Less May be More in the Management of Depression

A national study just published in the American Journal of Psychiatry says taking two medications for depression does not speed up recovery.

Although previous studies have suggested that combination therapy may be more effective than monotherapy, researchers at UT Southwestern Medical Center have now shown this is not the case. The condition, which affects approximately 19 million Americans each year, is a mood disorder in which feelings of sadness, loss, anger, or frustration interfere with everyday life for a long period of time. While the exact cause of depression is not known many researchers believe it is caused by chemical imbalances in the brain, which may be hereditary or caused by events in a person’s life.

The Combining Medication to Enhance Depression Outcomes, studied 665 patients aged 18-75 with major depressive disorder. It randomized patients into 3 groups who were then prescribed FDA approved antidepressant medications.

After 12 weeks of treatment, remission rates were similar across the three groups: 39%, 39% and 38%, respectively. Response rates were  about 52% in all three groups. After seven months of treatment, remission and response rates across the three groups remained similar, but side effects were more frequent in the third group.

These results show that, “Clinicians should not rush to prescribe combinations of antidepressant medications as first-line treatment for patients with major depressive disorder,” said Dr. Madhukar H. Trivedi, Principal Investigator of the study  and Professor of Psychiatry and Chief of the Division of Mood Disorders at UT Southwestern.The clinical implications are very clear – the extra cost and burden of two medications is not worthwhile as a first treatment step,” he concluded.

The next step is to study biological markers of depression to see if it is possible to predict response to antidepressant medication and, thus, improve overall outcomes.

Taking the Ouch out of Diabetes

New findings from UT Southwestern Medical Center researchers suggest that Type 1 diabetes could be converted to an asymptomatic, non-insulin-dependent disorder by eliminating the actions of a specific hormone.

Type 1 diabetes affects about 1 million people in the U.S.  In these people, the pancreatic islet cells that produce insulin are destroyed and sufferers must take insulin multiple times a day in order to metabolize blood sugar, regulate blood-sugar levels and prevent diabetic coma. They also must adhere to strict dietary restrictions.

These new studies in mice show that insulin becomes completely superfluous and its absence does not cause diabetes or any other abnormality when the actions of glucagon are suppressed.

Glucagon, a hormone produced by the pancreas, prevents low blood sugar levels in healthy individuals and causes high blood sugar in people with type 1 diabetes.

We’ve all been brought up to think insulin is the all-powerful hormone without which life is impossible, but that isn’t the case,” said Dr. Roger Unger, professor of internal medicine and senior author of the study appearing online and in the February issue of Diabetes.If diabetes is defined as restoration of glucose homeostasis to normal, then this treatment can perhaps be considered very close to a cure.

Insulin has been the gold standard for type 1 diabetes (insulin-dependent diabetes) since its discovery in 1922. But even optimal regulation of type 1 diabetes with insulin cannot restore normal glucose tolerance. These new findings demonstrate that elimination of glucagon restores glucose tolerance to normal.  In other words, if you don’t have glucagon, then you don’t need insulin.

Dr. Young Lee, assistant professor of internal medicine at UT Southwestern and lead author of the study, said the next step is to determine the mechanism behind this result.

““If we can find a way to block the actions of glucagon in humans, then maybe we can minimize the need for insulin therapy.”

Here at Word on Health, we’re sure that for those with diabetes, anything that reduces the need for injections has to be a positive.

Interfering Interferon

Word on Health heard some news this week that might just help asthma patients breathe easier.

Researchers at UT Southwestern Medical Center have found that interferon, a drug used to treat a variety of cancers such as leukemia and melanoma as well as multiple sclerosis and hepatitis; can block the development of certain immune cells known to cause asthma.

Known as T-helper 2 cells, under normal circumstances, they help protect against infections by releasing chemicals that induce inflammation. However in some people, these cells can promote allergic responses to normally harmless substances, including animal dander, pollens, and pollutants. Once Th2 cells become reactive to these substances, they promote all of the inflammatory processes common to allergic diseases like asthma and eczema.

The results which have just been published in the Journal of Immunology, suggest that interferon might be a viable, therapy for the treatment of asthma.

Dr. J. David Farrar (right) and research assistant Jonathan Huber

This finding is incredibly important, because humans are being treated with interferon for a variety of diseases, yet no one has tried treating asthma patients with interferon,” said J. David Farrar, PhD, Assistant Professor of Immunology and Molecular Biology at UT Southwestern and lead author of the study. “The current therapies for asthma are inhalers and steroids, both of which offer only temporary relief.”

In the current study, the researchers showed that interferon blocks the development of developing Th2 cells by targeting the very transcription factor that regulates their development and stability in the first place.

According to Farrar, “If you can stop a Th2 cell from ever developing, and if you can take a Th2 cell that has already become one and stop it from secreting these asthma-causing chemicals, then that’s really the ‘Holy Grail’ of treating asthma.”

Could this be an end to inhalers?  Only time and clinical trials will tell.