Thursday, August 27, 2009

Why Did Obese Individuals Tend To Eat More?

Modern lifestyle and unhealthy diet have made obesity to fast becoming an epidemic that worries many health professionals. This is because obesity will eventually lead to many undesired medical disorders like heart disease, diabetes, hypertension (high blood pressure), and even certain types of cancer.

Meanwhile, it seems that obese individuals tend to take in more food to the contrary that they are supposed to eat less to cut down their weight. Such phenomenon has aroused the curiosity of scientists and prompted them to find out the cause behind that.

Researchers from the University of Texas (UT), the Oregon Research Institute, and the Yale University School of Medicine, Connecticut, jointly found that obese persons may have fewer pleasure receptors in their brains, which require them to feed themselves with more of a rewarding substance like food or drugs so that they could experience the same level of pleasure as other people.

The findings of the study, which is one of the first to positively identify factors that increase people's weight gain risk in the future, were published in the month of October 2008 in the journal Science.

According to the researchers, human brain releases the so-called pleasure chemical dopamine, which is believed to be a reward to the body for consuming life-sustaining nutrition. They suspected weak reward centers in the brain prompt obese people to eat more, and they believed obese people might have fewer dopamine receptors causing them to overeat so as to compensate for this reward deficit.

A technique known as functional Magnetic Resonance Imaging (fMRI) was used to examine the extent to which pleasure receptors in individuals were activated in response to a taste of chocolate milkshake versus tasteless solution. The participants were then tested for the presence of a genetic variation that was linked to a lower number of the dopamine receptors. Changes in the participants’ BMI (body mass index) were tracked over a one-year period.

The researchers believed the results from the study are key for understanding weight gain and to helping at-risk obese individuals. By identifying changes in behavior or pharmacological options, it is hoped that the reward deficit could be corrected to prevent and treat obesity.

Friday, August 21, 2009

Tobacco Can Be Useful, Are You Sure?

Smoking and tobacco have always been linked to unhealthy news. Smokers not only have the higher chance of getting heart disease, lung cancers, and other ailments, the secondhand smoke originated from them could also cause harmful effects to the people around them. Many studies have confirmed the claim.

However, an interesting finding by researchers from the University of Verona have found a healthy use for tobacco after they genetically bled modified plants containing a medicine that could stop Type-1 diabetes.

They published their findings on March 19, 2009 in the journal BMC Biotechnology and indicated out that they had produced tobacco plants containing a potent anti-inflammatory protein known as interleukin-10 (IL-10), which could help patients with insulin-dependent Type-1 diabetes and other autoimmune diseases.

Agrochemical companies such as Bayer and Syngenta have been searching ways to produce complex protein drugs in plants but the progress has been slow.

The new finding is believed to mark the latest advance in the emerging field of molecular farming that might offer an alternative way of producing biotech drugs and vaccines at a cost cheaper than traditional factory systems do.

The European researchers believe the antibody medicines and vaccines, which are produced in cell cultures inside stainless steel fermenters, could eventually be grown more efficiently in fields. This is because plants are the world's most cost-effective protein producers. They have studied several different plants around the world, but tobacco is their firm favorite.

The researchers’ work has drawn the attention from tobacco giant Philip Morris, which is supporting a conference on plant-based medicine in Verona in June 2009.

Meanwhile, Swedish biotech company Diamyd has already been testing a conventionally produced GAD65 vaccine against diabetes in clinical trials. On the other hand, Protalix plans to submit its drug for regulatory approval in the United States and Israel in the 4th quarter of 2009.

Wednesday, August 19, 2009

What Is Piggyback Transplant for Heart Disease Patients?

Before knowing what piggyback transplant is, perhaps it is best to understand a term called cardiomyopathy.

Cardiomyopathy is a serious heart disease in which the heart muscle becomes inflamed and does not work as well as it should. In other words, the functions of the heart muscle are deteriorating. It can be caused by viral infection, heart attack, long-term and severe high blood pressure, alcoholism or other reasons that have not been identified yet. It is common in children in the first year of their life.

Simply replacing the ailing heart with a donor’s heart could not solve the problem. This is because the new heart could not adjust fast enough to handle the excess pressure built up in the lungs and it will fail.

One way the heart surgeon can do is to link the existing heart with a donor’s heart. In this so-called piggyback heart transplant, the surgeon inserts the new heart to the right side of the chest and attaches it parallel to the patient’s own heart. The 2 upper chambers on the left side of each heart must be lined up so that they could be merged.

The risks involved in such operations are similar to the traditional heart transplant, which include immune suppression problems and a chance of chronic rejection.

A British girl, who is now 16, is the world’s first heart transplant patient to recover fully after having her donor’s heart removed and functions restored to her original heart.

When she was 2 in 1995, she underwent a piggyback heart transplant and a new heart was inserted in parallel to her own failing heart. In 2006, she contracted cancer because of the immunosuppressant drugs she was taking to avoid organ rejection and the doctor removed the donor’s heart. At that time, her own heart had recovered sufficiently to work on its own. On July 14, 2009, her doctor reported in the Lancet medical journal that the girl has recovered fully from cancer since the surgery and has a normal cardiac function.

The girl’s success story certainly sparks hope for other patients with heart failure. The success indeed highlights the possibility for the patient’s own heart to make a full recovery if it is given adequate support to do so. Nevertheless, the road to recovery can never be an easy one. At one stage, the girl was forced to take 16 different medications to control her illness.

Friday, August 14, 2009

Why Should People Walk or Bike to Work?

Exercise forms an integral part in the prevention of heart disease and many other ailments. However, many of the working people are being pressured by heave workload that they can hardly find time to engage in any form of exercises or physical activities.

A large study in United States for health and commuting found that walking or biking to work, even partway, can boost physical fitness but sadly, very few Americans actually do it. In fact, only about 17 percent of workers walked or bicycled any portion of their commute.

According to experts, things like crumbling sidewalks, lack of bike paths and long distances have prevented American commuters from walking or biking to work.

Researchers from University of North Carolina at Chapel Hill examined the tests and questionnaires from 2,364 workers (middle-aged city dwellers) who were part of a larger federally funded study on heart disease risk. These participants, who lived in Chicago; Minneapolis; Birmingham, Alabama; and Oakland, California, were asked in 2005-2006 about their commuting habits in the past 12 months

It was found that those active commuters did better on treadmill tests of fitness, even after accounting for their leisure-time physical activity levels. This indeed suggested that commuter choices do make a difference.

In the study, the male active commuters also had healthier numbers for body mass index (BMI), blood pressure, insulin and blood fats (known as triglycerides). On the other hand, the researchers speculated that women walked or biked shorter distances and they may have done so less vigorously

The researchers acknowledged that the study has a chicken-and-egg problem. People, who are already active, could be the ones who walk or bike to work. In other words, fitness contributes to wanting to walk to work; nevertheless, the reverse might also be true.

Prior research has found that those countries having the highest levels of walking and biking also have the lowest levels of obesity. Nevertheless, little research has done to examine the health of Americans who walk or bike to work. The new study may be the first large US study of health and commuting.

Many cities in United States, workplaces are separated from homes that lengthen commutes. However, cities like Portland, Oregon, that build bike paths have higher rates of cycling. Meanwhile, companies can provide showers, changing areas and secure bike parking to encourage active commuting.

Tuesday, August 11, 2009

Using Stem Cell To Fix Damaged Heart!

If heart disease patients can make use of their own cells to repair their hearts, then people do not need to wait for donated hearts, which is always in short supply. Meanwhile, they also do not need to rely on dangerous medications to stop their body from rejecting the foreign organs.

This is the goal, which scientists have been striving to achieve. It seems that this dream is going to be realized in the very near future.

On July 20, 2009, a study that was published in the peer review journal Circulation revealed that researchers from the Mayo Clinic in Rochester, Minnesota have managed to reverse some of the damages caused by heart attack using stem cells that were induced from connective tissue cells. The proof-of-concept study on mice is the first attempt to use induced pluripotent stem (iPS) cells to treat heart disease.

Using the technique of nuclear reprogramming, the researchers believe they could reverse the fate of adult cells and customize on demand cardiovascular regenerative medicine. In fact, the research team genetically reprogrammed fibroblast cells, which contribute to the formation of connective tissues and scars, so that they became stem cells capable of developing into new heart muscle.

They transplanted these cells into mouse with damaged hearts and found that the cells had managed to stop progression of structural damage within 4 weeks. They also found that heart muscle performance that was lost after the heart attack was restored and tissue at the site of the damage was regenerated.

Stem cells do offer great potential for regenerative medicine as they can be coaxed into becoming lab-dish replacements for heart, liver, skin, eye, brain, nerve and other cells destroyed by disease, accident, war or normal wear-and-tear. In the meantime, they also have potential to cure diseases such as Parkinson's disease, Alzheimer's and Type-1 diabetes though research was limited because they were obtained from embryos.

In 2007, scientists discovered a way to reprogram adult skin cells into stem cells using embryos and exponentially increased the number of stem cells available for research purposes.

However, the iPS cells have not yet been approved for testing on humans and it will definitely take quite some time before it could be used in treatments.

Wednesday, August 05, 2009

Can Damage Heart Be Repaired?

It has long been thought that the heart does not have the ability to repair itself. In other words, when cells turn into fully formed adult heart muscle, they will stop dividing, and cannot replace damaged tissue caused by disease or deformity.

For heart attack patients with heart weakness, people with heart failure or heart disease children with congenital heart defects, their damaged heart muscle tissue normally does not regenerate.

However, researchers from the United States have found a way to repair the damage heart. What they discovered is that heart tissue could be re-grown and heart function improved in mice that were injected a growth factor without using stem cells. Such discovery is indeed a potential breakthrough for human cardiac care.

As published in the July 24, 2009 issue of journal Cell, the researchers from the Children's Hospital Boston and Harvard Medical School injected a substance known as neuregulin1 (NRG1), which is a protein, into the peritoneal cavity of live mice after a heart attack.

The injection was done once daily for a period of 12 weeks. It was found that heart regeneration was increase and pumping function (ejection fraction, assessed on echocardiograms) was improved when comparing to untreated control group.

NRG1 is one of the 4 proteins in the neuregulin family that acts on the EGFR family of receptors. It is essential for the normal development of the nervous system and the heart.

According to the researchers, this is the first regenerative therapy that may be applicable in a systemic way. In principle, human treatment could eventually be carried out with daily infusions of NRG1 at a clinic over a period of weeks.

Nevertheless, further research is still necessary to ensure such therapy is safe before it could be tested to human patients.

With many studies focusing on stem cells, the new finding does suggest that stem cells are not required and that stimulating differentiated cardiomyocytes to proliferate may just be a viable alternative too.

Saturday, August 01, 2009

Can Viagra Really Protect Hearts of People with Muscular Dystrophy?

Duchenne muscular dystrophy is an inherited wasting disease characterized by weakness and progressive degeneration of the muscles, including the heart muscle. Beginning at the age of 2 to 6, the disease will spread from the legs and pelvis to the whole body. Most people with such disease have to use a wheelchair by the age of about 12.

The heart of the affected patients will experience problems at around the age of 10 and this could progress quickly, affecting most victims by the age of 20. Such heart disease is responsible for the death among patients with muscular dystrophy.

Conducted by Canadian researchers from the Montreal Heart Institute, a study involving mice reported on May 12, 2008 in the Proceedings of the National Academy of Sciences that anti-impotence pills Viagra might protect the heart of people with muscular dystrophy.

Sildenafil, the active ingredient in Viagra, was given to mice with an animal version of Duchenne muscular dystrophy. The doses of the drug given were comparable to those prescribed to treat erectile dysfunction in men. It improved the heart performance of the mice by cutting the levels of damage to contracting heart muscle cells.

The heart of those mice to which sildenafil were not given did not function as well as normal mice, and they were more susceptible to stress-induced cell death.

According to the researchers, the drug did improve heart performance in the mice by preventing the breakdown of a naturally occurring chemical called cyclic guanosine monophosphate (cGMP), which is involved in a number of cellular signaling pathways.

Besides Viagra, Other impotence drugs like vardenafil sold under the brand name Levitra, and tadalafil sold under the name Cialis also affect the chemical cGMP.

Developed as a heart medication, sildenafil is widely prescribed for erectile dysfunction and pulmonary hypertension. No doubt, there is a lot of information on sildenafil that shows it would be relatively safe in adults but the researchers stressed that future human trials are necessary before doctors could prescribe it for heart trouble for those affected patients.

Although the findings indicated Viagra could potentially be used to prevent or delay heart failure in children with Duchenne muscular dystrophy, the researchers felt it would be premature to give Viagra to people with such disease.

Nevertheless, it is believed that discussions have begun among health experts about possible future studies using the drug in patients with muscular dystrophy.