While the news about red wine might sound great if you enjoy a glass of red wine with your evening meal, doctors are wary of encouraging anyone to start drinking alcohol. That's because too much alcohol can have many harmful effects on your body.
Still, many doctors agree that something in red wine appears to help your heart. It's possible that antioxidants, such as flavonoids or a substance called resveratrol, have heart-healthy benefits.
How is red wine heart healthy?
Red wine seems to have even more heart-healthy benefits than other types of alcohol, but it's possible that red wine isn't any better than beer, white wine or liquor for heart health. There's still no clear evidence that red wine is better than other forms of alcohol when it comes to possible heart-healthy benefits.
Antioxidants in red wine called polyphenols may help protect the lining of blood vessels in your heart. A polyphenol called resveratrol is one substance in red wine that's gotten attention.
Resveratrol in red wine
Resveratrol might be a key ingredient in red wine that helps prevent damage to blood vessels, reduces "bad" cholesterol and prevents blood clots.
Most research on resveratrol has been done on animals, not people. Research in mice given resveratrol suggests that the antioxidant might also help protect them from obesity and diabetes, both of which are strong risk factors for heart disease. However, those findings were reported only in mice, not in people. In addition, to get the same dose of resveratrol used in the mice studies, a person would have to drink over 60 liters of red wine every day.
Some research shows that resveratrol could be linked to a reduced risk of inflammation and blood clotting, both of which can lead to heart disease. More research is needed before it's known whether resveratrol was the cause for the reduced risk.
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Wednesday, March 9, 2011
Thursday, March 3, 2011
r Risk-based system to reduce unnecessary biopsies
OncologySTAT: How will we select men for biopsy in the future, and where are
we in terms of identifying molecular markers for aggressive prostate tumors?
Dr. Parker: I have no doubt that in the future we will be using risk
calculators based on multiple risk factors in order to decide who gets a
biopsy and who doesn't. Now, the adoption of these risk calculators has been
slow, partly because there are so many different risk calculators and no
consensus on which is better than any other, and partly because they have
not been extensively validated in separate cohorts. There is a pressing need
to validate these risk calculators and to see which of the currently
available risk calculators does the best job in different settings. I think
it is important that individual centers that do large numbers of prostate
biopsies should be auditing their results, seeking to validate these risk
calculators with a view to using them in future practice. So, in the very
near future, investigators should not be relying on PSA thresholds but
rather on the risk calculator that works best in their setting. There are a
large number of new markers that are coming through, which appear to predict
the risk of finding prostate cancer and, more importantly, the risk of
finding high-grade prostate cancer on biopsy. There is no doubt that some of
them will provide extra utility over and above the standard risk calculators
that are available today.
But, I'm also confident that none of these new markers is going to tell the
whole story. We should not expect any new marker to replace PSA and be used
on its own, to indicate who should get a biopsy and who shouldn't. Rather,
these new markers will need to be incorporated into existing risk
calculators. Among the novel markers, one of the best known is the urinary
PCA3 score, which looks promising. There are also a plethora of germline
genetic markers, which also appear to put men at increased risk of prostate
cancer, although, as yet, I'm not aware of any germline marker that is
associated with high-grade prostate cancer.
The fact that there are so many markers being evaluated underlines the need
for us to move from PSA-based decision-making to risk-based decision-making.
Right now, we have traditional risk factors, which I mentioned earlier, but
in 5 years' time, we are going to have a large number of new risk factors,
whether they are urinary markers, or blood markers, or germline genetic
markers. The only way we are going to make sense of all these new markers is
to use them as part of a risk-based approach.
So, again, the decision whether or not to have a prostate biopsy should be
made, in the future, not on a man's PSA level, but rather on the risk of
finding high-grade prostate cancer.
OncologySTAT: Then, aside from validating these different scoring systems
and validating more of the marker research, what are key, yet-unanswered
questions that need to be tested in clinical trials?
Dr. Parker: It will be important to know how effective these risk
calculators will be in avoiding unnecessary biopsies and reducing
over-diagnosis. Roobol et al have made a very nice first attempt at
estimating what the impact would be. They selected 10,000 men who took part
in the European randomized trial of prostate cancer screening, and described
what happened in the trial, given that biopsy was indicated for men with a
PSA level greater than 3 ng/mL. Then, they compared that with what would
have happened if they had used a risk threshold using the European risk
calculator.5
What they found was that about one-third of all the prostate biopsies would
have been avoided and that the number of indolent prostate cancers detected
would have been significantly reduced. Their work is a first step at showing
what could be gained from moving from a PSA-based system to a risk-based
system.
The other point to make is that while the immediate and obvious advantages
of using a risk-based system would be to reduce unnecessary biopsies and
reduce over-diagnosis, there is also a possible further benefit, because it
may be that we would be able to find harmful prostate cancers earlier,
before a man's PSA rises above the standard threshold, and finding it
earlier might improve the effectiveness of treatment. That is speculation,
but it is a further reason why we should be moving towards a risk
we in terms of identifying molecular markers for aggressive prostate tumors?
Dr. Parker: I have no doubt that in the future we will be using risk
calculators based on multiple risk factors in order to decide who gets a
biopsy and who doesn't. Now, the adoption of these risk calculators has been
slow, partly because there are so many different risk calculators and no
consensus on which is better than any other, and partly because they have
not been extensively validated in separate cohorts. There is a pressing need
to validate these risk calculators and to see which of the currently
available risk calculators does the best job in different settings. I think
it is important that individual centers that do large numbers of prostate
biopsies should be auditing their results, seeking to validate these risk
calculators with a view to using them in future practice. So, in the very
near future, investigators should not be relying on PSA thresholds but
rather on the risk calculator that works best in their setting. There are a
large number of new markers that are coming through, which appear to predict
the risk of finding prostate cancer and, more importantly, the risk of
finding high-grade prostate cancer on biopsy. There is no doubt that some of
them will provide extra utility over and above the standard risk calculators
that are available today.
But, I'm also confident that none of these new markers is going to tell the
whole story. We should not expect any new marker to replace PSA and be used
on its own, to indicate who should get a biopsy and who shouldn't. Rather,
these new markers will need to be incorporated into existing risk
calculators. Among the novel markers, one of the best known is the urinary
PCA3 score, which looks promising. There are also a plethora of germline
genetic markers, which also appear to put men at increased risk of prostate
cancer, although, as yet, I'm not aware of any germline marker that is
associated with high-grade prostate cancer.
The fact that there are so many markers being evaluated underlines the need
for us to move from PSA-based decision-making to risk-based decision-making.
Right now, we have traditional risk factors, which I mentioned earlier, but
in 5 years' time, we are going to have a large number of new risk factors,
whether they are urinary markers, or blood markers, or germline genetic
markers. The only way we are going to make sense of all these new markers is
to use them as part of a risk-based approach.
So, again, the decision whether or not to have a prostate biopsy should be
made, in the future, not on a man's PSA level, but rather on the risk of
finding high-grade prostate cancer.
OncologySTAT: Then, aside from validating these different scoring systems
and validating more of the marker research, what are key, yet-unanswered
questions that need to be tested in clinical trials?
Dr. Parker: It will be important to know how effective these risk
calculators will be in avoiding unnecessary biopsies and reducing
over-diagnosis. Roobol et al have made a very nice first attempt at
estimating what the impact would be. They selected 10,000 men who took part
in the European randomized trial of prostate cancer screening, and described
what happened in the trial, given that biopsy was indicated for men with a
PSA level greater than 3 ng/mL. Then, they compared that with what would
have happened if they had used a risk threshold using the European risk
calculator.5
What they found was that about one-third of all the prostate biopsies would
have been avoided and that the number of indolent prostate cancers detected
would have been significantly reduced. Their work is a first step at showing
what could be gained from moving from a PSA-based system to a risk-based
system.
The other point to make is that while the immediate and obvious advantages
of using a risk-based system would be to reduce unnecessary biopsies and
reduce over-diagnosis, there is also a possible further benefit, because it
may be that we would be able to find harmful prostate cancers earlier,
before a man's PSA rises above the standard threshold, and finding it
earlier might improve the effectiveness of treatment. That is speculation,
but it is a further reason why we should be moving towards a risk
Xgeva(denosumab)is more effective than Zometa® (
Xgeva Reduces Bone Complications From Prostate Cancer
Among men with bone metastases from prostate cancer, Xgeva™ (denosumab) was more effective than Zometa® (zoledronic acid) at delaying or preventing bone complications such as fracture. Results from this Phase III clinical trial were published in The Lancet.
Metastatic cancer refers to cancer that has spread to distant sites in the body. Several types of cancer—including prostate cancer—have a tendency to spread to the bone. Bone metastases can lead to serious problems such as fracture and spinal cord compression, and may require treatment with surgery or radiation therapy.
Bisphosphonate drugs such as Zometa have been commonly used to reduce the risk of complications from bone metastases. Xgeva is a newer type of drug that targets a protein known as the RANK ligand. This protein regulates the activity of osteoclasts (cells that break down bone). Xgeva was approved by the U.S. Food and Drug Administration (FDA) in 2010 for the prevention of bone complications in patients with bone metastases from solid (not blood-related) cancers, including prostate cancer.
To directly compare Xgeva to Zometa among prostate cancer patients with bone metastases, researchers conducted a Phase III clinical trial. The study enrolled 1,901 patients with metastatic, hormone-refractory prostate cancer. Study participants were assigned to receive either Xgeva or Zometa. Xgeva is given as a subcutaneous (under-the-skin) injection; Zometa is given intravenously (IV).
The objective of the study was to determine whether the occurrence of bone complications (“skeletal related events”) differed between the two study groups. The bone complications that were evaluated were fracture, radiation to the bone, surgery to the bone, and spinal cord compression.
The results of this study suggest that Xgeva is more effective than Zometa at delaying or preventing skeletal complications in prostate cancer patients with bone metastases.
Reference: Fizazi K, Carducci M, Smith M et al. Denosumab versus zoledronic acid for treatment of bone metastases in men with castration-resistant prostate cancer: a randomized, double-blind study. The Lancet. Early online publication February 25, 2011.
Among men with bone metastases from prostate cancer, Xgeva™ (denosumab) was more effective than Zometa® (zoledronic acid) at delaying or preventing bone complications such as fracture. Results from this Phase III clinical trial were published in The Lancet.
Metastatic cancer refers to cancer that has spread to distant sites in the body. Several types of cancer—including prostate cancer—have a tendency to spread to the bone. Bone metastases can lead to serious problems such as fracture and spinal cord compression, and may require treatment with surgery or radiation therapy.
Bisphosphonate drugs such as Zometa have been commonly used to reduce the risk of complications from bone metastases. Xgeva is a newer type of drug that targets a protein known as the RANK ligand. This protein regulates the activity of osteoclasts (cells that break down bone). Xgeva was approved by the U.S. Food and Drug Administration (FDA) in 2010 for the prevention of bone complications in patients with bone metastases from solid (not blood-related) cancers, including prostate cancer.
To directly compare Xgeva to Zometa among prostate cancer patients with bone metastases, researchers conducted a Phase III clinical trial. The study enrolled 1,901 patients with metastatic, hormone-refractory prostate cancer. Study participants were assigned to receive either Xgeva or Zometa. Xgeva is given as a subcutaneous (under-the-skin) injection; Zometa is given intravenously (IV).
The objective of the study was to determine whether the occurrence of bone complications (“skeletal related events”) differed between the two study groups. The bone complications that were evaluated were fracture, radiation to the bone, surgery to the bone, and spinal cord compression.
The results of this study suggest that Xgeva is more effective than Zometa at delaying or preventing skeletal complications in prostate cancer patients with bone metastases.
Reference: Fizazi K, Carducci M, Smith M et al. Denosumab versus zoledronic acid for treatment of bone metastases in men with castration-resistant prostate cancer: a randomized, double-blind study. The Lancet. Early online publication February 25, 2011.