



Archive for January 17th, 2011
First Published Friday, 20 March 2009
20 March 2009 by A C Grayling
AFTER John Locke published his Essay Concerning Human Understanding in 1690, he sent copies to various savants of his acquaintance, asking for comments and in particular for advice on whether he had left out anything essential – for if so, he could add it to a second edition. His correspondent William Molyneaux of Dublin replied that Locke needed to say something about personal identity: that is, what makes a person the same person throughout their life.
Belief in the idea of a substantial soul – a “you” that is separate from your body – was waning. In the absence of this metaphysical entity as a convenience for underpinning personal identity, what, asked Molyneaux, makes the retired general continuous with the eager subaltern of 40 years before, and he with the red-cheeked baby in his nurse’s arms 20 years before that? In response, Locke added a chapter to his second edition which instantly caused a storm of controversy and has been famous ever since in the annals of philosophy.
In that chapter Locke argued that a person’s identity over time resides in their consciousness (he coined this term, and here introduced it to the English language) of being the same self at a later time as at an earlier, and that the mechanism that makes this possible is memory. Whereas a stone is the same stone over time because it is the very same lump of matter – or almost, allowing for erosion – and an oak tree is identical with its originating acorn because it is the same continuous organisation of matter, a person is only the same through time if he or she is self-aware of being so. Memory loss interrupts identity, and complete loss of memory is therefore loss of the self.
The divines, represented by Edward Stillingfleet, Bishop of Worcester, took umbrage and attacked Locke for ignoring the immortal soul. In 1712 The Spectator magazine ran a front-cover demand that “the wits of Kingdom” should get together in conference to settle the matter of personal identity and selfhood, because the controversy was getting out of control. In 1739, when David Hume published the first volume of his Treatise on Human Nature, he stated that there is no such thing as the self, for if one conducts the empirical inquiry of introspecting – looking within oneself – to see what there is apart from current sensations, feelings, desires and thoughts, one does not find an extra something, a “self”, over and above these things, which owns them and endures beyond them.
Thus in 50 years the unreflective idea that each individual has an immortal soul as the basis of their selfhood had changed utterly. For millennia before Locke, no one had so much as raised the question. But it was no surprise that the question should suddenly become urgent as the Enlightenment dawned, with its central idea of the autonomous individual who is a bearer of rights and responsible for his or her own moral outlook; such an idea needs a robust idea of selfhood, and the philosophers eagerly tried to make sense of it.
Hume’s sceptical view did not prevail. Kant argued that logic requires a concept-imposing self to make experience possible, and the Romantics made the self the centre of each individual’s universe: “I am that which began,” wrote Swinburne in Hertha, “Out of me the years roll, out of me God and Man.” Without a deep idea of the self there could be no Freud or psychoanalysis.
So fundamental is the idea of the self to modern human consciousness that one would expect developments in neuroscience to have a direct bearing on it. And as Thomas Metzinger argues in his stimulating new book The Ego Tunnel, reviewed on page 44 of this issue, that is exactly what is happening – with surprising and often disconcerting results.
A C Grayling is a philosopher at Birkbeck, University of London
Source: Â http://www.newscientist.com/article/mg20127006.800-brain-science-and-the-search-for-the-self.html
First Published Saturday, 21 March 2009
Fwd:
*Kareem Dale, President Obama’s Special Assistant for Disability Policy, to
Speak at the 2009 Jacobus tenBroek Disability Law Symposium*
Don’t miss this opportunity to voice your concerns to Kareem Dale, Special
Assistant to the President for Disability Policy, at the 2009 Jacobus
tenBroek Disability Law Symposium on April 17th at the National Federation
of the Blind Jernigan Institute in Baltimore, Maryland. Mr. Dale will speak
on the Obama administration’ s policies on disability issues for
approximately thirty minutes followed by a forty-five minute question and
answer session. In addition to Mr. Dale, the presenters for the 2009
symposium are:
– Maura Healey, Assistant Attorney General and Chief, Office of Civil
Rights, Commonwealth of Massachusetts;
– Amy Robertson and Timothy Fox, Principals, Fox & Robertson, P.C.;
– Gerard Quinn, Professor of Law, National University of Ireland, Galway;
– Katherine Guernsey, International Lawyer and Adjunct Professor,
American University School of International Service;
– Samuel Bagenstos, Visiting Professor of Law, University of Michigan Law
School;
– Christine Griffin, Commissioner, United States Equal Employment
Opportunity Commission; and
– Peter Blanck, University Professor and Chairman, Burton Blatt Institute
at Syracuse University.
Ari Ne’eman, founding president of the Autistic Self-Advocacy Network, will
give the luncheon keynote address.
To view the full agenda, register online, or download the registration form
to register by mail or fax, visit the symposium web page at
http://www.nfb. org/nfb/Law_ Symposium. asp. Hotel information may also be
found on the symposium Web page.
The registration fee is $150; students may register for $20. A limited
number of scholarships to cover the registration fee will be available to
individuals with demonstrated financial need. Don’t miss this exciting
opportunity to interact with leading scholars, government officials, and
advocates and to make your voice heard. *The deadline to register is April
10, 2009.*
Symposium attendees will be provided documentation for CLE credit. Individuals
will be responsible for filing the application for CLE credit with their
state board.
The 2009 Jacobus tenBroek Disability Law Symposium is sponsored by the
National Federation of the Blind, the American Bar Association Commission on
Mental and Physical Disability Law, the Maryland Department of Disability,
the Texas Journal on Civil Liberties and Civil Rights, and the Legal Times.
For additional information about the symposium, contact:
Lou Ann Blake, Law Symposium Coordinator
National Federation of the Blind
Telephone: (410) 659-9314, ext. 2221
E-mail: lblake@nfb.org
—
Ari Ne’eman
President
The Autistic Self Advocacy Network
1660 L Street, NW, Suite 700
Washington, DC 20036
http://www.autistic advocacy. org
732.763.5530
First Published Saturday, 21 March 2009
By
Reviewed by John M. Grohol, Psy.D. on March 20, 2009
Friday, Mar 20 (Psych Central) —

Everyone is aware that alcohol affects the brain, but surprisingly, the specifics remain unclear.
One possibility is that alcohol may increase or decrease the release and the synthesis of endogenous opioid peptides — endorphins, enkephalins and dynorphins — in distinct brain regions important for drug addiction.
For the first time, a rodent study has confirmed that low to moderate levels of alcohol alter beta-endorphin release in the midbrain/Ventral Tegmental Area (VTA) region, producing the pleasant effects that likely reinforce alcohol consumption.
Results will be published in the June issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.
“Some of the functions of opioid peptides are similar to those of the opiate morphine,†explained Christina Gianoulakis, a professor in the departments of psychiatry and physiology at McGill University, and the study’s corresponding author.
“Like morphine, endogenous opioid peptides can induce analgesia and a mild euphoric effect, reduce anxiety, and may lead to a general feeling of well being. Therefore, increased release of endogenous opioid peptides in response to drinking could be partially responsible for the mild euphoric and anxiolytic effects associated with low to moderate amounts of alcoholic beverages.”
“The brain’s natural opioids have been implicated in many physiological functions such as pain and pleasure,†added Dzung Anh Le, a senior scientist at the Centre for Addiction and Mental Health, University of Toronto.
“Alcohol has long been thought to release these peptides, but previously the only way to confirm this was to rely on test tube experiments using extracted tissue samples, and findings from these studies were indirect and offered extremely limited interpretation.”
Le said that researchers suspected that dopamine was a key brain chemical in one of the most heavily implicated pathways likely involved in drug and alcohol addiction, the VTA.
“One mechanism by which alcohol produces its euphoric or rewarding effects is through the stimulation of natural opioid peptides in the VTA, which consequently activates dopamine in this critical pathway,†Le said.
“Until now, no one has been able to answer whether alcohol is actually capable of triggering opioid release in the VTA.”
Researchers injected male Sprague-Dawley rats with either saline or alcohol (0.8, 1.2, 1.6, 2.0, and 2.4 grams alcohol/kg of body weight). Using an in vivo microdialysis technique, study authors tracked the response of endorphins, enkephalins, and dynorphins at the level of the midbrain, including the VTA.
“We found that low to moderate but not high doses of alcohol increase the release of beta-endorphin in the VTA, one of the brain regions shown to be important for mediating the rewarding effect of alcohol,†said Gianoulakis.
“This supports a role of beta-endorphin in mediating some of the rewarding effects of alcohol. However, the same doses of alcohol that increase beta-endorphin release in the VTA have no significant effect on the release of enkephalins and dynorphins, the other two families of endogenous opioid peptides we examined.”
Gianoulakis said that readers should remember that it is the low to moderate doses of alcohol that are associated with mild euphoria, decreased anxiety and a general feeling of wellbeing. “On the other hand, high doses of alcohol are known to induce sedative and hypnotic effects, and often increase rather than decrease anxiety.”
“This research has confirmed a role of endogenous opioids in mediating alcohol addiction, and has delineated a pathway within which they may be involved,†said Le.
“It also goes further to specifically isolate an opioid peptide that may be most critically involved in a specific region of the brain. Endorphins are the natural peptides that most closely mimic the pharmacological properties of morphine, and of the three opioid families, they likely produce the greatest ‘high.”
Furthermore, Le added, methods used in this study are groundbreaking. “Dr. Gianoulakis and her team can track changes over time in living and freely moving animals,†he said.
“This has a profound implication on research in this area, as the effects of alcohol can be measured from an intact ‘living’ brain, in animals that are relatively uninhibited and unstressed within their environment.”
Both Gianoulakis and Le said these findings will help future treatment options.
“VTA beta-endorphin appears to play a significant role in alcohol reinforcement, and may partially explain the effectiveness of naltrexone — an opioid receptor antagonist currently used as treatment of alcoholism — in reducing alcohol consumption by some individuals,†said Gianoulakis.
“While current alcoholism treatment blocks opioids in a nonspecific fashion, this research suggests that a more targeted approach would be more beneficial,†said Le. “Researchers now have to specifically target endorphins in the VTA to see if it really does affect alcohol abuse and craving.”
“Readers should understand that drinking only low amounts of alcohol will increase endorphin release and produce pleasant effects,†said Gianoulakis.
“Thus, if after consumption of about two drinks of alcohol an individual does not experience the pleasant effects of alcohol, he or she should stop drinking. Consumption of high amounts of alcohol will not only fail to increase the release of endorphins, but may stimulate other systems in the brain that may lead to the development of anxiety and depression.”
Source: Blackwell Publishing
Source: Â http://psychcentral.com/news/2009/03/20/modest-alcohol-consumption-may-release-endorphins/4869.html
First Published Saturday, 21 March 2009
More Reasons to Eat Dark Chocolate
Can eating dark chocolate help lower your blood pressure? Studies reported in the Archives of Internal Medicine and Journal of the American Medical Association suggest the answer is “yes!”
Cocoa-rich dark chocolate may be as good at lowering blood pressure as some medications, according to two studies. But tea — green or black — doesn’t seem to have any significant effect.
A meta-analysis looked at 10 trials that studied the effects of polyphenol-rich tea and cocoa on blood pressure levels. The tea studies revealed no significant effect on blood pressure. But the cocoa studies found that people who ate 50–100 g of dark chocolate a day for two weeks had an average blood pressure decrease of 5/3 mm Hg.
In the second study, cocoa lowered blood pressure in 44 adults with untreated pre-hypertension or mild hypertension who received 6 g a day of dark chocolate or a matching amount of polyphenol-free white chocolate for 18 weeks.
Those eating dark chocolate had an average drop in blood pressure of 3/2 mm Hg, without any change in weight or cholesterol levels. This is one dietary change most people won’t have trouble making.
But beware: Chocolate is high in calories and eating too much can cause weight gain, which could undo cocoa’s blood pressure–lowering effect. So stick with the 6-g dose (0.25 oz) used in the second study; it was nearly as effective and contains only 30 calories.
[These studies were reported in the Archives of Internal Medicine (Volume 167, page 626) and the Journal of the American Medical Association (Volume 298, page 49).]
Another Reason To Go Easy on the Salt Shaker
You know that cutting back on salt is good for your blood pressure, but now there’s evidence it also prevents heart attack and stroke and death from cardiovascular disease.
Blood pressure levels tend to increase with higher intakes of sodium. By limiting your salt intake, you may be able to lower your systolic blood pressure by 2-8 mm Hg.
Salt added to foods during cooking and at the table makes up only about 10% of the sodium consumed in the typical American diet. A much larger proportion of the salt we consume comes from the sodium in processed foods like cold cuts; canned vegetables, meats, and soups; frozen dinners; cheeses; salad dressings; snack foods (such as potato chips); and fast food. Thus, reducing your salt intake means not only avoiding the saltshaker while cooking and at meals, but also reading food labels and choosing foods that are low in sodium.
And now there’s even more reason to go easy on the salt shaker, according to a study reported in the journal BMJ (volume 334, page 885). Researchers followed more than 3,100 adults with prehypertension. Participants who cut their sodium intake were 25% less likely to suffer a cardiovascular event (heart attack, stroke, or need for angioplasty or bypass surgery) or die of cardiovascular disease than those who stuck with their regular, often salt-laden diets. The findings come from two clinical trials that involved men and women 30-54 years old with high-normal blood pressure.
The participants were randomly assigned to either follow their usual diets or learn how to cut salt from their meals; those in the latter group lowered their sodium intake by 25-35%. During the five-year follow-up period, which began 10-15 years after the trials ended, the salt reducers had fewer heart attacks, strokes, and heart procedures, as well as a lower death rate.
Bottom line: These new findings show that the benefits of salt reduction extend beyond lowered blood pressure. So it’s even more important to follow experts’ advice on sodium: no more than 2,300 mg per day, and less than 1,500 mg if you have high blood pressure. Since processed foods are a major sodium source, always read product labels and opt for low-sodium versions whenever possible.
First Published Tuesday, 24 March 2009
Care for people with learning disabilities is under fire after a report found a litany of “significant and distressing failures” across the NHS and councils.
One man died as a result of failings in his care and it is likely that a second man’s death could have been avoided, the Health Service and Local Government Ombudsmen ruled.
Patients with learning difficulties were treated less favourably than others, resulting in “prolonged suffering and inappropriate care”, their report said.
And when their relatives complained about the care given to their loved ones, they were left “drained and demoralised and with a feeling of hopelessness”.
The charity Mencap said the conclusions were a “damning indictment” that confirmed an “appalling catalogue of neglect”.
The investigation was launched after Mencap made a complaint on behalf of the families of six vulnerable people who died in NHS or local authority care between 2003 and 2005.
The two ombudsmen called for an urgent review of health and social care for those with learning disabilities.
They found that Mark Cannon, 30, died as a consequence of public service failure by the Barking, Havering and Redbridge Hospitals NHS Trust and Havering Council in east London.
The ombudsmen concluded that he had been left in severe pain and great distress for prolonged periods, and was twice discharged from hospital without due concern for his safety.
The report – entitled Six Lives – found it was “likely” that the death of Martin Ryan, 43, another patient with learning disabilities, could have been avoided had his care and treatment not fallen so far below the required standard.
Mr Ryan, of Richmond, south west London, who had Down’s syndrome and epilepsy, went without food for 26 days while in hospital after suffering a stroke in November 2005.
The Health Service Ombudsman, Ann Abraham, concluded that Kingston Hospital NHS Trust gave him less favourable care because of his disability.
She found the failure to feed Mr Ryan for nearly four weeks “undoubtedly placed him at considerable risk of harm”.
Source(Includes Video): Â http://uk.news.yahoo.com/4/20090324/tuk-damning-report-on-disability-care-dba1618.html
