Associations between tooth loss and mortality patterns in the Glasgow Alumni Cohort
Tu et al. Heart.2007; 93: 1098-1103
ABSTRACT
Objective:
To use data from the Glasgow Alumni Cohort to investigate whether oral health in young adulthood is independently associated with later life cardiovascular disease (CVD) and cancer mortality.
Methods and results:
Of the original cohort (n = 15 322), 12 631 subjects were traced through the National Health Service Central Register.
Of these, 9569 men and 2654 women were 30 years or younger at baseline.
During up to 57 years of follow-up, 1432 deaths occurred among subjects with complete data, including 509 deaths from CVD and 549 from cancer.
After adjusting for potential confounders, no substantial association was found between the number of missing teeth (as a continuous variable) and all-cause mortality (hazard ratio (HR) for each extra missing tooth = 1.01; 95% confidence interval (CI) 1.00 to 1.02), CVD mortality (HR = 1.01; 95% CI 0.99 to 1.03) or cancer mortality (HR = 1.00; 95% CI 0.98 to 1.02).
When the number of missing teeth was treated as a categorical variable, there was evidence that students with nine or more missing teeth at baseline had an increased risk of CVD (HR = 1.35; 95% CI 1.03 to 1.77) compared with those with fewer than five missing teeth.
When the number of missing teeth was transformed using fractional polynomials, there seemed to be a non-linear relation between missing teeth and CVD mortality.
Conclusions:
Although some evidence was found to support the relation between tooth loss and CVD mortality, causal mechanisms underlying this association remain uncertain.
Showing posts with label Cancer. Show all posts
Showing posts with label Cancer. Show all posts
Tuesday, August 28, 2007
Thursday, July 26, 2007
Low LDL cholesterol levels tentatively linked to cancer risk
Cardiovascular News
Low LDL cholesterol levels tentatively linked to cancer risk
26 July 2007
MedWire News: An explorative analysis has found an association between the risk for cancer and achieved level of low-density lipoprotein (LDL) cholesterol in statin trials.
“This analysis doesn’t implicate the statin in increasing the risk of cancer,” stressed study author Richard Karas (Tufts University School of Medicine, Boston, Massachusetts, USA).
“The demonstrated benefits of statins in lowering the risk of heart disease remain clear; however, certain aspects of lowering LDL with statins remain controversial and merit further research.”
The investigators included statin-treated participants from 23 trials in their analysis, giving 309,506 person-years of follow-up.
The magnitude of LDL cholesterol reduction achieved by patients was not associated with cancer risk, or with the patients’ risk for elevated liver enzymes or rhabdomyolysis.
Their results are published in the Journal of the American College of Cardiology. In a related comment, journal editors Anthony DeMaria and Ori Ben-Yehuda (University of California at San Diego, USA) observed that over the past 5 years, “no other manuscript has stimulated such intense scrutiny and discussion.”
The only clear treatment-related effect that the researchers detected was an increasing risk for elevated liver enzymes with rising statin dose.
This rate of elevated liver enzymes rose from about 100 per 100,000 person-years with low statin doses to about 250 per 100,000 person-years with high doses. The absolute and percent LDL cholesterol reductions were not associated with the risk for cancer.
But the team found an inverse relationship between achieved LDL cholesterol levels and the risk for cancer, at an R2 of 0.43. In other words, 43% of the variance in cancer incidence could be accounted for by achieved cholesterol levels, although this was not adjusted for confounders.
In their discussion, Karas et al observe that their findings are consistent with epidemiologic studies showing a link between low cholesterol levels and cancer. But they also note that researchers who previously compiled a review of such studies failed to draw any definitive conclusions, and suggested that the proposed association could be due to confounding.
“One potential explanation is the possibility that low cholesterol levels are simply the effect of the disease rather than the cause, and is present before clinical manifestation of the cancer,” say Karas and team.
In an accompanying editorial, John LaRosa (State University of New York Downstate Medical Center, USA) noted that the link between LDL cholesterol levels and cancer can be further studied without the need for more trials, as many LDL-lowering studies have not published data on cancer.
“Lowering LDL represents an intervention of long duration, and we must continue to be vigilant in ensuring that its benefit clearly outweighs its risk,” he said.
“On the other hand, we must not allow that vigilance to deny the benefits of LDL lowering to those who need it.”
LINK:
Primary source: Journal of the American College of CardiologySource reference: Alsheikh-Ali AA et al. "Effect of the magnitude of lipid lowering on risk of elevated liver enzymes, rhabdomyolysis, and cancer." J Am Coll Cardiol 2007;50:409-418.
J Am Coll Cardiol 2007; 50: 409–418
Low LDL cholesterol levels tentatively linked to cancer risk
26 July 2007
MedWire News: An explorative analysis has found an association between the risk for cancer and achieved level of low-density lipoprotein (LDL) cholesterol in statin trials.
“This analysis doesn’t implicate the statin in increasing the risk of cancer,” stressed study author Richard Karas (Tufts University School of Medicine, Boston, Massachusetts, USA).
“The demonstrated benefits of statins in lowering the risk of heart disease remain clear; however, certain aspects of lowering LDL with statins remain controversial and merit further research.”
The investigators included statin-treated participants from 23 trials in their analysis, giving 309,506 person-years of follow-up.
The magnitude of LDL cholesterol reduction achieved by patients was not associated with cancer risk, or with the patients’ risk for elevated liver enzymes or rhabdomyolysis.
Their results are published in the Journal of the American College of Cardiology. In a related comment, journal editors Anthony DeMaria and Ori Ben-Yehuda (University of California at San Diego, USA) observed that over the past 5 years, “no other manuscript has stimulated such intense scrutiny and discussion.”
The only clear treatment-related effect that the researchers detected was an increasing risk for elevated liver enzymes with rising statin dose.
This rate of elevated liver enzymes rose from about 100 per 100,000 person-years with low statin doses to about 250 per 100,000 person-years with high doses. The absolute and percent LDL cholesterol reductions were not associated with the risk for cancer.
But the team found an inverse relationship between achieved LDL cholesterol levels and the risk for cancer, at an R2 of 0.43. In other words, 43% of the variance in cancer incidence could be accounted for by achieved cholesterol levels, although this was not adjusted for confounders.
In their discussion, Karas et al observe that their findings are consistent with epidemiologic studies showing a link between low cholesterol levels and cancer. But they also note that researchers who previously compiled a review of such studies failed to draw any definitive conclusions, and suggested that the proposed association could be due to confounding.
“One potential explanation is the possibility that low cholesterol levels are simply the effect of the disease rather than the cause, and is present before clinical manifestation of the cancer,” say Karas and team.
In an accompanying editorial, John LaRosa (State University of New York Downstate Medical Center, USA) noted that the link between LDL cholesterol levels and cancer can be further studied without the need for more trials, as many LDL-lowering studies have not published data on cancer.
“Lowering LDL represents an intervention of long duration, and we must continue to be vigilant in ensuring that its benefit clearly outweighs its risk,” he said.
“On the other hand, we must not allow that vigilance to deny the benefits of LDL lowering to those who need it.”
LINK:
Primary source: Journal of the American College of CardiologySource reference: Alsheikh-Ali AA et al. "Effect of the magnitude of lipid lowering on risk of elevated liver enzymes, rhabdomyolysis, and cancer." J Am Coll Cardiol 2007;50:409-418.
J Am Coll Cardiol 2007; 50: 409–418
Tuesday, July 24, 2007
Low Cholesterol Levels And Cancer
Low Cholesterol Levels And Cancer
Millions of Americans take statins to lower their cholesterol, but how low should you go" A number of scientific studies support the benefits of lowering low-density lipoprotein (LDL) cholesterol, and achieving low LDL cholesterol levels is one of the most important steps in preventing heart disease. New research, however, provides evidence for an association between low LDL levels and cancer risk.
The authors of the study, reported in the July 31, 2007, issue of the Journal of the American College of Cardiology (JACC), set out to understand how and why statins cause side effects, especially damage to the liver and muscle cells. The study findings support taking multiple medications rather than high-dose statins to minimize those side effects. The scientists did not expect to find the increased cancer risk (one additional incident per 1,000 patients) from low LDL levels, and additional studies have already begun to investigate this potential risk further. A key component in future studies will be to confirm the risk and to identify whether the risk may be a side effect of statins or just low LDL.
This analysis doesnt implicate the statin in increasing the risk of cancer, said lead author Richard H. Karas, M.D., F.A.C.C., professor of medicine at Tufts University School of Medicine. The demonstrated benefits of statins in lowering the risk of heart disease remain clear; however, certain aspects of lowering LDL with statins remain controversial and merit further research.
The scientists found one additional incident of cancer per 1,000 patients with low LDL levels when in comparison to patients with higher LDL levels. In their evaluation of randomized controlled statin trials published before November 2005, the scientists looked at 13 therapy arms consisting of 41,173 patients.
Scientists assessed absolute change and percentage of change in LDL reduction and the resulting achieved LDL levels in relation to rates of newly diagnosed cancer in each therapy arm. They also looked at the relationship between low, intermediate and high doses of statins and rates of newly diagnosed cancer. Eventhough they did not find a relationship between percent of change and absolute change in LDL levels, they observed higher rates of newly diagnosed cancer among patients with lower achieved LDL levels. In addition, the new cancers were not of any specific type or location.
Recent data from large-scale statin trials have shown that more intensive LDL lowering can provide significant cardiovascular benefits to higher-risk patients. In response to these findings, recent national guidelines have advocated for lower LDL goals and higher doses of statins to reach them. However, informal observations linking intensive LDL lowering and higher occurence rate of reported health problems, including liver and muscle toxicity and cancer, has introduced some concern over the safety of such therapys.
These concerns in part prompted the current study. However, the current findings are not definitive, as limitations of the study show. Scientists performed their analysis from summary data taken directly from published manuscripts of each trial. An analysis based on data for each individual patient would have yielded more specific and potentially more compelling results, said Dr. Karas.
These current findings provide insufficient evidence that there is any problem with LDL lowering that outweighs its significant benefits on vascular disease, said John C. La Rosa, M.D., who wrote an accompanying editorial in the July 31 issue of JACC. However, we must continue to be vigilant in ensuring that its benefit clearly outweighs its risk.
Eventhough the cancer risk was surprising, the scientists primarily sought to determine how and why statins cause side effects, especially damage to the liver and muscle cells. For this portion of the study, scientists analyzed 23 statin therapy arms that included 75,317 patients with a combined 309,506 years of follow up. A link between LDL lowering and liver or muscle irritation was not found. However, liver toxicity levels increased with higher statin dosage. Based on their findings, the scientists concluded that moderate-dose treatment with multiple medications including statins may prove to be preferable to high-dose treatment with statins alone. Dr. Karas emphasized that patients are advised to continue their statin therapys and, as always, consult their doctor before discontinuing use of any medication.
While these results raise important new questions about statin use, they do not demonstrate a causal relationship between statins and cancer, said James Dove, M.D., F.A.C.C., president of the American College of Cardiology. This study is hypothesis-generating, not hypothesis-proving.
Tuesday, June 12, 2007
Prostate cancer therapy may worsen heart threat
Prostate cancer therapy may worsen heart threat
Men at high cardiac risk should remedy those problems before tumor treatment starts, researchers say.
June 9, 2007
Standard treatment for prostate cancer — shutting off the body's production of androgen hormones — can shorten by 2 1/2 years the lives of men who are at high risk of developing heart disease, Boston researchers reported Friday.
The drugs used to suppress the hormones produce anemia, weight gain and insulin resistance, a constellation of factors known as metabolic syndrome.
These effects can sharply increase the risk of a fatal heart attack, especially in men already at high risk, Dr. Anthony D'Amico of Brigham and Women's Hospital in Boston reported in the Journal of Clinical Oncology.
Because the drugs can slow or halt the progression of a prostate tumor, researchers are not advocating that physicians stop using them.
Instead, they say, prostate cancer patients should be screened for cardiovascular risk, and those with risk factors should be aggressively treated for their potential heart disease before cancer therapy begins.
The medical field has come to realize "in the last year or two that hormone therapy has cardiovascular side effects and we need to pay attention to it," said Dr. Eric Klein of the Cleveland Clinic, who was not involved in the study. "I've already changed my practice."
The risk factors, he added, "are correctable and need to be corrected before treatment or concurrently."
The new study grew from a clinical trial of androgen suppression conducted by D'Amico. "I observed that there were a few men receiving treatment who died quickly of a heart attack," he said.
The 206-man sample in his study was not large enough, so he combined his results with data from studies in Canada, Australia and New Zealand. That brought the total number of men to 1,372, about half of whom received both radiation and hormone suppression therapy and half of whom received only radiation.
During the five years the men were tracked, 51 had fatal heart attacks, half of whom had had hormone suppression therapy. But the older men who received the therapy suffered their heart attacks about 2 1/2 years earlier, on average, than those who had not received it.
The heart attacks "occurred within the first six months to two years after treatment," D'Amico said.
"There wasn't an increased number of heart attacks, it is just that they occurred sooner."
The heart attacks affected about 2.5% of the men receiving treatment, he said.
The primary risk factors were diabetes and smoking. Obesity, high cholesterol levels and high blood pressure were also predictive.
D'Amico said he had begun referring high-risk cardiac patients for therapy, which includes aspirin, cholesterol-lowering statins, angioplasty and, for some, open-heart surgery.
"Hormonal therapy in men who need it is lifesaving," he said. But the cure rate "could be even higher if we screen the appropriate men for coronary risk factors."
Experts noted that oncologists had previously used estrogen in prostate cancer patients to suppress androgen hormones, but that use was abandoned in the late 1980s when clinical trials showed an increase in the risk of heart attacks.
Men at high cardiac risk should remedy those problems before tumor treatment starts, researchers say.
June 9, 2007
Standard treatment for prostate cancer — shutting off the body's production of androgen hormones — can shorten by 2 1/2 years the lives of men who are at high risk of developing heart disease, Boston researchers reported Friday.
The drugs used to suppress the hormones produce anemia, weight gain and insulin resistance, a constellation of factors known as metabolic syndrome.
These effects can sharply increase the risk of a fatal heart attack, especially in men already at high risk, Dr. Anthony D'Amico of Brigham and Women's Hospital in Boston reported in the Journal of Clinical Oncology.
Because the drugs can slow or halt the progression of a prostate tumor, researchers are not advocating that physicians stop using them.
Instead, they say, prostate cancer patients should be screened for cardiovascular risk, and those with risk factors should be aggressively treated for their potential heart disease before cancer therapy begins.
The medical field has come to realize "in the last year or two that hormone therapy has cardiovascular side effects and we need to pay attention to it," said Dr. Eric Klein of the Cleveland Clinic, who was not involved in the study. "I've already changed my practice."
The risk factors, he added, "are correctable and need to be corrected before treatment or concurrently."
The new study grew from a clinical trial of androgen suppression conducted by D'Amico. "I observed that there were a few men receiving treatment who died quickly of a heart attack," he said.
The 206-man sample in his study was not large enough, so he combined his results with data from studies in Canada, Australia and New Zealand. That brought the total number of men to 1,372, about half of whom received both radiation and hormone suppression therapy and half of whom received only radiation.
During the five years the men were tracked, 51 had fatal heart attacks, half of whom had had hormone suppression therapy. But the older men who received the therapy suffered their heart attacks about 2 1/2 years earlier, on average, than those who had not received it.
The heart attacks "occurred within the first six months to two years after treatment," D'Amico said.
"There wasn't an increased number of heart attacks, it is just that they occurred sooner."
The heart attacks affected about 2.5% of the men receiving treatment, he said.
The primary risk factors were diabetes and smoking. Obesity, high cholesterol levels and high blood pressure were also predictive.
D'Amico said he had begun referring high-risk cardiac patients for therapy, which includes aspirin, cholesterol-lowering statins, angioplasty and, for some, open-heart surgery.
"Hormonal therapy in men who need it is lifesaving," he said. But the cure rate "could be even higher if we screen the appropriate men for coronary risk factors."
Experts noted that oncologists had previously used estrogen in prostate cancer patients to suppress androgen hormones, but that use was abandoned in the late 1980s when clinical trials showed an increase in the risk of heart attacks.
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