ISLAMABAD  – Male pattern baldness is linked to an increased risk of coronary heart disease , but only if it’s on the top/crown of the head, a new study has revealed.
A receding hairline is not linked to an increased risk , the analysis indicates.
The researchers from University of Tokyo trawled the Medline and the Cochrane Library databases for research published on male pattern baldness and coronary heart disease , and came up with 850 possible studies, published between 1950 and 2012.
But only six satisfied all the eligibility criteria and so were included in the analysis. All had been published between 1993 and 2008, and involved just under 40,000 men. Three of the studies were cohort studies - meaning that the health of balding men was tracked for at least 11 years. Analysis of the findings from these showed that men who had lost most of their hair were a third more likely (32 percent) to develop coronary artery disease than their peers who retained a full head of hair.
When the analysis was confined to men under the age of 55-60, a similar pattern emerged. Bald or extensively balding men were 44 percent more likely to develop coronary artery disease .
Analysis of the other three studies, which compared the heart health of those who were bald / balding with those who were not, painted a similar picture.
It showed that balding men were 70 percent more likely to have heart disease and those in younger age groups were 84 percent more likely to do so.
Three studies assessed the degree of baldness using a validated scale (Hamilton scale). Analysis of these results indicated that the risk of coronary artery disease depended on baldness severity, but only if this was on the top/crown of the head, known as the vertex.
Extensive vertex baldness boosted the risk by 48 percent, moderate vertex baldness by 36 percent, and mild vertex baldness by 18 percent. By contrast, a receding hairline made very little difference to risk , the analysis showed.
New radiation therapy puts cancer into remission
Researchers at University of Missouri have developed a new form of radiation therapy that successfully puts cancer into remission in mice. This innovative treatment produced none of the harmful side-effects of conventional chemo and radiation cancer therapies. Clinical trials in humans could begin soon after the team led by Professor M. Frederick Hawthorne secures funding. “Since the 1930s, scientists have sought success with a cancer treatment known as boron neutron capture therapy (BNCT),” Hawthorne, a recent winner of the National Medal of Science awarded by President Obama in the White House, said.
“Our team at MU`s International Institute of Nano and Molecular Medicine finally found the way to make BNCT work by taking advantage of a cancer cell`s biology with nanochemistry,” he said.
Cancer cells grow faster than normal cells and in the process absorb more materials than normal cells. Hawthorne`s team took advantage of that fact by getting cancer cells to take in and store a boron chemical designed by Hawthorne.
When those boron-infused cancer cells were exposed to neutrons, a subatomic particle, the boron atom shattered and selectively tore apart the cancer cells, sparing neighboring healthy cells.
The physical properties of boron made Hawthorne`s technique possible. A particular form of boron will split when it captures a neutron and release lithium, helium and energy.
Like pool balls careening around a billiards table, the helium and lithium atoms penetrate the cancer cell and destroy it from the inside without harming the surrounding tissues.
Prostate cancer metastasis switch identified
A University of Colorado Cancer Center study has described for the first time a switch that regulates the production of the protein E-Cadherin, the loss of which is a prerequisite for prostate cancer metastasis. The transcription factor SPDEF turns on and off production, leading to metastasis or stopping it cold in models of prostate cancer.
“When E-Cadherin is lost, cells become `rouge` - they can detach from their surrounding tissues, move effortlessly through the circulatory system, grow and attach at new sites,” said Hari Koul, PhD, investigator at the CU Cancer Center and professor and director of Urology Research at the University of Colorado School of Medicine, the study`s senior author.
“In prostate tumors that had lost E-Cadherin, we put in SPDEF and the tumors once again expressed E-Cadherin. They were once again anchored in place and unable to metastasize. We can make these `rouge` cells back into epithelial-like cells and these epithelial cells stay anchored and lose the ability to migrate,” added Koul.
In fact, the work could have implications far beyond prostate cancer, as increasing evidence points to loss of E-Cadherin as a prerequisite for metastasis in many cancers.
Koul and colleagues first showed that E-Cadherin levels varied directly with the addition or subtraction of SPDEF. Then the group artificially knocked down E-Cadherin despite the presence of SPDEF and showed that cells remained able to migrate and invade new tissues (SPDEF didn`t by itself affect metastasis and was instead dependent on modulating E-Cadherin, which is the driver).
The group also showed a one-way switch - SPDEF regulates E-Cadherin, but E-Cadherin expression does nothing to affect levels of SPDEF. “Taken together, these studies paint a pretty compelling picture of SPDEF working in part through the modulation of E-Cadherin to inhibit prostate cancer metastasis,” Koul said.
“To the best of our knowledge these are the first studies demonstrating the requirement of SPDEF for expression of E-Cadherin,” he added.
Koul stated that his group is getting very close to turning off the loss of E-Cadherin in cancer cells by re-arming tumors with the gene that makes SPDEF and my testing small molecules that increase SPDEF in cancer cells.