Health for life

People with diabetes experience depression more often than people without diabetes.

Does having diabetes raise your risk of developing depression? Or is it the other way around ... Does experiencing depression raise your risk of developing diabetes?

No definitive answer to that question exists. In fact, the two may be inextricably intertwined. That did not deter a group of Johns Hopkins researchers from seeking to tease the two conditions apart. Their findings were reported in the June 18 issue of JAMA:

Examining A Bidirectional Association Between Depressive Symptoms And Diabetes

The study had two parts. The cohort used was the Multi-Ethnic Study of Atherosclerosis (MESA study), a group of US adults followed for about 3 years.

The first part involved 5201 participants without diabetes. Their findings:

"The crude incidence of type 2 diabetes over 3.2 years was 22.0 per 1000-person years for those with elevated depressive symptoms and 16.6 per 1000 person-years for those without elevated depressive symptoms."

So, there was a small increase in risk for diabetes in individuals experiencing depression. This difference, however, was partially lessened when lifestyle factors (smoking history, caloric intake, alcohol use, physical activity level) were considered. It is possible that the same lifestyle factors that put someone at risk for depression (physical inactivity, higher caloric intake with weight gain), also increase their risk for diabetes.

The second part involved 4847 participants without depressive symptoms. Their findings:

"Individuals with untreated type 2 diabetes were not at increased risk of developing elevated depressive symptoms, those with treated type 2 diabetes were at increased risk of developing elevated depressive symptoms. ... Treated type 2 diabetes was associated with a 52% higher odds of developing elevated depressive symptoms."

That last finding, where untreated patients did not experience depression but treated patients did, led the authors to conclude:

"Clinicians should be aware of increased risk of elevated depressive symptoms in individuals with treated type 2 diabetes and consider routine screening for depressive symptoms among these patients."

What is it about treatment for diabetes that raises risk for depression?

The authors speculate that psychological stress associated with diabetes management may contribute. Also, if youre being treated, youre likely to have a number of complications which by themselves could increase the risk for depression.

A diet high in omega-3 polyunsaturated fat lowers levels of problem enzyme

Columbia University Medical Center (CUMC) researchers have found that a diet high in saturated fat raises levels of endothelial lipase (EL), an enzyme associated with the development of atherosclerosis, and, conversely, that a diet high in omega-3 polyunsaturated fat lowers levels of this enzyme. The findings establish a "new" link between diet and atherosclerosis and suggest a novel way to prevent cardiovascular heart disease. In addition, the research may help to explain why the type 2 diabetes drug rosiglitazone (Avandia) has been linked to heart problems.

The study, conducted in mice, was published in the October 4 online edition of Atherosclerosis, Thrombosis, and Vascular Biology.

Like other lipases, EL plays a role in the metabolism of blood lipoproteins, which are complexes of lipids (fats) and proteins. EL, which is secreted by macrophages (a type of white blood cell) and other cells in arteries, was discovered in 1999. Studies have shown that elevated EL is associated with atherosclerosis and inflammation. Until now, however, little was known about how dietary fats might affect this enzyme, said study leader Richard Deckelbaum, MD, the Robert R. Williams Professor of Nutrition professor of pediatrics and of epidemiology and director of the Institute of Human Nutrition at CUMC.

In the current study, a strain of mice susceptible to atherosclerosis was fed a normal diet enriched with either palmitic acid (a common saturated fat) or eicosapentaenoic acid (an omega-3 fatty acid, or polyunsaturated fat, found in fish oil, among other foods). After 12 weeks, the mices aortas were examined for changes in the expression of EL and inflammatory factors. Aortas of mice fed the saturated fat diet showed a significant increase in EL and detrimental changes in inflammatory factors, while those of mice fed the polyunsaturated fat diet showed a significant decrease in EL and beneficial changes in inflammatory factors. Studies in cultured macrophages showed similar results.

"Our study identifies a new way in which the high-saturated-fat Western diet could lead to the development of atherosclerosis, though, of course, these results need to be confirmed in human studies," said Dr. Deckelbaum. "The findings might also explain some of the cardiovascular benefits that have been attributed to omega-3 fatty acids."

The researchers also found, in cell culture studies, that macrophages fed saturated fat showed increased expression of PPAR-gamma, a cell signaling molecule that plays a role in regulating lipid metabolism and inflammatory responses. This increase was blocked when the cells were fed an omega-3 fatty acid.

"These findings are intriguing, because we know that the diabetes drug rosiglitazone (sold under the brand name Avandia) is a strong PPAR-gamma activator and that it has been associated with an increased risk of heart disease," said Dr. Deckelbaum. "So we hypothesized that if rosiglitazone activates ppar-gamma, it might also activate EL, which would explain its effects on the heart."

In fact, when the macrophages were given rosiglitazone, the expression of EL increased markedly. The addition of omega-3 fatty acids to the cells blocked this increase. "This would suggest that besides raising LDL cholesterol levels, rosiglitazone can raise the risk of cardiovascular disease by increasing EL," said Dr. Deckelbaum. "In addition to its potential role in increasing arterial inflammatory responses, EL increases the anchoring of LDL to cell surfaces, which could be associated with increased LDL accumulation in coronary arteries."

Use of Avandia was severely restricted in 2010, when the drug was linked to the development of heart disease.

New research that looked at whether two commonly prescribed statin medicines, used to lower low-density lipoprotein (LDL) or bad cholesterol levels in the blood, can adversely affect cognitive function has found that one of the drugs tested caused memory impairment in rats.

Between six and seven million people in the UK1 take statins daily and the findings follow anecdotal evidence of people reporting that they feel that their newly prescribed statin is affecting their memory. Last year, the US Food and Drug Administration (FDA) insisted that all manufacturers list in their side effects that statins might affect cognitive function.

The study, led by scientists at the University of Bristol and published in the journal PLOS ONE, tested pravastatin and atorvostatin (two commonly prescribed statins) in rat learning and memory models. The findings show that while no adverse cognitive effects were observed in rat performance for simple learning and memory tasks for atorvostatin, pravastatin impaired their performance.

Rats were treated daily with pravastatin (brand name - pravachol) or atorvostatin (brand name - Lipitor) for 18 days. The rodents were tested in a simple learning task before, during and after treatment, where they had to learn where to find a food reward. On the last day of treatment and following one week withdrawal, the rats were also tested in a task which measures their ability to recognise a previously encountered object (recognition memory).

The studys findings showed that pravastatin tended to impair learning over the last few days of treatment although this effect was fully reversed once treatment ceased. However, in the novel object discrimination task, pravastatin impaired object recognition memory. While no effects were observed for atorvostatin in either task.

The results suggest that chronic treatment with pravastatin impairs working and recognition memory in rodents. The reversibility of the effects on stopping treatment is similar to what has been observed in patients, but the lack of effect of atorvostatin suggests that some types of statin may be more likely to cause cognitive impairment than others.

Neil Marrion, Professor of Neuroscience at Bristols School of Physiology and Pharmacology and the studys lead author, said: "This finding is novel and likely lects both the anecdotal reports and FDA advice. What is most interesting is that it is not a feature of all statins. However, in order to better understand the relationship between statin treatment and cognitive function, further studies are needed."