Neuroscience

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Breast milk is brain food You are what you eat, the saying goes, and now a study conducted by researchers at UC Santa Barbara and the University of Pittsburgh suggests that the oft-repeated adage applies not just to physical health but to brain power as well. In a paper published in the early online edition of the journal Prostaglandins, Leukotrienes and Essential Fatty Acids, the researchers compared the fatty acid profiles of breast milk from women in over two dozen countries with how well children from those same countries performed on academic tests. Their findings show that the amount of omega-3 docosahexaenoic acid (DHA) in a mother’s milk — fats found primarily in certain fish, nuts and seeds — is the strongest predictor of test performance. It outweighs national income and the number of dollars spent per pupil in schools. DHA alone accounted for about 20 percent of the differences in test scores among countries, the researchers found. On the other hand, the amount of omega-6 fat in mother’s milk — fats that come from vegetable oils such as corn and soybean — predict lower test scores. When the amount of DHA and linoleic acid (LA) — the most common omega-6 fat — were considered together, they explained nearly half of the differences in test scores. In countries where mother’s diets contain more omega-6, the beneficial effects of DHA seem to be reduced. More omega-3, less omega-6 “Human intelligence has a physical basis in the huge size of our brains — some seven times larger than would be expected for a mammal with our body size,” said Steven Gaulin, UCSB professor of anthropology and co-author of the paper. “Since there is never a free lunch, those big brains need lots of extra building materials — most importantly, they need omega-3 fatty acids, especially DHA. Omega-6 fats, however, undermine the effects of DHA and seem to be bad for brains.” Both kinds of omega fat must be obtained through diet. But because diets vary from place to place, for their study Gaulin and his co-author, William D. Lassek, M.D., a professor at the University of Pittsburgh’s Graduate School of Public Health and a retired assistant surgeon general, estimated the DHA and LA content — the good fat and the bad fat — in diets in 50 countries by examining published studies of the fatty acid profiles of women’s breast milk. The profiles are a useful measure for two reasons, according to Gaulin. First, because various kinds of fats interfere with one another in the body, breast milk DHA shows how much of this brain-essential fat survives competition with omega-6. Second, children receive their brain-building fats from their mothers. Breast milk profiles indicate the amount of DHA children in each region receive in the womb, through breastfeeding, and from the local diet available to their mothers and to them after they are weaned. The academic test results came from the Programme for International Student Assessment (PISA), which administers standardized tests in 58 nations. Gaulin and Lassek averaged the three PISA tests — math, science and reading ability — as their measure of cognitive performance. There were 28 countries for which the researchers found information about both breast milk and test scores. DHA content: best predictor of math test performance “Looking at those 28 countries, the DHA content of breast milk was the single best predictor of math test performance,” Gaulin said. The second best indicator was the amount of omega-6, and its effect is opposite. “Considering the benefits of omega-3 and the detriment of omega-6, we can get pretty darn close to explaining half the difference in scores between countries,” he added. When DHA and LA are considered together, he added, they are twice as effective at predicting test scores as either is alone, Gaulin said. Gaulin and Lassek considered two economic factors as well: per capita gross domestic product (a measure of average wealth in each nation) and per student expenditures on education. “Each of these factors helps explain some of the differences between nations in test scores, but the fatty acid profile of the average mother’s milk in a given country is a better predictor of the average cognitive performance in that country than is either of the conventional socioeconomic measures people use,” said Gaulin. From their analysis, the researchers conclude that both economic wellbeing and diet make a difference in cognitive test performance, and children are best off when they have both factors in their favor. “But if you had to choose one, you should choose the better diet rather than the better economy,” Gaulin said. The current research follows a study published in 2008 that showed that the children of women who had larger amounts of gluteofemoral fat “depots” performed better on academic tests than those of mothers with less. “At that time we weren’t trying to identify the dietary cause,” explained Gaulin. “We found that this depot that has been evolutionarily elaborated in women is important to building a good brain. We were content at that time to show that as a way of understanding why the female body is as evolutionarily distinctive as it is.” Now the researchers are looking at diet as the key to brain-building fat, since mothers need to acquire these fats in the first place. Their results are particularly interesting in 21st-century North America, Gaulin noted, because our current agribusiness-based diets provide very low levels of DHA — among the lowest in the world. Thanks to two heavily government-subsidized crops — corn and soybeans — the average U.S. diet is heavy in the bad omega-6 fatty acids and far too light on the good omega-3s, Gaulin said. Wrong kind of polyunsaturated fat “Back in the 1960s, in the middle of the cardiovascular disease epidemic, people got the idea that saturated fats were bad and polyunsaturated fats were good,” he explained. “That’s one reason margarine became so popular. But the polyunsaturated fats that were increased were the ones with omega-6, not omega-3. So our message is that not only is it advisable to increase omega 3 intake, it’s highly advisable to decrease omega-6 — the very fats that in the 1960s and ’70s we were told we should be eating more of.” Gaulin added that mayonnaise is, in general, the most omega-6-laden food in the average person’s refrigerator. “If you have too much of one — omega-6 — and too little of the other — omega 3 — you’re going to end up paying a price cognitively,” he said. The issue is a huge concern for women, Gaulin noted, because “that’s where kids’ brains come from. But it’s important for men as well because they have to take care of the brains their moms gave them. “Just like a racecar burns up some of its motor oil with every lap, your brain burns up omega-3 and you need to replenish it every day,” he said. (Image: Stacy Librandi)

Breast milk is brain food

You are what you eat, the saying goes, and now a study conducted by researchers at UC Santa Barbara and the University of Pittsburgh suggests that the oft-repeated adage applies not just to physical health but to brain power as well.

In a paper published in the early online edition of the journal Prostaglandins, Leukotrienes and Essential Fatty Acids, the researchers compared the fatty acid profiles of breast milk from women in over two dozen countries with how well children from those same countries performed on academic tests.

Their findings show that the amount of omega-3 docosahexaenoic acid (DHA) in a mother’s milk — fats found primarily in certain fish, nuts and seeds — is the strongest predictor of test performance. It outweighs national income and the number of dollars spent per pupil in schools.

DHA alone accounted for about 20 percent of the differences in test scores among countries, the researchers found.

On the other hand, the amount of omega-6 fat in mother’s milk — fats that come from vegetable oils such as corn and soybean — predict lower test scores. When the amount of DHA and linoleic acid (LA) — the most common omega-6 fat — were considered together, they explained nearly half of the differences in test scores. In countries where mother’s diets contain more omega-6, the beneficial effects of DHA seem to be reduced.

More omega-3, less omega-6

“Human intelligence has a physical basis in the huge size of our brains — some seven times larger than would be expected for a mammal with our body size,” said Steven Gaulin, UCSB professor of anthropology and co-author of the paper. “Since there is never a free lunch, those big brains need lots of extra building materials — most importantly, they need omega-3 fatty acids, especially DHA. Omega-6 fats, however, undermine the effects of DHA and seem to be bad for brains.”

Both kinds of omega fat must be obtained through diet. But because diets vary from place to place, for their study Gaulin and his co-author, William D. Lassek, M.D., a professor at the University of Pittsburgh’s Graduate School of Public Health and a retired assistant surgeon general, estimated the DHA and LA content — the good fat and the bad fat — in diets in 50 countries by examining published studies of the fatty acid profiles of women’s breast milk.

The profiles are a useful measure for two reasons, according to Gaulin. First, because various kinds of fats interfere with one another in the body, breast milk DHA shows how much of this brain-essential fat survives competition with omega-6. Second, children receive their brain-building fats from their mothers. Breast milk profiles indicate the amount of DHA children in each region receive in the womb, through breastfeeding, and from the local diet available to their mothers and to them after they are weaned.

The academic test results came from the Programme for International Student Assessment (PISA), which administers standardized tests in 58 nations. Gaulin and Lassek averaged the three PISA tests — math, science and reading ability — as their measure of cognitive performance. There were 28 countries for which the researchers found information about both breast milk and test scores.

DHA content: best predictor of math test performance

“Looking at those 28 countries, the DHA content of breast milk was the single best predictor of math test performance,” Gaulin said. The second best indicator was the amount of omega-6, and its effect is opposite. “Considering the benefits of omega-3 and the detriment of omega-6, we can get pretty darn close to explaining half the difference in scores between countries,” he added. When DHA and LA are considered together, he added, they are twice as effective at predicting test scores as either is alone, Gaulin said.

Gaulin and Lassek considered two economic factors as well: per capita gross domestic product (a measure of average wealth in each nation) and per student expenditures on education. “Each of these factors helps explain some of the differences between nations in test scores, but the fatty acid profile of the average mother’s milk in a given country is a better predictor of the average cognitive performance in that country than is either of the conventional socioeconomic measures people use,” said Gaulin.

From their analysis, the researchers conclude that both economic wellbeing and diet make a difference in cognitive test performance, and children are best off when they have both factors in their favor. “But if you had to choose one, you should choose the better diet rather than the better economy,” Gaulin said.

The current research follows a study published in 2008 that showed that the children of women who had larger amounts of gluteofemoral fat “depots” performed better on academic tests than those of mothers with less. “At that time we weren’t trying to identify the dietary cause,” explained Gaulin. “We found that this depot that has been evolutionarily elaborated in women is important to building a good brain. We were content at that time to show that as a way of understanding why the female body is as evolutionarily distinctive as it is.”

Now the researchers are looking at diet as the key to brain-building fat, since mothers need to acquire these fats in the first place.

Their results are particularly interesting in 21st-century North America, Gaulin noted, because our current agribusiness-based diets provide very low levels of DHA — among the lowest in the world. Thanks to two heavily government-subsidized crops — corn and soybeans — the average U.S. diet is heavy in the bad omega-6 fatty acids and far too light on the good omega-3s, Gaulin said.

Wrong kind of polyunsaturated fat

“Back in the 1960s, in the middle of the cardiovascular disease epidemic, people got the idea that saturated fats were bad and polyunsaturated fats were good,” he explained. “That’s one reason margarine became so popular. But the polyunsaturated fats that were increased were the ones with omega-6, not omega-3. So our message is that not only is it advisable to increase omega 3 intake, it’s highly advisable to decrease omega-6 — the very fats that in the 1960s and ’70s we were told we should be eating more of.”

Gaulin added that mayonnaise is, in general, the most omega-6-laden food in the average person’s refrigerator. “If you have too much of one — omega-6 — and too little of the other — omega 3 — you’re going to end up paying a price cognitively,” he said.

The issue is a huge concern for women, Gaulin noted, because “that’s where kids’ brains come from. But it’s important for men as well because they have to take care of the brains their moms gave them.

“Just like a racecar burns up some of its motor oil with every lap, your brain burns up omega-3 and you need to replenish it every day,” he said.

(Image: Stacy Librandi)

Filed under breast milk breastfeeding omega-3 cognitive performance health psychology neuroscience science

360 notes

Deconstructing the placebo response: Why does it work in treating depression? In the past three decades, the power of placebos has gone through the roof in treating major depressive disorder. In clinical trials for treating depression over that period of time, researchers have reported significant increases in patient’s response rates to placebos — the simple sugar pills given to patients who think that it may be actual medication. New research conducted by UCLA psychiatrists helps explain how placebos can have such a powerful effect on depression. “In short,” said Andrew Leuchter, the study’s first author and a professor of psychiatry at the UCLA Semel Institute for Neuroscience and Human Behavior, “if you think a pill is going to work, it probably will.” The UCLA researchers examined three forms of treatment. One was supportive care in which a therapist assessed the patient’s risk and symptoms, and provided emotional support and encouragement but refrained from providing solutions to the patient’s issues that might result in specific therapeutic effects. The other two treatments provided the same type of therapy, but patients also received either medication or placebos. The researchers found that treatment that incorporating either type of pill — real medication or placebo — yielded better outcomes than supportive care alone. Further, the success of the placebo treatment was closely correlated to people’s expectations before they began treatment. Those who believed that medication was likely to help them were much more likely to respond to placebos. Their belief in the effectiveness of medication was not related to the likelihood of benefitting from medication, however. “Our study indicates that belief in ‘the power of the pill’ uniquely drives the placebo response, while medications are likely to work regardless of patients’ belief in their effectiveness,” Leuchter said. The study appears in the current online edition of the British Journal of Psychiatry. At the beginning and end of the study, patients were asked to complete the Hamilton Rating Scale for Depression, giving researchers a quantitative assessment of how their depression levels changed during treatment. Those who received antidepressant medication and supportive care improved an average of 46 percent, patients who received placebos and supportive care improved an average of 36 percent, and those who received supportive care alone improved an average of just 5 percent. “Interestingly, while we found that medication was more effective than placebo, the difference was modest,” Leuchter said. The researchers also found that people who received supportive care alone were more likely to discontinue treatment early than those who received pills. People with major depressive disorder have a persistent low mood, low self-esteem and a loss of pleasure in things they once enjoyed. The disorder can be disabling, and it can affect a person’s family, work or school life, sleeping and eating habits, and overall health. In the double-blind study, 88 people ages 18 to 65 who had been diagnosed with depression were given eight weeks of treatment. Twenty received supportive care alone, 29 received a placebo with supportive care and 39 received actual medication with supportive care. The researchers measured the patients’ expectations for how effective they thought medication and general treatment would be, as well as their impressions of the strength of their relationship with the supportive care provider. “These results suggest a unique role for people’s expectations about their medication in engendering a placebo response,” Leuchter said. “Higher expectations of medication effectiveness predicted an improvement in placebo-treated subjects, and it’s important to note that people’s expectations about how effective a medication may be were already formed before they entered the trial.” Leuchter said the research indicates that factors such as direct-to-consumer advertising may be shaping peoples’ attitudes about medication. “It may not be an accident that placebo response rates have soared at the same time the pharmaceutical companies are spending $10 billion a year on consumer advertising.” (Image credit: © Chris Lamphear)

Deconstructing the placebo response: Why does it work in treating depression?

In the past three decades, the power of placebos has gone through the roof in treating major depressive disorder. In clinical trials for treating depression over that period of time, researchers have reported significant increases in patient’s response rates to placebos — the simple sugar pills given to patients who think that it may be actual medication.

New research conducted by UCLA psychiatrists helps explain how placebos can have such a powerful effect on depression.

“In short,” said Andrew Leuchter, the study’s first author and a professor of psychiatry at the UCLA Semel Institute for Neuroscience and Human Behavior, “if you think a pill is going to work, it probably will.”

The UCLA researchers examined three forms of treatment. One was supportive care in which a therapist assessed the patient’s risk and symptoms, and provided emotional support and encouragement but refrained from providing solutions to the patient’s issues that might result in specific therapeutic effects. The other two treatments provided the same type of therapy, but patients also received either medication or placebos.

The researchers found that treatment that incorporating either type of pill — real medication or placebo — yielded better outcomes than supportive care alone. Further, the success of the placebo treatment was closely correlated to people’s expectations before they began treatment. Those who believed that medication was likely to help them were much more likely to respond to placebos. Their belief in the effectiveness of medication was not related to the likelihood of benefitting from medication, however.

“Our study indicates that belief in ‘the power of the pill’ uniquely drives the placebo response, while medications are likely to work regardless of patients’ belief in their effectiveness,” Leuchter said.

The study appears in the current online edition of the British Journal of Psychiatry.

At the beginning and end of the study, patients were asked to complete the Hamilton Rating Scale for Depression, giving researchers a quantitative assessment of how their depression levels changed during treatment. Those who received antidepressant medication and supportive care improved an average of 46 percent, patients who received placebos and supportive care improved an average of 36 percent, and those who received supportive care alone improved an average of just 5 percent.

“Interestingly, while we found that medication was more effective than placebo, the difference was modest,” Leuchter said.

The researchers also found that people who received supportive care alone were more likely to discontinue treatment early than those who received pills.

People with major depressive disorder have a persistent low mood, low self-esteem and a loss of pleasure in things they once enjoyed. The disorder can be disabling, and it can affect a person’s family, work or school life, sleeping and eating habits, and overall health.

In the double-blind study, 88 people ages 18 to 65 who had been diagnosed with depression were given eight weeks of treatment. Twenty received supportive care alone, 29 received a placebo with supportive care and 39 received actual medication with supportive care.

The researchers measured the patients’ expectations for how effective they thought medication and general treatment would be, as well as their impressions of the strength of their relationship with the supportive care provider.

“These results suggest a unique role for people’s expectations about their medication in engendering a placebo response,” Leuchter said. “Higher expectations of medication effectiveness predicted an improvement in placebo-treated subjects, and it’s important to note that people’s expectations about how effective a medication may be were already formed before they entered the trial.”

Leuchter said the research indicates that factors such as direct-to-consumer advertising may be shaping peoples’ attitudes about medication. “It may not be an accident that placebo response rates have soared at the same time the pharmaceutical companies are spending $10 billion a year on consumer advertising.”

(Image credit: © Chris Lamphear)

Filed under placebo major depressive disorder depression mental health health medicine science

102 notes

Say ‘ahh’ to let your smartphone check for Parkinson’s disease Smartphones are designed to be curious. Having already learned about your friendships, your family and the pattern of your daily routine, designers are now interested in your health and fitness. A new crop of apps and wearable devices continuously measure and analyse vital signs such as movement and heart rate, claiming to count calories, optimise sleep quality and guide diet. While cynics might be tempted to dismiss these products as glorified pedometers for lycra-clad smartphone addicts, new research shows that the hardware inside existing consumer devices can already reliably detect degenerative, life-changing disorders, including Parkinson’s disease. Parkinson’s currently affects between seven to 10m people worldwide, and there is no cure. The disease can be diagnosed from a number of characteristic symptoms, including muscle tremor, changes in speech and difficulty of movement. However, diagnosis is challenging and usually involves regular visits to the doctor. It is estimated that one in five people with Parkinson’s are never diagnosed. Even if diagnosed, it can be difficult to accurately assess the how efficient treatment is in managing the disease. Read more

Say ‘ahh’ to let your smartphone check for Parkinson’s disease

Smartphones are designed to be curious. Having already learned about your friendships, your family and the pattern of your daily routine, designers are now interested in your health and fitness.

A new crop of apps and wearable devices continuously measure and analyse vital signs such as movement and heart rate, claiming to count calories, optimise sleep quality and guide diet. While cynics might be tempted to dismiss these products as glorified pedometers for lycra-clad smartphone addicts, new research shows that the hardware inside existing consumer devices can already reliably detect degenerative, life-changing disorders, including Parkinson’s disease.

Parkinson’s currently affects between seven to 10m people worldwide, and there is no cure. The disease can be diagnosed from a number of characteristic symptoms, including muscle tremor, changes in speech and difficulty of movement. However, diagnosis is challenging and usually involves regular visits to the doctor. It is estimated that one in five people with Parkinson’s are never diagnosed. Even if diagnosed, it can be difficult to accurately assess the how efficient treatment is in managing the disease.

Read more

Filed under parkinson's disease technology health science

179 notes

Autism rates steady for two decades

A University of Queensland study has found no evidence of an increase in autism in the past 20 years, countering reports that the rates of autism spectrum disorders (ASDs) are on the rise.

The study, led by Dr Amanda Baxter from UQ’s Queensland Centre for Mental Health Research at the School of Population Health, was a first-of-its-kind analysis of research data from 1990 to 2010. 

Dr Baxter said she and her colleagues found that rates had remained steady, despite reports that the prevalence of ASDs was increasing.

“We found that the prevalence of ASDs in 2010 was one in 132 people, which represents no change from 1990,” Dr Baxter said.

“We found that better recognition of the disorders and improved diagnostic criteria explain much of the difference in study findings over time.”

Part of the Global Burden of Disease project, this is the largest study to systematically assess rates and disability caused by ASDs in the community, using data collected from global research findings in the past 20 years.

ASDs are chronic, disabling disorders that stem from problems with brain development.

They affect people from a young age and are among the world’s 20 most disabling childhood conditions.

The study shows that about 52 million children and adults around the globe meet diagnostic criteria for an ASD.

Dr Baxter said researchers hoped the study would help guide health policy and improve support for those with ASD and their families.

“As ASDs cause substantial lifelong health issues, an accurate understanding of the burden of these disorders can inform public health policy as well as help allocate necessary resources for education, housing and employment,” she said.

The study, a collaboration with the University of Leicester and the University of Washington’s Institute for Health Metrics and Evaluation, is published in Psychological Medicine journal.

(Source: uq.edu.au)

Filed under autism ASD neurodevelopmental disorders health burden of disease psychology neuroscience science

377 notes

How we form habits and change existing ones Much of our daily lives are taken up by habits that we’ve formed over our lifetime. An important characteristic of a habit is that it’s automatic— we don’t always recognize habits in our own behavior. Studies show that about 40 percent of people’s daily activities are performed each day in almost the same situations. Habits emerge through associative learning. “We find patterns of behavior that allow us to reach goals. We repeat what works, and when actions are repeated in a stable context, we form associations between cues and response,” Wendy Wood explains in her session at the American Psychological Association’s 122nd Annual Convention. What are habits? Wood calls attention to the neurology of habits, and how they have a recognizable neural signature. When you are learning a response you engage your associative basal ganglia, which involves the prefrontal cortex and supports working memory so you can make decisions. As you repeat the behavior in the same context, the information is reorganized in your brain. It shifts to the sensory motor loop that supports representations of cue response associations, and no longer retains information on the goal or outcome. This shift from goal directed to context cue response helps to explain why our habits are rigid behaviors. There is a dual mind at play, Wood explains. When our intentional mind is engaged, we act in ways that meet an outcome we desire and typically we’re aware of our intentions. Intentions can change quickly because we can make conscious decisions about what we want to do in the future that may be different from the past. However, when the habitual mind is engaged, our habits function largely outside of awareness. We can’t easily articulate how we do our habits or why we do them, and they change slowly through repeated experience. “Our minds don’t always integrate in the best way possible. Even when you know the right answer, you can’t make yourself change the habitual behavior,” Wood says. Participants in a study were asked to taste popcorn, and as expected, fresh popcorn was preferable to stale. But when participants were given popcorn in a movie theater, people who have a habit of eating popcorn at the movies ate just as much stale popcorn as participants in the fresh popcorn group. “The thoughtful intentional mind is easily derailed and people tend to fall back on habitual behaviors. Forty percent of the time we’re not thinking about what we’re doing,” Wood interjects. “Habits allow us to focus on other things…Willpower is a limited resource, and when it runs out you fall back on habits.” How can we change our habits? Public service announcements, educational programs, community workshops, and weight-loss programs are all geared toward improving your day-to-day habits. But are they really effective? These standard interventions are very successful at increasing motivation and desire. You will almost always leave feeling like you can change and that you want to change. The programs give you knowledge and goal-setting strategies for implementation, but these programs only address the intentional mind. In a study on the “Take 5” program, 35 percent of people polled came away believing they should eat 5 fruits and vegetables a day. Looking at that result, it appears that the national program was effective at teaching people that it’s important to have 5 servings of fruits and vegetables every day. But the data changes when you ask what people are actually eating. Only 11 percent of people reported that they met this goal. The program changed people’s intentions, but it did not overrule habitual behavior. According to Wood, there are three main principles to consider when effectively changing habitual behavior. First, you must derail existing habits and create a window of opportunity to act on new intentions. Someone who moves to a new city or changes jobs has the perfect scenario to disrupt old cues and create new habits. When the cues for existing habits are removed, it’s easier to form a new behavior. If you can’t alter your entire environment by switching cities— make small changes. For instance, if weight-loss or healthy eating is your goal, try moving unhealthy foods to a top shelf out of reach, or to the back of the freezer instead of in front. The second principle is remembering that repetition is key. Studies have shown it can take anywhere from 15 days to 254 days to truly form a new habit. “There’s no easy formula for how long it takes,” Wood says. Lastly, there must be stable context cues available in order to trigger a new pattern. “It’s easier to maintain the behavior if it’s repeated in a specific context,” Wood emphasizes. Flossing after you brush your teeth allows the act of brushing to be the cue to remember to floss. Reversing the two behaviors is not as successful at creating a new flossing habit. Having an initial cue is a crucial component.

How we form habits and change existing ones

Much of our daily lives are taken up by habits that we’ve formed over our lifetime. An important characteristic of a habit is that it’s automatic— we don’t always recognize habits in our own behavior. Studies show that about 40 percent of people’s daily activities are performed each day in almost the same situations. Habits emerge through associative learning. “We find patterns of behavior that allow us to reach goals. We repeat what works, and when actions are repeated in a stable context, we form associations between cues and response,” Wendy Wood explains in her session at the American Psychological Association’s 122nd Annual Convention.

What are habits?

Wood calls attention to the neurology of habits, and how they have a recognizable neural signature. When you are learning a response you engage your associative basal ganglia, which involves the prefrontal cortex and supports working memory so you can make decisions. As you repeat the behavior in the same context, the information is reorganized in your brain. It shifts to the sensory motor loop that supports representations of cue response associations, and no longer retains information on the goal or outcome. This shift from goal directed to context cue response helps to explain why our habits are rigid behaviors.

There is a dual mind at play, Wood explains. When our intentional mind is engaged, we act in ways that meet an outcome we desire and typically we’re aware of our intentions. Intentions can change quickly because we can make conscious decisions about what we want to do in the future that may be different from the past. However, when the habitual mind is engaged, our habits function largely outside of awareness. We can’t easily articulate how we do our habits or why we do them, and they change slowly through repeated experience. “Our minds don’t always integrate in the best way possible. Even when you know the right answer, you can’t make yourself change the habitual behavior,” Wood says.

Participants in a study were asked to taste popcorn, and as expected, fresh popcorn was preferable to stale. But when participants were given popcorn in a movie theater, people who have a habit of eating popcorn at the movies ate just as much stale popcorn as participants in the fresh popcorn group. “The thoughtful intentional mind is easily derailed and people tend to fall back on habitual behaviors. Forty percent of the time we’re not thinking about what we’re doing,” Wood interjects. “Habits allow us to focus on other things…Willpower is a limited resource, and when it runs out you fall back on habits.”

How can we change our habits?

Public service announcements, educational programs, community workshops, and weight-loss programs are all geared toward improving your day-to-day habits. But are they really effective? These standard interventions are very successful at increasing motivation and desire. You will almost always leave feeling like you can change and that you want to change. The programs give you knowledge and goal-setting strategies for implementation, but these programs only address the intentional mind.

In a study on the “Take 5” program, 35 percent of people polled came away believing they should eat 5 fruits and vegetables a day. Looking at that result, it appears that the national program was effective at teaching people that it’s important to have 5 servings of fruits and vegetables every day. But the data changes when you ask what people are actually eating. Only 11 percent of people reported that they met this goal. The program changed people’s intentions, but it did not overrule habitual behavior.

According to Wood, there are three main principles to consider when effectively changing habitual behavior. First, you must derail existing habits and create a window of opportunity to act on new intentions. Someone who moves to a new city or changes jobs has the perfect scenario to disrupt old cues and create new habits. When the cues for existing habits are removed, it’s easier to form a new behavior. If you can’t alter your entire environment by switching cities— make small changes. For instance, if weight-loss or healthy eating is your goal, try moving unhealthy foods to a top shelf out of reach, or to the back of the freezer instead of in front.

The second principle is remembering that repetition is key. Studies have shown it can take anywhere from 15 days to 254 days to truly form a new habit. “There’s no easy formula for how long it takes,” Wood says. Lastly, there must be stable context cues available in order to trigger a new pattern. “It’s easier to maintain the behavior if it’s repeated in a specific context,” Wood emphasizes. Flossing after you brush your teeth allows the act of brushing to be the cue to remember to floss. Reversing the two behaviors is not as successful at creating a new flossing habit. Having an initial cue is a crucial component.

Filed under habits automatic processes prefrontal cortex attitudes health psychology neuroscience science

184 notes

US Alzheimer’s Rate Seems to Be Dropping The rate of Alzheimer’s disease and other dementias is falling in the United States and some other rich countries — good news about an epidemic that is still growing simply because more people are living to an old age, new studies show. An American over age 60 today has a 44 percent lower chance of developing dementia than a similar-aged person did roughly 30 years ago, the longest study of these trends in the U.S. concluded. Dementia rates also are down in Germany, a study there found. "For an individual, the actual risk of dementia seems to have declined," probably due to more education and control of health factors such as cholesterol and blood pressure, said Dr. Kenneth Langa. He is a University of Michigan expert on aging who discussed the studies Tuesday at the Alzheimer’s Association International Conference in Copenhagen. The opposite is occurring in some poor countries that have lagged on education and health, where dementia seems to be rising. More than 5.4 million Americans and 35 million people worldwide have Alzheimer’s, the most common form of dementia. It has no cure and current drugs only temporarily ease symptoms. A drop in rates is a silver lining in the so-called silver tsunami — the expected wave of age-related health problems from an older population. Alzheimer’s will remain a major public health issue, but countries where rates are dropping may be able to lower current projections for spending and needed services, experts said. Recent studies from the Netherlands, Sweden and England have suggested a decline, and the new research extends this look to some other parts of the world. Read more (Image: Thinkstock)

US Alzheimer’s Rate Seems to Be Dropping

The rate of Alzheimer’s disease and other dementias is falling in the United States and some other rich countries — good news about an epidemic that is still growing simply because more people are living to an old age, new studies show.

An American over age 60 today has a 44 percent lower chance of developing dementia than a similar-aged person did roughly 30 years ago, the longest study of these trends in the U.S. concluded.

Dementia rates also are down in Germany, a study there found.

"For an individual, the actual risk of dementia seems to have declined," probably due to more education and control of health factors such as cholesterol and blood pressure, said Dr. Kenneth Langa. He is a University of Michigan expert on aging who discussed the studies Tuesday at the Alzheimer’s Association International Conference in Copenhagen.

The opposite is occurring in some poor countries that have lagged on education and health, where dementia seems to be rising.

More than 5.4 million Americans and 35 million people worldwide have Alzheimer’s, the most common form of dementia. It has no cure and current drugs only temporarily ease symptoms.

A drop in rates is a silver lining in the so-called silver tsunami — the expected wave of age-related health problems from an older population. Alzheimer’s will remain a major public health issue, but countries where rates are dropping may be able to lower current projections for spending and needed services, experts said.

Recent studies from the Netherlands, Sweden and England have suggested a decline, and the new research extends this look to some other parts of the world.

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Filed under alzheimer's disease dementia health neuroscience science

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Alzheimer’s disease drug-development pipeline: few candidates, frequent failures Introduction Alzheimer’s disease (AD) is increasing in frequency as the global population ages. Five drugs are approved for treatment of AD, including four cholinesterase inhibitors and an N-methyl-D-aspartate (NMDA)-receptor antagonist. We have an urgent need to find new therapies for AD. Methods We examined Clinicaltrials.gov, a public website that records ongoing clinical trials. We examined the decade of 2002 to 2012, to better understand AD-drug development. We reviewed trials by sponsor, sites, drug mechanism of action, duration, number of patients required, and rate of success in terms of advancement from one phase to the next. We also reviewed the current AD therapy pipeline. Results During the 2002 to 2012 observation period, 413 AD trials were performed: 124 Phase 1 trials, 206 Phase 2 trials, and 83 Phase 3 trials. Seventy-eight percent were sponsored by pharmaceutical companies. The United States of America (U.S.) remains the single world region with the greatest number of trials; cumulatively, more non-U.S. than U.S. trials are performed. The largest number of registered trials addressed symptomatic agents aimed at improving cognition (36.6%), followed by trials of disease-modifying small molecules (35.1%) and trials of disease-modifying immunotherapies (18%). The mean length of trials increases from Phase 2 to Phase 3, and the number of participants in trials increases between Phase 2 and Phase 3. Trials of disease-modifying agents are larger and longer than those for symptomatic agents. A very high attrition rate was found, with an overall success rate during the 2002 to 2012 period of 0.4% (99.6% failure). Conclusions The Clinicaltrials.gov database demonstrates that relatively few clinical trials are undertaken for AD therapeutics, considering the magnitude of the problem. The success rate for advancing from one phase to another is low, and the number of compounds progressing to regulatory review is among the lowest found in any therapeutic area. The AD drug-development ecosystem requires support. Full Article (Image: Shutterstock)

Alzheimer’s disease drug-development pipeline: few candidates, frequent failures

Introduction

Alzheimer’s disease (AD) is increasing in frequency as the global population ages. Five drugs are approved for treatment of AD, including four cholinesterase inhibitors and an N-methyl-D-aspartate (NMDA)-receptor antagonist. We have an urgent need to find new therapies for AD.

Methods

We examined Clinicaltrials.gov, a public website that records ongoing clinical trials. We examined the decade of 2002 to 2012, to better understand AD-drug development. We reviewed trials by sponsor, sites, drug mechanism of action, duration, number of patients required, and rate of success in terms of advancement from one phase to the next. We also reviewed the current AD therapy pipeline.

Results

During the 2002 to 2012 observation period, 413 AD trials were performed: 124 Phase 1 trials, 206 Phase 2 trials, and 83 Phase 3 trials. Seventy-eight percent were sponsored by pharmaceutical companies. The United States of America (U.S.) remains the single world region with the greatest number of trials; cumulatively, more non-U.S. than U.S. trials are performed. The largest number of registered trials addressed symptomatic agents aimed at improving cognition (36.6%), followed by trials of disease-modifying small molecules (35.1%) and trials of disease-modifying immunotherapies (18%). The mean length of trials increases from Phase 2 to Phase 3, and the number of participants in trials increases between Phase 2 and Phase 3. Trials of disease-modifying agents are larger and longer than those for symptomatic agents. A very high attrition rate was found, with an overall success rate during the 2002 to 2012 period of 0.4% (99.6% failure).

Conclusions

The Clinicaltrials.gov database demonstrates that relatively few clinical trials are undertaken for AD therapeutics, considering the magnitude of the problem. The success rate for advancing from one phase to another is low, and the number of compounds progressing to regulatory review is among the lowest found in any therapeutic area. The AD drug-development ecosystem requires support.

Full Article

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Filed under alzheimer's disease drug development health science

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Watching TV and Food Intake: The Role of Content Obesity is a serious and growing health concern worldwide. Watching television (TV) represents a condition during which many habitually eat, irrespective of hunger level. However, as of yet, little is known about how the content of television programs being watched differentially impacts concurrent eating behavior. In this study, eighteen normal-weight female students participated in three counter-balanced experimental conditions, including a ‘Boring’ TV condition (art lecture), an ‘Engaging’ TV condition (Swedish TV comedy series), and a no TV control condition during which participants read (a text on insects living in Sweden). Throughout each condition participants had access to both high-calorie (M&Ms) and low-calorie (grapes) snacks. We found that, relative to the Engaging TV condition, Boring TV encouraged excessive eating (+52% g, P = 0.009). Additionally, the Engaging TV condition actually resulted in significantly less concurrent intake relative to the control ‘Text’ condition (−35% g, P = 0.05). This intake was driven almost entirely by the healthy snack, grapes; however, this interaction did not reach significance (P = 0.07). Finally, there was a significant correlation between how bored participants were across all conditions, and their concurrent food intake (beta = 0.317, P = 0.02). Intake as measured by kcals was similarly patterned but did not reach significance. These results suggest that, for women, different TV programs elicit different levels of concurrent food intake, and that the degree to which a program is engaging (or alternately, boring) is related to that intake. Additionally, they suggest that emotional content (e.g. boring vs. engaging) may be more associated than modality (e.g. TV vs. text) with concurrent intake. Full Article (Image: ThinkStock)

Watching TV and Food Intake: The Role of Content

Obesity is a serious and growing health concern worldwide. Watching television (TV) represents a condition during which many habitually eat, irrespective of hunger level. However, as of yet, little is known about how the content of television programs being watched differentially impacts concurrent eating behavior. In this study, eighteen normal-weight female students participated in three counter-balanced experimental conditions, including a ‘Boring’ TV condition (art lecture), an ‘Engaging’ TV condition (Swedish TV comedy series), and a no TV control condition during which participants read (a text on insects living in Sweden). Throughout each condition participants had access to both high-calorie (M&Ms) and low-calorie (grapes) snacks. We found that, relative to the Engaging TV condition, Boring TV encouraged excessive eating (+52% g, P = 0.009). Additionally, the Engaging TV condition actually resulted in significantly less concurrent intake relative to the control ‘Text’ condition (−35% g, P = 0.05). This intake was driven almost entirely by the healthy snack, grapes; however, this interaction did not reach significance (P = 0.07). Finally, there was a significant correlation between how bored participants were across all conditions, and their concurrent food intake (beta = 0.317, P = 0.02). Intake as measured by kcals was similarly patterned but did not reach significance. These results suggest that, for women, different TV programs elicit different levels of concurrent food intake, and that the degree to which a program is engaging (or alternately, boring) is related to that intake. Additionally, they suggest that emotional content (e.g. boring vs. engaging) may be more associated than modality (e.g. TV vs. text) with concurrent intake.

Full Article

(Image: ThinkStock)

Filed under obesity food consumption eating habits television TV health science

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Study finds association between maternal exposure to agricultural pesticides, autism in offspring

Pregnant women who lived in close proximity to fields and farms where chemical pesticides were applied experienced a two-thirds increased risk of having a child with autism spectrum disorder or other developmental delay, a study by researchers with the UC Davis MIND Institute has found. The associations were stronger when the exposures occurred during the second and third trimesters of the women’s pregnancies.

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The large, multisite California-based study examined associations between specific classes of pesticides, including organophosphates, pyrethroids and carbamates, applied during the study participants’ pregnancies and later diagnoses of autism and developmental delay in their offspring. It is published online today in Environmental Health Perspectives.

“This study validates the results of earlier research that has reported associations between having a child with autism and prenatal exposure to agricultural chemicals in California,” said lead study author Janie F. Shelton, a UC Davis graduate student who now consults with the United Nations. “While we still must investigate whether certain sub-groups are more vulnerable to exposures to these compounds than others, the message is very clear: Women who are pregnant should take special care to avoid contact with agricultural chemicals whenever possible.”

California is the top agricultural producing state in the nation, grossing $38 billion in revenue from farm crops in 2010. Statewide, approximately 200 million pounds of active pesticides are applied each year, most of it in the Central Valley, north to the Sacramento Valley and south to the Imperial Valley on the California-Mexico border. While pesticides are critical for the modern agriculture industry, certain commonly used pesticides are neurotoxic and may pose threats to brain development during gestation, potentially resulting in developmental delay or autism.

The study was conducted by examining commercial pesticide application using the California Pesticide Use Report and linking the data to the residential addresses of approximately 1,000 participants in the Northern California-based Childhood Risk of Autism from Genetics and the Environment (CHARGE) Study. The study includes families with children between 2 and 5 diagnosed with autism or developmental delay or with typical development. It is led by principal investigator Irva Hertz-Picciotto, a MIND Institute researcher and professor and vice chair of the Department of Public Health Sciences at UC Davis. The majority of study participants live in the Sacramento Valley, Central Valley and the greater San Francisco Bay Area.

Twenty-one chemical compounds were identified in the organophosphate class, including chlorpyrifos, acephate and diazinon. The second most commonly applied class of pesticides was pyrethroids, one quarter of which was esfenvalerate, followed by lambda-cyhalothrin permethrin, cypermethrin and tau-fluvalinate. Eighty percent of the carbamates were methomyl and carbaryl.

For the study, researchers used questionnaires to obtain study participants’ residential addresses during the pre-conception and pregnancy periods. The addresses then were overlaid on maps with the locations of agricultural chemical application sites based on the pesticide-use reports to determine residential proximity. The study also examined which participants were exposed to which agricultural chemicals.

“We mapped where our study participants’ lived during pregnancy and around the time of birth. In California, pesticide applicators must report what they’re applying, where they’re applying it, dates when the applications were made and how much was applied,” Hertz-Picciotto said. “What we saw were several classes of pesticides more commonly applied near residences of mothers whose children developed autism or had delayed cognitive or other skills.”

The researchers found that during the study period approximately one-third of CHARGE Study participants lived in close proximity – within 1.25 to 1.75 kilometers – of commercial pesticide application sites. Some associations were greater among mothers living closer to application sites and lower as residential proximity to the application sites decreased, the researchers found.

Organophosphates applied over the course of pregnancy were associated with an elevated risk of autism spectrum disorder, particularly for chlorpyrifos applications in the second trimester. Pyrethroids were moderately associated with autism spectrum disorder immediately prior to conception and in the third trimester. Carbamates applied during pregnancy were associated with developmental delay.

Exposures to insecticides for those living near agricultural areas may be problematic, especially during gestation, because the developing fetal brain may be more vulnerable than it is in adults. Because these pesticides are neurotoxic, in utero exposures during early development may distort the complex processes of structural development and neuronal signaling, producing alterations to the excitation and inhibition mechanisms that govern mood, learning, social interactions and behavior.

“In that early developmental gestational period, the brain is developing synapses, the spaces between neurons, where electrical impulses are turned into neurotransmitting chemicals that leap from one neuron to another to pass messages along. The formation of these junctions is really important and may well be where these pesticides are operating and affecting neurotransmission,” Hertz-Picciotto said.

Research from the CHARGE Study has emphasized the importance of maternal nutrition during pregnancy, particularly the use of prenatal vitamins to reduce the risk of having a child with autism. While it’s impossible to entirely eliminate risks due to environmental exposures, Hertz-Picciotto said that finding ways to reduce exposures to chemical pesticides, particularly for the very young, is important.

“We need to open up a dialogue about how this can be done, at both a societal and individual level,” she said. “If it were my family, I wouldn’t want to live close to where heavy pesticides are being applied.”

(Source: ucdmc.ucdavis.edu)

Filed under autism ASD pregnancy pesticides health neurotransmission science

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How a new approach to funding Alzheimer’s research could pay off More than 5 million Americans suffer from Alzheimer’s disease, the affliction that erodes memory and other mental capacities, but no drugs targeting the disease have been approved by the U.S. Food and Drug Administration since 2003. Now a paper by an MIT professor suggests that a revamped way of financing Alzheimer’s research could spur the development of useful new drugs for the illness. “We are spending tremendous amounts of resources dealing with this disease, but we don’t have any effective therapies for it,” says Andrew Lo, the Charles E. and Susan T. Harris Professor of Finance and director of the Laboratory for Financial Engineering at the MIT Sloan School of Management. “It really imposes a tremendous burden on society, not just for the afflicted, but also for those who care for them.” Lo and three co-authors propose creating a public-private partnership that would fund research for a diverse array of drug-discovery projects simultaneously. Such an approach would increase the chances of a therapeutic breakthrough, they say, and the inclusion of public funding would help mitigate the risks and costs of Alzheimer’s research for the private sector. There would be a long-term public-sector payoff, according to the researchers: Government funding for Alzheimer’s research would pale in comparison to the cost of caring for Alzheimer’s sufferers in public health-care programs. The paper’s model of the new funding approach calls for an outlay of $38.4 billion over 13 years for research; the costs of Medicare and Medicaid support for Alzheimer’s patients in 2014 alone is estimated to be $150 billion. “Having parallel development would obviously decrease the waiting time, but it increases the short-run need for funding,” Lo says. “Given how much of an urgent need there is for Alzheimer’s therapies, it has to be the case that if you develop a cure, you’re going to be able to recoup your costs and then some.” In fact, the paper’s model estimates a double-digit return on public investment over the long run. Lo adds: “Can we afford it? I think a more pressing question is, ‘Can we afford not to do something about this now?’” Modeling the odds of success The paper, “Parallel Discovery of Alzheimer’s Therapeutics,” was published today in Science Translational Medicine. Along with Lo, the co-authors of the piece are Carole Ho of the biotechnology firm Genentech, Jayna Cummings of MIT Sloan, and Kenneth Kosik of the University of California at Santa Barbara. The main hypothesis on the cause of Alzheimer’s involves amyloid deposition, the buildup of plaques in the brain that impair neurological function; most biomedical efforts to tackle the disease have focused on this issue. For the study, Ho and Kosik, leading experts in Alzheimer’s research, compiled a list of 64 conceivable approaches to drug discovery, addressing a range of biological mechanisms that may be involved in the disease. A fund backing that group of research projects might expand the chances of developing a drug that could, at a minimum, slow the progression of the disease. On the other hand, it might not increase the odds of success so much that pharmaceutical firms and biomedical investment funds would plow money into the problem. “Sixty-four projects are a lot more than what’s being investigated today, but it’s still way shy of the 150 or 200 that are needed to mitigate the financial risks of an Alzheimer’s-focused fund,” Lo says. The model assumes 13 years for the development of an individual drug, including clinical trials, and estimates the success rates for drug development. Given 150 trials, the odds of at least two successful trials are 99.59 percent. Two successful trials, Lo says, is what it would take to make the investment — a series of bonds issued by the fund — profitable and attractive to a broad range of investors. “With a sufficiently high likelihood of success, you can issue debt to attract a large group of bondholders who would be willing to put their money to work,” Lo says. “The enormous size of bond markets translates into enormous potential funding opportunities for developing these therapeutics.” Stakeholders everywhere To be clear, Lo says, Alzheimer’s drug development is a very difficult task, since researchers often have to identify a pool of potential patients well before symptoms occur, in order to see how well therapies might work on delaying the onset of the disease. Compared with the development of new drugs to treat other diseases, “Alzheimer’s drug development is more expensive, takes longer, and needs a larger sample of potential patients,” Lo acknowledges. However, since the number of Americans suffering from Alzheimer’s is projected to double by 2050, according to the Alzheimer’s Association, an advocacy group, Lo stresses the urgency of the task at hand.”

How a new approach to funding Alzheimer’s research could pay off

More than 5 million Americans suffer from Alzheimer’s disease, the affliction that erodes memory and other mental capacities, but no drugs targeting the disease have been approved by the U.S. Food and Drug Administration since 2003. Now a paper by an MIT professor suggests that a revamped way of financing Alzheimer’s research could spur the development of useful new drugs for the illness.

“We are spending tremendous amounts of resources dealing with this disease, but we don’t have any effective therapies for it,” says Andrew Lo, the Charles E. and Susan T. Harris Professor of Finance and director of the Laboratory for Financial Engineering at the MIT Sloan School of Management. “It really imposes a tremendous burden on society, not just for the afflicted, but also for those who care for them.”

Lo and three co-authors propose creating a public-private partnership that would fund research for a diverse array of drug-discovery projects simultaneously. Such an approach would increase the chances of a therapeutic breakthrough, they say, and the inclusion of public funding would help mitigate the risks and costs of Alzheimer’s research for the private sector.

There would be a long-term public-sector payoff, according to the researchers: Government funding for Alzheimer’s research would pale in comparison to the cost of caring for Alzheimer’s sufferers in public health-care programs. The paper’s model of the new funding approach calls for an outlay of $38.4 billion over 13 years for research; the costs of Medicare and Medicaid support for Alzheimer’s patients in 2014 alone is estimated to be $150 billion.

“Having parallel development would obviously decrease the waiting time, but it increases the short-run need for funding,” Lo says. “Given how much of an urgent need there is for Alzheimer’s therapies, it has to be the case that if you develop a cure, you’re going to be able to recoup your costs and then some.” In fact, the paper’s model estimates a double-digit return on public investment over the long run.

Lo adds: “Can we afford it? I think a more pressing question is, ‘Can we afford not to do something about this now?’”

Modeling the odds of success

The paper, “Parallel Discovery of Alzheimer’s Therapeutics,” was published today in Science Translational Medicine. Along with Lo, the co-authors of the piece are Carole Ho of the biotechnology firm Genentech, Jayna Cummings of MIT Sloan, and Kenneth Kosik of the University of California at Santa Barbara.

The main hypothesis on the cause of Alzheimer’s involves amyloid deposition, the buildup of plaques in the brain that impair neurological function; most biomedical efforts to tackle the disease have focused on this issue. For the study, Ho and Kosik, leading experts in Alzheimer’s research, compiled a list of 64 conceivable approaches to drug discovery, addressing a range of biological mechanisms that may be involved in the disease.

A fund backing that group of research projects might expand the chances of developing a drug that could, at a minimum, slow the progression of the disease. On the other hand, it might not increase the odds of success so much that pharmaceutical firms and biomedical investment funds would plow money into the problem.

“Sixty-four projects are a lot more than what’s being investigated today, but it’s still way shy of the 150 or 200 that are needed to mitigate the financial risks of an Alzheimer’s-focused fund,” Lo says.

The model assumes 13 years for the development of an individual drug, including clinical trials, and estimates the success rates for drug development. Given 150 trials, the odds of at least two successful trials are 99.59 percent. Two successful trials, Lo says, is what it would take to make the investment — a series of bonds issued by the fund — profitable and attractive to a broad range of investors.

“With a sufficiently high likelihood of success, you can issue debt to attract a large group of bondholders who would be willing to put their money to work,” Lo says. “The enormous size of bond markets translates into enormous potential funding opportunities for developing these therapeutics.”

Stakeholders everywhere

To be clear, Lo says, Alzheimer’s drug development is a very difficult task, since researchers often have to identify a pool of potential patients well before symptoms occur, in order to see how well therapies might work on delaying the onset of the disease.

Compared with the development of new drugs to treat other diseases, “Alzheimer’s drug development is more expensive, takes longer, and needs a larger sample of potential patients,” Lo acknowledges.

However, since the number of Americans suffering from Alzheimer’s is projected to double by 2050, according to the Alzheimer’s Association, an advocacy group, Lo stresses the urgency of the task at hand.”

Filed under alzheimer's disease drug development health medicine neuroscience science

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