Medical News Today News Article: "Gene Linked To Increased Risk Of Developing Inflammatory Arthritis May Also Increase Patients' Risk Of Dying From Cardiovascular Disease
01 Feb 2008
People with rheumatoid arthritis (RA), an inflammatory autoimmune disease, tend to die younger and, largely from cardiovascular disease (CVD). One explanation for this increasingly recognized fact is that inflammation promotes atherosclerosis. A marker of inflammation, elevation of the C-reactive protein (CRP) level has been shown to predict CVD in the general population. However, other highly inflammatory diseases - Crohn's, for example - do not carry the same high risk of premature death from heart disease.
To identify other possible suspects, researchers in the United Kingdom investigated whether genetic variants linked to the likelihood of developing RA might also make patients more likely to die from CVD. Led by Dr. Tracey M. Farragher at the University of Manchester and funded by the Arthritis Research Campaign (arc), the study focused on two genes - HLA-DRB1and PTPN22 - and their interactions with known RA risk factors. The evidence, presented in the February 2008 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), implicates HLA-DRB1 genotypes, already associated with RA susceptibility and severity, as a predictor of premature death from CVD for inflammatory arthritis patients. For RA patients in particular, having the shared epitope (SE) - a group of HLA-DRB1 alleles with kindred amino acid traits - plus anti-cyclic citrullinated peptide (anti-CCP) antibodies and current smoking is an especially deadly combination."
Showing posts with label Genetics. Show all posts
Showing posts with label Genetics. Show all posts
Friday, February 1, 2008
Saturday, January 19, 2008
Study Locates Cholesterol Genes; Finds Surprises About Good, Bad Cholesterol
Study Locates Cholesterol Genes; Finds Surprises About Good, Bad Cholesterol
ScienceDaily (Jan. 17, 2008) — An international study of 20,000 people found seven new genes that influence blood cholesterol levels, a major factor in heart disease, and confirmed 11 other genes previously thought to influence cholesterol.
full story
ScienceDaily (Jan. 17, 2008) — An international study of 20,000 people found seven new genes that influence blood cholesterol levels, a major factor in heart disease, and confirmed 11 other genes previously thought to influence cholesterol.
full story
Friday, October 5, 2007
Why Lonely People Get Sick More Often
Why Lonely People Get Sick More Often
New research suggests that social isolation alters the immune system at the genetic level, raising the risk of serious disease. Oh, and the definition of loneliness might surprise you.
WEB EXCLUSIVE
By Sarah Kliff
Newsweek
Updated: 4:51 p.m. ET Sept. 13, 2007
Sept. 13, 2007 - We all know about heartache. For some, feeling alone can be physically painful. And a strong body of recent research has established that it’s not just in our minds. Chronic social isolation is linked to heart disease—it stresses the entire cardiovascular system—and can also hurt our ability to fend off colds and other viruses. But the cause of those connections has been unclear. Is it that lonely people have fewer social resources, meaning no one to rely on when they fall ill, or can the sensation of loneliness change their biology?
A study out this week suggests that it’s the latter: loneliness actually changes how the body functions at a molecular level. The research links feelings of social isolation to an alteration in the activity of specific genes—ones that put lonely people at higher risk for serious disease. And the study, published in the current issue of Genome Biology, also points to the startling fact that it is the perception of loneliness that triggers the adverse health conditions, independent of how much social interaction an individual actually has. Even someone with hundreds of “friends” on Facebook or at the office might think of herself as a lonely person.
So how can feeling lonely translate into poor health? Researchers believe that chronic social isolation sets off a biological chain reaction that causes normal immune responses to malfunction. It starts with the lonely individual’s outlook on the world, in which, typically, other people are perceived as threatening. This makes social interactions—going to a party, for example—more stressful. “Chronically lonely people have a subjective theory of the world that says that people can’t be trusted,” says Steven Cole, assistant professor at the UCLA School of Medicine and the study’s lead author. “It’s not that they’re hostile; they just perceive the world as somewhat more threatening.”
That perception cues the body to produce a stress hormone called cortisol. In a healthy immune system, cortisol tells a group of genes to shut down the body’s inflammatory response. But in a person who’s chronically stressed or anxious due to loneliness, that process is altered. Here’s how it works: for most people a low level of inflammation is normal; it means the body is performing general maintenance and responding to minor, sometimes unnoticeable threats. However, high levels of inflammation are worrisome. In autoimmune diseases, for example, the body attacks its own tissues and causes an increase in inflammation. Inflammation is also linked to a number of serious health risks, including cancer. Cole and his colleagues found that lonely individuals consistently had higher levels of inflammation even though they were producing a slightly higher level of cortisol—the hormone that should be shutting down the inflammatory response. The receptors, Cole says, were not responding properly, probably because they were receiving a constant stream of cortisol. “If you send a signal to a receptor all day long it will stop listening,” says Cole. “Essentially, it’s like the immune system saying that cortisol is crying wolf."
That accounts for the higher levels of inflammation the researchers observed in chronically lonely individuals. But they also found other faulty immune responses: lonely people produced fewer antibodies, which the body uses to tag pathogens, like bacteria and viruses. They also had a lower antiviral response; a group of genes involved in fighting viruses were not expressing themselves as much. “The risky parts of the immune system are going too hard, and the health-protective parts are not going hard enough,” says Cole.
Interestingly, what causes that imbalance isn’t how many pals an individual has or the number of social interactions. Rather, the loneliness that leads to these adverse health conditions is tied to how individuals perceive their social situations. “Loneliness is inherently subjective,” says Steven Asher, a psychology professor at Duke University who was not affiliated with the study. Asher has spent decades studying friendship and loneliness and says that an individual’s level of social interaction does not necessarily say anything about his or her loneliness.
“You can measure how many friends they have, and whether they provide support, but the only way you can know if somebody is lonely is to ask them,” says Asher. He has observed individuals with many friends who will report being lonely and, on the opposite side, those with few friends who do not. And, like Cole, Asher has found that lonely individuals tend to have a distinctly different outlook on social interactions. “We find that people who are lonely are more socially anxious,” Asher says. “They’re definitely feeling more stress and more anxiety.”
So what should lonely guys and gals do if they’re worried about their health? Harvard Medical School experts suggest talk therapy. For those who want to tackle the loneliness head on, helping others can be a fantastic way to make essential social connections. Tutoring in a subject you know at a local school or any kind of volunteer work can provide all-around benefits and bring you close to people of like mind. Even just one new but meaningful contact can make all the difference. And to manage creeping stress, you can take some basic relaxation measures like meditation or paced breathing.
URL: http://www.msnbc.msn.com/id/20762868/site/newsweek/page/0/
New research suggests that social isolation alters the immune system at the genetic level, raising the risk of serious disease. Oh, and the definition of loneliness might surprise you.
WEB EXCLUSIVE
By Sarah Kliff
Newsweek
Updated: 4:51 p.m. ET Sept. 13, 2007
Sept. 13, 2007 - We all know about heartache. For some, feeling alone can be physically painful. And a strong body of recent research has established that it’s not just in our minds. Chronic social isolation is linked to heart disease—it stresses the entire cardiovascular system—and can also hurt our ability to fend off colds and other viruses. But the cause of those connections has been unclear. Is it that lonely people have fewer social resources, meaning no one to rely on when they fall ill, or can the sensation of loneliness change their biology?
A study out this week suggests that it’s the latter: loneliness actually changes how the body functions at a molecular level. The research links feelings of social isolation to an alteration in the activity of specific genes—ones that put lonely people at higher risk for serious disease. And the study, published in the current issue of Genome Biology, also points to the startling fact that it is the perception of loneliness that triggers the adverse health conditions, independent of how much social interaction an individual actually has. Even someone with hundreds of “friends” on Facebook or at the office might think of herself as a lonely person.
So how can feeling lonely translate into poor health? Researchers believe that chronic social isolation sets off a biological chain reaction that causes normal immune responses to malfunction. It starts with the lonely individual’s outlook on the world, in which, typically, other people are perceived as threatening. This makes social interactions—going to a party, for example—more stressful. “Chronically lonely people have a subjective theory of the world that says that people can’t be trusted,” says Steven Cole, assistant professor at the UCLA School of Medicine and the study’s lead author. “It’s not that they’re hostile; they just perceive the world as somewhat more threatening.”
That perception cues the body to produce a stress hormone called cortisol. In a healthy immune system, cortisol tells a group of genes to shut down the body’s inflammatory response. But in a person who’s chronically stressed or anxious due to loneliness, that process is altered. Here’s how it works: for most people a low level of inflammation is normal; it means the body is performing general maintenance and responding to minor, sometimes unnoticeable threats. However, high levels of inflammation are worrisome. In autoimmune diseases, for example, the body attacks its own tissues and causes an increase in inflammation. Inflammation is also linked to a number of serious health risks, including cancer. Cole and his colleagues found that lonely individuals consistently had higher levels of inflammation even though they were producing a slightly higher level of cortisol—the hormone that should be shutting down the inflammatory response. The receptors, Cole says, were not responding properly, probably because they were receiving a constant stream of cortisol. “If you send a signal to a receptor all day long it will stop listening,” says Cole. “Essentially, it’s like the immune system saying that cortisol is crying wolf."
That accounts for the higher levels of inflammation the researchers observed in chronically lonely individuals. But they also found other faulty immune responses: lonely people produced fewer antibodies, which the body uses to tag pathogens, like bacteria and viruses. They also had a lower antiviral response; a group of genes involved in fighting viruses were not expressing themselves as much. “The risky parts of the immune system are going too hard, and the health-protective parts are not going hard enough,” says Cole.
Interestingly, what causes that imbalance isn’t how many pals an individual has or the number of social interactions. Rather, the loneliness that leads to these adverse health conditions is tied to how individuals perceive their social situations. “Loneliness is inherently subjective,” says Steven Asher, a psychology professor at Duke University who was not affiliated with the study. Asher has spent decades studying friendship and loneliness and says that an individual’s level of social interaction does not necessarily say anything about his or her loneliness.
“You can measure how many friends they have, and whether they provide support, but the only way you can know if somebody is lonely is to ask them,” says Asher. He has observed individuals with many friends who will report being lonely and, on the opposite side, those with few friends who do not. And, like Cole, Asher has found that lonely individuals tend to have a distinctly different outlook on social interactions. “We find that people who are lonely are more socially anxious,” Asher says. “They’re definitely feeling more stress and more anxiety.”
So what should lonely guys and gals do if they’re worried about their health? Harvard Medical School experts suggest talk therapy. For those who want to tackle the loneliness head on, helping others can be a fantastic way to make essential social connections. Tutoring in a subject you know at a local school or any kind of volunteer work can provide all-around benefits and bring you close to people of like mind. Even just one new but meaningful contact can make all the difference. And to manage creeping stress, you can take some basic relaxation measures like meditation or paced breathing.
URL: http://www.msnbc.msn.com/id/20762868/site/newsweek/page/0/
Left Main Heart Disease Runs in the Family
Familial aggregation of left main coronary artery disease and future risk of coronary events in asymptomatic siblings of affected patients
Primary source: European Heart Journal Advance Access published online on October 3, 2007
Fischer M, et al "Familial aggregation of left main coronary artery disease and future risk of coronary events in asymptomatic siblings of affected patients"
Aims: Recently, we observed in a hypothesis-generating exploratory search on the heritability of coronary morphology that left main coronary disease (LMD) was frequently shared by siblings with coronary artery disease (CAD). Thus, our aims were, first, to test specifically the familial aggregation of LMD and second, to investigate whether LMD is a stronger predictor for future incident events than other manifestations of CAD in seemingly healthy siblings of CAD patients.
Methods and results: Coronary angiograms of 1801 patients (n = 882 from the initial exploratory study and 919 additional angiograms) were analysed from families with 2 affected CAD siblings. We estimated the heritability using the variance-component methodology and sibling recurrent risks by logistic regression analysis. Moreover, we studied 1369 healthy siblings of CAD patients with known coronary morphology who had a subsequent coronary event by conducting a prospective, nested case–control study. LMD-frequency was comparable in our initial exploratory study (11%) and the new sample (12%). The heritability of LMD was significant in the exploratory 48%, P = 0.010, in the subsequent 45%, P = 0.045, and in the total study sample 49%, P = 0.002. The sibling recurrent risk ratio to present with LMD was 3.6 [CI 1.7–7.1] when another sibling was affected by LMD. In the prospective study on initially healthy family members of CAD patients, 79 siblings experienced an event during follow-up. LMD was more frequently found in families with an event than in families without (13.9 vs. 6.4%, P = 0.036). The relative risk for initially asymptomatic siblings of patients with LMD to suffer from a coronary event was 2.5 [CI 1.1–5.8] compared with siblings of patients with other manifestations of CAD.
Conclusion: These data confirm our initial observation of familial aggregation of LMD. Moreover, in apparently healthy siblings of patients with LMD, this heritable component results in a risk increase for future events that is greater than that of a strong positive family history by itself.
Primary source: European Heart Journal Advance Access published online on October 3, 2007
Fischer M, et al "Familial aggregation of left main coronary artery disease and future risk of coronary events in asymptomatic siblings of affected patients"
Aims: Recently, we observed in a hypothesis-generating exploratory search on the heritability of coronary morphology that left main coronary disease (LMD) was frequently shared by siblings with coronary artery disease (CAD). Thus, our aims were, first, to test specifically the familial aggregation of LMD and second, to investigate whether LMD is a stronger predictor for future incident events than other manifestations of CAD in seemingly healthy siblings of CAD patients.
Methods and results: Coronary angiograms of 1801 patients (n = 882 from the initial exploratory study and 919 additional angiograms) were analysed from families with 2 affected CAD siblings. We estimated the heritability using the variance-component methodology and sibling recurrent risks by logistic regression analysis. Moreover, we studied 1369 healthy siblings of CAD patients with known coronary morphology who had a subsequent coronary event by conducting a prospective, nested case–control study. LMD-frequency was comparable in our initial exploratory study (11%) and the new sample (12%). The heritability of LMD was significant in the exploratory 48%, P = 0.010, in the subsequent 45%, P = 0.045, and in the total study sample 49%, P = 0.002. The sibling recurrent risk ratio to present with LMD was 3.6 [CI 1.7–7.1] when another sibling was affected by LMD. In the prospective study on initially healthy family members of CAD patients, 79 siblings experienced an event during follow-up. LMD was more frequently found in families with an event than in families without (13.9 vs. 6.4%, P = 0.036). The relative risk for initially asymptomatic siblings of patients with LMD to suffer from a coronary event was 2.5 [CI 1.1–5.8] compared with siblings of patients with other manifestations of CAD.
Conclusion: These data confirm our initial observation of familial aggregation of LMD. Moreover, in apparently healthy siblings of patients with LMD, this heritable component results in a risk increase for future events that is greater than that of a strong positive family history by itself.
Wednesday, July 25, 2007
Specific Gene Suppressor Described As A 'Dictator With A Conscience'
Specific Gene Suppressor Described As A 'Dictator With A Conscience'
25 Jul 2007 University of New South Wales (UNSW) researchers have uncovered an important naturally occurring mechanism in the body where "bad" cells that cause blockages in our blood vessels are kept under strict growth control, while "good" cells that keep our blood vessels free of clots and growths are left unaffected.
The discovery is expected to benefit those who will need heart coronary bypass surgery, an angioplasty -- the mechanical widening of a narrowed or totally blocked blood vessel -- or will undergo haemodialysis.
Professor Levon Khachigian, from UNSW's Centre for Vascular Research, who previously pioneered "molecular assassin" drug technology, describes this novel mechanism he discovered as "a molecular dictatorship with a conscience".
"The dictator is a specific gene suppressor called YY1, which has the therapeutically appealing capacity to differentiate between certain cell types when it goes about its activity," says Professor Khachigian.
This key finding has just been published in the world's premier cardiovascular research journal, Circulation Research.
Professor Khachigian's research provides new hope in tackling the global problems of coronary bypass graft failure, and restenosis -- the closing or narrowing of an artery that was previously opened by a procedure such as angioplasty.
"While the most effective way to head off restenosis is a drug-coated stent, the drugs that sit on these stents inhibit the growth of good cells as well as the bad.
"If you had to have catheter intervention to re-open an occluded artery, for sustained symptom-free benefit you would be hoping for suppressed smooth muscle cell growth, without affecting endothelial cell growth," says Professor Khachigian.
"And that's exactly what happens when we simply top up blood vessels with the body's natural reserves of YY1."
Article adapted by Medical News Today from original press release.
25 Jul 2007 University of New South Wales (UNSW) researchers have uncovered an important naturally occurring mechanism in the body where "bad" cells that cause blockages in our blood vessels are kept under strict growth control, while "good" cells that keep our blood vessels free of clots and growths are left unaffected.
The discovery is expected to benefit those who will need heart coronary bypass surgery, an angioplasty -- the mechanical widening of a narrowed or totally blocked blood vessel -- or will undergo haemodialysis.
Professor Levon Khachigian, from UNSW's Centre for Vascular Research, who previously pioneered "molecular assassin" drug technology, describes this novel mechanism he discovered as "a molecular dictatorship with a conscience".
"The dictator is a specific gene suppressor called YY1, which has the therapeutically appealing capacity to differentiate between certain cell types when it goes about its activity," says Professor Khachigian.
This key finding has just been published in the world's premier cardiovascular research journal, Circulation Research.
Professor Khachigian's research provides new hope in tackling the global problems of coronary bypass graft failure, and restenosis -- the closing or narrowing of an artery that was previously opened by a procedure such as angioplasty.
"While the most effective way to head off restenosis is a drug-coated stent, the drugs that sit on these stents inhibit the growth of good cells as well as the bad.
"If you had to have catheter intervention to re-open an occluded artery, for sustained symptom-free benefit you would be hoping for suppressed smooth muscle cell growth, without affecting endothelial cell growth," says Professor Khachigian.
"And that's exactly what happens when we simply top up blood vessels with the body's natural reserves of YY1."
Article adapted by Medical News Today from original press release.
Subscribe to:
Posts (Atom)