The endless string of good news about Vitamin D never ceases:

Vitamin D found in fish boosts brain power

Eating fish – long considered ‘brain food’ – may really be good for the old grey matter, as is a healthy dose of sunshine, new research suggests.

University of Manchester scientists in collaboration with colleagues from other European centres have shown that higher levels of vitamin D – primarily synthesised in the skin following sun exposure but also found in certain foods such as oily fish – are associated with improved cognitive function in middle-aged and older men.

The study, published in the Journal of Neurology, Neurosurgery and Psychiatry, compared the cognitive performance of more than 3,000 men aged 40 to 79 years at eight test centres across Europe.

The researchers found that men with higher levels of vitamin D performed consistently better in a simple and sensitive neuropsychological test that assesses an individual’s attention and speed of information processing.

“Previous studies exploring the relationship between vitamin D and cognitive performance in adults have produced inconsistent findings but we observed a significant, independent association between a slower information processing speed and lower levels of vitamin D,” said lead author Dr David Lee, in Manchester’s School of Translational Medicine.

“The main strengths of our study are that it is based on a large population sample and took into account potential interfering factors, such as depression, season and levels of physical activity.

“Interestingly, the association between increased vitamin D and faster information processing was more significant in men aged over 60 years, although the biological reasons for this remain unclear.”

“The positive effects vitamin D appears to have on the brain need to be explored further but certainly raise questions about its potential benefit for minimising ageing-related declines in cognitive performance.”

Something that I can definitely attest to is the phenomenon that once you endure the learning of one foreign language, the acquisition of other foreign languages becomes easier. I always felt the case was that one ‘learnt how to learn a language’. Now it’s been proven in a scientific study.

I strongly recommend language learning as a hobby. in my experience, it offers insight and opens up new ways of thinking about your mother tongue, too, as well as improving memory and ‘overall brain functionality’.

Exposure to 2 languages carries far-reaching benefits

People who can speak two languages are more adept at learning a new foreign language than their monolingual counterparts, according to research conducted at Northwestern University. And their bilingual advantage persists even when the new language they study is completely different from the languages they already know.

“It’s often assumed that individuals who’ve learned multiple languages simply have a natural aptitude for learning languages,” said Viorica Marian, associate professor of communication sciences and disorders at Northwestern University. “While that is true in some cases, our research shows that the experience of becoming bilingual itself makes learning a new language easier.”

In the first study to explore a possible advantage in bilinguals who learned a second language at a parent’s knee, Northwestern researchers asked three groups of native English speakers — English-Mandarin bilinguals, English-Spanish bilinguals and monolinguals — to master words in an invented language that bore no relationship to English, Spanish or Mandarin.

They found that the bilingual participants — whether English-Mandarin or English-Spanish speakers – mastered nearly twice the number of words as the monolinguals.

And they believe the bilingual advantage is likely to generalize beyond word learning to other kinds of language learning, including learning new words in one’s own language and a very basic ability to maintain verbal information.

“After learning another language, individuals can transfer language learning strategies they’ve acquired to subsequent language learning and become better language learners in general,” said Northwestern School of Communication’s Marian.

Marian and Margarita Kaushanskaya, now assistant professor of communicative disorders at University of Wisconsin-Madison, are co-authors of “The Bilingual Advantage in Novel World Learning.” Their study will be published in the August issue of Psychonomic Bulletin and Review.

The study has important implications for educators who are considering the appropriate age at which to introduce foreign language instruction as well as for parents who in increasing numbers have an option to enroll their children in dual language immersion programs.

“We’re seeing that exposure to two languages early in life carries far-reaching benefits,” said co-author Kaushanskaya. “Our research tells us that children who grow up with two languages wind up being better language learners later on.”

Although there are more opportunities today for children to participate in dual language immersion programs than in the past, parents often avoid them for fear that dual language instruction may end up confusing or distracting their children and inhibit subject learning.

In research presented in the May issue of the Journal of Experimental Psychology, however, the two co-authors demonstrate that bilinguals actually are better able than monolinguals to inhibit irrelevant information while learning a new language. Repressing irrelevant information, after all, is something bilinguals do every time they speak.

What’s more, the majority of the world’s population outside the United States is bilingual or multilingual, Marian noted. In the U.S., approximately one out of five American households speaks a language other than English at home, according to the U.S. Census. And, with higher birth rates among Hispanics relative to the rest of the population, that proportion is rapidly growing.

Previous research already indicates that individuals who have formally studied two or more languages as adults more easily acquire a new language than monolinguals. New research even indicates that the onset of Alzheimer’s disease in bilinguals is, on average, delayed by four years compared to monolinguals.

The Northwestern researchers chose to study bilinguals who learned a second language at an early age and in a non-classroom study to avoid suggestions that their subjects simply were exceptionally talented or motivated foreign language learners.

For their study in Psychonomic Bulletin and Review, the researchers controlled for age, education, English language vocabulary size and, in the case of bilinguals, second language proficiency. Sixty Northwestern University students in their early twenties — 20 monolinguals, 20 early English-Mandarin speakers and 20 early English-Spanish speakers – participated.

All participants were tested twice for word mastery in the invented language. The initial test took place immediately after they heard and repeated the invented language words. The second test occurred a week later.

Researchers have debunked one of the most insidious myths about this much-maligned but highly beneficial drug in an article from Dermatology Times:

Isotretinoin and suicide: Epidemiological study shows no association

London, Ontario, Canada — Suicidal behavior among patients taking isotretinoin represents an uncommon, idiosyncratic phenomenon, according to the author of a recent study of nationally representative patient data spanning a decade.

Read more…

Eating fatty fish once a week reduces men’s risk of heart failure

Omega-3 fatty acids in fish oils are also beneficial

BOSTON – Eating salmon or other fatty fish just once a week helped reduce men’s risk of heart failure, adding to growing evidence that omega-3 fatty acids are of benefit to cardiac health. Led by researchers at Beth Israel Deaconess Medical Center (BIDMC) and reported in today’s on-line issue of the European Heart Journal, the findings represent one of the largest studies to investigate the association.

“Previous research has demonstrated that fatty fish and omega-3 fatty acids help to combat risk factors for a range of heart-related conditions, such as lowering triglycerides [fats in the blood] reducing blood pressure, heart rate and heart rate variability,” explains first author Emily Levitan, PhD, a research fellow in the Cardiovascular Epidemiology Research Center at BIDMC. “Collectively, this may explain the association with the reduced risk of heart failure found in our study.”

A life-threatening condition that develops when the heart can no longer pump enough blood to meet the body’s needs, heart failure (also known as congestive heart failure) is usually caused by existing cardiac conditions, including high blood pressure and coronary artery disease. Heart failure is the leading cause of hospitalization among patients 65 and older, and is characterized by such symptoms as fatigue and weakness, difficulty walking, rapid or irregular heartbeat, and persistent cough or wheezing.

The researchers followed 39,367 Swedish men between the ages of 45 and 79 from 1998 to 2004. The researchers recorded details of the men’s diet and tracked the men’s outcome through Swedish inpatient hospital registers and cause-of-death registers. During this period, 597 men in the study (with no previous history of heart disease or diabetes) developed heart failure. Thirty-four men died.

Analysis of their numbers showed that the men who ate fatty fish (herring, mackerel, salmon, whitefish and char) once a week were 12 percent less likely to develop heart failure, compared with men who ate no fatty fish. Although this association did not reach statistical significance, notes Levitan, the researchers also found a statistically significant association with the intake of marine omega-3 fatty acids, which are found in cod liver and other fish oils: The men who consumed approximately 0.36 grams a day were 33 percent less likely to develop heart failure than the men who consumed little or no marine omega-3 fatty acids.

“We divided the men into five groups based on their intake of fatty fish,” explains Levitan. “The first group consumed little or no fatty fish; at the other end of the spectrum, the fifth group consumed significant quantitities, three or more servings per week. We found that while the ‘middle group’ – who ate one serving per week – had a 12 percent reduced risk of heart failure, the next two groups, who ate either two servings a week or three or more servings a week, had nearly the same heart failure risk as the men who ate no fish at all.”

The findings were similar when the researchers looked at fish oil consumption: Among five groups based on fish oil consumption, the middle group, who consumed 0.36 grams per day of omega-3 fatty acids showed a 33 percent reduced risk of heart failure, while the men who consumer greater quantities (approximately 0.46 grams per day or 0.71 grams per day) had a risk of heart failure similar to the men who consumed little or no fish oils.

“The higher rates of heart failure in men who consumed the most fatty fish or marine omega-3 fatty acids compared with the men who had moderate consumption may be due to chance,” explains Levitan. Alternatively, she explains, the men who ate more fish may already be in poor health, and may be trying to improve their health through fish consumption.

“Our study reinforces the current recommendations for moderate consumption of fatty fish,” notes Levitan. “Current guidelines from the American Heart Association recommend eating fatty fish twice a week. It will be important, going forward, to replicate these findings in other populations, particularly those including women, as our study looked at men only.”

Think memory worsens with age? Then yours probably will…

Thinking your memory will get worse as you get older may actually be a self-fulfilling prophecy. Researchers at North Carolina State University have found that senior citizens who think older people should perform poorly on tests of memory actually score much worse than seniors who do not buy in to negative stereotypes about aging and memory loss.

In a study published earlier this month, psychology professor Dr. Tom Hess and a team of researchers from NC State show that older adults’ ability to remember suffers when negative stereotypes are “activated” in a given situation. “For example, older adults will perform more poorly on a memory test if they are told that older folks do poorly on that particular type of memory test,” Hess says. Memory also suffers if senior citizens believe they are being “stigmatized,” meaning that others are looking down on them because of their age.

“Such situations may be a part of older adults’ everyday experience,” Hess says, “such as being concerned about what others think of them at work having a negative effect on their performance – and thus potentially reinforcing the negative stereotypes.” However, Hess adds, “The positive flip side of this is that those who do not feel stigmatized, or those in situations where more positive views of aging are activated, exhibit significantly higher levels of memory performance.” In other words, if you are confident that aging will not ravage your memory, you are more likely to perform well on memory-related tasks.

The study also found a couple of factors that influenced the extent to which negative stereotypes influence older adults. For example, the researchers found that adults between the ages of 60 and 70 suffered more when these negative stereotypes were activated than seniors who were between the ages of 71 and 82. However, the 71-82 age group performed worse when they felt stigmatized.

Finally, the study found that negative effects were strongest for those older adults with the highest levels of education. “We interpret this as being consistent with the idea that those who value their ability to remember things most are the most likely to be sensitive to the negative implications of stereotypes, and thus are most likely to exhibit the problems associated with the stereotype.”

“The take-home message,” Hess says, “is that social factors may have a negative effect on older adults’ memory performance.”

Hess is the lead author on the study, “Moderators of and Mechanisms Underlying Stereotype Threat Effects on Older Adults’ Memory Performance.” Co-authors on the study are former NC State students Joey T. Hinson and Elizabeth A. Hodges. The study was published online April 1 by Experimental Aging Research.

Longer life is accompanied by fewer degenerative diseases…

A biochemical pathway that helps keep cells alive when oxygen is low also plays a role in longevity and resistance against some diseases of old age, according to a report to be published April 16 in the journal Science.
A cell’s protective reaction to a drop in oxygen is called the hypoxic response. Researchers at the University of Washington (UW) have found that nematode worms live longer if their genetic make-up permits their cells to turn on the hypoxic response under normal oxygen conditions.
Not only do these worms live longer, the researchers noted, their cells are relatively free from the toxic proteins that accumulate and clump together as an animal ages.
Dr. Matt Kaeberlein, UW assistant professor of pathology and the senior author on the study, said that defining cellular mechanisms that prevent accumulation of these proteins may point to new therapeutic targets for devastating diseases that often accompany old age in people. Toxic protein aggregations, he explained, are seen in the brain cells of those with Alzheimer’s disease, Huntington’s disease, and several other degenerative conditions that afflict the elderly.
The co-lead authors, Dr. Ranjana Mehta and Dr. Katy Steinkraus, uncovered the life-extending role of the hypoxic response while studying the mechanism by which dietary restriction slows aging in nematodes. Dietary restriction has been shown to increase life span in many different organisms, including worms, flies and mice. Kaeberlein’s group had previously found that dietary restriction also protects against toxic protein aggregation in nematode models of Huntington’s and Alzheimer’s diseases. To their surprise, however, genetic experiments mapped the hypoxic response to a previously unknown longevity pathway, different from dietary restriction.
“The research findings suggest that the hypoxic response promotes longevity and reduces the accumulation of toxic proteins by a mechanism that is distinct from both dietary restriction and insulin-like signaling. It appears to be an alternative pathway,” Kaeberlein said. “However, we don’t know if future studies might reveal that all of these different genetic pathways converge somewhere down the line into a common mechanism for delaying the effects of age.”
The key factor that controls the hypoxic response is called HIF. HIF is regulated by another protein called VHL-1, which tags HIF to be destroyed by a cellular machine called the proteasome. Destruction of HIF by VHL-1 keeps the hypoxic response “off” when oxygen is present. The UW researchers bred worms that could not produce VHL-1, leading to persistence of HIF even in the presence of high oxygen levels. They found that these worms, which were able to turn on the hypoxic response under normal oxygen conditions, lived about 30 percent longer than worms whose cells made VHL-1.
They also found that animals lacking VHL-1 were resistant to the toxic proteins known to cause Alzheimer’s and Huntington’s diseases, and that their cells accumulated less of an age-pigment called lipofuscin. Lipofuscin is thought to be one indicator of an animal’s health during aging. According to Kaeberlein, “These observations may suggest that the hypoxic response not only increases life span, but also lengthens health span and protects against the molecular processes that lead to neurodegenerative diseases in people.” Health span refers to the period of an organism’s life that is relatively free of disease.
The authors note that the hypoxic response, including HIF and VHL-1, is very well conserved in organisms from nematodes to humans, raising the possibility that modulating HIF activity may be useful for treating some age-associated diseases, and perhaps even slowing aging, in people. Kaeberlein cautions, however, that “mutation of VHL-1 is associated with a variety of tumors, and any therapies targeted toward activation of HIF would most likely need to be specific for cells that are not rapidly dividing, such as brain cells or muscle cells.”
“What we’re focused on now,” says Mehta, “is figuring out how HIF is protecting the animals from aging.” In both worms and people, HIF regulates the activity of several factors involved in growth and resistance to stress. “One or more of these factors must be the key.”
Kaeberlein agrees. “This is a completely new pathway for aging and age-associated disease. If we can understand at a very detailed level how HIF is slowing aging, we may be able to use that information to develop effective therapies for treating age-associated diseases in people.”

Yuan et al. have identified another anti-cancer effect of the “longevity” protein SIRT1. By speeding the destruction of the tumor promoter c-Myc, SIRT1 curbs cell division. The study will be published online April 13 (www.jcb.org) and will appear in the April 20 print issue of the Journal of Cell Biology.

The yeast and nematode equivalents of SIRT1 are fountains of youth that stretch lifespan. Whether SIRT1 slows aging in mammals isn’t certain, but it’s beneficial in other ways. The protein tunes up metabolism, reducing blood levels of glucose and insulin, and might forestall neurodegenerative illnesses such as Alzheimer’s disease and ALS. Given its pro-life credentials, you might expect SIRT1 to inhibit cancer. And several studies suggest that it does. But other work indicates that the protein aids tumors. For example, SIRT1 chops off acetyl groups, which can inactivate the tumor suppressor p53.

Yuan et al. determined SIRT1’s effect on the transcription factor c-Myc, whose expression surges in many breast, colon, and liver cancers. The two proteins are tangled in a regulatory loop, the team found. c-Myc latched onto SIRT1’s promoter, spurring cells to manufacture more SIRT1. In turn, SIRT1 detached acetyl groups from c-Myc, hastening its breakdown. To test SIRT1’s effects on tumor growth, the researchers implanted cancerous cells expressing c-Myc into nude mice that lack immune defenses. Boosting production of SIRT1 blocked tumor formation.

How deacetylation of c-Myc sparks its destruction is still a mystery. The researchers say that the results don’t necessarily conflict with studies suggesting that SIRT1 is pro-tumor. Whether SIRT1 promotes or prevents cancer probably depends on the situation.

Scientists at the Buck Institute for Age Research have identified a protein that plays a key role in the life-extending effects of calorie restriction.

Press release follows:

Buck scientists identify a key protein that may explain the anti-aging and anti-cancer benefits of dietary restriction

Novato, CA, May 21, 2009. A protein that plays a key role in tumor formation, oxygen metabolism and inflammation is involved in a pathway that extends lifespan by dietary restriction. The finding, which appears in the May 22, 2009 edition of the on-line journal PLoS Genetics, provides a new understanding of how dietary restriction contributes to longevity and cancer prevention and gives scientists new targets for developing and testing drugs that could extend the healthy years of life.

The protein is HIF-1 (hypoxia-inducible factor 1). It helps cells survive by turning on when oxygen levels are low. HIF-1 is also active in some forms of human cancer. HIF-1 overexpression is frequently detected in solid tumors; inhibition of HIF-1 has been proved to be an efficient way to prevent cancer growth. Now, scientists at the Buck Institute for Age Research have shown that HIF-1 is also a key player in dietary restriction. HIF-1 is involved in a molecular pathway known to regulate cell growth and metabolism in response to nutrients and growth factors.

Previous studies on HIF-1 have mainly focused on its roles in oxygen metabolism and tumor development, said Buck faculty member Pankaj Kapahi, PhD, lead author of the study. Kapahi says the study encourages the investigation of HIF-1 in nutrient sensing pathways. The data in this study also points to HIF-1 as a likely target for regulating the protective effects of dietary restriction in mammals, said Kapahi. Dietary restriction is one of the most robust methods for extending lifespan and delaying age-related disease among various species.

Kapahi says the molecular mechanisms involved in how dietary restriction slows cancer and extends lifespan have been largely unknown. This study gets us closer to understanding that process and gives us better targets for both designing and testing drugs which could mimic the effects of dietary restriction in humans, said Kapahi.

The research involved nematode worms that were genetically altered to both under and over-express HIF-1. The animals, which are the most-often used model to study aging, were fed different diets. Animals that were designed to over-express HIF-1 did not get the benefit of lifespan extension even though their diets were restricted. Animals that under-expressed HIF-1 lived longer, even when they had a nutrient-rich diet. Furthermore, it was found that the lifespan extension resulting from dietary restriction required activity in signaling pathways in the endoplasmic reticulum, the part of the cell involved in processing and the proper folding of proteins. This finding supports the theory that aging stems from the effects of misfolded proteins and opens up a rich area of investigation to examine the mechanisms by which stress in the endoplasmic reticulum affects lifespan.

Contributors to this work:
Other Buck Institute researchers involved in the study include Di Chen, and Emma Lynn Thomas. The work was supported by the Ellison Medical Foundation, the Larry L. Hillblom Foundation, the American Federation for Aging Research, the Bill and Rita Haynes Foundation, and the National Institute on Aging.

About the Buck Institute:
The Buck Institute is the only freestanding institute in the United States that is devoted solely to basic research on aging and age-associated disease. The Institute is an independent nonprofit organization dedicated to extending the healthspan, the healthy years of each individuals life. The National Institute of Aging designated the Buck a Nathan Shock Center of Excellence in the Basic Biology of Aging, one of just five centers in the country. Buck Institute scientists work in an innovative, interdisciplinary setting to understand the mechanisms of aging and to discover new ways of detecting, preventing and treating conditions such as Alzheimers and Parkinsons disease, cancer and stroke. Collaborative research at the Institute is supported by new developments in genomics, proteomics and bioinformatics technology.

Press release from Tufts University School of Nutrition

BOSTON (May 18, 2009) Curcumin, the major polyphenol found in turmeric, appears to reduce weight gain in mice and suppress the growth of fat tissue in mice and cell models. Researchers at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University (USDA HNRCA) studied mice fed high fat diets supplemented with curcumin and cell cultures incubated with curcumin.

“Weight gain is the result of the growth and expansion of fat tissue, which cannot happen unless new blood vessels form, a process known as angiogenesis.” said senior author Mohsen Meydani, DVM, PhD, director of the Vascular Biology Laboratory at the USDA HNRCA. “Based on our data, curcumin appears to suppress angiogenic activity in the fat tissue of mice fed high fat diets.”

Meydani continued, “It is important to note, we don’t know whether these results can be replicated in humans because, to our knowledge, no studies have been done.”

Turmeric is known for providing flavor to curry. One of its components is curcumin, a type of phytochemical known as a polyphenol. Research findings suggest that phytochemicals, which are the chemicals found in plants, appear to help prevent disease. As the bioactive component of turmeric, curcumin is readily absorbed for use by the body.

Meydani and colleagues studied mice fed high fat diets for 12 weeks. The high fat diet of one group was supplemented with 500 mg of curcumin/ kg diet; the other group consumed no curcumin. Both groups ate the same amount of food, indicating curcumin did not affect appetite, but mice fed the curcumin supplemented diet did not gain as much weight as mice that were not fed curcumin.

“Curcumin appeared to be responsible for total lower body fat in the group that received supplementation,” said Meydani, who is also a professor at the Friedman School of Nutrition Science and Policy at Tufts. “In those mice, we observed a suppression of microvessel density in fat tissue, a sign of less blood vessel growth and thus less expansion of fat. We also found lower blood cholesterol levels and fat in the liver of those mice. In general, angiogenesis and an accumulation of lipids in fat cells contribute to fat tissue growth.”

Writing in the May 2009 issue of the Journal of Nutrition, the authors note similar results in cell cultures. Additionally, curcumin appeared to interfere with expression of two genes, which contributed to angiogenesis progression in both cell and rodent models.

“Again, based on this data, we have no way of telling whether curcumin could prevent fat tissue growth in humans.” Meydani said. “The mechanism or mechanisms by which curcumin appears to affect fat tissue must be investigated in a randomized, clinical trial involving humans.”

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This study was funded by a grant from the United States Department of Agriculture. Asma Ejaz, a graduate student who worked on this project received a scholarship grant from the Higher Education Commission of Pakistan.

Ejaz A, Wu, D, Kwan P, and Meydani M. Journal of Nutrition. May 2009; 139 (5): 1042-1048. “Curcumin Inhibits Adipogenesis in 3T3-L1 Adipocytes and Angiogenesis and Obesity in C57/BL Mice. 919-925.”

A little over a month ago I conducted a personal experiment where I took 25mg/day doxycycline hyclate in an effort to improve the quality of my skin by reducing collagen breakdown via the inhibition of Matrix-Metalloproteinases (MMPs).

For the duration of the experiment, I consumed approximately 25mg doxycycline in the morning on top of my usual stack of supplements. Unfortunately, due to laziness and lack of time, I don’t have any objective observational data of the effects (i.e., comparative photos taken under identical conditions), so I’ll instead talk about how things appeared. I wouldn’t normally be satisfied with such subjective measurement, but the outcome was so resoundingly bad that I don’t think it matters! :/

Initially, I was perplexed that an ulcer I developed in my mouth was seeming to take far longer than normal to heal; however, this may have something to do with my expectation that healing, especially of oral wounds, would be accelerated.

The one important factor that I intended to measure was if doxycycline supplementation would do anything to increase the production of collagen in the skin. As someone who has experienced the obvious and profound (and positive) effect of oral retinoids on skin texture and quality, I was somewhat disappointed in doxycycline’s effect. Not only was there no (subjective) reduction in the number, severity, or depth of the photo-aging induced wrinkles on my face, but the doxycycline appeared to be making the condition worse!

About two weeks into the experimental period, I was continually dismayed every time I looked into the mirror at what appeared to be a ‘thinning’ of the skin on my face, particularly noticeable on my forehead, as well as more noticeable wrinkles and an overall reduction in any remnants of the youthful glow that Father Time has yet to wrestle from me. Even within the short duration of the experiment, the skin on my face started to take on that ‘papery’ stiffness one associates with the skin of the elderly.

It really was difficult to persist with the regimen in the face of what I felt to be outright failure of my idea, but I did anyway.

About ten days after ceasing the medication, I already feel my skin has mostly regained its normal texture, but I can’t be sure because I didn’t carry out any real quantitative analysis. It has definitely reverted to its normal elasticity.

All in all, I recommend not employing doxycycline to improve the quality of one’s skin. As for why this happened, I can only speculate. If we assume that doxycycline does in fact inhibit the breakdown of collagen, I suppose it could have caused a ’stiffening’ of the skin, which then caused it to appear more wrinkly and deeply lined. The perceived reduction in facial subcutaneous fat my have just been my interpretation of the changed texture. Perhaps it skews the ratio of collagen to elastin, again resulting in a reduced elasticity of the skin.

Regardless, I seem to have discovered for myself why there is apparently no research taking place regarding doxycycline as a potential ‘cosmaceutical’!