Be mindful, of the benefits of mindfulness:

Mindfulness has gotten a lot of press coverage over the last few years, and may well represent an extremely beneficial, cost effective, long term, low side effect treatment for a whole range of common stress, motivation, focus and affective related disorders. Here is a compilation of a few articles on the subject:

http://www.sciencedaily.com/releases/2013/06/130604114001.htm

"Although we've known that meditation can reduce anxiety, we hadn't identified the specific brain mechanisms involved in relieving anxiety in healthy individuals,"
For the study, 15 healthy volunteers [TOOO SMALL!!!!! ] with normal levels of everyday anxiety were recruited for the study. These individuals had no previous meditation experience or anxiety disorders. All subjects participated in four 20-minute classes to learn a technique known as mindfulness meditation. In this form of meditation, people are taught to focus on breath and body sensations and to non-judgmentally evaluate distracting thoughts and emotions… Researchers found that meditation reduced anxiety ratings by as much as 39 percent.

The study revealed that meditation-related anxiety relief is associated with activation of the anterior cingulate cortex and ventromedial prefrontal cortex, areas of the brain involved with executive-level function. During meditation, there was more activity in the ventromedial prefrontal cortex, the area of the brain that controls worrying. In addition, when activity increased in the anterior cingulate cortex -- the area that governs thinking and emotion -- anxiety decreased.”

http://www.sciencedaily.com/releases/2013/06/130619195139.htm

Mindfulness meditation can increase wellbeing and reduce stress in school children

Mindfulness = a mental training that develops sustained attention that can change the ways people think, act and feel

522 pupils, aged between 12 and 16 years, from 12 secondary schools [took] part in the study. 256 pupils at six of the schools were taught the Mindfulness in Schools Project's curriculum, a nine week introduction to mindfulness designed for the classroom." The other 266 pupils at the other six schools did not receive the mindfulness lessons, and acted as a control group.

Our mindfulness curriculum aims to engage even the most cynical of adolescent audience with the basics of mindfulness. We use striking visuals, film clips and activities to bring it to life without losing the expertise and integrity of classic mindfulness teaching."

All the pupils were followed up after a three month period. The follow-up was timed to coincide with the summer exam period -- which is a potential time of high stress for young people. The researchers found that those children who participated in the mindfulness programme reported fewer depressive symptoms, lower stress and greater wellbeing than the young people in the control group. Encouragingly, around 80% of the young people said they continued using practices taught in MiSP's mindfulness curriculum after completing the nine week programme. Teachers and schools also rated the curriculum as worthwhile and very enjoyable to learn and teach.

We found that those young people who took part in the programme had fewer low-grade depressive symptoms, both immediately after completing the programme and at three-month follow-up. This is potentially a very important finding, given that low-grade depressive symptoms can impair a child's performance at school, and are also a risk factor for developing adolescent and adult depression."

"These findings are likely to be of great interest to our overstretched schools who are trying to find simple, cost effective and engaging ways to promote the resilience of their students -- and of their staff too -- at times when adolescence is becoming increasingly challenging, staff under considerable stress, and schools under a good deal of pressure to deliver on all fronts...The next step is to carry out a randomised controlled trial into the MiSP curriculum, involving more schools, pupils and longer follow-ups."

Pain killers interfere with antidepressants:

http://www.healthcentral.com/depression/treatment-579181-5.html

In two studies, scientists found that taking antidepressants raises levels of cytokines in a person’s body. These cytokines then boost the levels of a protein called p11. This protein makes more serotonin receptors on the surface of cells. Having more of these receptors makes it easier for them to interact with serotonin. Serotonin is the primary brain chemical that SSRIs are designed to affect. Increasing serotonin usually reduces depression.

painkillers interfered with the production of these cytokines. This reduced the levels of p11 protein, which then reduced serotonin receptors on cells.  Thus, there were fewer serotonin receptors for the brain chemical to work on, and this kept the SSRI antidepressants from working at full strength.

scientists found evidence that non-steroidal anti-inflammatory drugs (NSAIDs) significantly reduce the effectiveness of selective serotonin reuptake inhibitor antidepressants (SSRIs) In fact, NSAIDs were associated with a 10 percent drop in depression remission rates, from 55 percent to 45 percent.What this means is that if you take NSAIDs and SSRI antidepressants together, there’s a 10 percent greater chance you’ll still suffer from depression, even if you’re taking a medication to treat it.

People who suffer from chronic pain could be prescribed other kinds of antidepressants such as tricyclic antidepressants or buproprion (Wellbutrin), which work on neurotransmitters in the brain, but not in the same way.  Or, people with depression could be given other types of medications to treat their pain.

http://www.pnas.org/content/early/2011/04/20/1104836108.abstract

In contrast to the levels detected in serum, we found that frontal cortical levels of certain cytokines (e.g., TNFα and IFNγ) were increased by serotonergic antidepressants and that these effects were inhibited by antiinflammatory agents. The antagonistic effect of antiinflammatory agents on antidepressant-induced behaviors was confirmed by analysis of a dataset from a large-scale real-world human study, “sequenced treatment alternatives to relieve depression” (STAR*D), underscoring the clinical significance of our findings. Our data indicate that clinicians should carefully balance the therapeutic benefits of antiinflammatory agents versus the potentially negative consequences of antagonizing the therapeutic efficacy of antidepressant agents in patients suffering from depression.

Jasmine triggers GABA receptors!!

http://www.sciencedaily.com/releases/2010/07/100708104320.htm
the two fragrances Vertacetal-coeur (VC) and the chemical variation (PI24513) have the same molecular mechanism of action and are as strong as the commonly prescribed barbiturates or propofol.They soothe, relieve anxiety and promote sleep... vertacetal-coeur (VC) and the chemical variation (PI24513) were the strongest: they were able to increase the GABA effect by more than five times and thus act as strongly as the known drugs. The "cross check" with genetically modified GABA receptors in transgenic mice which no longer responded to propofol confirmed that the mechanism of action is the same: the altered receptor also no longer responded to the fragrances.

"Applications in sedation, anxiety, excitement and aggression relieving treatment and sleep induction therapy are all imaginable. The results can also be seen as evidence of a scientific basis for aromatherapy." By changing the chemical structure of the scent molecules, the researchers hope to achieve even stronger effects

Herbal extract may extend lifespan independently of calorie restriction mechanism (SIRT)

http://www.sciencedaily.com/releases/2013/06/130618125112.htm

herbal extract  of a yellow-flowered mountain plant(Rhodiola rosea)  long used for stress relief was found to increase the lifespan of fruit fly populations by an average of 24 percent, independent of calorie restriction pathways

Rhodiola rosea, also known as golden root…Rhodiola works in a manner completely unrelated to dietary restriction and affects different molecular pathways.

The researchers proved this by putting flies on a calorie-restricted diet. It has been shown that flies live longer when the amount of yeast they consume is decreased. Jafari and Schriner expected that if Rhodiola functioned in the same manner as dietary restriction, it would not work in these flies. But it did. They also tested Rhodiola in flies in which the molecular pathways of dietary restriction had been genetically inactivated. It still worked.

Not only did Rhodiola improve lifespan an average of 24 percent in both sexes and multiple strains of flies, but it also delayed the loss of physical performance in flies as they aged and even extended the lives of old flies. Jafari's group previously had shown that the extract decreased the natural production of reactive oxygen species molecules in the fly mitochondria and protected both flies and cultured human cells against oxidative stress.

Rhodiola has already shown possible health benefits in humans, such as decreasing fatigue, anxiety and depression; boosting mood, memory and stamina; and preventing altitude sickness. Grown in cold climates at high elevations, the herb has been used for centuries by Scandinavians and Russians to reduce stress. It's also thought to have antioxidant properties.

Jafari's research group is currently exploring the plant's potential to kill cancer cells, improve Alzheimer's disease and help stem cells grow.

Rhodiola is readily available online and in health food stores. Jafari, though, has analyzed several commercial products and found them to not contain sufficient amounts of the reputed active compounds -- such as rosavin and salidroside -- that characterize high-quality products.

Sapolsky on chronic stress and hippocampal damage:
 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC60045/

Chronic stress causes prolonged Cortisol release from the adrenals, which in turn feeds back to the hypothalamus and has a negative feedback on the cortisol release, as one would expect. However, there is more to this than a simple negative feedback loop. The hippocampus seems to have a negative influence upon the hypothalamic release of CRH, in turn lowering cortisol levels. Unfortunately, the sustained levels of cortisol, if an organism is chronically stressed, seem to inhibit the hippocampus through 3 possible mecahnisms described by sapolsky:
1)Temporary (reversible) retraction of hippocampal dendritic connections
2)Ihnibition of neurogenesis in the hippocampus
3)Hippocampal neurotoxicity = a loss of preexisting hippocampal neurons

This explains the loss of hippocampal volume that is common in severly depressed patients that express high cortisol levels, and might explain the permanency of various functional/mood/ learning losses as a result of depression working through permanent hippocampal damage.




The potentially good news is that anti depressants (Tianeptine - and SSRE [enhancer]) - and possibly other (SSRI's) [despite the seeming incongruity] increase BDNF, which in turn inhibits the effect of cortisol upon the hippocampus thereby preserving its integrity.
"Although the best known of these are the specific serotonin reuptake inhibitors such as Prozac, other efficacious drugs also block the reuptake of norepinephrine and/or dopamine. Nicely commensurate with the involvement of serotonin, there is some evidence that increased serotonin availability can stimulate cell proliferation in the hippocampus However, tianeptine is a distinctly atypical antidepressant (with, reputedly, only limited clinical efficacy), which increases serotonin reuptake. Thus, it decreases synaptic serotonin concentrations, rather than enhancing them."



It may well be then, that antidepressants not only help the patient now, but if they can both lower stress now, and lower the deleterious effects of stress upon the hippocampus, that the patient is less likely to have lasting permanent damage to the hippocampus, and with it permanent damage to learning and mood centres!

It is worth mentioning that a few still think some sort of neurogenesis issue in the hippocampus could lead to depression, not the other way around, but they are a minority and evidence appears scarce.

I will leave you with the great man's words himself:
"Obviously, more research is needed. It would be a boon to biological psychiatry if any antidepressants can prevent some of the neurobiological correlates of depression, in addition to alleviating the affective symptoms. But findings such as these also support the frequent uphill battle for those who study depression, or suffer from it, namely convincing others that this is a real biological disorder, rather than some sort of failure of fortitude or spirit."