ScienceDaily (Jan. 3, 2006) — Passive smoking almost doubles the risk of the progressively degenerative eye disease, age related macular degeneration, shows research in the British Journal of Ophthalmology.
The macula lies at the centre of retina at the back of the eye. It's crucial for fine central vision, which is essential for tasks, such as reading and driving.
The risk of macular degeneration increases once someone is over the age of 60. It is a leading cause of partial sightedness and blindness in many European countries and the USA.
The researchers base their findings on 435 people with end stage macular degeneration and 280 partners who lived with them.
They found that the more a person smoked, the greater were their chances of developing age related macular degeneration, and the results showed that it was the amount smoked rather than whether someone had ever smoked that was critical.
Regularly smoking a pack or more a day for 40 years almost tripled the risk of age related macular degeneration compared with those who did not smoke, the research showed.
Smoking increased the risk of both types of macular degeneration (geographic atrophy and choroidal neovascularisation).
Giving up for 20 years or more cut the risk to levels comparable with those for non-smokers, the research found
The risks were also increased for partners who were non-smokers, and had lived with a smoker for five years or more. Their risk nearly doubled.
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Citation: Smoking and age related macular degeneration: the number of pack years of cigarette smoking is a major determinant of risk for both geographic atrophy and choroidal neovascularisation Br J Ophthalmol 2006; 90: 73-80
Adapted from materials provided by BMJ Specialty Journals.
BMJ Specialty Journals (2006, January 3). Passive Smoking Almost Doubles Risk Of Degenerative Eye Disease. ScienceDaily. Retrieved January 8, 2008, from http://www.sciencedaily.com /releases/2006/01/060102123337.htm
Monday, January 7, 2008
Smoking Doubles Risk Of Degenerative Eye Condition
ScienceDaily (Apr. 15, 2005) — Smoking doubles the risk of the progressive and irreversible eye condition, macular degeneration, and may account for almost 30,000 cases in the UK, suggests research in the British Journal of Ophthalmology.
The risk of macular degeneration increases with age and is the most common cause of blindness in the
The findings are based on a representative sample of over 4,000 people, aged 75 and older, from 49 general practices across
The participants all underwent a series of detailed eye tests and were asked about their smoking habits, and if they had given up, how long ago. After taking into account other risk factors, such as alcohol consumption and cardiovascular disease, the results showed that current smokers were twice as likely to be visually impaired as non-smokers.
Those who had kicked the habit more than 20 years previously were not at risk.
Based on the numbers of people in the
"An increased risk of [age related macular degeneration], which is the most commonly occurring cause of blindness in the United Kingdom, is yet another reason for people to stop smoking and governments to develop public health campaigns against this hazard," conclude the authors.
Adapted from materials provided by British Medical Journal.
High Insulin Levels Increase Inflammatory Markers And Beta-amyloids, May Contribute To Alzheimer's
ScienceDaily (Aug. 12, 2005) — CHICAGO -- Moderately elevated levels of insulin increase the levels of inflammatory markers and beta-amyloid in plasma and in cerebrospinal fluid, and these markers may contribute to Alzheimer's disease, according to a new study posted online today from Archives of Neurology, one of the JAMA/Archives journals. The study will be published in the October print edition of the journal.
According to background information in the article, "conditions of insulin resistance and hyperinsulinemia are associated with elevated levels of inflammatory markers and increase the risk for Alzheimer disease (AD). Inflammation has been proposed as a key pathogenic factor for AD."
Mark A. Fishel, M.D., from the University of Washington, Seattle, and colleagues, raised blood insulin levels (while maintaining normal blood sugar levels) in 16 healthy older adults ranging in age from 55 to 81 years, and then measured the changes in levels of inflammatory markers, modulators, and beta-amyloid (a protein associated with AD) in plasma and cerebrospinal fluid.
"Moderate peripheral hyperinsulinemia (increased levels of insulin) provoked striking increases in CNS (central nervous system) inflammatory markers," the authors report. "Our findings suggest that insulin-resistant conditions such as diabetes mellitus and hypertension may increase the risk for AD, in part through insulin-induced inflammation."
"Although this model has obvious relevance for diabetes mellitus, hyperinsulinemia and insulin resistance are widespread conditions that affect many nondiabetic adults with obesity, impaired glucose tolerance, cardiovascular disease, and hypertension. Our results provide a cautionary note for the current epidemic of such conditions, which, in the context of an aging population, may provoke a dramatic increase in the prevalence of AD. More encouragingly, greater understanding of insulin's role in AD pathogenesis may lead to novel and more effective strategies for treating, delaying, or even preventing this challenging disease," the authors conclude.
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(Arch Neurol. 2005; 62: 1-6. Available pre-embargo for the media at www.jamamedia.org) Editor's Note: This work was supported by the Department of Veterans Affairs,
Adapted from materials provided by JAMA and Archives Journals.
Cytokine Resistance Contributes To Pathology Of Type 2 Diabetes
ScienceDaily (Jun. 15, 2007) — In a study appearing this month in the Journal of Immunology, researchers at the University of Illinois describe how an impaired anti-inflammatory response plays a role in the pathology of type 2 diabetes.
Type 2 diabetes is classified as a metabolic disorder, but a growing number of researchers are beginning to think of it also as a disease of the innate immune system. Inflammation, a key component of the early immune response, is chronically elevated in people with type 2 diabetes. While the pro-inflammatory pathways of type 2 diabetes have received much attention, the anti-inflammatory side of the equation is less well known.
The new study focused on a number of cytokines, protein signals that bind to specific receptors on cells and set off a cascade of biochemical reactions within the cell. Interleukins, interferons, tumor necrosis factors and some growth factors are among the cytokines that direct many aspects of the immune response. Cytokines are secreted by many types of cells, including the immune cells known as macrophages.
In earlier studies, the researchers had shown that macrophages in diabetic and obese (diabese) mice secrete more pro-inflammatory and less anti-inflammatory cytokines than those of nondiabese mice. The team, led by pathology professor and department head Gregory Freund, also had demonstrated that human monocytes cultured under type 2 diabetic conditions had impaired interleukin-4 signaling. Interleukin 4 (IL-4) is an important player in the immune response in that it steers macrophages toward the production of other anti-inflammatory cytokines. It also inhibits secretion of the pro-inflammatory cytokines.
When IL-4 binds to its receptor on a target cell, it sets off one of two cascades of intracellular events.
The first of these signal transduction pathways, the Jak-STAT pathway, is well studied and well understood. The second, called the insulin receptor substrate 2 / phosphatidylinositol-3 kinase (IRS-2/PI3K) pathway, was more of a mystery, and of greater interest to Freund and his colleagues.
What drew them to this pathway was its potential role in the anti-inflammatory response, and its similarity to the cascade initiated when cells respond to insulin.
“One of the actions of diabetes is to create intracellular insulin resistance,” Freund said. “Some of the cytokines that work on cells share the same pathways as the insulin receptor.” Since diabetes causes insulin resistance, Freund said, “shouldn’t there be a resistance to cytokines, too? And that is what we found.”
The research team showed, for the first time, that the IRS-2 signaling arm of the interleukin-4 pathway directed the up-regulation of a key anti-inflammatory molecule in primary macrophages, and that this pathway was disrupted in type 2 diabetic conditions. They also showed that the loss of IL-4 function in diabese mice caused chronic over-expression of an important suppressor of cytokine signaling (SOCS) protein. This SOCS-3 protein aborts the cascade of events that normally leads to insulin uptake and/or cytokine signaling in a balanced inflammatory response.
This study supports earlier findings that inflammation is a key part of the pathology of diabetes, Freund said. Pro-inflammatory cytokines are elevated in type 2 diabetes, but the anti-inflammatory mechanisms are also impaired, leading to a multitude of major and minor health issues in the diabese.
“They get a cold. They get injured. Something happens. And it’s worse in those people with obesity or diabetes and lasts longer than it does in others,” Freund said. “Why? The imbalance may be the elevation in pro-inflammation. But it probably also includes a loss of anti-inflammatory function.”
This research was supported by grants from the National Institutes of Health, American Heart Association, and the
Adapted from materials provided by University of Illinois at Urbana-Champaign.
Pro-inflammatory Enzyme Linked To Diabetes; Immune System's Macrophages May Be Key To Treatment
ScienceDaily (Feb. 3, 2005 ) — An enzyme that initiates inflammation has been directly linked to insulin resistance and resulting type II diabetes by researchers at the UCSD School of Medicine. In addition, the team suggests that inhibition of the enzyme in the immune system’s macrophages may be a new diabetes therapy.
Published in the February 2005 issue of the journal Nature Medicine, the study describes research in mice that identifies enzyme IkB kinase ß (Ikk-ß) as a central coordinator of inflammatory responses in the liver and macrophages, the immune system cells which attack infections.
Both control mice and mice with Ikk-ß deleted in specific types of cells were fed a high-fat diet that normally causes metabolic syndrome and type II diabetes. While the control mice developed the diabetes and insulin-resistant symptoms, mice in which the Ikk-ß was deleted from microphages retained their healthy insulin levels.
“The potential for a new diabetes treatment is great,” said one of the study’s senior authors, Jerrold Olefsky, M.D., chief of UCSD’s Division of Endocrinology and Metabolism in the Department of Medicine, and associate dean for scientific affairs for the
Affecting 18.2 million Americans, diabetes is a disease in which the body does not produce or properly use insulin, a hormone necessary to convert sugar, starches and other food into energy needed for daily life. Previous studies in the past few years have implicated inflammation as playing a role in diabetes, but just how this occurred was unknown.
The researchers generated mice without Ikk-ß in liver cells that play a direct role in insulin-regulated glucose metabolism, and in systemic myeloid cells, pivotal players in inflammatory responses as they produce macrophages.
In response to challenges with a high-fat diet, mice with Ikk-ß deficient myeloid cells retained insulin sensitivity in all target tissues. Because the myeloid cells (and their macrophages) are systemic – able to travel throughout the body – they were identified by the researchers as the best target for diabetes treatments.
The mice lacking Ikk-ß only in the liver retained their insulin sensitivity in the liver but became insulin resistant in fat and muscle. Other tissue, such as muscle, was not tested in this study, because a previous study has shown that deletion of Ikk-ß in muscle has no effect on obesity-induced insulin resistance and type II diabetes, although muscle is a major insulin-responsive tissue.
In addition to Olefsky, a senior author of the paper was Michael Karin, Ph.D., UCSD professor of pharmacology, an American Cancer Society Research Professor, and the scientist who first discovered IKK and its subunits. The paper was a collaborative effort between the diabetes lab of Olefsky and Karin’s molecular signaling lab in the department of pharmacology.
Additional authors included first author Melek C. Arkan, UCSD Department of Pharmacology; and Andrea L. Hevener, UCSD Division of Endocrinology and Metabolism, Department of Medicine; Florian R. Freten, Shin Maeda, Zhi-Wei Li, UCSD Division of Endocrinology and Metabolism, Department of Medicine; Jeffrey M. Long, Ph.D., and Anthony Wynshaw-Boris, M.D., Ph.D., UCSD Departments of Pediatrics and Medicine; and Giuseppe Poli, S. Luigi Hospital, University of Turin, Italy. The study was funded by the National Institutes of Health.
Adapted from materials provided by University Of California - San Diego.
Type 2 Diabetes: Inflammation, Not Obesity, Cause Of Insulin Resistance
ScienceDaily (Nov. 7, 2007) — Researchers at the University of California, San Diego (UCSD) School of Medicine have discovered that inflammation provoked by immune cells called macrophages leads to insulin resistance and Type 2 diabetes. Their discovery may pave the way to novel drug development to fight the epidemic of Type 2 diabetes associated with obesity, the most prevalent metabolic disease worldwide.
In recent years, it has been theorized that chronic, low-grade tissue inflammation related to obesity contributes to insulin resistance, the major cause of Type 2 diabetes. In research done in mouse models, the UCSD scientists proved that, by disabling the macrophage inflammatory pathway, insulin resistance and the resultant Type 2 diabetes can be prevented.
In recent years, it has been theorized that chronic, low-grade tissue inflammation related to obesity contributes to insulin resistance, the major cause of Type 2 diabetes. In research done in mouse models, the UCSD scientists proved that, by disabling the macrophage inflammatory pathway, insulin resistance and the resultant Type 2 diabetes can be prevented.
The findings of the research team, led by principle investigators Michael Karin, Ph.D., Professor of Pharmacology in UCSD's Laboratory of Gene Regulation and Signal Transduction, and Jerrold Olefsky, Distinguished Professor of Medicine and Associate Dean for Scientific Affairs, will be published as the feature article of the November 7 issue of Cell Metabolism.
"Our research shows that insulin resistance can be disassociated from the increase in body fat associated with obesity," said Olefsky.
Macrophages, found in white blood cells in the bone marrow, are key players in the immune response. When these immune cells get into tissues, such as adipose (fat) or liver tissue, they release cytokines, which are chemical messenger molecules used by immune and nerve cells to communicate. These cytokines cause the neighboring liver, muscle or fat cells to become insulin resistant, which in turn can lead to Type 2 diabetes.
The UCSD research team showed that the macrophage is the cause of this cascade of events by knocking out a key component of the inflammatory pathway in the macrophage, JNK1, in a mouse model. This was done through a procedure called adoptive bone marrow transfer, which resulted in the knockout of JNK1 in cells derived from the bone marrow, including macrophages.
With this procedure, bone marrow was transplanted from a global JNK1 knockout mouse (lacking JNK1 in all cell types) into a normal mouse that had been irradiated to kill off its endogenous bone marrow. This resulted in a chimeric mouse in which all tissues were normal except the bone marrow, which is where macrophages originate. As a control, the scientists used normal, wild-type mice as well as mice lacking JNK1 in all cell types. These control mice were also subjected to irradiation and bone marrow transfer.
The mice were all fed a high-fat diet. In regular, wild-type mice, this diet would normally result in obesity, leading to inflammation, insulin resistance and mild Type 2 diabetes. The chimeric mice, lacking JNK1 in bone marrow-derived cells, did become obese; however, they showed a striking absence of insulin resistance -- a pre-condition that can lead to development of Type 2 diabetes.
"If we can block or disarm this macrophage inflammatory pathway in humans, we could interrupt the cascade that leads to insulin resistance and diabetes," said Olefsky. "A small molecule compound to block JNK1 could prove a potent insulin-sensitizing, anti-diabetic agent."
The research also proved that obesity without inflammation does not result in insulin resistance. Olefsky explained that when an animal or a human being becomes obese, they develop steatosis, or increased fat in the liver. The steatosis leads to liver inflammation and hepatic insulin resistance.
The chimeric mice did develop fatty livers, but not inflammation. "Their livers remained normal in terms of insulin sensitivity," said Olefsky, adding that this shows that insulin resistance can also be disassociated from fatty liver.
"We aren't suggesting that obesity is healthy, but indications are promising that, by blocking the macrophage pathway, scientists may find a way to prevent the Type 2 diabetes now linked to obesity and fatty livers," Olefsky said.
Co-first authors of the paper are Giovanni Solinas, UCSD Department of Pharmacology and Cristian Vilcu, UCSD Division of Endocrinology and Metabolism.
Additional contributors include Jun-Li Luo, Willscott Naugler and Sergei Grivennikov, UCSD Department of Pharmacology; Jaap G. Neels, and Gautam K. Bandyopadhyay, UCSD Division of Endocrinology and Metabolism; Anthony Wynshaw-Boris, UCSD Departments of Pediatrics and Medicine; and Miriam Scadeng, UCSD Department of Radiology.
This research was supported by National Institutes of Health grants ES004151, ES006376, DK033651 and DK074868. Additional funding was provided by a fellowship from the Swiss National Science Foundation, a University of California Discovery Grant and Mentor-Based Postdoctoral Fellowships from the American Diabetes Association.
Adapted from materials provided by University of California - San Diego.
University of California - San Diego (2007, November 7). Type 2 Diabetes: Inflammation, Not Obesity, Cause Of Insulin Resistance. ScienceDaily. Retrieved January 8, 2008, from http://www.sciencedaily.com /releases/2007/11/071106133106.htm
Diabetes, Depression Together Increase Risk For Heart Patients
ScienceDaily (Mar. 11, 2007 ) — Having both depression and type 2 diabetes increases the risk of death for heart patients. Each factor had been known to increase the risk of heart disease deaths by itself, but together they're even more deadly.
In an analysis of more than 900 patients with established coronary artery disease,
The study showed that among type 2 diabetes patients, having high depression scores increased the risk of dying by 20 to 30 percent compared to patients with similar depression scores but no type 2 diabetes.
"We found a trend showing that the probability of death increases as the level of depression increases in diabetic patients with coronary artery disease," said Duke researcher Anastasia Georgiades, Ph.D. "Our data appear to show an important interaction between type 2 diabetes and depression, meaning that physicians should closely monitor their heart patients who have both of these disorders."
"There is some sort of synergistic effect between type 2 diabetes and depression that we don't fully understand," Georgiades said. "In our analysis, we controlled for factors that could influence mortality, such as heart disease severity and age. For whatever reasons, these patients were still at higher risk of dying, and future research will aim to investigate the mechanisms for this association."
The research was supported by the National Heart, Lung, Blood Institute.
The researchers followed 933 heart patients for more than four years and correlated the 135 deaths that occurred during that period with the presence of type 2 diabetes and depression alone and together.
Georgiades said there are some possible explanations for the link between depression and diabetes.
"Patients with type 2 diabetes typically have an extensive self-care regimen involving special diet, medications, exercise and numerous appointments with their doctor," she said. "It may be that such patients who are depressed might not be as motivated to carry out all these activities, thereby putting them at higher risk."
Depression has also been linked to other cardiovascular risk factors such as insulin resistance, hypertension, obesity, increased cigarette smoking, alcohol abuse and physical inactivity.
Adapted from materials provided by Duke University Medical Center.
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