Vitamin D levels may have different effects on atherosclerosis in blacks, whites

Washington, March 15 (ANI): Supplementing vitamin D in those with atherosclerosis or “hardening of the arteries,” may have different effects in black and white patients, suggests a study.

Experts at the Wake Forest University School of Medicine found that the supplement could actually do harm in black individuals.

Principal investigator Barry I. Freedman, John H. Felts III Professor and chief of the section on nephrology at the School of Medicine, said: “In black patients, lower levels of vitamin D may not signify deficiency to the same extent as in whites. We should use caution when supplementing vitamin D in black patients while we investigate if we are actually worsening calcium deposition in the arteries with treatment.”

The team based their research on the relationship between circulating vitamin D levels and arterial calcium in 340 black men and women with type 2 diabetes.

Freedman, an affiliate of the Maya Angelou Center for Health Equity, part of the School of Medicine, continued: “We found that higher circulating levels of vitamin D in blacks were associated with more calcium in the artery walls. This is the opposite effect of what is felt to occur in white patients and shows that the accepted “normal” range of vitamin D may be different between blacks and whites.

Freedman further warned physicians to practice caution when supplementing vitamin D levels in blacks.

Freedman added: “Doctors frequently prescribe supplemental vitamin D. However, we do not know all of its effects and how they may differ between the races. The bottom line is that racial differences in calcium handling are seen and black and white patients have differing risk for bone and heart disease. We should more clearly determine the effects of supplementing vitamin D in black patients with low levels based on existing criteria and should not assume that the effects of supplementation will be the same between the races.”

The study has been published in the Journal of Clinical Endocrinology and Metabolism. (ANI)

Popular stomach acid reducer ups patients’ risk of developing pneumonia threefold

Washington, September 15 (ANI): Researchers at Wake Forest University School of Medicine have found that a popular stomach-acid reducer, which is used to prevent stress ulcers in critically ill patients who need breathing machine support, triples the likelihood of contracting pneumonia among such patients.

Hospital-acquired pneumonia-the leading cause of infection-related deaths in critically ill patients-increases hospital stays by an average of seven to nine days, cost of care, and the risk of other complications.

“As best we can tell, patients who develop hospital-acquired pneumonia or ventilator-acquired pneumonia have about a 20 to 30 percent chance of dying from that pneumonia. It’s a significant event,” said senior study author Dr. David L. Bowton, professor and head of the Section on Critical Care in the Department of Anesthesiology.

During the study, the researchers compared treatment with two drugs that decrease stomach acid: ranitidine, marketed under the name ZantacTM, and pantoprazole, marketed under the name ProtonixTM or PrilosecTM.

Both drugs decrease stomach acid, but the newer pantoprazole is considered more powerful, and has become the drug of choice in many hospitals.

However, upon the analysis of 834 patient charts, the researchers came to the conclusion that the risk of developing pneumonia was thee times more in the hospitalised cardiothoracic surgery patients who had been treated with pantoprazole.

“We conducted this study, in part, because we thought we were seeing more pneumonias than we were used to having,” said study co-author Marc G. Reichert, pharmacy coordinator for surgery at Wake Forest University Baptist Medical Center.

The researchers say that their study suggests some other steps to keep critically ill patients from developing ventilator-associated pneumonia.

Bowton suggests that doctors consider whether an acid reducer is needed at all, and, in cases where it is needed, ranitidine is recommended because of the apparent decreased risk in developing pneumonia.

Doctors should stop using the drug as soon as the risk of bleeding passes – once the patient is off the breathing machine and eating, either on his/her own or through a feeding tube.

“Stopping the drugs earlier appears to be the best thing for patients,” Reichert said.

The study has been published in a recent issue of CHEST. (ANI)

Key component in preeclampsia development identified

Washington, Sep 5 (ANI): Researchers at Wake Forest University School of Medicine have found a key contributor in the development of preeclampsia in pregnant women – a condition that can result in miscarriage and maternal death.

The researchers in the study focused on identifying the differences in the uteri of pregnant women with and without preeclampsia and how the mother’s tissues vary from the immediately adjacent foetus’ tissue in preeclamptic women.

“Preeclampsia is a very serious condition that affects 7 to 10 percent of all pregnancies in the United States. It can be devastating to both mother and baby, and currently there is no cure except to deliver the fetus. Our finding brings us one step closer to understanding the condition by getting a picture of what is happening at the maternal and fetal interface,” said Dr. K. Bridget Brosnihan, the lead investigator for the study.

Preeclampsia is a rapidly progressive condition that impacts multiple body systems, causing high blood pressure, decreased liver function and, in the most severe cases, affecting the activity of the brain, resulting in seizures.

If left untreated, preeclampsia can lead to serious, even fatal, complications for both mother and baby.

Despite numerous studies, researchers have only closed down on one possible pathway-the renin-angiotensin system (RAS), which regulates blood pressure and fluid retention.

The RAS, when operating normally, forms a hormone called angiotensin II- a potent vasoconstrictor that binds to angiotensin II receptors throughout the body, including in the maternal uterine “bed” and the fetal placenta.

It causes the muscular walls of blood vessels to contract, narrowing the diameter of the vessels and increasing blood pressure.

In normal pregnancy, the uterus has lower RAS activity, producing less angiotensin II, which results in the blood vessels remaining dilated.

This leads to lower blood pressure and allows more oxygen and nutrients to pass from the mother’s uterus to the placenta and foetus, which is beneficial for its development.

However, in preeclamptic women, the activity of the RAS is increased in the uterus, yet the mother’s vessels remain dilated and the fetus’ vessels constrict more than normal.

Brosnihan and colleagues focused on uncovering the reason for this in the current study and found that the angiotensin II receptors are not detectable in the uteri of pregnant or preeclamptic women.

In normal pregnancy, this does not present a problem because there is less angiotensin II being produced, making the receptors less important.

However, in preeclamptic women, where uterine angiotensin II is high, the hormone does not bind to its receptors in the uterus as it should.

Instead, it passes through to the vessels of the foetal placenta and constricts the foetus’ vessels, limiting the foetus’ oxygen and nutrient intake and often causing low birth weight.

The only known way to cure preeclampsia is delivery of the baby.

Inhibitors of the RAS are known to have bad effects on the foetus, so controlling the system is difficult in preeclamptic women, said Brosnihan.

“It is very hard to control parts of this system to prevent preeclampsia without hurting the baby. Our study provides some insight into maternal factors that may augment the disease. Hopefully, one day, we will be closer to finding a cure,” said Brosnihan.

The study has been published in the September issue of Endocrinology. (ANI)

Mutation in high blood pressure-regulating gene linked to inherited kidney disease

Washington, August 19 (ANI): A collaborative study has shown that a mutation in a gene that helps regulate high blood pressure is a cause of inherited kidney disease.

The discovery made by researchers Wake Forest University School of Medicine, Charles University in Prague, and colleagues provides insight into a protein, renin, that is important in blood pressure regulation, and reveals the cause of one type of inherited kidney disease occurring in adults and children.

Dr. Anthony Bleyer, professor of internal medicine-nephrology at the School of Medicine, points out that a mutation in the gene that encodes renin was first identified as the cause of an hereditary kidney disease by a research group led by Dr. Stanislav Kmoch, at Charles University in Prague.

Working with Kmoch and Dr. Suzanne Hart, at the National Institutes of Health, Bleyer identified the condition among American families in his study group of families with rare, inherited kidney disease.

The researchers revealed that families identified with the specific genetic mutation investigated in this study suffered from anaemia in childhood, and progressive kidney disease resulting in the need for dialysis, a mechanical way to cleanse the blood.

Children typically have relatively low blood pressure. Adults suffer from gout and worsening kidney disease.

“There are many families with inherited kidney disease that do not know the cause and may suffer from this condition. We are interested in helping these families identify the cause of kidney disease that runs in their family,” Bleyer said.

The researcher further revealed that the research team had identified a potential treatment for the disease, and a clinical trial was under way at Wake Forest University School of Medicine.

Understanding how the mutation in the renin gene affects these families also provides insight into how renin works in healthy individuals, for the low levels of renin in children with this condition appear to cause anaemia.

The researchers say that the importance of renin in maintaining a normal blood count, and preventing anaemia in childhood was not previously known.

They plan to continue researching renin with hopes of better understanding how the protein functions in health and disease.

A research articled describing their study has been published in the American Journal of Human Genetics. (ANI)

How long-lasting memories form in the brain

Washington, Aug 12 (ANI): A research team, led by Indian-origin boffin, has come closer to understanding how fleeting moments are sealed into life-long memories.

According to the researchers, the findings may one day help scientists develop treatments to prevent and treat conditions such as post-traumatic stress disorder.

“Although many things are known about memories that form from repeat experiences, not much is known with regard to how some memories form with just one exposure,” said Ashok Hegde, from Wake Forest University School of Medicine and the lead investigator on the study.

Hegde said that scientists do know that people tend to remember extremely happy or sad occasions vividly because of the emotional connection.

Extreme emotions trigger the release of a chemical in the brain called norepinephrine, which is related to adrenaline. That norepinephrine somehow helps memories last a long time – some even a lifetime.

In the current study, Hegde and colleagues looked at how norepinephrine helps female mice remember the scent of their male partners after being exposed to it just once during mating.

The researchers studied the neural circuitry in the accessory olfactory bulb, the part of the brain where memory of the male partner’s scent is stored.

They found that norepinephrine, released in mice while mating, activates an enzyme called Protein Kinase C (PKC), specifically, the “alpha” isoform of PKC, in the accessory olfactory bulb.

The PKC enzyme has about a dozen forms, or isoforms, that exist in the brains of mammals, including humans.

“The fact that PKC-alpha is activated through the release of norepinephrine is an important discovery. It explains how strong memories form for specific sensory experiences,” Hegde said.

In female mice, the information about the partner’s scent is carried by a chemical called glutamate and the fact that mating has occurred is conveyed by the release of norepinephrine, Hegde explained.

Previous studies have found that glutamate and norepinephrine together, but not individually, cause strong memory formation for the male’s scent.

“No one knew how this happened. Our findings indicate that the PKC-alpha enzyme tells the nerve cells in the brain that these two chemicals have arrived together. PKC-alpha is like the bouncer who lifts the rope blocking the entrance to an exclusive club for strong memories when glutamate and norepinephrine arrive together. If they arrive alone, they can’t get past the velvet rope,” Hegde said.

Hegde said that when memory is stored in the brain, the connections between nerve cells, called synapses, change. Strong memories are formed when synapses become stronger through structural changes that occur at the synapse. PKC-alpha works with glutamate and norepinephrine to create those changes.

The study is available online and is scheduled to appear in an upcoming issue of Neuroscience. (ANI)

Regular moderate alcohol intake cuts dementia risk in older adults

Washington, July 14 (ANI): Regular moderate alcohol intake offers long-term cognitive protection and reduces the risk of dementia in older adults, according to a new study.

This is the largest, longest U.S. study to look at the effects of regular alcohol intake on dementia in seniors, both with and without memory problems.

For the study, researchers at Wake Forest University School of Medicine examined and interviewed 3,069 individuals, 75 years or older and most without any memory or thinking problems, about their drinking habits.

Participants were asked about beer, wine, and liquor. The researchers then categorized the individuals as abstainers (non-drinkers), light drinkers (one to seven drinks per week), moderate drinkers (eight to 14 drinks per week), or heavy drinkers (more than 14 drinks per week). All types of alcohol were included.

The study subjects were then examined and interviewed every six months for six years to determine changes in their memory or thinking abilities and to monitor who developed dementia.

The researchers found that individuals, who had no cognitive impairment at the start of the study and drank eight to 14 alcoholic beverages per week, or one to two per day, experienced an average 37 percent reduction in risk of developing dementia compared to individuals who did not drink at all and were classified as abstainers.

For older adults who started the study with mild cognitive impairment, however, consumption of alcohol, at any amount, was associated with faster rates of cognitive decline.
n addition, those who were classified in the heavy drinker category, consuming more than 14 drinks per week, were almost twice as likely to develop dementia during the study compared to non-drinkers with mild cognitive impairment.

“We were excited to see that even in older adults, moderate alcohol intake decreases the risk of dementia. It is important to note, however, that our study found a significantly higher risk of dementia for heavy drinkers who started the study with mild cognitive impairment,” said Kaycee Sink, M.D., M.A.S (Masters of Advanced Studies in clinical research), a geriatrician and senior author of the study.

The study has been presented at the Alzheimer’s Association 2009 International Conference on Alzheimer’s Disease (ICAD), in Vienna on July 13. (ANI)

Gene that switches on during epilepsy development identified

Washington, Apr 23 (ANI): Researchers at Wake Forest University School of Medicine have identified a gene that switches on during development of epilepsy.

The discovery made while studying mice may help explain how some people without a genetic predisposition to epilepsy can develop the disorder.

In a study published this month in the Journal of Neuroscience, senior researcher Dwayne W. Godwin, Ph.D., a professor of neurobiology and anatomy, and colleagues, report discovering that a gene, already known to predispose people who inherit an active form of it to certain forms of epilepsy, can actually be “switched on” in animals that do not appear to have inherited the active form, and therefore a genetic predisposition, to the condition.

The gene codes a calcium channel in the brain that underlies seizures, so the finding may reveal a mechanism by which epilepsy develops in those with no apparent genetic predisposition to it.

“Epilepsy is a terrible disorder that affects millions of kids and adults all over the world,” Godwin said.

“There are many different forms of epilepsy with different symptoms. We don’t know why some people acquire epilepsy – the cause isn’t always clear from the person’s genetic makeup. We do know that in some forms of epilepsy, once someone has a seizure they tend to have more. Our findings from this study suggest that something about the brain changes that can lead to this increased tendency to have a seizure. Our study shows that an important change occurs in calcium channels that help to transmit this abnormal activity throughout the brain,” the expert added.

Calcium channels come in a variety of forms throughout the body and are responsible for several key functions, depending on their placement and quantity. The calcium channels in the brain are normally embedded within the membrane of brain cells, where they allow passage of calcium ions into the cell and are responsible for the electrical activity of the brain.

The passage of calcium ions into cells determines how excitable the cells are, and how easily abnormal activity spreads through the brain.

If, as in epilepsy, a particular channel shows up where it is not supposed to or appears in too many or too few numbers, the function that channel is responsible for can become abnormal. Researchers know that during epileptic seizures, these calcium channels in the brain, responsible for generating electrical brain rhythms, become highly active.

For the study, researchers used a mouse model to observe changes in tissue from regions of the brain that are involved in seizures, the hippocampus and the thalamus. They measured these changes at different time intervals as the mice developed epilepsy. The researchers found that after an initial seizure, more of this particular kind of calcium channel begins to be expressed where it wasn’t before, and the presence of the channel caused brain activity to become increasingly abnormal and epileptic.

“Calcium channels underlie valuable functions. But in the wrong place, at the wrong time, or in the wrong amount, their presence can be disruptive. In the context of brain circuits, the brain cells that have too many copies of the channel get over excited and respond abnormally,” Godwin said.

While the hippocampus is usually targeted in studies of epilepsy, the new channels were being made in a region of the brain called the thalamus. The thalamus is connected to the hippocampus and is involved in the spread of seizures throughout the brain.

“Certain kinds of channels are normal and expected in the thalamus, but after an initial seizure more copies of a channel that isn’t normally found in this brain region begin to appear,” explained graduate student John Graef, the first author on the study.

“The brain activity then becomes dominated by the new copies of this channel. It helps explain how seizures can develop and spread,” the expert added. (ANI)

No link between osteoporosis drugs, irregular heartbeat

Washington, Apr 7 (ANI): Commonly used osteoporosis drugs have not been found to increase the risk of irregular heartbeat, say research team led by Indian-origin scientist from Wake Forest University School of Medicine.

Bisphosphonates, found in prescription drugs reduces the risk of fractures, especially those of the spine and hips in older patients, however studies have revealed that they might cause problems with heart rhythm, thereby increasing the risk of stroke or heart attack.

“Some trials show there could be a potential link between the use of bisphosphonates and the development of serious heart rhythm problems, but in our study the link wasn’t conclusive,” said Sonal Singh from Wake Forest University School of Medicine and lead investigator for the study.

“So we urge that additional investigations be conducted,” she added.

During the study, the researchers analyzed the data from previous observational studies and clinical trials to determine the link between bisphosphonate therapy and irregular heart beat.

Although bisphosphonate use was associated with a significant increase in the incidence of “serious” heart rhythm disturbances, but when they included “non-serious” cases in their analysis, they found no overall increased risk of atrial fibrillation.

“We found no risk of stroke and cardiovascular mortality in the trials. That was very reassuring,” said Singh.

The study appears in Drug Safety. (ANI)

Early weight gain leads to mobility problems in old age

Washington, Apr 7 (ANI): People who gain weight early in life are three times more likely to develop mobility problems in old age, even if they eventually lose weight, says a new study from Wake Forest University School of Medicine.

Lead researcher Denise Houston added that dropping weight later in life could lead to problems with mobility because weight loss later in life is usually involuntary and the result of an underlying chronic condition.

She suggests that carrying extra weight can strain joints, hinder exercise and lead to chronic conditions, such as diabetes, arthritis and heart disease that are directly related to the development of mobility limitations.

“In both men and women, being overweight or obese put them at greater risk of developing mobility limitations in old age, and the longer they had been overweight or obese, the greater the risk,” said Houston.

“We also found that, if you were of normal weight in old age but had previously been overweight or obese, you were at greater risk for mobility limitations,” she added.

The researchers looked at 2,845 people who were on average 74 years old. The researchers defined mobility limitation as difficulty walking a quarter-mile or climbing 10 steps.

The researchers found that women who were overweight or obese with a BMI of 25 or greater from their mid-20s to their 70s were nearly three times more likely to develop mobility limitations than women who were normal weight throughout.

The risk for men was slightly less – they were about 1.6 times more likely to develop mobility limitations, according to the study.

The study also found that women who were obese with a BMI of 30 or greater, at age 50, but not in their 70s, were 2.7 times more likely to develop mobility limitations compared to women who were not obese throughout. ,

Men who were obese at 50, but not in their 70s, were 1.8 times more likely to develop mobility limitations than men who never carried the extra weight.

“The data suggest that interventions to prevent overweight and obesity in young and middle-aged adults may be useful in preventing or delaying the onset of mobility limitations later in life,” she added.

The study appears in American Journal of Epidemiology. (ANI)

Blood protein may hold key to stopping cancer progression

Washington, April 1 (ANI): Scientists at Wake Forest University School of Medicine have reached a step closer to developing a new drug to inhibit tumour growth in cancer patients, and potentially help in the healing of wounds.

The researchers looked at angiogenesis – the body’s formation of new blood vessels from existing blood vessels – and how some blood proteins are involved in that process and affect blood vessel growth during a study.

They found that a protein called ferritin binds to and cripples the ability of another blood protein, called HKa, to shut down blood vessel growth.

The researcher point out that new blood vessels supply a steady stream of nutrients and oxygen, which are essential for tumour growth.

According to them, their study showed that the binding of the two proteins actually assists in new blood vessel formation by removing HKa’s influence, and therefore promotes tumour growth.

Based on their observations, the researchers hypothesised that if the binding of ferritin and Hka could somehow be prevented, it would help block the growth of tumours.

The finding also has possible implications for wound care, as the healing of wounds needs blood vessel growth.

Thus, according to the researchers, it is possible that by increasing the binding of ferritin to HKa, one could increase the rate at which a serious wound heals.

“It’s been known for a long time that levels of ferritin are increased in people with tumours, but it’s never been understood why that happens,” said Dr. Suzy V. Torti, the study’s lead investigator, an associate professor of biochemistry and an expert in iron biology at the School of Medicine.

“Ferritin appears to play an important role in blood vessel formation. Further, the interaction between ferritin and HKa may represent a new area of interest for possible drug development,” Torti added.

During the study, mice were injected with prostate cancer cells to determine how ferritin and HKa affected the formation of new blood vessels.

The mice injected with the cancer cells grew tumours.

However, upon mixing HKa with the tumour cells, the researchers found that the blood vessel formation was inhibited. hen the team added ferritin to the mixture of HKa and cancer cells, the blood vessel formation was restored, and it allowed the tumours to grow again.

“Blood vessels can either be helpful, for example in wound healing, or they can be harmful, for example by favouring tumour growth,” Torti said.

“Our new finding is that the interaction between ferritin and HKa can influence blood vessel formation. This finding could serve as the basis for strategies to either inhibit or stimulate blood vessels. This opens up a new realm of potential ways to treat tumors or other conditions that depend on new blood vessel formation,” Torti added.

The study has been reported in the Proceedings of the National Academy of Sciences. (ANI)

Yoga cuts depression by half in breast cancer patients

Washington, Feb 25 (ANI): Yoga not only provides emotional benefits to women with breast cancer, but also reduces their chances of depression, says a new study.

The study, published in a special issue of Psycho-Oncology focusing on physical activity, found that women undertaking a ten week program of 75 minute Restorative Yoga (RY) classes gained positive differences in aspects of mental health such as depression, positive emotions, and spirituality (feeling calm/peaceful) compared to the control group.

RY is a gentle type of yoga, which is similar to other types of yoga classes, moving the spine in all directions but in a more passive and gentle way. Props such as cushions, bolsters, and blankets provide complete physical support for total relaxation with minimal physical effort, and so people in differing levels of health can practice yoga more easily.

Forty-four women took part in the study, with 22 undertaking the yoga classes and 22 in the waitlist control group. All of the women had breast cancer; 34 percent were actively undergoing cancer treatment while the majority had already completed treatment.

All participants completed a questionnaire at the beginning and end of the ten-week program, asking them to evaluate their quality of life through various measures. The results clearly showed that the women who had been given the RY classes experienced a wide range of benefits compared to the control group (who were later all invited to attend identical RY classes).

“Evidence from systematic reviews of randomised trials is quite strong that mind-body therapies improve mood, quality of life, and treatment-related symptoms in people with cancer. Yoga is one mind-body therapy that is widely available and involves relatively reasonable costs,” said lead researcher Suzanne Danhauer, Ph.D., based at Wake Forest University School of Medicine.

“Given the high levels of stress and distress that many women with breast cancer experience, the opportunity to experience feeling more peaceful and calm in the midst of breast cancer is a significant benefit,” the expert added.

The study found that women who started with higher negative emotions and lower emotional well-being derived greater benefit from the gentle yoga intervention compared to the control group.

Women in the gentle yoga group also demonstrated a significant within-group improvement in fatigue, while no such change was noted for the control group. (ANI)

Compound used in BP drugs may benefit brain tumour patients

Washington, Feb 19 (ANI): Researchers from at Wake Forest University Baptist Medical Centre have found that a compound used in blood pressure medication may help prevent cognitive loss after radiation therapy in brain tumour patients.

In the study conducted using a rat model, the researchers assumed that that a compound similar to the anti-hypertensive drug losartan can prevent the cognition loss that has been closely-associated with radiation therapy for brain tumour treatment.

The researchers hope that the same theory could easily be applied in a human clinical trial setting because the drug used has a long-established safety profile in patients who have taken it to treat high blood pressure.

“We need to kill cancer cells but also prevent or reduce treatment-related side effects,” said Mike E. Robbins, Ph.D., a professor in the department of radiation oncology at the Brain Tumour Centre of Excellence, part of Wake Forest University School of Medicine.

“One very interesting feature of this compound is that it has never shown any pro-tumor effects. If anything, it appears to have anti-tumor properties.

“We’re very close to having a compound that will protect the normal brain from cognitive injury as a result of radiation and, at the same time, we may very well increase the likelihood of one day curing brain cancer patients of their tumours,” he added.

Previous studies had shown that radiation may lead to the overproduction of angiotensin II (Ang II), a peptide that has been associated with decline of brain function.

Blocking the binding of Ang II to the Ang type I receptor in patients receiving radiation, researchers suggest that they could prevent or hinder cognitive decline.

In the study involving 80 rats, each group was divided in half to either receive radiation or no treatment.

Then, each of those halves was divided into two more groups: one that received L-158,809, the compound similar to losartan, in its drinking water, and one group that received plain drinking water. The rats that received the drug received it before, during and for different time intervals – 14, 28 or 54 weeks – post-radiation.

In addition, a small group of rats continued to receive the drug for only five weeks after radiation.

They found that administering L-158,809 before, during and for as little as five weeks after radiation either prevents or lessens the severity of radiation-induced cognitive impairment.

“This study provides hope that we may be able to take a drug that has been prescribed to millions of individuals with essentially very little morbidity and give it to cancer patients and stop them from experiencing cognitive impairment as a result of brain radiation,” said Robbins.

The findings appear in the International Journal of Radiation, Biology, Physics. (ANI)

New biomarker for fatal prostate cancer identified

Washington, Feb 14 (ANI): After reporting excess calcium as an indicator of prostate cancer, researchers at Wake Forest University School of Medicine and the University of Wisconsin have now identified an even more accurate biomarker of the life-threatening disease-high levels of ionised serum calcium.

The new finding can help provide some direction for men diagnosed with prostate cancer, about whether their cancer is likely to be fatal or not.

“Scientists have known for many years that most prostate cancers are slow-growing and that many men will die with, rather than of, their prostate cancer,” said Dr. Gary G. Schwartz, senior author of the study.

He added: “The problem is, how can we determine which cancers pose a significant threat to life and need aggressive treatment versus those that, if left alone, are unlikely to threaten the patient’s life? These findings may shed light on that problem.”

This is the first time that any study has examined fatal prostate cancer risk in relation to pre-diagnostic levels of ionised serum calcium.

The researchers found that men in the highest third of ionised serum calcium levels were three times more likely to die of prostate cancer than those with the least amount of ionised serum calcium.

Also, they confirmed a previous finding of a doubling of risk for fatal prostate cancer among men whose level of total serum calcium falls in the highest third of the total serum calcium distribution.

Ionised serum calcium is the biologically active part of total serum calcium. About 50 percent of total serum calcium is inactive, leaving only the ionised serum calcium to directly interact with cells.

Dr. Halcyon G. Skinner, of the University of Wisconsin, the study’s lead author, said that the findings had both scientific and practical implications.

Scientifically, it helps focus research on what it is about calcium that may promote prostate cancer.

And practically speaking, the finding may offer some guidance to men trying to decide whether or not to seek treatment for a recent prostate cancer diagnosis.

If confirmed, the findings could also lead to the general reduction of over-treatment of prostate cancer.

“These results do not imply that men need to quit drinking milk or avoid calcium in their diets,” Schwartz added.

The study appears in the journal Cancer Epidemiology, Biomarkers and Prevention. (ANI)