Though our mind can only affect certain body processes it can have a lot more to do with healing than we have been able to identify until recently. Evidence based medicine and the idea that the mind has effect on healing are not at odds at all. This article is a good example of how evidence based practices can be used to examine the mind’s effect on healing.
Background Placebo treatment can significantly influence subjective symptoms. However, it is widely believed that response to placebo requires concealment or deception. We tested whether open-label placebo (non-deceptive and non-concealed administration) is superior to a no-treatment control with matched patient-provider interactions in the treatment of irritable bowel syndrome (IBS). Methods Two-group, randomized, controlled three week trial (August 2009-April 2010) conducted at a single academic center, involving 80 primarily female (70%) patients, mean age 47±18 with IBS diagnosed by Rome III criteria and with a score ≥150 on the IBS Symptom Severity Scale (IBS-SSS). Patients were randomized to either open-label placebo pills presented as “placebo pills made of an inert substance, like sugar pills, that have been shown in clinical studies to produce significant improvement in IBS symptoms through mind-body self-healing processes” or no-treatment controls with the same quality of interaction with providers. The primary outcome was IBS Global Improvement Scale (IBS-GIS). Secondary measures were IBS Symptom Severity Scale (IBS-SSS), IBS Adequate Relief (IBS-AR) and IBS Quality of Life (IBS-QoL). Findings Open-label placebo produced significantly higher mean (±SD) global improvement scores (IBS-GIS) at both 11-day midpoint (5.2±1.0 vs. 4.0±1.1, p <.001) and at 21-day endpoint (5.0±1.5 vs. 3.9±1.3, p = .002). Significant results were also observed at both time points for reduced symptom severity (IBS-SSS, p = .008 and p = .03) and adequate relief (IBS-AR, p = .02 and p = .03); and a trend favoring open-label placebo was observed for quality of life (IBS-QoL) at the 21-day endpoint ( p = .08). Conclusion Placebos administered without deception may be an effective treatment for IBS. Further research is warranted in IBS, and perhaps other conditions, to elucidate whether physicians can benefit patients using placebos consistent with informed consent. Trial Registration ClinicalTrials.gov NCT01010191
This is fascinating, using virtual reality to treat depression. I wonder if it could work the other way. Some people I know seem to relate to most everything in the first person. If they see a movie, they imagine it is happening to them; if you make an analogy, they think you are talking about them; if they read some tragedy in the newspaper, they imagine that it happened to them. Every bad thing in the world that they hear about happens to them, personally. Such people often experience much pain and suffering, which they are eager to share with others.
This might make a difference in our lives soon.
SPINY GRASS AND SCRAGGLY PINES creep amid the arts-and-crafts buildings of the Asilomar Conference Grounds, 100 acres of dune where California’s Monterey Peninsula hammerheads into the Pacific. It’s a rugged landscape, designed to inspire people to contemplate their evolving place on Earth. So it was natural that 140 scientists gathered here in 1975 for an unprecedented conference.They were worried about what people called “recombinant DNA,” the manipulation of the source code of life. It had been just 22 years since James Watson, Francis Crick, and Rosalind Franklin described what DNA was—deoxyribonucleic acid, four different structures called bases stuck to a backbone of sugar and phosphate, in sequences thousands of bases long. DNA is what genes are made of, and genes are the basis of heredity.Preeminent genetic researchers like David Baltimore, then at MIT, went to Asilomar to grapple with the implications of being able to decrypt and reorder genes. It was a God-like power—to plug genes from one living thing into another. Used wisely, it had the potential to save millions of lives. But the scientists also knew their creations might slip out of their control. They wanted to consider what ought to be off-limits.
Caffeine acts through neuronal adenosine A2A receptors to prevent mood and memory dysfunction triggered by chronic stressJune 23rd, 2015 by Donald Steiny
This abstract is technical and it may not be obvious what it is saying, but it is great news for coffee drinkers (and tea drinkers too). One of the neural circuits in our uses a neurotransmitter called glutamate. When too much of this activity happens it fries the neurons which is not a Good Thing. We like our neurons and want them to stay healthy. Some things have a protective effect, like NAC (N-Acetyl Cystine). Well, it turns out that another thing that protects your neurons from frying is caffeine!
It is stress that causes your glutamate receptors to go nuts and start frying themselves. When that happens we get depressed (it is depressing to know you are frying neurons, isn’t it?). Drugs like lamotrigine, which is used for the depressed phase of bipolar disorder, also protect the neurons from getting fried by stress.
It helps preserve your memory.
So, we have yet another reason to drink lots of coffee. Yay! I am going to go refill my coffee cup right now.
Caffeine acts through neuronal adenosine A2A receptors to prevent mood and memory dysfunction triggered by chronic stress
Manuella P. Kastera,b,1, Nuno J. Machadoa,1, Henrique B. Silvaa,1, Ana Nunesa,1, Ana Paula Ardaisa,c, Magda Santanaa, Younis Baqid,e, Christa E. Müllerd, Ana Lúcia S. Rodriguesb, Lisiane O. Porciúnculac, Jiang Fan Chenf, Ângelo R. Toméa,g, Paula Agostinhoa,h, Paula M. Canasa, and Rodrigo A. Cunhaa,h,2Author AffiliationsEdited by Bruce S. McEwen, The Rockefeller University, New York, NY, and approved May 11, 2015 (received for review December 3, 2014)
Significant epidemiological studies show that individuals exposed to repeated stress, a major trigger of depression, increase their caffeine intake, which correlates inversely with the incidence of depression. However, the mechanism underlying this protective effect is unknown. We used an animal model of chronic unpredictable stress (CUS) to show that caffeine prevents the maladaptive changes caused by CUS in a manner mimicked by the selective blockade of adenosine A2A receptors (A2AR). CUS enhanced A2AR in synapses, and the selective elimination of neuronal A2AR abrogated CUS modifications. Moreover, A2AR blockade also afforded a therapeutic benefit, paving the way to consider A2AR blockers as a strategy to manage the negative impact of chronic stress on mood and memory.
The consumption of caffeine (an adenosine receptor antagonist) correlates inversely with depression and memory deterioration, and adenosine A2A receptor (A2AR) antagonists emerge as candidate therapeutic targets because they control aberrant synaptic plasticity and afford neuroprotection. Therefore we tested the ability of A2AR to control the behavioral, electrophysiological, and neurochemical modifications caused by chronic unpredictable stress (CUS), which alters hippocampal circuits, dampens mood and memory performance, and enhances susceptibility to depression. CUS for 3 wk in adult mice induced anxiogenic and helpless-like behavior and decreased memory performance. These behavioral changes were accompanied by synaptic alterations, typified by a decrease in synaptic plasticity and a reduced density of synaptic proteins (synaptosomal-associated protein 25, syntaxin, and vesicular glutamate transporter type 1), together with an increased density of A2AR in glutamatergic terminals in the hippocampus. Except for anxiety, for which results were mixed, CUS-induced behavioral and synaptic alterations were prevented by (i) caffeine (1 g/L in the drinking water, starting 3 wk before and continued throughout CUS); (ii) the selective A2AR antagonist KW6002 (3 mg/kg, p.o.); (iii) global A2AR deletion; and (iv) selective A2AR deletion in forebrain neurons. Notably, A2AR blockade was not only prophylactic but also therapeutically efficacious, because a 3-wk treatment with the A2AR antagonist SCH58261 (0.1 mg/kg, i.p.) reversed the mood and synaptic dysfunction caused by CUS. These results herald a key role for synaptic A2AR in the control of chronic stress-induced modifications and suggest A2AR as candidate targets to alleviate the consequences of chronic stress on brain function.chronic stress adenosine A2A receptor caffeine synaptic dysfunction mood dysfunction
Footnotes1M.P.K., N.J.M., H.B.S., and A.N. contributed equally to this work.2To whom correspondence should be addressed. Email: email@example.com.Author contributions: M.P.K., P.A., P.M.C., and R.A.C. designed research; A.L.S.R. provided important advice in planning experiments; M.P.K., N.J.M., H.B.S., A.N., A.P.A., M.S., Â.R.T., P.A., and P.M.C. performed research; Y.B., C.E.M., and J.F.C. contributed new reagents/analytic tools; M.P.K., N.J.M., H.B.S., A.N., A.P.A., A.L.S.R., L.O.P., Â.R.T., P.A., P.M.C., and R.A.C. analyzed data; and N.J.M. and R.A.C. wrote the paper.