We have known for a long time that there are close links between depression, aging and heart disease, but the nature of the link has remained elusive. Most of the smart money has been on inflammation, but there could be other candidates.

New research in the journal Brain, Behavior and Immunity has linked an increase in two inflammatory proteins in the immune system with a latent viral infection and proposes a chain of events that might accelerate cardiovascular disease. It is possible that the same process may be involved in a number of other ailments that can afflict us, as we get older. The findings also suggest that chronic depression may play a key role in initiating the cascade that can lead to the development of coronary artery disease.

It has been known for some time that increased levels of the proinflammatory cytokines, TNF-α and IL-6, predict mortality and morbidity. High levels of each of them are found in the plasma and in atherosclerotic lesions of people with cardiovascular disease.

The levels of IL-6 in the body increase as the immune system ages. Some of the IL-6 is generated by immune cells - macrophages - that go to the site of an infection or injury. Earlier work by the team also showed that increases in psychological stress and depression could substantially raise the levels of IL-6 and TNF-α in the body.

Increased stress and depression can also trigger latent viruses to reactivate and begin reproducing inside cells. The viruses of greatest interest are some herpes viruses such as the Epstein-Barr virus (EBV). We know that up to 90% of the people in North America have been infected by EBV by the time they are adults.

If EBV begins to multiply in cells in the body, it produces a protein called dUTpase that, in turn, can stimulate macrophages to make yet more IL-6.

The researchers developed a model to test these linkages by using endothelial cells that line the inside of veins in umbilical cord tissue. I spent years working with these cells myself, and they provide an excellent substrate for examining vascular responses and the interaction between blood vessels and macrophages when exposed to the virus as well as the dUTpase protein.

As expected, the production of IL-6, as well as TNF-a, were increased just as they would be as part of the inflammatory process in the body. Such chronic incidents of inflammation are integral to the onset of atherosclerosis and an array of other diseases.

This work suggests a new way of thinking about how vascular diseases develop. We carry around these latent herpes viruses in our bodies virtually all our lives and periodically they can hurt us as we age, develop depression or, perhaps a nutritional imbalance.

Taken together with the recent data on the physical effects of loneliness, if you want to live a long and healthy life:

• Watch you mood: depression can kill you
• Stay socially engaged: loneliness can be fatal
• Maintain a balanced diet
• Take some physical exercise every day
• Learn – and practice! – some simple stress management techniques. You can obtain some at RichardGPettyMD.com

It is fascinating to see a medicine or a therapy that is used for one thing being applied in a completely different area. A good example is thalidomide, a drug that was introduced in 1957 to treat morning sickness. It was pulled from the market because it could cause terrible fetal malformations. Years later it was discovered that it could be very helpful in the treatment of multiple myeloma, leprosy and Behcet’s disease.

Now a new study has shown that people treated with the antibiotic minocycline within six to 24 hours after a stroke (cerebrovascular accident) had significantly fewer disabilities.

In the study 152 men and women received either an oral dose of minocycline or placebo for five days following stroke. People who received minocycline were treated on average within 13 hours of the onset of the stroke compared to 12 hours for the placebo group. Patients were followed up for three months.

People treated with minocycline had significantly better outcomes than those treated with placebo. By three months, the minocycline group performed four times better than the placebo group on the National Institutes of Health Stroke Scale, which measures vision, facial palsy, movement, and speaking ability.

Minocycline appears to be neuroprotective and to prevent programmed cell death or apoptosis.

This could turn out to be very important because current stroke treatments only work during the first few hours after the onset of symptoms, and many people do not get to the hospital in time to be treated.

Insulin may have some extremely important roles in the mind as well as the body.

Though best known for its role in promoting glucose uptake into cells, insulin has at least five hundred known functions in the human body. For many years nobody was sure whether insulin was important to the brain: neurons in the brain are unusual in that they do not need insulin to enter them. But then we discovered that insulin acts on other important metabolic processes in neurons. In the brain it also does duty as a chemical messenger and as a growth factor, and brain insulin signaling is crucial for the creation of memory. Over the years a number of theorists have suggested that some neurological and psychiatric illnesses could be a result of disturbances in insulin-related processes in the brain.

It is now beginning to look as if they may have been correct.

Some recent evidence has suggested that Alzheimer’s disease and diabetes mellitus share a number of common pathways and Alzheimer’s disease is associated with peripheral insulin resistance.

New research has been published by investigators from Northwestern University in the FASEB Journal - the journal of the Federation of American Societies for Experimental Biology – that may finally nail down the reason why insulin signaling may stop working in Alzheimer’s disease.

The research team used mature cultures of neurons from the hippocampus of the brain to study synapses – the connection between neurons - that have been implicated in learning and memory mechanisms. They wanted to examine the effect of a toxic protein, known to attack memory-forming synapses, that is called “ADDL” for “amyloid ß-derived diffusible ligand.” ADDLS are small, soluble aggregated proteins that accumulate in the earliest stages of Alzheimer’s disease. The researchers had previously found that ADDLs bind very specifically at synapses, which in turn initiates deterioration of their function, shape and composition. They now went on and studied the synapses and their insulin receptors before and after ADDLs were introduced. Regions of the nerve with normal numbers of insulin receptors have no ADDL binding, but when the ADDLs are added they remove insulin receptors from nerve cells, effectively making them insulin resistant.

And an insulin resistant neuron cannot participate in the formation of memories.

This finding implies that there is a fundamental connection between diabetes and Alzheimer’s disease, and this may in turn help us to see whether existing diabetes treatments might protect neurons from ADDLs and improve insulin signaling in people with Alzheimer’s disease.

The first type of diabetes is Type 1, a.k.a. insulin-dependent or juvenile onset. The second is Type 2, a.k.a. non-insulin-dependent diabetes. So is Alzheimer’s Type 3?

It has also been known for some time that physical exercise is one of the factors that may help reduce the chance of developing Alzheimer’s disease, and we may now have a mechanism by which it can help.

This is an extraordinarily interesting and important discovery that should lead to a whole new research angle, perhaps with medicines that are already available.

The Howard Hughes Medical Institute (HHMI) has agreed to support Springer’s Open Choice program. What that means is that if articles are accepted for publication after a process of rigorous peer-review, they will immediately be published with full open access and deposited in repositories such as PubMed Central, at a flat-rate fee per article of $3,000. Springer’s Open Choice program applies to all its journals.

HHMI has a strong commitment to ensuring public access to original research articles. Beginning with papers submitted for publication after January 1, 2008, HHMI will require its scientists to publish their original research articles in journals that allow the articles and supplementary materials to be made freely accessible in a public repository within six months of publication.

HHMI is the largest private funder of biomedical research in the United States and commits more than $500 million a year for research and distributes $80 million in grant support for science education.

HHMI investigators already publish a significant number of research articles in open access journals or in journals with open access options. Under the new policy, HHMI will pay up to $2,000 in open access charges per article with the balance coming from laboratory budgets or other sources.

It is wonderful that one of the largest and most prestigious research institutes in the world, is actively supporting open-access publishing and backing up their words with significant funding

I know that there are going to be a ton of exceptions, but I was extremely interested to see a study in the journal Biology Letters that seems to indicate that a deep male voice may attract women more than a great physique or an attractive face. Men with deep voices are also much more likely to have more children than men who do not have deep voices.

The investigators used an interesting analogy, sating that a man’s deep voice is a bit like a peacock’s tail: it has no survival value, but attracts the female of the species. Testosterone masculinizes the voice at puberty.

The research team interviewed 52 women and 49 men aged 18-55, from the Swahili–speaking Hadza tribe in Tanzania. They chose the Hadza tribe because their lifestyles reflect those of our hunter-gatherer ancestors. The females gather berries and search for wild plants. The males collect honey and hunt animals. Even though the Hadza are monogamous, extra-marital sex is common, but there is no birth control.

During the interviews, which took place in Swahili, the voices of the men and women were recorded. On studying the recording later they found that the deep voiced men had fathered more children than the non-deep voiced men. The man with the deepest voice had ten surviving children, while the one with the highest pitched voice had three.

Coren Apicella, the lead author, suggested that perhaps the males with the lower pitched voices had higher testosterone levels, which attracted them more to females or made them more attractive to them. It is also possible that men with higher testosterone levels start reproducing earlier in life. They may also be better hunters, since testosterone may have an impact on muscle mass, and a better hunter would bring more food, allowing their wives to have shorter inter-birth intervals.

It is possible that if vocal dimorphism evolved partly due to mate selection, then in the past men and women may have had more similar voices.

I don’t suppose that anyone is going to be too interested to hear this, but your humble reporter has always had a very deep voice…