Exercise May Help Maintain Weight Loss

FRIDAY, Sept. 4 (HealthDay News) — For dieters, the benefits of exercise may go beyond calories burned, a new study suggests.

Exercise may ward off weight gain after dieting by reducing appetite, preventing fat cells from accumulating and by prompting the body to burn calories from fat before burning calories from carbohydrates, reducing feelings of hunger, research finds.

The study was published recently in the American Journal of Physiology — Regulatory, Integrative and Comparative Physiology.

Researchers put obesity-prone rats on a high-fat diet for 16 weeks, during which time they ate whatever they wanted and did not exercise.

Later, rats were put on a low-fat, low-calorie diet to shed 14 percent of their body weight. Rats were then kept on the diet for eight weeks to maintain their lower weight.

During the maintenance phase, half the rats exercised on a treadmill while the other half were sedentary.

Afterward, rats were permitted to eat as much low-fat food as they wanted. One group continued to exercise while the other didn’t.

After two months, the rats that exercised regained less weight, burned more fat in the morning and more carbohydrates later in the day, accumulated fewer fat cells and gained less abdominal fat compared to the sedentary rats.

Since less energy is needed to store fat than to store carbohydrates, burning carbohydrates first burns less calories overall, according to researchers from the University of Colorado Denver.

In rats that exercised, burning fat first may also help to dampen feelings of hunger.

Exercise also protected against the increase in fat cells that often occurs when weight is regained. While the sedentary rats accumulated new fat cells soon after they started regaining the weight, the rats that exercised didn’t.

New fat cells increase fat storage capacity in the abdomen, according to the study. The increase in fat cells may also help explain why sedentary rats ended up heavier than even before they dieted.

Though weight gain seems to be clear-cut — when more calories are consumed than calories burned, you gain weight — research is showing that a person’s body weight, appetite and metabolism are determined by an interplay of physiological, psychological, cognitive and lifestyle factors.

Previous research found that many dieters regain weight because calorie restriction can cause physiological signals, such as hunger, to go into overdrive, triggering overeating and weight gain.

Exercise may help in maintaining weight loss by altering what’s known as “defended” weight, or the body weight each person’s physiology and metabolism seeks to maintain, and may also make diets easier to follow, according to the study.

The study also calls into question a widely accepted belief that the number of fat cells cannot be altered by dietary or lifestyle changes, researchers said.
SOURCE: American Physiological Society, news release, Sept. 2, 2009

Einstein scientists move closer to a safer anthrax vaccine

September 4, 2009 – (BRONX, NY) – Researchers at Albert Einstein College of Medicine of Yeshiva University have identified two small protein fragments that could be developed into an anthrax vaccine that may cause fewer side effects than the current vaccine.

The research is significant because anthrax is considered a major bioterrorism threat. The current anthrax vaccine is intended mainly for members of the armed forces serving in areas considered high risk and for individuals involved in homeland biosecurity.

“Our research was motivated by the fact that the current anthrax vaccine has significant limitations and there is great need for a better one,” says lead author Nareen Abboud, Ph.D., an Einstein postdoctoral fellow and lead author of the study, which appears in the current issue of The Journal of Biological Chemistry. The study’s senior author is Arturo Casadevall, M.D., Ph.D., Leo and Julia Forchheimer Professor and chairman of microbiology & immunology.

Anthrax, a disease caused by the bacterial species Bacillus anthracis, occurs when anthrax spores (the microbe’s dormant stage) are inhaled, ingested or enter the body through an open wound. Anthrax is a common disease among grazing animals such as cows, goats, and sheep but can also result from bioterrorism.

Eighty to 90 percent of people infected through inhalation will die if not treated, according to the U.S. Department of Health and Human Services. In 2001, five people died after inhaling anthrax spores contained in envelopes mailed to U.S. lawmakers and media personnel. Typical treatment post-exposure includes the antibiotics ciprofloxacin, doxycycline and penicillin.

Anthrax results in part from toxic proteins, or toxins, that the multiplying bacteria secrete. The current anthrax vaccine employs one of these proteins, which elicits protective antibodies when injected into people.

While this 40-year-old vaccine can prevent di

Haemostasis or normal blood clotting is essential for survival

From public health scares about the risk of deep vein thrombosis (DVT) on long-distance flights to high rates of pulmonary embolism (PE) in patients recovering from major surgery, venous thromboembolism (VTE) is a well-publicised, serious health issue.^{1, 2}
expand…
Patients undergoing major orthopaedic surgery for total hip or total knee replacement or surgery for fracture of the hip are at particularly high risk of DVT. Undertreatment remains a problem, despite ample evidence that primary preventive therapy effectively reduces the risk of DVT, PE, and fatal PE.^{3, 57}

Thrombosis complications also play a major role in cardiovascular disease. Blood clots in coronary arteries cause acute coronary syndrome, and blood clots that form in the heart are the major cause of stroke in people with atrial fibrillation.^{4, 5}

Coagulation schematic

Abnormal haemostasis

The coagulation cascade

An evolving model

The intrinsic and extrinsic pathway model

The cell-based model

Propagation of clotting: the central role of Factor Xa

Final step: fibrin formation

Fibrinolysis: restoring blood flow

Fibrinolysis, as the term implies, is the process that dissolves fibrin. It leads to clot dissolution. Plasminogen is the precursor of plasmin, which breaks up fibrin clots. During initial clot formation, plasminogen activators are inhibited. Over time, endothelial cells begin to secrete tissue plasminogen activators to start dissolving the clot as the structural integrity of the blood vessel wall is restored. Medications that convert plasminogen to plasmin are used to treat acute, life-threatening thrombotic disorders, such as myocardial infarction.⁶

Vitamin C Deficiency Impairs Early Brain Development, Guinea Pig Study Finds

New research at LIFE – Faculty of Life Sciences at University of Copenhagen shows that vitamin C deficiency may impair the mental development of new-born babies.

In the latest issue of the well-known scientific journal The American Journal of Clinical Nutrition, a group of researchers headed by professor Jens Lykkesfeldt shows that guinea pigs subjected to moderate vitamin C deficiency have 30 per cent less hippocampal neurones and markedly worse spatial memory than guinea pigs given a normal diet. Like guinea pigs, human beings are dependent on getting vitamin C through their diet, and Jens Lykkesfeldt therefore speculate that vitamin C deficiency in pregnant and breast-feeding women may also lead to impaired development in foetuses and new-born babies.

The brain retains vitamin C

Several factors indicate that the neonatal brain, in contrast to other tissue, is particularly vulnerable to even a slight lowering of the vitamin C level. The highest concentration of vitamin C is found in the neurons of the brain and in case of a low intake of vitamin C, the remaining vitamin is retained in the brain to secure this organ. The vitamin thus seems to be quite important to brain activity. Tests have shown that mouse foetuses that were not able to transport vitamin C develop severe brain damage. Brain damage which resembles the ones found in premature babies and which are linked to learning and cognitive disabilities later in life.

Widespread vitamin C deficiency

In some areas in the world, vitamin C deficiency is very common – population studies in Brazil and Mexico have shown that 30 to 40 per cent of the pregnant women have too low levels of vitamin C, and the low level is also found in their foetuses and new-born babies. It is not yet known to what extent new-born babies in Denmark or the Western World suffer from vitamin C deficiency but a conservative estimate would be 5 to 10 per cent based on the occurrence among adults.

“We may thus be witnessing that children get learning disabilities because they have not gotten enough vitamin C in their early life. This is unbearable when it would be so easy to prevent this deficiency by giving a vitamin supplement to high-risk pregnant women and new mothers” says Jens Lykkesfeldt whose research group is currently studying how early in pregnancy vitamin C deficiency affects the embryonic development of guinea pigs and whether the damage may be reversed after birth.

Brain Cancer

What is brain cancer?

Brain cancer is a disease of the brain in which cancer cells (malignant) arise in the brain tissue. Cancer cells grow to form a mass of cancer tissue (tumor) that interferes with brain functions such as muscle control, sensation, memory, and other normal body functions. Tumors composed of cancer cells are called malignant tumors, and those composed of noncancerous cells are called benign tumors. Cancer cells that develop from brain tissue are called primary brain tumors while tumors that spread from other body sites to the brain are termed metastatic brain tumors. Statistics suggest that brain cancer occurs infrequently and is likely to develop in about 22,000 new people per year in 2009, with about 13,000 deaths as estimated by the National Cancer Institute (NCI).

Not all brain tumors are alike, even if they arise from the same type of brain tissue. Tumors are assigned a grade depending on how the cells in the tumor appear microscopically. The grade also provides insight as to the cell’s growth rate. NCI lists the following grades:

• Grade I: The tissue is benign. The cells look nearly like normal brain cells, and they grow slowly.
• Grade II: The tissue is malignant. The cells look less like normal cells than do the cells in a grade I tumor.
• Grade III: The malignant tissue has cells that look very different from normal cells. The abnormal cells are actively growing (anaplastic).
• Grade IV: The malignant tissue has cells that look most abnormal and tend to grow quickly.

The most common primary brain tumors are usually named for the brain tissue type from which they originally developed. These are gliomas, meningiomas, pituitary adenomas, vestibular schwannomas, and primitive neuroectodermal tumors (medulloblastomas). Gliomas have several subtypes which include astrocytomas, oligodendrogliomas, ependymomas, and choroid plexus papillomas. When the grades are coupled with the tumor name, it gives doctors a better understanding about the severity of the brain cancer. For example, a grade III (anaplastic) glioma is an aggressive tumor, while an acoustic neuroma is a grade I benign tumor. However, even benign tumors can cause serious problems if they grow big enough to cause increased intracranial pressure or obstruct vascular structures or cerebrospinal fluid flow.

What is metastatic brain cancer?

Cancer cells that develop in a body organ such as the lung (primary cancer tissue type) can spread via the bloodstream or lymphatic system to other body organs such as the brain. Tumors formed by such cancer cells that spread (metastasize) to other organs are called metastatic tumors. Metastatic brain cancer is a mass of cells (tumor) that originated in another body organ and has spread into the brain tissue. Metastatic tumors in the brain are more common than primary brain tumors. They are usually named after the tissue or organ where the cancer first developed (for example, metastatic lung or breast cancer tumors in the brain, which are the most common types found).

What causes brain cancer?

Primary brain tumors arise from many types of brain tissue (for example, glial cells, astrocytes, and other brain cell types). Metastatic brain cancer is caused by the spread of cancer cells from a body organ to the brain. However, the causes for the change from normal cells to cancer cells in both metastatic and primary brain tumors are not fully understood. Data gathered by research scientists show that people with certain risk factors are more likely to develop brain cancer. Individuals with risk factors such as having a job in an oil refinery, as a chemist, embalmer, or rubber-industry worker show higher rates of brain cancer. Some families have several members with brain cancer, but heredity as a cause for brain tumors has not been proven. Other risk factors such as smoking, radiation exposure, and viral infection (HIV) have been suggested but not proven to cause brain cancer. There is no good evidence that brain cancer is contagious, caused by head trauma, or caused by cell phone use. Although many lay press and Web articles claim that aspartame (artificial sweetener) causes brain cancer, as of 2009, the FDA maintains that it does not cause brain cancer and base their findings on over 100 toxicological and clinical studies regarding the sweetener’s safety.

Why don’t brain tumors respond to medication?

Malignant brain tumors often fail to respond to promising new medication. Researchers in Heidelberg have discovered a mechanism and a tumor marker for the development of this resistance. A “death receptor” can possibly provide information as to how great the chances of success are for chemotherapy. At the same time, it offers a new approach for promising brain tumor therapy.

Dr. Wolf Mller, senior consultant in the Neuropathology Department at the Institute of Pathology of Heidelberg University Hospital, and his team were able to show that certain brain tumors (astrocytomas) can deactivate a crucial protein on their cell surface, the so-called death receptor. The medication docks onto this receptor and causes the cells to die. An intact “death receptor” can thus serve as a tumor marker for whether or not a therapy has a chance of success. The study was conducted with funding from the Tumor Center of Heidelberg/Mannheim and was published in the journal Clinical Cancer Research.

Primary brain tumors that develop from brain cells, in particular their most malignant variant the glioblastoma, have a very poor prognosis. Although various kinds of therapies are attempted, patients with a glioblastoma usually die within two years of diagnosis. The researchers are thus working at high speed to become more familiar with the biology of these tumors in order to develop more efficient treatment.

“Death receptor” can be switched on and off

The researchers in Heidelberg examined various primary brain tumors (astrocytomas, which also include glioblastomas) and discovered that the gene for the death receptor DR4 was switched off in up to 75 percent of cases by what is known as “promoter methylation”. This means that methyl groups accumulate at the segment of the gene that is crucial for its activity (expression). The gene’s information can thus no longer be read, the gene is silenced.

The death receptor DR4 is an attracti
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Stroke: Surgery Safer Than Angioplasty?

Stroke: Surgery Safer Than Angioplasty?

Better Long-Term Outcomes Seen With Carotid Artery Surgery, Study Shows

By Salynn Boyles
WebMD Health News

Reviewed By Louise Chang, MD

Aug. 28, 2009 — Surgery is safer and slightly more effective than balloon angioplasty for preventing strokes, new research shows.

Two newly published investigations join a growing body of research showing worse outcomes in patients who have balloon angioplasty to clear the clogged neck arteries that supply oxygen-rich blood to the brain.

The findings could have a big impact on clinical practice, especially in the United States where balloon angioplasty is now performed far more often than surgery to open blocked or narrowed carotid arteries.

Both procedures carry their own risk of stroke, but it has not been clear if one was safer or worked better than the other.

“Taking all the studies together, the risk of stroke is now clearly higher with angioplasty,” stroke researcher Peter M. Rothwell, MD, PhD, tells WebMD. “What these two (new) papers now also show is that the long-term outcome is also worse with angioplasty. This is therefore a double-blow for angioplasty.”

Angioplasty Considered Safer

Narrowing of the carotid artery because of buildup of fatty plaque is one of the main risk factors of stroke.

The plaque can either be removed surgically or the narrowed artery can be opened by inflating a tiny balloon threaded up to the neck through a narrow catheter inserted into a groin artery. These days, a wire mesh stent is almost always inserted during angioplasty to keep the artery open.

Balloon angioplasty with stenting has become the procedure of choice in the U.S. in recent years, largely because it has been considered safer than surgery, says Larry B. Goldstein, MD, who directs Duke University Medical Center’s stroke center.

It is now clear that this is not the case, Goldstein tells WebMD.

The new studies, both performed by the same international research team, include the longest follow-up yet of patients treated with surgery or angioplasty for coronary artery disease.

Researchers followed 251 patients who had surgery and 253 who had angioplasty for up to 11 years, lead investigator Martin M. Brown, MD, tells WebMD.

Eight years later, slightly more angioplasty patients than surgery patients (11.3% vs. 8.6%) had experienced strokes, although the difference wasn’t statistically significant.

The angioplasty group also had more minor strokes within the first 30 days of having the procedure, compared to the surgery group (eight vs. one). The surgery group had more cases of cranial nerve palsy (22 vs. zero), a temporary nerve injury, and hematoma that needed surgery or longer stay in the hospital (17 vs. three).

In the second study, the researchers used ultrasound imaging to look for plaque buildup in the carotid arteries of 213 patients following surgery and 200 following angioplasty.

After five years, three times as many angioplasty patients had severe artery blockage (31% vs. 10%). “Patients who had angioplasty with stents had a lower risk of plaque recurrence than those who had angioplasty alone.

“The trials make it clear that surgery is the best option, but it is important to understand that the difference is not that great,” lead investigator Martin M. Brown, MD, tells WebMD. “Patients who can’t have surgery or don’t want it are still likely to do well.”

Surgery, Angioplasty or No Treatment

Because recruitment for the trials occurred before stents were routinely used with angioplasty, the results are not all that relevant to patients who have the procedure today, Goldstein says.

“One criticism is that the procedures used then are somewhat outdated, but this is an issue with any long-term interventional study,” he says. “The technology tends to move faster than the sciences.”

Another pressing question is whether too many procedures to clear clogged carotid arteries are being performed in the United States, he says.

The benefits of treatment are well established for patients with symptoms associated with carotid artery disease, but this is not the case for patients who have no symptoms, Goldstein says.

“If you have symptomatic high-grade narrowing of the carotid arteries, the risk of stroke can be as high as 26% over two years with no intervention,” he says. “The stroke risk for someone with asymptomatic disease is on the order of 1% to 2%.”

He tells WebMD that in the U.S. the majority of angioplasty with stenting procedures for carotid artery disease are performed on asymptomatic patients.

“The question now is who, if anybody, with asymptomatic disease should have anything done to their carotid artery, because the risk of causing harm is not small,” he says.

SOURCES: The Lancet Neurology, Aug. 29, online. Larry B Goldstein, MD, professor of medicine, director, Duke Stroke Center, Duke University Medical Center. Peter M. Rothwell, MD, PhD, John Radcliffe Hospital, Oxford, England. Martin M. Brown, MD, The National Hospital for Neurology and Neurosurgery, London. News release, The Lancet Neurology. WebMD Medical Reference: “Carotid Artery Disease.”

©2009 WebMD, LLC. All Rights Reserved.

How Bad Feelings Can Harm Your Health

By Ed Edelson
HealthDay Reporter

How bad feelings affect your humour

THURSDAY, Aug. 27 (HealthDay News) — A depressed emotional state — feelings of hopelessness and apathy — could have a direct effect on your physical health, new research indicates.

A study of stroke survivors found a slower rate of recovery among those experiencing apathy, caring little about themselves and the world around them. And a study of healthy middle-aged women found an association between hopelessness and unexpected thickening of the carotid artery, the main blood vessel to the brain.

Both findings are reported in the Aug. 27 issue of Stroke.

The apathy study was triggered by a 2006 paper on Parkinson’s disease in a different journal, said Nancy E. Mayo, a professor of medicine at McGill University in Montreal, and lead author of the apathy study. “It said that if patients were apathetic the best thing was just to leave them alone,” she said. “I was incensed that the author said we just shouldn’t care.”

So Mayo launched a study in which 408 family caregivers of stroke survivors filled out apathy questionnaires every four months, asking whether the survivor “waits for someone to do things that he or she can do for self,” or “just sits and watches” and the like.

It’s an admittedly imperfect method of measurement, Mayo said, “but we used what we had.” Reports indicated that a third of the stroke survivors had minor apathy through the first year, with 3% having high levels of apathy. Apathy worsened for 7% of the survivors, and eased for 7% during the year.

Measurements of physical function showed that “even very minor apathy had just as strong an impact on recovery as major apathy,” Mayo said. Answers about the quality of life of the stroke survivors, such as their engagement in social activities, found lesser improvement among those whose apathy worsened.

It’s not clear what can be done to help in such a situation, Mayo said, in large part because very little research has been done on apathy. “You can’t fix what you can’t measure,” she said. “This is a first attempt to sort things out. Since no one is paying attention, it is not surprising there are no treatments for it.”

Drug therapy is a vague possibility, along with behavioral therapy. “We don’t have anything that has evidence-based data other than being kind and enthusiastic,” Mayo said. “Were looking at clues from addiction research. There needs to be a lot of work.”

The report on the physical effect of hopelessness was an offshoot of a nationwide study of cardiovascular disease in women, said study author Susan A. Everson-Rose, an associate professor of medicine at the University of Minnesota.

She and her colleagues singled out 559 menopausal women with no history of cardiovascular disease to answer a two-item questionnaire about their expectations regarding future goals.

A previous study led by Everson-Rose, using the same questionnaire in Finnish men, found an association between hopelessness and cardiovascular disease outcome, she said, as did another study in women with documented cardiovascular disease.

This new study found a direct relationship between rising hopelessness and thickening of the lining of the carotid artery, a risk factor for stroke. Overall, women measuring higher on the hopelessness scale had .02 millimeters more thickening, equal to the amount caused by one year of aging. Women with the highest hopeless scores had an average .06 millimeters greater thickening than those with the lowest scores.

“This doesn’t necessarily mean that hopelessness had a direct physical effect, since it could be operating through mechanisms we didn’t measure,” Everson-Rose said.

But there is a clinical message, she said: “Physicians should tell patients that emotional states can have a physical effect, and that they should seek appropriate treatment for them. Psychiatric treatment for severe depression and hopelessness is warranted.”

SOURCES: Nancy E. Mayo, Ph.D, professor, medicine, McGill University, Montreal; Susan A. Everson-Rose, Ph.D, associate professor, medicine, University of Minnesota, Minneapolis; Aug. 27, 2009, Stroke

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