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In our work with coaching and consulting clients, we found ourselves discussing Emotional Intelligence (EI) almost daily, and these conversations left us wanting data-based answers to the question of how leaders perceive the importance of EI. After reviewing existing studies, many of which established a strong link between performance and EI, we conducted original research with 265 leaders. We analyzed their views of leadership and EI by job level in organization, years of leadership experience, gender, and personality type, as measured by the Myers-Briggs Type Indicator (MBTI) ®. This study is unique in describing how leaders define, value, and develop their Emotional Intelligence — in their own words.

What elements of leadership do executives, managers, and consultants consider most important to success?

When leaders hear “Emotional Intelligence,” what do they think it means?

Do leaders believe Emotional Intelligence can be developed? If so, how?

How emotionally intelligent do they think they already are?

How do perspectives on leadership and Emotional Intelligence vary by job level, experience, personality type, and gender?

265 leaders participated by invitation in this extensive online survey. One-third are executives, another third directors or managers, and the rest are primarily business owners and consultants. Descriptive statistics were developed for the entire data set. Narrative responses were coded by independent raters and analyzed for statistical significance.

Excerpts of Findings

Release 1: What Makes a Successful Leader?
This report covers findings on which capacities — related and not related to Emotional Intelligence — participants associate with successful leadership.

• Vision topped the list of critical leadership capacities for nearly all leaders. Two other “applied EI” capacities — Relationship Building and People Development — were ranked in the top 5, along with Strategic Thinking and Execution.
• Of the remaining 15 capacities studied, all the EI items — including Self-Awareness, Empathy, and Adaptability — were rated as more important than the traditional leadership capacities, such as External/Market Orientation, Financial Acumen, and Planning.
• However, leaders of different personality type, job level, and experience rated many capacities quite differently. For example, Executives were more than twice as likely to value Optimism as were Managers/Directors or Consultants. Regardless of job level, participants of different personality type showed substantial variation in what they consider important to successful leadership.

Release 2: Leaders Speak Out on Emotional Intelligence
This report describes how leaders define and develop EI.

• Most leaders believe Emotional Intelligence is about building relationships and using emotions wisely, reading people, and being aware of their own emotions. These responses are consistent across levels, experience, and personality.
• Nearly all leaders believe EI can be developed and are able to offer recommendations developing EI. These recommendations vary substantially by years of leadership experience. For example, the more experienced the leader, the more likely to recommend training, coaching, feedback, and self-directed development.
• When leaders describe how they develop their own EI, years of experience is far less significant in differentiating their responses. Instead, leaders of different personality types (MBTI) develop their own EI very differently. For example, people with Feeling Perceiving preferences (FP’s) are nearly three times more likely than people with Thinking Perceiving preferences (TP’s) to cite training/group experiences as important in developing their EI.
• Surprisingly, gender matters not at all in any of our findings. Men and women provided similar answers in describing EI, how it can be developed, how they develop their own EI, and how they rate their own EI.

Release 3, expected fall 2004, will address how these leaders rate various aspects of their own Emotional Intelligence.

Excerpts of Implications

• Leaders at all levels are open to developing Emotional Intelligence, but they talk about it quite differently than do many consultants and EI theorists. Leadership coaches, HR professionals, and others who help people develop their EI should adjust their language and initial focus to reflect aspects of EI that resonate most with executives and managers – relationships, reading people, self-awareness, rather than empathy, self-confidence, and self-control.
• “Soft skills” development programs would benefit from a richer view of what leaders actually value. In particular, leaders are deeply interested in resources that help them extract the learning from their own experiences.
• Multiple types of EI development programs are needed to advance leaders of different personality types. MBTI is a significant predictor of the how leaders describe developing their own EI. For example, group learning is indispensable to some types and anathema to others.
• To excel at the highly-ranked Relationship Management capacities, leaders should develop their EI “building block” capabilities of self-awareness, reading others, and adaptability. This study shows that leaders may underestimate the importance of these basics in performing the complex capabilities they highly value.
• When assessing development needs or engaging in succession planning, leaders should be aware of blind spots or stereotypes they may hold. To the extent that executives view their own strength profiles as especially desirable, they may overlook leaders with different and perhaps complementary strengths. Also, look beyond common MBTI stereotypes. For example, J’s and P’s were indistinguishable in how they valued Execution, Achievement Drive, and Adaptability.
• Loosen assumptions about gender differences. Men and women answer questions about EI with astonishing similarity.

When the mood strikes, a kiss can catch us in a mix of tastes, textures, mysteries—and scents.  We kiss nervously, flirtingly, angrily, or excitedly.  And a kiss is not just all about sex: Hollywood celebs throw us air kisses, mobsters impart the kiss of death, and an astronaut kisses the soil after a safe return home.  So why, then, are we so taken with the kiss?

Scientists agree our lips evolved first for eating—and then later for speech.  Yet, with a kiss, a different kind of ‘hunger’ applies.  Kisses set off a whirlwind of neuro-chemical messages yielding anything from sensations of touch to sexual arousal; feelings of closeness to even a wave of euphoria.

However, kissing is not a solo affair, and kissing transmits external messages as well.  The bringing together of two bodies sets off messages just as powerful with your partner (whether they are precisely the same feelings is another matter altogether).  Kisses pack quite a punch: even one can transmit much information about the potential of a relationship.  Research proves that kisses are so powerful that a ‘first kiss’ gone badly can derail even the most promising of relationships.

Scientists believe that lip-locking evolved as a means to promote mate-selection.  Kisses transmit olfactory, tactile and postural types of information tapping into both the conscious and unconscious mind that drives decisions, including a genetically-compatible mate!  Some researchers believe that a kiss can even disclose the extent to which a partner might commit to raising children—central to our specie’s survival.

Nearly 50 years ago, British zoologist and author Desmond Morris posited that kissing probably evolved from primates: mothers chew food for their young, and then feed them mouth-to-mouth.  And since chimps still feed this way, early man probably did so, as well. 

This press of outturned lips against lips may have later progressed as a way to comfort children in times of hunger—and eventually becoming a general expression of affection.  (Leave it to us humans to take these first parental kisses down the myriad of paths we have today!)

It is believed that unseen chemical messengers named pheromones helped along the evolution of the intimate kiss.  Both animals and plants use pheromones to communicate: insects, for example, emit pheromones to signal alarms, point out a food trail or announce sexual attraction.

In 1995, a Swiss researcher showed why pheromones are so important in humans, too.  He had women sniff t-shirts worn by men, and asked which smelled best.  The results were startling: the women did not choose randomly, which was discovered by comparing the DNA of the women and men.  Instead, women overwhelmingly picked the scent of man whose histocompatibility complex (MHC)—the genes that forge our immune systems—differed from their own.  (Different MHC’s mean less immune overlap, and the increased likelihood of healthy, disease-resistant kids.)  Thus, kissing may be a woman’s way of assessing a potential mate’s immune compatibility—without investing an excessive amount of time, energy in (and not to mention sexual activity with) a man.

However, these scientists aren’t telling the average person anything new: when it comes time to close your eyes and lean in, we all know that a kiss is never just a kiss.

Why are our immune systems overreacting causing allergies, pain, inflammation and killing health cells? by Rob Stein.

Secrets of Sales Success, free seminar on June 21 in Vallejo CA.

About.

On Tuesday, May 6, at New York City’s cavernous Javitz Center, Dr. BJ Casey, PhD, took the stage to discuss why some of us are anxious — how we develop fear and anxiety responses neurobiologically, that is. Dr. Casey, a professor of developmental psychobiology and Director of the Sackler Institute at Weill Cornell Medical College, was speaking to a large room of psychiatrists, psychologists, and researchers at the American Psychiatric Association’s 167th Annual Meeting. “Thank you,” she announced, “I hope you’ve had some coffee. It’s a difficult time after lunch.”

As many as 18% of US adults^[1] and upwards of 30% of young people^[2] suffer from some form of anxiety, making it the most prevalent mental health disorder in the country. Depending on the type of anxiety and time course of symptoms, adults with anxiety are typically treated with various combinations of fast-acting anxiolytics (namely, benzodiazepines); other pharmacotherapies, such as antidepressants, and psychotherapy, particularly cognitive-behavioral therapy (CBT).

Similar strategies are used in children and adolescents, with CBT being the primary evidence-based behavioral therapy used in this population. The idea is to identify the cause of the anxiety and replace associated negative behaviors and thinking patterns with positive ones. Exposure-based therapy, a type of CBT, is considered one of the more effective approaches to treating pediatric anxiety, though it still only carries a 50%-60% success rate.^[3] The technique involves gradually and repeatedly exposing a patient to an anxiety- or fear-inducing stimulus or situation until they are able to overcome the negative associations and reactions — in other words, attempting to desensitize them to anxiety-causing cues.

Anxiety often goes undiagnosed, and therefore untreated, in children and adolescents. Left untreated, it can lead to chronic and debilitating mental and physical illness. Casey and a number of her colleagues feel that patient outcomes can be improved, not only through improved recognition but also by personalizing treatment. If researchers can untangle the web of connections occurring in the developing brain, and how certain developmental patterns increase or decrease anxiety risk, clinicians would then be able to better determine which patients are more likely to respond to a particular treatment.

The adolescent brain is frantic with activity and influences. “Regional synaptic pruning and changes in myelination are occurring at a time when the brain is being marinated in gonadal hormones,” Casey stated. She continued, “We also see peaks in neurotrophins and neurochemicals that are important to emotional and fear regulation.” Neurotrophins are proteins that control neuronal development and function.

Casey then pointed out that although most brain imaging studies in adolescents have looked at the cortex, the deep, more primitive brain structures also play a key role in development, particularly in terms of learning the emotional significance of environmental cues. By the early 2000s, numerous laboratories were looking at how different brain regions, both primitive and cortical, interact with each other during development.

Early Experiences and Later Life Anxiety

So how do the various developing brain regions contribute to our emotional development? And how do our adolescent experiences steer brain maturation and contribute to later-life fear and anxiety? The answer resides partially in the amygdala, part of the subcortical limbic system and a key player in emotion regulation. Also involved is the prefrontal cortex (PFC), the anterior part of our cerebral cortex responsible for complex thought and emotion processing.

Numerous studies have shown that fearful cues lead to heightened amygdala activity. And as Casey pointed out, the PFC relays inhibitory signals to the amygdala as part of our fear regulation circuit. With repeated exposures to an initially fearful stimulus that turns out to be unthreatening, increased signaling from the PFC dampens amygdala activity. As a result, output to the autonomic nervous system is dampened, and we feel less fear.

Of course, the neurobiology of human anxiety is far more complex than a signal circuit: Sensory inputs project to the amygdala’s lateral nucleus, where fear memories are maintained, and projections from the amygdala’s central nucleus also influence our autonomic and endocrine responses to fear. But it’s the relationship between the amygdala and the PFC that controls our ability to habituate to cues that might otherwise lead to anxiety and fear.

Work by Hare and colleagues (including Casey)^[4] found that in children who rate themselves as having high anxiety, a fearful stimulus results in initial recruitment of amygdala activity as expected. However with repeated presentations of the same cue, the activity doesn’t return to baseline, as it does in nonanxious control subjects. Their ability to habituate is impaired. Casey then explained the possible reasons why. Like so many mental and medical conditions, the culprit can be environmental, genetic, and oftentimes both.

To identify possible environmental influences on anxiety, Casey and her group turned to the often traumatic experience of an orphanage upbringing.^[5] They wanted to assess how adversity early in life impacts emotion regulation, in a sense using an orphanage childhood as a proxy for disorganized parenting.

They looked at children raised in overseas orphanages who were adopted and relocated to the New York City area. Study subjects were between 5 and 15 years old and had been in the United States for at least 2 years, to ensure that they had had time to adjust to the new environment.

First, they were presented with a series of neutral visual cues on a screen. Next, a fear-inducing face was flashed, to which the subjects were asked not to pay attention. A higher percentage of those who grew up in orphanages exhibited increased amygdala activity in response to the fear cue; in controls, increased activity in the PFC was seen, presumably suppressing attention toward the fear cue.

An important part of emotional regulation is our ability to suppress inappropriate reactions — in other words, to not waste our attention on emotional cues that have no significant relevance to a situation. Those who grew up in orphanages were unable to redirect their attention and ignore fearful cues.

The study also revealed how these findings might relate to real-world functioning. When the child participants came into the laboratory, they were asked to leave their adoptive parent to play a game with an experimenter for 10-15 minutes. When they came back, Casey’s team would monitor their interactions with their adoptive parents; those with greater amygdala activity made significantly less eye contact following this separation and reunion with their parent.

Casey cautioned that a drawback of human naturalistic experiments is the lack of control over prenatal history and genetic background. So the findings of dysregulated fear could be due to factors other than the “disorganized parenting” of the orphanage experience.

To help disentangle causality, her group ran a parallel study^[5] mimicking the orphanage experience in mice. Nesting material was removed from cages, and maternal behavior was monitored. The mothers spent more time foraging for nesting than with their pups. Mothers whose nesting wasn’t removed spent more time grooming their litter.

This model was then used to assess fear habituation, using a similar approach as in the human experiment.^[6] “How do you get mice to ignore a potential threat?” asked Casey. “As it turns out, they really like sweetened condensed milk,” she followed. The mice were put in a “home” cage equipped with a milk nozzle. When moved to a new cage with a light, considered a threat by the rodents, they froze for a period of time before going after the milk.

This slower latency time in the presence of stress was correlated with heightened amygdala activity. This pattern of increased latency and amygdala activity remained even after the stressor was removed 20 days later and even after development of the PFC in adulthood, suggesting long-term dysregulation of emotion with early adversity.

Genetic Contributions

Genetic influences also appear to be a major contributor to fear and anxiety. Of particular importance appears to be the gene encoding for brain-derived neurotrophic factor (BDNF), a neurotrophin responsible for neuronal growth, differentiation, and survival.

Casey’s Cornell colleague Dr. Frances Lee has developed a new strain of mouse carrying a BDNF polymorphism in which methionine is substituted for valine. This BDNF Val66Met knock-in model results in decreased neurotrophin activity, biologically recapitulating the effects of the human polymorphism.^[7] The mice mimic the “wallflower at the school dance,” according to Casey: When tested in an open field task, they spent more time near the walls, an indication of anxiety-like behavior.^[8]

Fatima Soliman, Casey and Lee’s joint MD, PhD, student, performed a related study in the mice and humans with the BDNF Val66Met polymorphism,^[9] looking at Pavlovian conditioning to fear cues and their ability to extinguish negative associations. The mice received a minor foot shock paired with a neutral audible tone, whereas the humans were played an intrusive sound — Casey likened it to that “obnoxious alarm clock” — paired with innocuous images of colored squares. Next, the conditioned stimuli were presented repeatedly without the noxious stimulus, and subjects were monitored for fear responses (in mice, freezing; in humans, sweating).

Wild-type mice were found to freeze at first, but not after numerous tone presentations; BDNF Val66Met mice exhibited freezing behavior that did not extinguish with subsequent trials. Similar findings were seen in humans with the polymorphism, present in roughly 30% of those of white persons.

A single polymorphism is unlikely to fully account for the complexities of human fear and associated neurodevelopmental aberrations, and with twice as many presentations, they eventually learned. However, in subjects carrying a substituted methionine in the BDNF gene, fear doesn’t extinguish as readily in response to repeated nonthreatening cues; in those with a valine, it extinguishes more easily. Using neuroimaging, the authors showed that polymorphism carriers exhibited more amygdala and less PFC activity with subsequent cue presentations.

Clinical Implications and Manipulating Memory

The ultimate goal of this work is, of course, to treat patients suffering from anxiety. The data suggest that it might be possible to predict who will respond to certain therapies on the basis of their genetic profile and its correlation with fear extinction.

One study^[10] showed that adults with posttraumatic stress disorder who have the BDNF Val66Met polymorphism do not respond well to exposure CBT. Collaborative work between Casey and Lee looked at fear conditioning across all ages to determine whether certain age groups are better or less able to extinguish fear memories.^[11]

In response to the same negative cues as in their previous work, preadolescent and adult mice showed considerable fear extinction, whereas adolescent mice showed little to none. Humans showed a similar response pattern. Using expression of the c-Fos gene — an indirect marker of neuronal activity — the investigators showed that the PFC is not heavily recruited in adolescents; hence, their fear does not extinguish as well with repeated presentation of empty threat cues.

These data suggest that individuals of certain ages may not be as responsive to exposure-based CBT. Examination of existing clinical data by Casey and her colleague Dr. John Walkup indicate that this may be the case, but further research is needed, Collectively, this work provides evidence for whom and when exposure forms of CBT may be most effective.^[12]

Bringing it back to the neurobiological underpinnings of anxiety, Casey concluded by highlighting ongoing work in her laboratory looking at how anxiety might be alleviated by bypassing the reliance on the crucial projections from the PFC to the amygdala that are still developing during adolescence and altering fear memories themselves at the level of the amygdala. “Memory is not static, but dynamic,” said Casey. “When we learn something, we store it in memory. But every time we retrieve it, we update it with new information. We can attach new meaning to that memory.”

Is altering a memory that easy? Possibly. Casey and her colleagues wanted to attenuate fear memories by altering the memory during the so-called memory “reconsolidation window,” which appears to be between 10 minutes and a few hours after retrieval of an existing memory. Building on work in adults by Monfils and colleagues^[13] and Schiller and colleagues,^[14] they first applied their reliable unpleasant noise/colored square method to induce fear acquisition. Before extinction training of the fear memory, they presented the square that had been paired with unpleasant noise as a reminder.

After waiting 10-15 minutes — to coincide with the reconsolidation window — extinction learning was initiated. Those not exposed to the reminder cue before extinction learning showed an arousal response when retested the next day. Those reminded did not.

“This finding suggests that one way to work around exposure-resistant fear and anxiety is by taking advantage of this period of reconsolidation,” said Casey, nearing the end of her talk. It’s not that CBT doesn’t work across the board in adolescents, but rather that the correct type and timing of the CBT are essential.

Casey suggests that clinicians build on the reconsolidation window findings in the clinic. First, the patient comes in to the clinic and is reminded of why they are there (reminder cue). Then, clinicians establish a positive and safe rapport with the patient for 10-15 minutes — waiting for that critical window of apparent plasticity (reconsolidation window) — and then they initiate exposure therapy. “Many clinicians are already doing this,” Casey commented, “but [previously], we just didn’t have the evidence for why this timing may be so effective for some and not others.”

Following Casey’s talk, during the Q&A session, an audience member asked whether the data presented during the previous hour suggest that the “preadolescent anxious kid inevitably becomes the adolescent anxious kid.”

Casey’s response suggested that all hope is not lost — that intervening early before the circuitry becomes hard-wired may be the best hope for alleviating anxiety. This will require better and earlier identification of those at risk in order to intervene and ultimately prevent the anxiety from escalating. “I treat a lot of college students with social phobia who are terrified to speak in classes,” she responded, “If they’d gotten exposure therapy earlier, would they by more amenable to therapy now? It’s possible. But we just don’t know.”

The Hastings Center has updated and expanded its landmark 1987 consensus guidelines for ethical care of terminally ill patients. Oxford University Press published this second edition of The Hastings Center Guidelines for Decisions on Life-Sustaining Treatment and Care Near the End of Life.

“As the population ages, more people are living with chronic diseases,” Hastings Center President and guidelines working group member Mildred Z. Solomon, EdD, said in a news release. “Advances in medicine have created both benefits and burdens, including problems of quality, safety, access, and cost. We need to help patients and families better navigate their choices, and physicians and healthcare leaders must build systems of care that are wiser and more compassionate.”

The guidelines target all healthcare professionals involved in caring for terminally ill patients. They discuss ethical and legal options in the United States for use of life-sustaining technologies, offer comprehensive guidance on informing patients and surrogates of their options, and include detailed strategies to optimize healthcare delivery.

Issues in end-of-life care include confusion and conflict over decision-making, poor patient–clinician communication, insufficient pain and symptom relief, and use of treatments offering minimal benefit. Consequences of poor care include reduced quality of life, greater family stress, and increased costs of healthcare without added value

A physician’s offer or a family’s request to “do everything” may neither respect the patient’s rights nor ensure good care. Recognizing religious, cultural, psychological, and social factors affecting medical decision-making can help clinicians provide appropriate, respectful care, according to the guidelines.

“The guidelines offer a reliable framework for these discussions, and for education, policy-making, and redesign of care,” lead author Nancy Berlinger, PhD, a research scholar at the Hastings Center, said in the news release. “They also encourage healthcare leaders and administrators to support better outcomes for patients by building more effective forms of care delivery and integrating care near the end of life into organizational safety and improvement initiatives.”

Changes from the 1987 Guidelines

• Recommendations based on the past 25 years of “empirical research, clinical innovation, legal and policy developments, and evolution of professional consensus”;

• discussion of decision-making for and about children near the end of life;

• issues specific to patients with disabilities, including the effect of their perspectives on physcian–patient communication and management decisions;

• recent evidence regarding brain injuries and neurological states, how they affect prognosis, and laypersons’ misperceptions and unrealistic expectations due to media influences;

• information regarding physician-assisted suicide and how it differs from treatment refusal;

• discussion of controversy regarding palliative sedation;

• acknowledgement that cost is an ethical issue in healthcare decision-making;

• request that hospitals and healthcare organizations develop transparent policies on cost management to avoid bedside rationing; and

• integration of “the insights of ethics and law, medicine and other healthcare professions; the experience of patients and family caregivers; and patient advocacy.”

The 1987 edition of the guidelines set the ethical and legal framework for US medical decision-making and was cited in the Supreme Court’s 1990 Cruzan decision. This established patients’ constitutional right to refuse life-sustaining medical treatments and affirmed that surrogates could make decisions for patients lacking that capacity.

In the news release, Kathleen M. Foley, MD, chair of the Society of Memorial Sloan-Kettering Cancer Center, refers to the new guidelines as “the sourcebook for how the ethics of life-sustaining treatment and care at the end of life should be taught, institutionalized, and translated into clinical teaching and practice.”

Physicians continue to provide high-intensity care for terminally ill patients even though they do not want the same aggressive treatment for themselves at the end of life.

This conclusion comes from a study presented at the recent meeting of the American Geriatrics Society, which was widely reported in the lay press. The study was published onlineMay 28 in PLoS One.

The findings on physician attitudes about end-of-life care are particularly important because of the “silver tsunami” of older adults who will be needing end-of-life care in the United States and around the world, said lead author Vyjeyanthi S. Periyakoil, MD, director of palliative care education and training at Stanford University School of Medicine in California.

“We have seen large advances in modern biomedicine that have increased longevity but have failed to improve, significantly, a person’s health or quality of life in the 2 years prior to death,” she told Medscape Medical News.

“This results in millions of Americans living with a tremendous burden of major chronic diseases at the end of life,” she explained.

There is also a big disparity between what Americans say they want at the end of life and the care they actually receive, Dr. Periyakoil noted.

“The overwhelming majority of patients, at least 80%, wish to avoid extreme measures to prolong their lives, but their wishes are often overridden,” she said.

“Most patients want to die a peaceful death at home without being a burden to their families, emotionally or financially. But what they want and what they get depends not so much on their preferences or advanced directives, but on their local healthcare system and individual doctors’ practice styles,” she added.

Why the Disconnect?

Dr. Periyakoil and her colleagues sought to determine what factors influence whether physicians choose to pursue aggressive end-of-life treatment for their patients when they would not want it for themselves.

They also looked at how physicians’ attitudes about advance directives have changed since 1990, when the Self-Determination Act was passed, giving patients more control over their end-of-life care.

The study involved 2 cohorts. The first comprised 1081 physicians who completed a Web-based advanced directive form and a 14-item advance directive attitude survey at Stanford Hospital & Clinics and the Veterans Affairs Palo Alto Health Care System in 2013.

The second comprised 790 internal medicine and family medicine physicians from Arkansas who were asked the same 14 survey questions in 1989 but who did not complete an advance directive form (JAMA. 1989;262:2415-2419).

Responses from the 2 cohorts were compared.

“We hypothesized that because advance directives are routine and an accepted healthcare practice, current-day doctors’ attitudes would be much more positive toward them than those in the 1989 group,” Dr. Periyakoil said.

Surprisingly, attitudes changed very little over time.

Because the 1989 and 2013 cohorts were different, “you might argue that we were comparing apples and oranges,” she explained.

There were more women in the 2103 cohort than the 1989 cohort (51.4% vs 7.5%). In the 2013 cohort, 48.9% of respondents reported being an ethnic minority; ethnic diversity for the 1989 cohort was not reported.

In 2103, attitudes about advance directives varied significantly by ethnic group. White and black doctors had similar positive attitudes about advance directives; Hispanic/Latino doctors had the least positive attitudes about advanced directives.

Attitudes also differed by subspecialty in 2013. Physicians from emergency medicine, physical medicine and rehabilitation, pediatrics, and obstetrics and gynecology were more positively disposed to advance directives than physicians from radiology and nuclear medicine, surgery, orthopedics, and radiation oncology.

Differences between the emergency medicine and radiation oncology specialties were notable (success rate difference [SRD], 0.305), as were differences between pediatrics and radiation oncology (SRD, 0.304), emergency medicine and orthopedics (SRD, 0.283), and obstetrics and gynecology and radiation oncology (SRD, 0.280).

HICAGO (Reuters) – By law, Dr. Richard Pazdur, the U.S. Food and Drug Administration’s cancer drug czar, is not allowed to consider the cost of treatments his agency reviews, only whether they are safe and effective.

But Pazdur is not blind to escalating drug prices and the growing debate over how to place an appropriate value on cancer drugs, which can cost $100,000 a year or more.

“It’s very difficult for me to talk about,” Pazdur said in an interview at the American Society of Clinical Oncology meeting in Chicago, where the issue of value has been a consistent theme among the world’s top cancer doctors.

Instead, he recounts a story about buying his first house in Detroit in 1982.

“I was very nervous. I asked the realtor if I was paying the correct price. She said to me, ‘Rick, the price is what anybody is willing to pay for it.'”

In his view, the same applies to cancer drugs.

“Everybody knows that these are expensive drugs,” he said. “Obviously, we can’t just continue going on with escalating prices of drugs. That’s not a regulatory decision or anything profound from the FDA. It’s just the reality of the situation.”

Pazdur said the solution will likely take “a national dialog” involving all stakeholders – insurers, patients, doctors, lawmakers.

At the ASCO meeting this week, that dialog has already begun. In a forum on drug costs, Dr. Ezekiel Emanuel, the architect of President Barack Obama’s healthcare law, said costs can no longer be ignored. Emanuel reminded his well-heeled audience that the median household income in the United States is $52,000.

“It’s not a lot of money, especially compared to almost everything we do for cancer patients,” he said. Just one costly cancer drug “wipes out the median income household.”

And while the FDA may be barred from considering cost, Dr. John Marshall of Georgetown Lombardi Comprehensive Cancer Center, said the agency might reconsider its standards of deciding which drugs offer enough benefit to win approval.

“Is a $30,000-a-month drug that improves survival by 1.4 months effective? By an FDA standard, yes, if it meets the safety and efficacy data bar. But you would never swipe your VISA card for that kind of advantage,” Marshall said.

Pazdur said FDA cannot suddenly raise the bar on drug approvals, but he said the treatments he is seeing now, based on better science, are already far more effective than ever.

Since 2012, when FDA began implementing its so-called Breakthrough Therapy Designation program, 45% of the drugs that have been granted that designation have been cancer drugs.

“We’re seeing drugs that have higher response rates even in very refractory (drug resistant) populations,” he said. “That is really making us look at how we develop drugs and how we evaluate drugs.”

Better drugs could translate into a shorter regulatory process, cutting the cost of drug development.

“If we can speed approvals, drugs will cost less,” Marshall said.

Although the death rate from stroke is declining, it is rising for other neurologic diseases such as Alzheimer disease and Parkinson disease (PD). Unlike in Alzheimer’s, we can pinpoint the abnormality in the brain that leads to PD, a substantial destruction of the dopamine-producing neurons in the substantia nigra. By the time an individual has lost 50%-70% of the dopamine-producing neurons in this region, the symptoms of PD, such as tremor, slowness of movement, rigidity, and impaired balance and coordination, are already apparent. You might think that simply giving dopamine would resolve the symptoms, but any of the initial benefits of dopamine soon erode, leaving the patient trapped in a body that is increasingly less responsive. We also know that PD is associated with neuroinflammation. Therefore, we need a therapy known to both increase dopamine and reduce neuroinflammation. Does any such therapy exist? Yes, and it comes from therapeutic levels of omega-3 fatty acids. I say “therapeutic,” because if you give placebo levels of omega-3 fatty acids to patients with PD, you get placebo effects.

Omega-3 fatty acids have the unique ability to cross the blood-brain barrier that most drugs don’t have. They are also known to increase dopamine levels and reduce neuroinflammation in the brain.^[1,2] Furthermore, the omega-3 fatty acid eicosapentaenoic acid (EPA) has been shown to reduce the motor impairments and neuroinflammation in animal models in which the symptoms of PD can be rapidly induced by a drug known as MPTP.^[3]

Why don’t we see any clinical trials using high-dose omega-3 fatty acids? Previous trials have all used placebo doses of omega-3 fatty acids — in particular, EPA. I know this because I have published many peer-reviewed articles on the use of high-dose omega-3 fatty acids rich in EPA in the treatment of attention-deficit/hyperactivity disorder (ADHD), major childhood depression, and age-related macular degeneration (AMD).^[4-6] Once you give a therapeutic dose of omega-3 fatty acids, especially EPA, you get therapeutic effects. The common reason given for not using high-dose omega-3 fatty acids is the mistaken belief that the patients will bleed to death. That is simply not true, especially if you monitor the ratio of arachidonic acid (AA) to EPA in the blood. As long as the AA/EPA ratio remains above 1.5 (as it is for the Japanese population, whose diet is rich in omega-3 fatty acids through fish consumption), you are not going to have any bleeding problems. But as you get closer to that AA/EPA ratio, you start to see dramatic improvements in neurologic function.

Another problem with human trials is that you have to treat the patients like lab rats. That is, you have to control their entire diet and in particular the levels of omega-6 fatty acids that they are consuming. Whereas omega-3 fatty acids are anti-inflammatory, omega-6 fatty acids are proinflammatory. In fact, increased intake of AA (an omega-6 fatty acid) appears to be correlated with an increased incidence of PD.^[7] Another recent study indicated that if you simultaneously reduce omega-6 fatty acids while increasing the omega-3 fatty acids in the diet, the clinical results are significantly improved.^[8,9] Maybe that’s asking too much for patients with PD or any patient with a neurologic problem. As a result, we simply continue to look for a “magic drug” that allows patients to eat whatever they want. I don’t think that this is a productive research route for treating PD, let alone other neurologic diseases such as Alzheimer’s, ADHD, AMD, or even chronic headaches.

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