure.Indeed, although some studies suggest a short-term effect of directly translocated UFP through the activation of the coagulation cascade via contact activation, as demonstrated in vitro (Kilinc et al. 2010), evidence seems to favor a more prominent role for inflammatory changes related to chronic PM exposure. Microvesicles are circulating vesicles released from stimulated or apoptotic cells in the vasculature, or during thrombogenesis in the bone marrow, with a mean diameter smaller than 1 ?m. Through their surface expression ofreferencesubjectsexposurecoagulatory changesauthor + yearntypemean age(SD or range)gender(% male)controlled exposuretype of air pollutionexposure timesignificant changesno significant changes(Seaton et al.
2006)13healthy subjects34 (20-56)46yeswood smoke4hFVIIIfbg, FVII, D-dim, vWF(Ruckerl et al.



Management of type 2 diabetes in general practice
Seven steps to dental health options
04.01.2015 Ictm Diabetes


Comments

  1. ZAYKA

    Day, dr and I agreed going to a forty-50 net carb might these uncomfortable side.

    04.01.2015

  2. 59

    Given a number of diets of varying macronutrient striking pattern.

    04.01.2015

  3. SADE_QIZ

    Need to know is how low do you need your daily tasty you won't uncontrolled high blood pressure.

    04.01.2015