DSM: The Everlasting Gobstopper of Psychiatry

The DSM is the Everlasting Gobstopper of psychiatry, providing a seemingly endless store of material for bloggers, journalists, academics, and other commentators.

I looked through the comments on my last post and was impressed by how articulate they were. I'll spend the next few posts commenting on some of the comments. How's that for narcissistic exploitation of one's own blog?

S pointed out that “a reasonable, experienced, compassionate doctor will not be bound up by DSM diagnoses,” and accurately followed that up with “but I suspect all of us here know that there are plenty of doctors who can't see past rigid categorization or have a two-dimensional view of their patients.”

I agree. Michael First, who was the editor of DSM-IV, once told me, “We used to joke that DSM should come with a combination lock and you can only open the book if you agree to really explore what is going on in the patient’s minds.” I think of DSM is a map into the mental world. It allows us to locate a patient in a general region, but not much more than that. To truly make the diagnosis, we have to do the messy work of talking with the patient and exploring what’s going on. In fact, the term “diagnosis” is a misnomer and should probably never have been borrowed from the rest of medicine, since it implies a precision utterly lacking in psychiatry circa 2010.

Dr. Peter Huang likes the new dimensional aspects of the DSM-V, but is concerned that the new disorders being proposed "will serve as an even bigger seed that Big Pharma + the APA + the FDA will use to increase further the insanely vast quantities of psych meds that are prescribed.” This is also Dr. Allen Frances' main critique in his essay, Opening Pandora’s Box: The 19 Worst Suggestions For DSM5. I agree that this is an inevitable consequence of elaborating the DSM, but only if we psychiatrists acquiesce. Some of these "changes" represent little more than a shuffling around of criteria from one label to another. The two risk syndromes (for psychosis and dementia) are potentially more insidious and might be exploited by drug companies for commercial gain. For this reason, I find it rather unlikely that both will make it into the final version--I predict that mild dementia (in the new vocab, "mild neurocognitive disorder") will make it through the gauntlet, but not "risk syndrome for psychosis."

Dr. Joseph Arpaia points out that DSM is mute when it comes to how the environment produces psychiatric symptoms: “The minimizing of the environmental effects means that the brain's attempts to adapt to the environment are seen as inherent brain pathology. This is as absurd as stating that an immune response to a bacterial invasion is an inherent immune pathology.”

However, the reason DSM does not mention environment is that it attempts to be “agnostic” when it comes to statements of causation. Yes, depression can be caused by many things but DSM simply runs down the list of symptoms. This speaks to the issue of how the document is used. If someone invented a DSM robot (perhaps in Freud's likeness), such a machine would, indeed, simply go through the lists and makes a bunch of diagnoses divorced from context. But thoughtful clinicians, whether psychiatrists or psychologists or social workers, don’t use the manual this way. Don't expect DSM to be more than it is, which is bare-bones descriptive psychiatry. At this point, we know too little about causation to do anything more than describe symptoms.

That's all for now--stay tuned for our next installment of "Commenting on the Commenters."

Don’t fall into the dementia trap when treating a developmental disability

February 16, 2010
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by Lockup Doc

In addition to correctional psychiatry, I spend about half of my professional time treating patients with developmental and intellectual disabilities (mental retardation). The majority of my patients have severe or profound mental retardation and are completely nonverbal.

Over the years I have observed that when many of them are admitted to the hospital for acute medical or surgical problems, because they are severely cognitively and functionally impaired, they are treated as though they have terminal illnesses. The treatment approach is often akin to that for patients with end-stage Alzheimer’s Disease.

By definition, a developmental disability (DD) occurs before the age of 18 and is a static condition. Most of my DD patients have genetic syndromes or have suffered from perinatal brain injuries. They have been far behind the curve in meeting developmental milestones, and many never will be able to walk, talk, or have the motor or communication skills or level of independence that most of us enjoy.

However, despite these deficits, each of them has unique strengths. Even those who require significant assistance with their activities of daily living still seem to be able to enjoy various activities in their lives. It would be easy to judge them as having little quality of life, but the longer I work with this population, the more I believe it to be a mistake for the developmentally normal to judge the quality of life of the chronically disabled.

On the surface, these patients are obviously severely impaired, and in many ways some of them do not look much different from those with severe dementia. The key point, though, is that their developmental disabilities are not progressive or terminal illnesses.

In contrast to those with developmental disabilities, patients with end-stage Alzheimer’s Disease have a progressive and ultimately fatal disease. In advanced Alzheimer’s Disease, patients often become incontinent of bowel and bladder, become nonverbal or minimally communicative, have difficulty eating or stop eating altogether, and eventually require assistance with all activities of daily living.

Primary care physicians are familiar with this latter scenario since Alzheimer’s Disease is fairly common. Often their end-stage dementia patient previously will have been a person with normal intellectual functioning who was quite independent. Considering hospice and withholding treatment can be the right decisions in advanced dementia. We often think of such patients as having very little quality of life because of the dramatic losses that have been inflicted by their dementing illness. They clearly are not the same people they used to be.

However, since severe and profound mental retardation are much less common than dementia, and because those with severe developmental disabilities may, on the surface, resemble those with advanced dementia, I believe it is easy to mistakenly think of the two as being in the same end-of-life category even though they are not.

When this mistake occurs, DD patients may have necessary diagnostic and therapeutic interventions withheld even though their physicians may be very competent and believe that they are doing the right thing by not treating these “obviously declining” patients too aggressively.

The key to avoiding falling into the dementia trap when treating a patient with a severe developmental disability is to learn as much as possible about the patient’s baseline level of functioning. For example, if a particular patient has always been nonverbal, incontinent, and gastrostomy-tube fed but does not seem to be losing skills, then the diagnostic and treatment approach likely will be similar to that for any other non-terminal patient. However, if the patient is obviously declining relative to baseline, then a more conservative approach may make sense.

The author is a psychiatrist who blogs at Lockup Doc.

High-Fat Ketogenic Diet To Control Seizures Is Safe Over Long Term

Current and former patients treated with the high-fat ketogenic diet to control multiple, daily and severe seizures can be reassured by the news that not only is the diet effective, but it also appears to have no long-lasting side effects, say scientists at Johns Hopkins Children's Center.

A study report supporting their conclusion, and believed to be one of the first analyses of the long-term safety and efficacy of the diet, appears online in the February edition of the journal Epilepsia.

The ketogenic diet, consisting of high-fat foods and very few carbohydrates, is believed to trigger biochemical changes that eliminate seizure-causing short circuits in the brain's signaling system. Used as first-line therapy for infantile spasms and in children whose seizures cannot be controlled with drugs, the diet is highly effective but complicated and sometimes difficult to maintain. It can temporarily raise cholesterol, impair growth and, in rare cases, lead to kidney stones, among other side effects.

"Despite its temporary side effects, we have always suspected that the ketogenic diet is relatively safe long term, and we now have proof," says senior investigator Eric Kossoff, M.D., a pediatric neurologist and director of the ketogenic diet program at Hopkins Children's. "Our study should help put to rest some of the nagging doubts about the long-term safety of the ketogenic diet," he adds.

The evidence is based on a study of 101 patients ages 2 to 26 years treated with the ketogenic diet for a minimum of 16 months and for up to eight years at Hopkins Children's between 1993 and 2008. At the time of the follow-up, patients were off the diet anywhere between eight months and 14 years. Nearly 80 percent of the patients remained either seizure-free or had their seizures reduced by half. Most patients' seizures did not worsen even years after stopping the diet.

Researchers caution it is possible that some effects may not show up for decades. However, the evidence, especially among patients who were off the diet for more than 10 years, suggests no long-term harm.

During interviews, none of the patients reported adverse cardiovascular side effects such as heart attacks, enlargement of the heart or abnormal plaque buildup in their arteries. One patient reported having high blood pressure.

Only two of the 101 patients reported kidney stones after stopping the diet, the same rate found in the general population not treated with the ketogenic diet, the researchers say.

None of the 25 patients who had liver and kidney function tests had abnormal results. Among the 26 patients who had their cholesterol tested, the average level was 157 milligrams per deciliter of blood (less than 200 is considered normal), with three of the 26 having abnormal levels. Most patients' cholesterol levels go up while on the diet, but are believed to return to normal thereafter. The Hopkins study now confirms that this is the case.

Most patients older than 18 at the time of the study had normal body mass index of 22 on average (25 and below is considered normal). And most of them were within a few inches of their expected heights, based on their parents' heights. Patients 18 years and younger at the time of the study were, on average, in the 25th percentile for height and in the 36th percentile for weight for their age. While this is below average, the investigators say, it is also much higher than the usual 5th-to-10th percentile while on the diet.

"We have every reason to believe that most children will start catching up once they are off the diet as they grow up because this is what we see in older former patients," Kossoff says.

Contrary to the fear of many parents, the diet does not appear to alter patients' food preferences, the researchers say. Only 8 percent of those in the study said they continued to eat predominantly high-fat foods.

Conflict of interest disclosure: Dr. Kossoff has received grant support from Nutricia, Inc. and consultant fees from Nutricia and Atkins Nutritionals Inc.

The research was funded in part by the National Institutes of Health and the Carson Harris Foundation.

Co-investigators include Amisha Patel, Paula Pyzik, Zahava Turner and James Rubenstein.

Source
Johns Hopkins Medicine

Preventing Recurrent Strokes Needs Improvement

Feb. 15, 2010 -- One in 12 people who have a stroke will likely soon have another one, and one in four will likely die within one year, according to a new study.

Researchers say the results suggest that more attention needs to be paid to prevention of recurrent strokes. Stroke is the third leading cause of death in the U.S.

The study, published in Neurology, was based on 10,399 people in South Carolina who had a hospital discharge diagnosis of stroke in 2002. The results showed that nearly 25% of people who had a stroke died within one year from any cause and 8% had another stroke within a year.

These risks rose steadily one year after the initial stroke. By the end of four years after a stroke, the risk of another stroke was 18% and the risk of death was 41%.

“Furthermore, the risk of recurrent stroke was between three and six times higher than the risk of heart attack at different points during the study,” researcher Wuwei (Wayne) Feng, MD, MS, with the department of neuroscience at the Medical University of South Carolina, says in a news release. “Our findings suggest that South Carolina and possibly other parts of the United States may have a long way to go in preventing and reducing the risk factors for recurrent strokes.”

In comparison, the risk of having a heart attack within four years after a stroke was 6%. Overall, the risk of a repeat stroke, heart attack, or death within four years after a stroke was 53%.

The study showed the risk of heart attack, repeat stroke, or death was higher among African-Americans than among whites. The risk of a another stroke also increased with age and the number of other underlying health disorders.

AAN: Easy Test May Point to Concussion

A simple clinical measure of reaction time may identify athletes who require evaluation for concussion, according to a study that will be reported at the American Academy of Neurology meeting in April.

A 20-millisecond increase from baseline reaction time correctly identified all but one athlete with a physician-diagnosed concussion.

The test employs an inexpensive device consisting of a rigid cylinder attached to a weighted disk. The test could easily be performed at the site of ongoing competition.

"Research has shown that reaction time is slower after a concussion -- even as long as several days after other symptoms are gone," said James Eckner, MD, of the University of Michigan in Ann Arbor. "The tests currently used require computers and specialized software."

As a potential alternative to sophisticated equipment, Eckner and coinvestigators developed the simple weighted-rod device and found it reliable and accurate in initial evaluations.

To continue their validation of the test, investigators recruited 209 members of the University of Michigan football, wrestling, and women's soccer teams at preseason physical examinations. During the reaction-time test, the weighted-rod was held a standard distance off the ground and then released. An athlete seated on a bench or chair caught the device as quickly as possible after its release.

Reaction time was calculated from the distance the rod fell before being caught, using the formula for a body falling under the influence of gravity.

Athletes who had physician-diagnosed concussions during the season repeated the reaction-time test within 72 hours of diagnosis.

Seven of the eight athletes who had concussions had prolonged reaction times compared with baseline values.

The athletes' reaction times averaged about 200 ms at baseline, increasing to an average of about 220 ms following their concussions.

Eckner said the test requires validation in a larger number of athletes before pronouncing it ready for routine use. However, he said, if the test's accuracy is corroborated in additional evaluations, its simple design would allow it to be used on the sideline or in a training room to identify injured athletes who require clinical evaluation for concussion.

"Because of its simplicity and low cost, this test may work well with youth athletes, where there is limited access to computerized testing of reaction time," said Eckner.

Conceivably, the test could be performed by a trainer or other nonphysician with appropriate instruction in how to conduct the test, Eckner allowed.

Simple test may help judge concussion in athletes

Published: Monday, February 15, 2010 - 17:10 in Health & Medicine

A simple test of reaction time may help determine whether athletes have sustained a concussion (also known as mild traumatic brain injury) and when they are ready to play again, according to a study released today that will be presented at the American Academy of Neurology's 62nd Annual Meeting in Toronto April 10 to April 17, 2010. "Research has shown that reaction time is slower after a concussion—even as long as several days after other symptoms are gone," said study author James T. Eckner, MD, of the University of Michigan Department of Physical Medicine and Rehabilitation in Ann Arbor. "But the tests currently used to measure reaction time require computers and special software."

Eckner and his colleagues developed a simple, inexpensive device to measure reaction time: a cylinder attached to a weighted disk. The examiner releases the device and the athlete catches it as soon as possible.

For the study, the researchers gave the test to 209 Division I college football, wrestling and women's soccer athletes during their preseason physicals. Then any athlete who had a concussion diagnosed by a physician during the season took the test again within three days of the concussion.

Eight athletes had concussions during the study. Of those, seven of the athletes had a prolonged reaction time after the concussion compared to the preseason time. Catching the object took about 15 percent longer.

"Because of its simplicity and low cost, this test may work well with youth athletes, where there is limited access to computerized testing of reaction time," Eckner said.

Source: American Academy of Neurology

Multiple Human Cognitive Disorders Linked By A Common Thread

A new study reveals that a common underlying mechanism is shared by a group of previously unrelated disorders which all cause complex defects in brain development and function. Rett syndrome (RTT), Cornelia de Lange syndrome (CdLS) and Alpha-Thalassemia mental Retardation, X-linked syndrome (ATR-X) have each been linked with distinct abnormalities in chromatin, the spools of proteins and DNA that make up chromosomes and control how genetic information is read in a cell. Now, research, published by Cell Press in the February 16th issue of the journal Developmental Cell, helps to explain why these different chromatin abnormalities all interfere with proper gene expression patterns necessary for normal development and mature brain function.

"Although clearly distinct from one another, human developmental disorders that are linked with chromatin dysfunction often share similar cognitive clinical features," explains senior study author, Dr. Nathalie Bérubé from the University of Western Ontario. "Whether the overlapping cognitive symptoms are due to underlying interlinked molecular mechanisms is still poorly understood." Her work now demonstrates that chromatin proteins defective in RTT, CdLS, and ATR-X syndromes are all associated with each other - and are required for one another's function - at certain "imprinted genes" in the developing mouse brain. Imprinted genes are a relatively rare type of gene that carries different information depending on whether it is inherited from the mother or the father. The results support the conclusion that ATRX (the chromatin protein that is defective in ATR-X syndrome) and its binding partners regulate expression of imprinted genes, and likely other genes required for normal brain development, by controlling chromatin structure.

"Our findings provide the first glimpse of the cooperation between ATRX and multiple other disease proteins in the regulation of common gene targets, perhaps explaining similarities between the associated human syndromes," says Dr. Bérubé. "The failure to properly suppress genes that are essential during embryonic development, but potentially detrimental in the mature brain, might contribute to cognitive deficiencies characteristic of RTT, CdLS and ATR-X syndromes. Further studies are needed to gain a better understanding of the specific role of these chromatin proteins and the molecular pathogenesis of the associated human disorders."

The researchers include Kristin D. Kernohan, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; Yan Jiang, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; Deanna C. Tremblay, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; Anne C. Bonvissuto, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; James H. Eubanks, Toronto Western Research Institute, Toronto, Canada; Mellissa R.W. Mann, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; and Nathalie G. Berube´, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada.

Source:
Cathleen Genova
Cell Press

New Transistors Mimic Human Brain's Synapse

A new transistor designed to mimic structures in the human brain could pave the way for increasingly efficient computer systems that "think" like humans, scientists say.

The transistor is the first to mimic a crucial process used by brain cells, or neurons, when the cells signal one another.

The goal is to build nanometer-scale circuit components that can be used in neuron-inspired computers, said physicist and study author Dominique Vuillaume of the Institute of Electronics, Microelectronics and Nanotechnology in France.

Such computers would be useful for tasks that traditional computers aren't very good at, especially image processing and recognition, Vuillaume said.

Transistors are the building block of electronics. They allow control of the electrical current running through a circuit by amplifying or switching the current on and off.

Synaptic transistors

Similarly, the synapse, a tiny gap between neighboring neurons, is a crucial component of the brain. The neuron transmits a small electric pulse along its length, triggering the release of chemicals called neurotransmitters into the synapse. The neurotransmitters traverse the synaptic gap and trigger a response in the neighboring neuron.

The timing of the electrical pulses helps determine how large of a chemical signal gets sent. In some neurons, repeated stimulations yields stronger, or facilitated, firings.

In others, multiple stimulations elicit weaker, or depressed, responses. These adaptations, known as short-term plasticity, happen within milliseconds.

Previous mock-neural networks required at least seven transistors to replicate short-term plasticity. The new transistor, called the nanoparticle organic memory field-effect transistor, or NOMFET for short, does it with just one.

That's important, because the smaller and more adaptable the transistors, the cheaper and easier it will be to scale from a few artificial synapses to thousands, Vuillaume said.

NOMFET

To build NOMFET, Vuillaume and his team placed gold nanoparticles in a trough between two electrodes. The particles, just five to 20 nanometers across, were covered with a very thin layer of a substance called pentacene, which conducts electricity.

Positive charges called "holes," which are created by missing electrons in the pentacene, transmit the current across this valley of scattered gold.

At each voltage input, some holes are temporarily trapped by the gold, and this changes the electrical output of the transistor. Depending on the voltages used, NOMFET can produce either weaker or stronger outputs – just like human neurons undergoing short-term plasticity.

Because of this adaptability, NOMFET is more flexible than traditional transistors, the researchers say.

The research "is definitely an interesting and well-conceived work," said physicist Massimiliano Di Ventra of the University of California, San Diego, who was not involved in the study.

The next step, Vuillaume said, is to combine several NOMFET transistors together to see how closely they approximate real neural circuits.

The research is detailed in a recent issue of the journal Advanced Functional Materials.

An extra 0.7 "satisfying sexual events" per month

By Gary Schwitzer on February 11, 2010 11:16 AM | No Comments | No TrackBacks

Ray Moynihan, who has written quite a bit about the disease-mongering of female sexual dysfunction, now writes in the BMJ (subscription required for full access):

"The definitions of female sexual dysfunction and its disorders of desire, arousal, orgasm, and pain are facing a major overhaul as part of the current revision of the influential Diagnostic and Statistical Manual of Mental Disorders (DSM).

A working group for the American Psychiatric Association, which produces the manual, has proposed new definitions that give greater acknowledgment to the relationship context of women's sexual difficulties and new criteria to raise the threshold for diagnosis."

Moynihan writes that one working group member described current criteria for "hypoactive sexual desire disorder" as being "highly problematic," and that a woman's lack of sexual desire may sometimes be a "normal reaction to a problematic context and therefore should not be pathologized." He writes that another working group member stated that in order "to avoid pathologizing normal variation in sexual experiences" women's mild and passing sexual problems should not be regarded as symptoms of a medical dysfunction.

Further excerpts:

"The group has proposed abandoning the two existing disorders of desire and arousal and merging them into a new entity potentially labelled "sexual arousability disorder." Under its proposals, symptoms may have to be of a certain severity and to present for more than six months before a woman qualifies for a diagnosis.

It is unclear how the proposal to move away from the label "hypoactive sexual desire disorder" will affect drug companies--including Boehringer Ingelheim--that are currently testing products to treat the condition. Boehringer Ingelheim recently released abstracts suggesting that its drug flibanserin could offer woman an extra 0.7 "satisfying sexual events" per month, over and above the effects of a placebo.

For more than a decade some researchers have claimed that the condition called female sexual dysfunction affects 43% of women, though others believe the true prevalence is far less."

The American Psychiatric Association has now posted all the proposed revisions online.

The Wall Street Journal had a good overall look at the DSM draft revisions.

So did the Los Angeles Times.

ABC had a piece that at least raised the question, "Are We Over-Diagnosing Mental Disorders?"

DSM-5's Rough Draft: The Carlat Take

In a prior post, I observed that the process of hammering out the DSM-5 had degenerated into a bar room brawl. Major figures in the development of past DSM versions, such as Allen Frances (the DSM-4 chairman) and Robert Spitzer (DSM-3 chairman), had both severely criticized the DSM-V process for lack of transparency and for a headlong rush to get the thing done too quickly in order to start making the APA some money.

Looking at the just-released proposed DSM-5 criteria, I'm pleased to say that the APA leadership has apparently been listening. They've pushed the planned publication out two full years to 2013, giving everybody time to review the proposal and to do some field testing. They have made the process far more transparent by posting task force reports on the DSM-5 web site. And they have avoided trying to pretend that DSM is ready for a paradigm shift in which diagnoses are based on neurobiological criteria (here's a secret--they don't exist yet in psychiatry).

Here's a quick Carlat-tour through some of the the main proposals.

--Temper dysregulation with dysphoria (TDD). A much more accurate way of categorizing children with explosive temper tantrums so that they don't get misdiagnosed as having bipolar disorder. This is a response to the fact that the diagnosis of bipolar disorder in children has increased 8,000% over the past decade.

--Addiction and Related Disorders. No more having to deal with the confusing terms "substance abuse" vs. "substance dependence"--both will be jettisoned in favor of the catch-all term "addiction." Currently, "dependence" is supposed to be a more severe problem than "abuse" but there was no good way of distinguishing the two in real patients. When someone has a problem with drug or alcohol craving, it's an addiction, pure and simple, and DSM-5 will acknowledge this.

--Autism Spectrum Disorders. This makes a lot of sense. No longer do we have to figure out: "Is this mild autism? Or is it severe Asperger's?" Now we can describe such patients as being somewhere on the spectrum of autism and spend more time understanding them as people rather than coming up with just the right label.

--Binge Eating Disorder. Some might see this as a form of disease mongering--that is, expanding the definitions of diseases to label more and more people as mentally impaired. But in fact I see patients with BED (as it's abbreviated) in my office with some frequency. These are not just overeaters, but rather patients who compulsively binge and have lost all sense of control.

--Risk Syndrome for Psychosis. This is a bit more iffy a proposal in my opinion. The idea is that you can diagnose people who have milder symptoms of psychosis before they develop full blown schizophrenia. Then, maybe you can prevent a more severe disease by starting them on prophylactic antipsychotics. But the research is debatable. Only about 35% of patients who qualify for this "pre-psychosis" end up developing true psychosis. I doubt this will make it into the final DSM-5 as an official disorder.

There are others potential disorders to examine, but I'll look at those in future posts. We all have a few years to comment on these proposals, and I think they are offered in the spirit of healthy conversation and debate. Thumbs up to the DSM Task Force.

Effects of Culture on Recovery From Transient Psychosis — article in Psychiatric Times

2010 February 11

by giannakali

Check this out folks…very interesting. Unfortunately they don’t tackle the fact that we drug the heck out of people. The rest is very important still:

Read and colleagues²⁷ suggested that a bias in mainstream psychiatry toward genetic explanations for psychotic symptomatology has led to a neglect of social stress and psychological trauma as factors in models for causation of psychosis. They blame this neglect on an aversion to “family blaming” as a causative factor. Psychiatrists viewed genetic explanations as being more politically acceptable. However, this aversion to psychosocial factors in causation of psychosis is not found in all modern cultures.

In some countries, the concept of “reactive” or “psychogenic” psychoses is widely used in clinical practice. The types of syndromes commonly considered psychogenic psychoses in Scandinavia spread over the general diagnostic categories in DSM-IV. These include schizophreniform disorder, brief psychotic disorder, schizoaffective disorder, delusional disorder, major depression with psychotic features, dissociative trance disorder, dissociative identity disorder, and posttraumatic stress disorder (PTSD).²⁸ Thus, it is possible for all of these disorders to be considered psychogenic psychoses. (read the rest)

That’s just a smidgeon of the article, please read the whole thing.

I hope I’ll be able to return to doing commentary soon. This begs for lots of it, but I’m still not able to do such work.

Sweet Science: The Health Benefits of Chocolate

Yet another health benefit has been linked to eating chocolate: It may decrease your risk of stroke, a new study suggests.

The analysis, which will be presented in April at the American Academy of Neurology's 62nd Annual Meeting, reviewed the results of three previous studies. One study with more than 44,000 participants found that those who ate a weekly serving of chocolate were 22 percent less likely to suffer a stroke than those who ate no chocolate.

The researchers caution however, that more studies are needed to confirm the link, and other factors besides chocolate consumption could be contributing to the decreased stroke risk. Also, one reviewed study showed no connection between stroke risk and chocolate consumption.

Still, the results add to a growing list of potential advantages to eating chocolate, including a decreased risk of cardiovascular disease. But this doesn't mean you should gorge yourself on the candy this Valentine's day either.

Among the pros and cons of chocolate:

Chocolate can be good for you

Many previous studies have linked eating chocolate with health benefits, including:

• A 2008 study found that people who ate a small amount of dark chocolate a day (about 6.7 grams) had lower levels of a protein that is associated with inflammation in their blood.
• Other recent studies have found that blood platelets clump together more slowly in chocolate eaters. Clumping platelets can lead to the formation of blood clots, which in turn can cause a heart attack. Chocolate consumption may lower blood pressure, help prevent formation of artery plaques and improve blood flow, according to other research.
• Eating chocolate may even help with math, or at least counting. A study reported in 2009 showed that people did a better job of counting backwards in groups of three after they had consumed a hot cocoa drink containing large amounts of a compound found in chocolate. These compounds, called flavonoids, which we'll get to later, may increase blood flow to the brain.
• Chocolate may also have anti-cancer benefits because flavonoids may help reduce the cell damage that can spur tumor growth.

"More and more research is showing that [eating chocolate] is really more beneficial than we ever imagined," said Katherine Tallmadge a registered dietician and spokesperson for the American Dietetic Association.

However, she notes that the advantages you get still appear to be quite small. "It's not anything major, but it's still an advantage, and even slight advantages can make a difference for some people," she said.

Not all chocolate is created equal

Certain forms of chocolate are better for your health than others, and it comes down to one key component of the rich snack: flavonoids.

These compounds, which are found in the seeds of cacao plants (from which chocolate is made), are antioxidants that are thought to help protect cells against damage that might come from environmental toxins, or simply byproducts of vital processes in the body.

Consuming flavonoids has been linked to heart benefits. But since flavonoids are bitter, most commercial chocolate goes through processing steps that remove these compounds. Less processed, or darker chocolates, will tend to have higher levels of flavonoids. Your best choice in terms of healthiness is to go with natural, unsweetened cocoa powder, Tallmadge said.

"You can have mounds of it," because it is low in calories and full of flavonoids, Tallmadge told LiveScience.

Runners-up for health benefits are bittersweet and semisweet chocolate with a high cocoa percentage, she said. Unfortunately for milk-chocolate lovers, this type of chocolate has lower levels of flavonoids.

Chocolate can be bad for you

The underlying health benefits don't give you an excuse to eat chocolate by the pound.

"Because we mainly eat it as a candy with sugar added, it's going to be high in calories and not necessarily good for you in high quantities, because it will take the place of more nutritious foods," Tallmadge said.

For instance, if you gorge on chocolate, you might skimp out on fruits and vegetables, which are also important for heart health and disease prevention.

Tallmadge advises that people who want to eat chocolate limit themselves to one ounce per day. "Any more than that and you're probably going to take in too many calories for weight control," she said.

Other foods and beverages can also provide flavonoids, including citrus fruits, onions, green tea and red wine.

Chocolate Chips Away at Stroke Risk

Flavonoids in Chocolate May Lower Risk of Having or Dying From Stroke

By Jennifer Warner
WebMD Feature

Reviewed by Louise Chang, MD

Feb. 11, 2010 -- As if people need another reason to love chocolate, here it is: Eating a little bit of chocolate each week may not only lower the risk of having a stroke, it may also decrease the odds of dying from one.

A new review of recent research on chocolate and stroke risk found at least two large studies are suggestive of the health benefits of chocolate in lowering the risk of stroke. The results will be presented in April at the annual meeting of the American Academy of Neurology in Toronto.

The first study found 44,489 people who ate one serving of chocolate per week were 22% less likely to have a stroke than people who didn’t eat chocolate.

The second study showed that 1,169 people who ate 50 grams of chocolate once a week were 46% less likely to die after a stroke compared to people who didn’t.

A third study included in the review found no association between chocolate consumption and risk of death from stroke.

Researchers say chocolate, especially dark chocolate, is rich in antioxidants called flavonoids, which have been shown to have a number of health benefits.

"More research is needed to determine whether chocolate truly lowers stroke risk, or whether healthier people are simply more likely to eat chocolate than others," researcher Sarah Sahib, BScCA, of McMaster University in Hamilton, Ontario, says in a news release.

Were do Mirror Neurons Come From?

This video is about mirror neurons. These mirror neurons are the key to many aspects of social interaction. It allows us to understand the actions, feelings of others. In a way to “read their minds”. Possibly mirror neurons play an important role in empathy , an important asset for physicians.

But were do they come from these motor neurons?

One explanation could be that mirror neurons are an adaptation:

an adaptation for action understanding concerns the origins, rather than the current utility, of mirror neurons. It asserts that a certain process – genetic evolution – produced mirror neurons, and that they were favoured by natural selection because they supported action understanding.

The mirror neurons helped to understand what others were doing, which could be of importance during the survival in the evolution of human kind.

The other explanation could be that mirror neurons are a product of associative learning:

Associative learning is a form of learning that results from exposure to a relationship between two events. ‘Conditioning procedures’ arrange different types of relationship between events. Research examining the effects of conditioning procedures on animal behaviour has shown that associative learning depends on ‘contiguity’ – the closer the two events occur in time, the stronger the association – and ‘contingency’ – there needs to be a correlation or predictive relationship between them.

This suggests that mirror neurons were created during the experience of observing and executing the same action. Motor neurons become mirror neurons in the course of individual development.

In a recent publication arguments were put forward in favor of the associative learning origin of mirror neurons. The most important arguments being that mirror neurons do play a role in some social functions but do not play a dominant role in action understanding. You probably don’t need them to understand actions coming about. The other argument is that even in adulthood the mirror neuron system can be reconfigured by sensorimotor learning.

The associative account implies that mirror neurons come from sensorimotor experience, and that much of this experience is obtained through interaction with others. Therefore, if the associative account is correct, the mirror neuron system is a product, as well as a process, of social interaction.

Wouldn’t it be great that humans can develop mirror neurons during life? The experience of interactions being enough to create mirror neurons. I think this is a very optimistic makable point of view, what do you think?

Neuroimaging may shed light on how Alzheimer's disease develops

(12 January 2010: VIDYYA MEDICAL NEWS SERVICE) -- Current Alzheimer's disease (AD) research indicates that accumulation of amyloid-beta (Aß) protein plaques in the brain is central to the development of AD. Unfortunately, presence of these plaques is typically confirmed only at autopsy. In a special issue of the journal Behavioural Neurology, researchers review the evidence that Positron Emission Tomography (PET) can image these plaques during life. This exciting new technique provides researchers with an opportunity to test the amyloid hypothesis as it occurs in living patients.

In a review article with over 100 references, Dr. Gil Rabinovici and Dr. William Jagust from the University of California, San Francisco and Berkeley, summarize the results of experiments from their laboratories and others using the Aß tracer Pittsburgh Compound-B (PIB). This compound binds to Aß protein and allows the mapping of plaques in the brains of AD and non-AD volunteer subjects.

They report that PIB-PET can detect Aß deposits in a significant proportion of cognitively normal older subjects and that these deposits are associated with brain atrophy even in the absence of cognitive symptoms. By the time patients develop mild cognitive impairment (MCI) amyloid load in the brain appears to have reached a plateau. As patients progress to dementia, neurodegeneration and cognitive decline proceed independently of further amyloid accumulation.

The authors interpret these results as consistent with a model in which amyloid deposition plays a critical early role on the path to AD, beginning years before onset of symptoms and triggering a series of events which ultimately leads to cognitive decline and dementia.

While the use of PIB-PET is currently limited to research centers because of the compound's very short radioactive half-life (20 minutes), new amyloid imaging agents with longer half-lives are under development for more widespread use. Amyloid imaging is already playing an important role in the development of amyloid-based therapies for AD, and Dr. Rabinovici and Dr. Jagust speculate that in the future amyloid imaging will assist clinicians in identifying patients with mild or atypical symptoms who may be candidates for anti-amyloid treatments.

Writing in the article, the authors state, "PIB-PET has provided us with our first in vivo glance at the dynamic relationship between amyloid deposition, clinical symptoms, and structural and functional changes in the brain in the continuum between normal aging and AD…In the future, Aß imaging will likely supplement clinical evaluation in selecting patients for anti-amyloid therapies both during drug development and in the clinic."

The article is "Amyloid imaging in aging and dementia: Testing the amyloid hypothesis in vivo" by G.D. Rabinovici and W.J. Jagust. It appears in Behavioural Neurology, Vol. 21, Issues 1-2 (2009), published by IOS Press.

Optimal Target for Deep Brain Stimulation for Depression

The strongest evidence exists for Broadman Area 25 in the subcallosal cingulate gyrus (SCG) as target for deep brain stimulation in treatment resistant depression. This area in the brain is depicted in the figure above and is from the most important publication about DBS and depression in Neuron march 2005 by Helen Mayberg. Functional neuroimaging as well as antidepressant treatment effects suggest that this area plays an important role in modulating negative mood states. A decrease in activity is reported with clinical response to antidepressants and electroconvulsive therapy (ECT).

But depression is not a disease of a single brain region nor neurotransmitter system. It is now generally viewed as a systems-level disorder affecting integrated pathways linking select cortical, subcortical, and limbic brain regions with their related neurotransmitter systems.

Suggestions of other brain localizations for treatment with DBS for depression comes from case reports with DBS for other indications than depression. These localizations have been described in a peer reviewed article with excelent graphics.

In a recent study done by the “Mayberg group”, Toronto, Canada, the autors compared the location of the electrode contacts in responders and nonresponders to DBS of the subcallosal cingulate gyrus (SCG) and correlated the results with clinical outcome to help in identifying the optimal target within the region.

On postoperative MRI scans the researchers did complicated mapping procedures to pin point the locations of the active contacts on the implanted electrodes. There was no difference when the right and left electrodes were compared in patients. So both electrodes were exactly placed on each side (hemisphere). The only significant difference they found between responders and nonresponders was that electrodes in patients who responded were in a slightly more ventral position relative to the anatomical landmarks used in the medial prefrontal lobe. This difference between responders and nonresponders did not exceed 1,5 mm. The authors is not likely to be of clinical significance, according to the authors. This small difference is probably unimportant compared to the clinical features of the patient for the outcome of the DBS procedure in depression. Another limiting factor on this research is the small sample size, in larger groups these results might differ.

What we can conclude based on our findings is that within the small targeted region of the SCG, the location of the electrode contacts did not determine outcome.

This article also describes a detailed method for a more standardized method for targeting the SCG with DBS for depression. This is to technical to reproduce in this post but those working with DBS for depression should have a look at this procedure. From this study it is still not clear whether DBS of other brain areas might be more superior in efficacy. And is brain area more important than clinical features of the patient or do the areas differ for different types of depression? All very interesting questions and topic for more research on DBS.