Lack of nutrients and metabolic syndrome linked to different subtypes of depression

A low intake of folate and vitamin B12 increases the risk of melancholic depressive symptoms, according to a study among nearly 3,000 middle-aged and elderly Finnish subjects. On the other hand, non-melancholic depressive symptoms are associated with an increased risk for the metabolic syndrome. Based on these new observations, melancholic and non-melancholic depression may be separate depressive subtypes with different etiologies in terms of proinflammation and diet. The study was the first to look at these depressive sub-types separately.

"The findings have practical implications in the care of patients with depressive symptoms. For example, it may be wise to avoid medication causing weight gain among patients with non-melancholic depression, whereas melancholic depressive symptoms may call for a closer look at the quality of the patient’s diet," says Mr Jussi Seppälä, MD, Chief of the Department of Psychiatry of the Hospital District of Southern Savo.

Melancholic depression involves typical depressive symptoms, such as a depressed mood. Non-melancholic depression is characterized by other types of symptoms, such as low self-esteem and feelings of worry and anxiety.

Among subjects with the highest folate intake, the risk for melancholic depressive symptoms was almost 50 per cent lower than among those with the lowest intake. In addition, among those with the highest vitamin B12 levels, the risk for melancholic depressive symptoms was almost three times lower than among those with the lowest levels. Both findings are new. A similar association with non-melancholic depressive symptoms was not observed.

Another novel observation is that the risk for the metabolic syndrome was twofold among those with non-melancholic depressive symptoms, as compared to those with melancholic symptoms or those with no depressive symptoms.

Mr Seppälä’s doctoral thesis “Depressive symptoms, metabolic syndrome and diet" was published at the University of Eastern Finland. The study was conducted as part of the Finnish Type 2 Diabetes Prevention Programme. The findings were originally published in Journal of Affective Disorders.

Researchers define key events early in the process of cellular aging

For the first time, scientists at Fred Hutchinson Cancer Research Center have defined key events that take place early in the process of cellular aging.

Together the discoveries, made through a series of experiments in yeast, bring unprecedented clarity to the complex cascade of events that comprise the aging process and pave the way to understanding how genetics and environmental factors like diet interact to influence lifespan, aging and age-related diseases such as cancer and neurodegenerative disorders.

The findings, including unexpected results that link aspects of aging and lifespan to a mechanism cells use to store nutrients, are described in the Nov. 21 issue of Nature by co-authors Daniel Gottschling, Ph.D., a member of the Hutchinson Center’s Basic Sciences Division, and Adam Hughes, Ph.D., a postdoctoral fellow in the Gottschling Lab.

The work began with Hughes and Gottschling searching for the source of age-related damage in mitochondria.

“Normally, mitochondria are beautiful, long tubes, but as cells get older, the mitochondria become fragmented and chunky,” said Gottschling, also an affiliate professor in the Department of Genome Sciences at the University of Washington. “The changes in shape seen in aging yeast cells are also observed in certain human cells, such as neurons and pancreatic cells, and those changes have been associated with a number of age-related diseases in humans.”

What causes mitochondria to become distorted and dysfunctional as cells age had long been a mystery, but Gottschling and Hughes have discovered that specific changes in the vacuole lead directly to their malfunctioning.The researchers found the acidity of a structure in yeast cells known as the vacuole is critical to aging and the functioning of mitochondria – the power plants of the cell. They also describe a novel mechanism, which may have parallels in human cells, by which calorie restriction extends lifespan.

Omega-3 Supplements May Slow A Biological Effect of Aging

Taking enough omega-3 fatty acid supplements to change the balance of oils in the diet could slow a key biological process linked to aging, new research suggests.

The study showed that most overweight but healthy middle-aged and older adults who took omega-3 supplements for four months altered a ratio of their fatty acid consumption in a way that helped preserve tiny segments of DNA in their white blood cells.

These segments, called telomeres, are known to shorten over time in many types of cells as a consequence of aging. In the study, lengthening of telomeres in immune system cells was more prevalent in people who substantially improved the ratio of omega-3s to other fatty acids in their diet.

Omega-3 supplementation also reduced oxidative stress, caused by excessive free radicals in the blood, by about 15 percent compared to effects seen in the placebo group.

“The telomere finding is provocative in that it suggests the possibility that a nutritional supplement might actually make a difference in aging,” said Jan Kiecolt-Glaser, professor of psychiatry and psychology at Ohio State and lead author of the study.

New gene-therapy approach could improve obesity treatment

Medical researchers at the University of Alberta have found a new way of using gene therapy to treat obesity. The treatment was successful, resulting in less weight gain, higher activity levels and decreased insulin resistance in lab models on a high-fat, high-sugar diet.

Faculty of Medicine & Dentistry researcher Jason Dyck, who works in the Department of Pediatrics and the Department of Pharmacology, published his findings this week in the peer-reviewed journal Nutrition and Diabetes. His team found a way to deliver the obesity treatment via DNA as opposed to a virus, which has had limited success in the past, especially over the long term. The results they demonstrated corroborated findings by other researchers who conducted short-term studies or used more risky methods of gene delivery.

“I think our findings may bring this treatment one step closer to clinical trials, as this approach appears to be much safer than conventional forms of gene therapy,” said Dyck.

The obesity treatment focused on increasing levels of adiponectin, a hormone secreted from fat cells. As a person gains weight and fat cells get larger, the body secretes less of this hormone. People who are thin secrete high levels of this hormone.

“This hormone seems to be protective against a number of diseases, including diabetes and cardiovascular disease, as well as weight gain,” says Dyck. “But as you gain weight, less adiponectin is secreted and you lose the beneficial effects associated with this hormone.”

Lab animal models fed a high-fat, high-sugar diet that were given this treatment gained less weight, burned more calories, were more active, used more oxygen, and were better protected against glucose intolerance and insulin resistance than those that were fed the same diet but didn’t get the anti-obesity treatment. Dyck hopes other research teams will move his work forward.

New research from the Hebrew University of Jerusalem shows that a carefully scheduled high-fat diet can lead to a reduction in body weight and a unique metabolism in which ingested fats are not stored, but rather used for energy at times when no food is available.

The results were published in FASEB Journal under the title ‘Timed high-fat diet resets circadian metabolism and prevents obesity.’

Previous research has established that disrupting mammals’ daily rhythms, or feeding them a high-fat diet, disrupts metabolism and leads to obesity. The researchers wanted to determine the effect of combining a high-fat diet with long-term feeding on a fixed schedule. They hypothesized that careful scheduling of meals would regulate the biological clock and reduce the effects of a high-fat diet that, under normal circumstances, would lead to obesity.

For 25 years, the rhesus monkeys were kept semi-starved, lean and hungry. The males’ weights were so low they were the equivalent of a 6-foot-tall man who tipped the scales at just 120 to 133 pounds. The hope was that if the monkeys lived longer, healthier lives by eating a lot less, then maybe people, their evolutionary cousins, would, too. Some scientists, anticipating such benefits, began severely restricting their own diets.

The results of this major, long-awaited study, which began in 1987, are finally in. But it did not bring the vindication calorie restriction enthusiasts had anticipated. It turns out the skinny monkeys did not live any longer than those kept at more normal weights. Some lab test results improved, but only in monkeys put on the diet when they were old. The causes of death — cancer, heart disease — were the same in both the underfed and the normally fed monkeys.

The connections between the rising rates of chronic disease and the production and consumption of modern foods can no longer be ignored. Our food supply is not healthy, nor is it sustainable. It has changed so dramatically that we have yet to adapt to the changes. Our food supply has been completely adulterated over the past few decades alone, more drastically than during any other time in history.

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