Low-carb diet speeds initial weight loss

In a Research of overweight and obese people, those who went on a low carbohydrate diet lost more weight -- and more fat -- than their peers who went on a low-fat, portion-controlled diet.
After 12 weeks on the low-carb plan, study participants had lost an average of 4.9 kilograms (10.8 pounds), compared to 2.5 kg (5.5 pounds) for their peers on the low-fat diet.

However, after the weight-maintenance phase of the study, which lasted another 24 weeks, differences between the two groups in weight loss and fat mass remained, but were no longer statistically significant.

The findings confirm that the low-carb diet tested in the study is a "reasonable alternative" to cutting fat and controlling portions in order to maintain a healthy weight, Dr. Kevin C. Maki of Radiant Research in Chicago and colleagues conclude.

The approach Maki's team tested -- a reduced-glycemic-load (RGL) diet -- required people to restrict their carbohydrate intake and eat more low glycemic index (GI) foods, meaning foods that produce a relatively small, gradual increase in blood sugar levels. Low GI foods generally are rich in fiber, consist of more complex carbohydrates, and include vegetables, beans and whole grains.

Research participants on the RGL diet did not eat certain high-carb foods, such as fruits and starches, for the first two weeks, and also abstained from alcohol, after which they introduced low-GI foods and were allowed to drink moderate amounts of alcohol. But they were allowed to eat as much of the permitted foods as they wanted. Those on the low-fat diet were instructed to reduce their energy intake 500 to 800 calories per day by eliminating high-fat foods and controlling portion sizes.

After 12 weeks, study participants in either group could continue on the weight loss diet or switch to a weight maintenance plan.

At 12 weeks, the low-carb group had lost significantly more weight, and also more fat -- 1.9 kg (4.2 pounds) of fat vs. 0.9 kg (2 pounds) for the low-fat diet group.

By 36 weeks, the low-carb group had kept off 4.5 kg (10 pounds), compared to 2.6 kg (5.7 pounds) for the low-fat group, not a huge difference.

Low-carb diet participants had maintained a 2 kg (4.4 pounds) loss of fat weight, compared to 1.3 kg (2.9 pounds) for the low fat group, which again was not a significant difference.

The researchers say more research is needed to clarify the mechanisms responsible for the greater initial losses of body weight and fat associated with the RGL diet, to evaluate the persistence of these losses over longer treatment periods, and to obtain greater insight into strategies that would improve long-term weight-loss maintenance."

Source: www.medical-health-care-information.com

Antibiotics too often prescribed for sinus woes

U.S. doctors are consistently overprescribing antibiotics for sinus infections, a new study finds, but even the physician who led the research doesn't see how the problem can be eliminated.
That's because when it comes to treatments for sinus trouble, antibiotics are the best of a bad lot, said Dr. Donald A. Leopold, chairman of the department of otolaryngology at the University of Nebraska Medical Center.

"We as physicians don't have very good medications for chronic rhinosinusitis," he said. "The only other drugs in contention are topical steroids, and they are not great. As a group I suggest we are frustrated at not having good drugs. It would be great if we had better medications for this chronic inflammation."

Another factor is what patients demand, Leopold said. "Many patients call up and ask for specific antibiotics," he said. "The patients know these names. They have been marketed to them, so they know the drugs are available. And antibiotics do give some relief."
His team published their findings in the March issue of Archives of Otolaryngology Head and Neck Surgery.

According to the report, two national studies show that Americans made more than 17 million visits to health-care facilities for sinus infection between 1999 and 2002. At least one antibiotic was prescribed in nearly 83 percent of cases of acute rhinosinusitis and in nearly 70 percent of cases of the chronic, longer-running version of the condition, in which symptoms persist for at least 12 weeks.

The problem is that antibiotics are effective only against bacteria, but many sinus infections are due to other causes, such as viral infections, allergies or hormonal changes. The often-repeated standard wisdom is that use of antibiotics in such cases should be avoided to reduce the emergence of dangerous resistant bacterial strains.

But it's hard to preach that wisdom to someone with a drippy, hurting sinus who wants immediate relief, Leopold acknowledged. Because more effective drugs are lacking, "patients are desperate, physicians are desperate, and it is not a happy situation," he said.
Consider the case of the working physician called on to treat such a patient, said Dr. Neil L. Kao, vice chairman of the rhinitis/sinusitis committee of the American College of Allergy, Asthma and Immunology. He happens to be just such a working physician, in private practice in Greenville, S.C.

There are ways to determine whether a sinus infection is bacterial, Kao said. One is to do endoscopy, running a tube into the nose to obtain a sample of mucus from the sinus. Another is nasal cytology, examining a swab from the lining of the nose. A third is to take an X-ray.
"The problem with all of these is that they are expensive and time-consuming," Kao said. "The differences between symptoms caused by an allergy, bacterial infection, viral infection and a common cold are few. For us, even specialist doctors, when you see someone with acute nasal symptoms, it is hard to tell the cause. And the truth is that most of the people diagnosed with sinusitis go to primary care doctors."

Public awareness about antibiotic resistance is increasing, but most people suffering from cough, drip, lack of sleep and other sinus symptoms are likely to come in demanding an antibiotic, Kao said.

And so the physician often makes the practical choice of giving what the patient wants, with a chance of relief, over the more abstract issue of antibiotic resistance, he said.

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Blood pressure drugs may fight lung cancer

Drugs commonly used to control high blood pressure may also shrink lung tumors.

As prescribed, the medicines -- known as angiotensin-converting enzyme (ACE) inhibitors -- keep blood pressure in check by boosting levels of the "angiotensin (1-7)" hormone, thereby prompting dilation of blood vessel walls.

Blood pressure patients taking ACE inhibitors also have lower rates of lung cancer, noted a team from Wake Forest University School of Medicine in Winston-Salem, N.C.

Investigating further, they found that angiotensin (1-7) cuts back on levels of cycloxygenase-2 (cox-2), an enzyme that promotes cell growth and is often elevated in lung cancer patients.
In the team's latest experiment, boosting angiotensin (1-7) levels in mice shrank lung cancer tumors by 30 percent.

"We are cautiously optimistic, but you know how these things go," said study co-author Patricia E. Gallagher, a researcher at Wake Forest's hypertension and vascular research center. "So many of these drugs go to trial, and while they work great in animals, when you get to the patient population, they're just not as effective. But to this point, we can say that, in mice, we got a reduction in cox-2 and a big reduction in tumor size without any toxic side effects."
The findings are reported in the March 15 issue of Cancer Research.

According to the American Cancer Society, lung cancer remains the leading cause of cancer death among men and women, killing more Americans than colon, breast, and prostate cancer combined. Because they are typically diagnosed at a later stage of disease, 6 in 10 lung cancer patients will die within the first year following diagnosis. Five-year survival is just 14 percent, and an estimated 170,000 Americans die each year from the disease.

In their study, the Gallagher team worked with a group of two- to four-week-old mice that had received transplanted lung cancer cells derived from a 58-year-old patient. The tumors were allowed to grow for 32 days.

Rather than testing ACE inhibitors themselves, the researchers injected half the mice with the angiotensin (1-7) hormone for a 28-day treatment period. The remaining mice received saline.
The experiment stimulated blood levels of angiotensin (1-7) in the mice to concentrations equivalent to those found in humans being treated with ACE inhibitors.

Subsequent dissections revealed that cox-2 levels diminished significantly in the treated mice, while lung tumors shrank by 30 percent. In contrast, tumors in mice receiving the saline solution grew to 2.5 times their pre-treatment size.

Gallagher and her colleagues uncovered no evidence of toxic side effects among the angiotensin (1-7) mice. The rodents displayed no apparent changes in body weight, heart rate or blood pressure, the researchers said.

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FDA oks new drug for advanced breast cancer

U.S. regulators approved on Tuesday a new drug that in clinical trials delayed breast cancer progression in women no longer responding to Herceptin, a drug effective against tumors with too much of a protein called HER-2.

When given in combination with chemotherapy, the new drug, Tykerb (lapatinib), did a better job of curtailing cancer growth than did the chemo drug alone.

"Today's approval is a step forward in making new treatments available for patients who have progression of their breast cancer after treatment with some of the most effective breast cancer therapies available," Dr. Steven Galson, director of the U.S. Food and Drug Administration's Center for Drug Evaluation and Research, said in a prepared statement. "New targeted therapies such as Tykerb are helping expand options for patients."

Tykerb, which comes in pill form, is made by GlaxoSmithKline, which funded the clinical trial. The results of the trial were initially announced last June at the American Society of Clinical Oncology annual meeting, in Atlanta.

About 8,000 to 10,000 American women die from metastatic HER2-positive breast cancer each year, the FDA said.

Tykerb, among a class of drugs called kinase inhibitors, deprives tumor cells of signals they need to grow. But it differs from other cancer drugs in that it actually enters cells and blocks the function of the HER2 protein, the agency said.

The drug was tested in a trial involving 400 women with advanced or metastatic breast cancer that was HER2 positive. Common side effects included diarrhea, nausea, vomiting, and rash. A small percentage of participants also had a decrease in heart function that may have been characterized by shortness of breath. This condition generally was reversible, the agency said.
Some 20 percent to 25 percent of breast cancers have abnormally high levels of the HER2/neu receptor and, as a result, are generally more aggressive. Herceptin (trastuzumab) blocks activity of the receptor by binding to the part of the receptor outside the cell. Tykerb, by contrast, binds to a part of the receptor inside the cell.

The clinical trial included a plan for an independent data monitoring committee to analyze data at the halfway point to see if the benefits were larger than anticipated, in which case the committee would recommend the study be closed.

On March 20, 2006, the monitoring committee made a unanimous recommendation to terminate the trial because the results were so encouraging.

Women in the combined therapy group had almost double the time to disease progression as did women receiving Xeloda alone: 36.9 weeks vs. 19.7 weeks.

Responding to the FDA's approval of Tykerb, Dr. Len Lichtenfeld, deputy chief medical officer of the American Cancer Society, said in a prepared statement: "The approval of Tykerb is a significant step forward because it once again demonstrates the promise of targeted therapies, where we take our understanding of how cancer cells work and apply that knowledge to new drug development. We now have a new drug that offers promise and hope to women who have a more aggressive form of breast cancer, where until very recently we had little to offer. And we now have two drugs that are effective in treating this particular form of the disease.

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Lung cancer screens may not save lives

A new research suggests that screening smokers and former smokers for lung cancer doesn't save lives or prevent advanced disease and may lead to unneeded and harmful treatment. But it's not the final word on CT scans.

Some experts have hoped that the scans, which are a special kind of X-ray that can detect tiny lung abnormalities, will prevent lung cancer deaths by getting people into treatment earlier. But there hasn't been convincing evidence of that.

A large and authoritative scientific study won't be completed for a few years. Without that evidence, the American Cancer Society doesn't recommend the test, which costs $300 to $400, and most insurance companies won't pay for it.

The latest research, appearing in Wednesday's Journal of the American Medical Association, analyzed lung cancer deaths and cases of advanced lung cancer among 3,246 smokers and former smokers who had annual CT scans for about four years.

Researchers compared deaths and advanced cancer cases with rates predicted by a mathematical model. The model — based on a person's age, gender, asbestos exposure and smoking history — has proven valid in previous studies.

The model predicted there would be 33.4 cases of advanced cancer; there were 42. The model predicted 38.8 lung cancer deaths; there were 38.

"We don't see a trace of evidence that a single life was saved, that a single case of advanced cancer was avoided," said study co-author Dr. Peter Bach of Memorial Sloan-Kettering Cancer Center in New York.

CT screening did increase diagnosis and treatment. The people screened were three times more likely to be diagnosed with lung cancer and 10 times more likely to have lung surgery than predicted.

Bach said it's likely the cancers found by scans were so slow-growing they might never have caused death. Meanwhile, scanning missed the fast-growing, fatal cancers, which popped up between the annual scans.

"It's like taking a photo of the night sky when you're looking for a shooting star," Bach said.
Because CT scanning led to more biopsies and surgeries, patients were at risk of complications such as lung punctures, bleeding and infection, Bach said.

"Getting screened for lung cancer with CT scanning is not only unproven, it's potentially a risky endeavor," he said.

Lung cancer is the leading cause of cancer death in the United States and worldwide. About 213,380 Americans will be diagnosed with lung cancer in 2007, and the disease is expected to kill 160,390. Smoking is the main culprit.

Last year, another study was more encouraging about the potential for CT screening. It found that people whose early tumors were detected and promptly removed had an estimated 10-year survival rate of 92 percent.

An author of that study, Dr. Claudia Henschke of New York-Presbyterian Hospital/Weill Cornell Medical Center, said the new findings don't detract from the benefit found in her study. She said both studies should encourage discussion of how best to evaluate screening tools.
Any alternative to CT scans for lung cancer screening is many years away.

Dr. David Johnson, at Nashville's Vanderbilt-Ingram Cancer Center, who wasn't involved in either study, said the new research adds a note of caution about CT scans as smokers, former smokers and their doctors wait for results from the National Cancer Institute's study of 50,000 people coming in a few years.

In the meantime, Johnson doesn't recommend routine CT scans. "There's nothing more powerful to protect yourself from lung cancer than stopping smoking," he said. "CT scanning is not the answer. Stopping smoking is the answer."

Source: www.medical-health-care-information.com

Treating depression improves diabetes control

A new found of type 2 diabetics with depression confirms that depression has a negative impact on glycemic (blood sugar) control, researchers report, and "affirms the importance of depression management in diabetic patients in its potential to improve glycemic control."
Researchers from Missouri treated 93 patients with type 2 diabetes and depression with the antidepressant bupropion (Wellbutrin).

"We selected bupropion because it is capable of reducing depression and weight simultaneously and hypothesized that these effects would be accompanied by improved glycemic control in diabetic patients with major depressive disorder," the team explains in the journal Diabetes Care.

In support of their hypothesis, "antidepressant treatment produced benefits beyond just mood improvement," first author Dr. Patrick J. Lustman from Washington University School of Medicine, St. Louis, told Reuters Health. "Patients also lost weight, improved self-management of their diabetes, and improved their glucose control (A1C levels)."

Of these short-term improvements, only depression improvement predicted maintenance of improved blood sugar control in the subsequent 6 months, the researchers found.
"This confirms our hypothesis that depression improvement can produce better glycemic control, independent of favorable changes in weight and diabetes self care," Lustman noted. "Improvement in depression was the key to achieving longer term improvements in glucose control."

Lustman concludes that the data "point to the importance of weight-independent physiological factors (insulin sensitivity, inflammation) that improve during depression relief and contribute to better long-term control of diabetes."

Erectile dysfunction drugs may trump nitroglycerin for heart protection

Erectile dysfunction drugs may be better than nitroglycerin in protecting the heart from damage before and after a severe heart attack, Virginia Commonwealth University researchers report.

During a heart attack, the heart is deprived of oxygen, which can result in significant damage to heart muscle and tissue. After the attack, most patients require treatment to reduce and repair the damage and improve their chances of survival. With the exception of early reperfusion, there are no available therapies that are truly effective in protecting or repairing such damage clinically.

Rakesh C. Kukreja, Ph.D., professor of medicine and Eric Lipman Chair of Cardiology at VCU, and colleagues compared nitroglycerin with two erectile dysfunction drugs -- Viagra®, generically known as sildenafil, and Levitra®, generically known as vardenafil -- to determine the effectiveness of each for heart protection following a heart attack. Nitroglycerin is a drug used to treat angina, or chest pain. It is a vasodilator and opens blood vessels in order to improve the flow of blood to a patient's heart.

The research team reported that in an animal model, sildenafil and vardenafil reduce damage in the heart muscle when given after a severe heart attack. In contrast, nitroglycerin failed to reduce the damage in the heart when administered under similar conditions. The findings were published in the Journal of Molecular and Cellular Cardiology, the official publication of the International Society for Heart Research.

"Erectile dysfunction drugs can prevent damage in the heart not only when given before a heart attack, as we discovered previously, but also lessen the injury after the heart attack," said Kukreja, who is the lead author of the study.

According to Kukreja, the protective effects on the heart produced by these erectile dysfunction drugs may be potentially useful as adjunct therapy in patients undergoing elective procedures, including coronary artery bypass graft, coronary angioplasty or heart transplantation. In addition, he said another potential application could be to prevent the multiple organ damage that occurs following cardiac arrest, resuscitation or shock.

"Preserving heart function is critical to optimal cardiac outcomes," said George W. Vetrovec, M.D., chair of cardiology at the VCU Pauley Heart Center. "These agents have significant potential to enhance patient outcomes, particularly in high risk circumstances, such as acute heart attacks."

For several years, Kukreja and his colleagues have studied a class of erectile dysfunction drugs known as phosphodiesterase-5 inhibitors as part of ongoing research into heart protection. The team first investigated sildenafil, and then vardenafil, and found that both compounds were protective when given before a heart attack under experimental conditions.

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HIV drug resistance spurred by widely used Hepatitis B drug

A Johns Hopkins study has proven false established medical practice that an antiretroviral drug widely used to treat hepatitis B liver infections was safe to use on its own in patients co-infected with HIV. Their findings demonstrate that treatment with entecavir leads to cross-resistance to other antiviral drugs used to treat the AIDS virus.

"Our results show that entecavir is no different from any other that has been shown to be active against HIV - it breeds resistance rapidly, despite its ability to reduce the amount of HIV in the body," says senior study author and infectious disease specialist Chloe Thio, M.D.

Researchers say the findings, presented at the 2007 Conference on Retroviruses and Opportunistic Infections (CROI) in Los Angeles, have serious implications for the more than 4 million people worldwide believed to be infected with both viral illnesses but who need to treat their hepatitis B and are not yet on anti-HIV drugs.

Authors of the study have informed the U.S. Food and Drug Administration of their results so that prescribing physicians can be notified and so that drug labeling can be changed. They have also notified Bristol-Myers Squibb, which makes and sells entecavir under the brand name Baraclude.

"The alert should go out to co-infected people to consult with their physicians immediately about entecavir to see if it is the right drug to treat their hepatitis B in the first place and to evaluate alternative therapies," says Thio, an associate professor of medicine at The Johns Hopkins University School of Medicine.

This says she has stopped prescribing entecavir as her first option in treating hepatitis B in co-infected patients who are not already using drugs to suppress HIV.

"The good news is that co-infected patients already on HIV therapy can still use entecavir to treat their hepatitis B, but the bad news is that there are now fewer options for treating hepatitis B first," she adds. Hepatitis B infection attacks the liver and can lead to cirrhosis, liver cancer or even death from liver failure.

Entecavir, first marketed in March 2005, has been a leading treatment for chronic forms of hepatitis B, which can be fatal to almost a quarter of those infected if it is left untreated. The drug's label information currently states that is has no clinical effects on HIV.

According to Thio, some co-infected patients decide first to treat their hepatitis B infection if HIV has not yet weakened their immune system and to avoid the debilitating side effects of anti-HIV medications.

In the Hopkins study, researchers found in both laboratory and clinical tests that within six months of entecavir therapy, a so-called M184V mutation of HIV develops. This says viruses with this mutation are known to be resistant to lamivudine, better known as 3TC, a medication that prevents HIV replication and "is a cornerstone of most drug-combination therapies used to fight the immune system disease." Because lamivudine is in the same category of HIV therapies as another widely used drug, emtricitabine, its effectiveness is also compromised by entecavir, she says.

This began to investigate entecavir's effects on HIV in fall 2006 after noticing reports of anti-HIV activity in two co-infected patients, one at the Johns Hopkins Moore Clinic, which specializes in HIV/AIDS care, and another at a San Diego medical center. The patients (and there is now a third case) were taking only entecavir yet showed a tenfold decrease in the amount of HIV in their blood.

Previous studies had shown entecavir not to have any significant effects on HIV, about they were based on older tests that could not quantify the effects of HIV on individual immune cells or detect mutations. Thio believed that the recent patient cases called for a more thorough investigation with more advanced techniques.

She and her team combined various concentrations of entecavir with 100,000 human immune cells from a healthy blood donor, then infected them with an HIV test virus and measured the number of cells infected over time.

The lab test, developed at Hopkins by study co-author Robert Siliciano, M.D., Ph.D., a professor at Hopkins and a Howard Hughes Medical Institute investigator, specifically tests what drugs affect HIV and can be tailored to probe effects on any particular mutant of HIV.

Lab results showed that entecavir, in concentrations less than a tenth of what is used in humans, cut the number of newly infected cells in half. However, at increasing concentrations, the drug had no greater impact on suppressing HIV replication. HIV is a virus renowned for its ability to change form and thus evade or develop resistance to therapies designed to stop its action.

Similar testing with entecavir, immune cells and the M184V form of HIV showed that the drug did not stop the virus from infecting the cells. This provided evidence, scientists say, that the drug specifically fostered development of this mutation in HIV, later confirmed by clinical testing.

When researchers tested the blood of one of the co-infected patients for the M184V mutation, they found none in samples taken at the start of entecavir thereapy. But they did find it in 61 percent of viral samples tested after four months of therapy, and 96 percent at six months.

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