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Another famous long-running study (Framingham Heart Study) finds more bad news for middle-aged coach-potatoes (that is, those who don't exercise or have poor physical fitness). It's an observational study (thus they found an association), but the finding is pretty damn convincing: that poor physical fitness (basically a sedentary life-style) may be linked to a smaller brain size (brain volume) 20 years later. The reason this is significant is because shrinking brain volume means that accelerated brain aging is occurring.

Researcher Nicole Spartano said: "Brain volume is one marker of brain aging. Our brains shrink as we age, and this atrophy is related to cognitive decline and increased risk for dementia. So, this study suggests that people with poor fitness have accelerated brain aging." Bottom line: if you don't get much exercise or lead a sedentary life-style, then increase your activity levels for hopefully better brain health decades later. Just getting out daily (or several times a week) and walking briskly would improve fitness. From Medical Xpress:

Couch potatoes may have smaller brains later in life

Poor physical fitness in middle age may be linked to a smaller brain size 20 years later, according to a study published in the February 10, 2016, online issue of Neurology, the medical journal of the American Academy of Neurology."We found a direct correlation in our study between poor fitness and brain volume decades later, which indicates accelerated brain aging," said study author Nicole Spartano, PhD, with Boston University School of Medicine in Boston.

For the study, 1,583 people enrolled in the Framingham Heart Study, with an average age of 40 and without dementia or heart disease, took a treadmill test. They took another one two decades later, along with MRI brain scans. The researchers also analyzed the results when they excluded participants who developed heart disease or started taking beta blockers to control blood pressure or heart problems; this group had 1,094 people. 

The participants had an average estimated exercise capacity of 39 mL/kg/min, which is also known as peak VO2, or the maximum amount of oxygen the body is capable of using in one minute. Exercise capacity was estimated using the length of time participants were able to exercise on the treadmill before their heart rate reached a certain level. For every eight units lower a person performed on the treadmill test, their brain volume two decades later was smaller, equivalent to two years of accelerated brain aging. When the people with heart disease or those taking beta blockers were excluded, every eight units of lower physical performance was associated with reductions of brain volume equal to one year of accelerated brain aging.

The study also showed that people whose blood pressure and heart rate went up at a higher rate during exercise also were more likely to have smaller brain volumes two decades later. Spartano said that people with poor physical fitness often have higher blood pressure and heart rate responses to low levels of exercise compared to people with better fitness. Spartano noted that the study is observational. It does not prove that poor physical fitness causes a loss of brain volume; it shows the association. (Link to study in journal Neurology.)

More evidence that traditional toys and books are superior to electronic toys in both verbal parent-child interactions and non-verbal interactions for young children. Parent-child verbal interactions are so important because they teach young children language, lay the groundwork for literacy skills, teach role-playing, teach emotional and social skills such as turn-taking and accepting others' leads. In other words, put down the electronic gadgets and go spend time talking and interacting with your young child with old style traditional toys and books. From Science Daily:

How does type of toy affect quantity, quality of language in infant playtime?

Electronic toys for infants that produce lights, words and songs were associated with decreased quantity and quality of language compared to playing with books or traditional toys such as a wooden puzzle, a shape-sorter and a set of rubber blocks, according to an article published online by JAMA Pediatrics.

Anna V. Sosa, Ph.D., of Northern Arizona University, Flagstaff, and colleagues conducted a controlled experiment involving 26 parent-infant pairs with children who were 10 to 16 months old. Researchers did not directly observe parent-infant play time because it was conducted in participants' homes. Audio recording equipment was used to pick up sound. Participants were given three sets of toys: electronic toys (a baby laptop, a talking farm and a baby cell phone); traditional toys (chunky wooden puzzle, shape-sorter and rubber blocks with pictures); and five board books with farm animal, shape or color themes.

While playing with electronic toys there were fewer adult words used, fewer conversational turns with verbal back-and-forth, fewer parental responses and less production of content-specific words than when playing with traditional toys or books. Children also vocalized less while playing with electronic toys than with books, according to the results.

Results also indicate that parents produced fewer words during play with traditional toys than while playing with books with infants. Parents also used less content-specific words when playing with traditional toys with their infants than when playing with books. The authors note results showed the largest and most consistent differences between electronic toys and books, followed by electronic toys and traditional toys.

"These results provide a basis for discouraging the purchase of electronic toys that are promoted as educational and are often quite expensive. These results add to the large body of evidence supporting the potential benefits of book reading with very young children. They also expand on this by demonstrating that play with traditional toys may result in communicative interactions that are as rich as those that occur during book reading. ... However, if the emphasis is on activities that promote a rich communicative interaction between parents and infants, both play with traditional toys and book reading can be promoted as language-facilitating activities while play with electronic toys should be discouraged," the study concludes.

EDITORIAL: "Electronic toys that make noises or light up are extremely effective at commanding children's attention by activating their orienting reflex. This primitive reflex compels the mind to focus on novel visual or auditory stimuli. The study by Sosa in this issue of JAMA Pediatrics suggests that they may do more than just command children's attention; they appear to reduce parent-child verbal interactions. Why does this matter? Conversational turns during play do more than teach children language. They lay the groundwork for literacy skills, teach role-playing, give parents a window into their child's developmental stage and struggles, and teach social skills such as turn-taking and accepting others' leads.

Verbal interactions of course are only part of the story. What is missing from this study is a sense of how nonverbal interactions, which are also an important source of social and emotional skills, varied by toy type," write Jenny S. Radesky, M.D., of the University of Michigan Medical School, Ann Arbor, and Dimitri A. Christakis, M.D., M.P.H., of Seattle Children's Hospital and a JAMA Pediatrics associate editor, in a related editorial.

A large study found that using antidepressants during the second or third trimester of pregnancy increases the risk that the child will have autism by 87%,  especially if the mother takes selective serotonin reuptake inhibitors (SSRIs). A drawback was that the study looked at associations rather than actual cause (which would have meant randomly assigning women to either treatment or no treatment - which is unethical). From Medical Xpress:

Taking antidepressants during pregnancy increases risk of autism by 87 percent

Using antidepressants during pregnancy greatly increases the risk of autism, Professor Anick Bérard of the University of Montreal and its affiliated CHU Sainte-Justine children's hospital revealed today. Prof. Bérard, an internationally renowned expert in the fields of pharmaceutical safety during pregnancy, came to her conclusions after reviewing data covering 145,456 pregnancies.

"The variety of causes of autism remain unclear, but studies have shown that both genetics and environment can play a role," she explained. "Our study has established that taking antidepressants during the second or third trimester of pregnancy almost doubles the risk that the child will be diagnosed with autism by age 7, especially if the mother takes selective serotonin reuptake inhibitors, often known by its acronym SSRIs." Her findings were published today in JAMA Pediatrics.

Bérard and her colleagues worked with data from the Quebec Pregnancy Cohort and studied 145,456 children between the time of their conception up to age ten. In addition to information about the mother's use of antidepressants and the child's eventual diagnosis of autism, the data included a wealth of details that enabled the team to tease out the specific impact of the antidepressant drugs. 

"We defined exposure to antidepressants as the mother having had one or more prescription for antidepressants filled during the second or third trimester of the pregnancy. This period was chosen as the infant's critical brain development occurs during this time," Prof. Bérard said. "Amongst all the children in the study, we then identified which children had been diagnosed with a form of autism by looking at hospital records indicating diagnosed childhood autism, atypical autism, Asperger's syndrome, or a pervasive developmental disorder. Finally, we looked for a statistical association between the two groups, and found a very significant one: an 87% increased risk." 

The findings are hugely important as six to ten percent of pregnant women are currently being treated for depression with antidepressants. In the current study, 1,054 children were diagnosed with autism (0.72% of the children in the study), on average at 4.5 years of age. Moreover, the prevalence of autism amongst children has increased from 4 in 10,000 children in 1966 to 100 in 10,000 today. While that increase can be attributed to both better detection and widening criteria for diagnosis, researchers believe that environmental factors are also playing a part.

"It is biologically plausible that anti-depressants are causing autism if used at the time of brain development in the womb, as serotonin is involved in numerous pre- and postnatal developmental processes, including cell division, the migration of neuros, cell differentiation and synaptogenesis - the creation of links between brain cells," Prof. Bérard explained. "Some classes of anti-depressants work by inhibiting serotonin (SSRIs and some other antidepressant classes), which will have a negative impact on the ability of the brain to fully develop and adapt in-utero".

New research showed that eight days after a concussion, the concussed athletes (football players) looked and felt like they had recovered (clinical recovery), but MRIs showed that there were still neurophysiological abnormalities (significant blood flow decrease) in their brains. They did not look at if and when the blood flow returned to normal, but that research also needs to be done.

It is very disturbing to look at both this research and also the finding that the off-season is not enough for high school football players to recover from the repeated hits (not concussions, but sub-concussive hits) that they receive during the football season (Nov. 24, 2015 post). Do student football players really know and understand the dangers to their brains from the repeated hits and also concussions that occur in football? From Medical Xpress:

Reduced blood flow seen in brain after clinical recovery of acute concussion

Some athletes who experience sports-related concussions have reduced blood flow in parts of their brains even after clinical recovery, according to a study presented today at the annual meeting of the Radiological Society of North America (RSNA). The results suggest a role for MRI in determining when to allow concussed athletes to return to competition.

Decisions to clear concussed athletes to return to action are typically based on symptoms and cognitive and neurological test results. However, there is increasing evidence that brain abnormalities persist beyond the point of clinical recovery after injury. To find out more, researchers from the Medical College of Wisconsin in Milwaukee studied concussed football players with arterial spin labeling, an advanced MRI method that detects blood flow in the brain.

Dr. Wang and colleagues studied 18 concussed players and 19 non-concussed players. They obtained MRI of the concussed players within 24 hours of the injury and a follow-up MRI eight days after the injury and compared results with those of the non-concussed players. Clinical assessments were obtained for both groups at each time point, as well as at the baseline before the football season.

The concussed players demonstrated significant impairment on clinical assessment at 24 hours post-injury, but returned to baseline levels at eight days. In contrast to clinical manifestation, the concussed players demonstrated a significant blood flow decrease at eight days relative to 24 hours post-injury, while the non-concussed players had no change in cerebral blood flow between the two time points.

"In eight days, the concussed athletes showed clinical recovery," Dr. Wang said. "However, MRI showed that even those in clinical recovery still had neurophysiological abnormalities. Neurons under such a state of physiologic stress function abnormally and may become more susceptible to second injury." "For years, we've relied on what athletes are telling us," Dr. McCrea said. "We need something more objective, and this technology may provide a greater measurement of recovery."

This past week there was discussion of the number of high school football players that die annually while playing football (at least 5). But the bigger risk - because it involves so many players - is the damage to brains that occurs from concussions and from just being hit in football. The response from football enthusiasts is that there are safeguards now - that football players don't play after a concussion until they "heal" (show no obvious symptoms). But do they really heal? And much of the damage is from repeated hits, without having a concussion (sub-concussive blows or hits), what about the damage from that?

This study found that repeated head hits in football can cause changes in brain chemistry and metabolism, even in high school players not diagnosed with concussions. And even after the lengthy off-season (somewhere between two and five months after the season has ended)—the majority of players are still showing that they had not fully recovered. The researchers also made it clear that 2 weeks is not enough time to heal from a concussion. Scary long-term implications - what is happening to brains that never truly heal from past seasons as the players start playing in the next season? From Futurity:

High School Football: Teen Brains Don't Heal During Offseason

Brain scans of high school football players taken before, during, and after the season raise concerns they don’t fully recover from repeated head hits. The researchers used an imaging technique called proton magnetic resonance spectroscopy (1H MRS) to study the brains of 25 high school football players and compared them to the brains of teenagers involved in non-contact sports. The findings suggest repeated head hits in football can cause changes in brain chemistry and metabolism, even in players not diagnosed with concussions. 

We are seeing damage not just to neurons, but also to the vasculature and glial cells in the brain,” says Eric Nauman, professor of mechanical engineering, basic medical sciences, and biomedical engineering at Purdue University. “I was particularly disturbed that when you get to the offseason—we are looking somewhere between two and five months after the season has ended—the majority of players are still showing that they had not fully recovered.”

The 1H MRS data provide details about the blood flow, metabolism, and chemistry of neurons and glial cells important for brain function. The data also revealed a “hypermetabolic response” during the preseason, as though the brain was trying to heal connections impaired from the previous season. “We found that in the preseason for the football players in our study, one part of the brain would be associating with about 100 other regions, which is much higher than the controls,” says Thomas Talavage,  professor of electrical and computer engineering and biomedical engineering and co-director of the Purdue MRI Facility.

“The brain is pretty amazing at covering up a lot of changes. Some of these kids have no outward symptoms, but we can see their brains have rewired themselves to skip around the parts that are affected.”

One of the research papers shows that knowing a player’s history of specific types of hits to the head makes it possible to accurately predict “deviant brain metabolism,” suggesting that sub-concussive blows can produce biochemical changes and potentially lead to neurological problems, which indicates a correlation between players taking the heaviest hits and brain chemistry changes.

The data shows that the neurons in the motor cortex region in the brains of football players produced about 50 percent less of the neurotransmitter glutamine compared to controls. “We are finding that the more hits you take, the more you change your brain chemistry, the more you change your brain’s ability to move blood to the right locations,” Nauman says.

“Recent proton magnetic resonance spectroscopy studies argue that the recommended two-week window of rest is insufficient for full metabolic recovery after concussion,” Nauman says. “Those returning to play prior to full recovery could incur a second concussion with symptoms and metabolic changes more lasting than the first.”

 Drink coffee daily -  3 to 5 cups of either regular or decaffeinated - and live longer by lowering your risk of premature death from cardiovascular disease, neurological disease, type 2 diabetes, and suicide. Yes, it was an observational study, but the results are similar to what other studies are finding. From Medical Xpress:

Moderate coffee drinking may lower risk of premature death

People who drink about three to five cups of coffee a day may be less likely to die prematurely from some illnesses than those who don't drink or drink less coffee, according to a new study by Harvard T.H. Chan School of Public Health researchers and colleagues. Drinkers of both caffeinated and decaffeinated coffee saw benefits, including a lower risk of death from cardiovascular disease, neurological diseases, type 2 diabetes, and suicide.

"Bioactive compounds in coffee reduce insulin resistance and systematic inflammation," said first author Ming Ding, a doctoral student in the Department of Nutrition. "That could explain some of our findings. However, more studies are needed to investigate the biological mechanisms producing these effects."

Researchers analyzed health data gathered from participants in three large ongoing studies: 74,890 women in the Nurses' Health Study; 93,054 women in the Nurses' Health Study 2; and 40,557 men in the Health Professionals Follow-up Study. Coffee drinking was assessed using validated food questionnaires every four years over about 30 years. During the study period, 19,524 women and 12,432 men died from a range of causes.

In the whole study population, moderate coffee consumption was associated with reduced risk of death from cardiovascular disease, diabetes, neurological diseases such as Parkinson's disease, and suicide. Coffee consumption was not associated with cancer deaths. The analyses took into consideration potential confounding factors such as smoking, body mass index, physical activity, alcohol consumption, and other dietary factors.

Could this be? Fungal infection being the cause of Alzheimer's disease? Noteworthy from a recent study conducted in Spain: all the Alzheimer's disease (AD) patients had evidence of fungal infections in their brains, central nervous systems, and vascular systems, but none were found in the control subjects (those without Alzheimer's disease). Many of the symptoms of AD (such as inflammation of the central nervous system and activation of the immune system) match those with long-lasting fungal infections. A "microbial cause" has long been suggested as a cause of AD, and interestingly other studies have also found fungal infections in AD patients. The research so far has found several fungal species in AD patients (including Candida albicans). The researchers mention that in one study anti-fungal treatment reversed clinical symptoms of AD in 2 patients (but it was written off  as misdiagnosis).

Another possibility that immediately occurs to  explain the findings is that perhaps Alzheimer's disease somehow results in fungal infections - that the AD makes them more prone to fungal infection. In case you're wondering - all the AD patients and control patients studied had died - this is why their brain tissue could be studied so thoroughly. Excerpts from a research article by D. Pisa et al in Nature:

Different Brain Regions are Infected with Fungi in Alzheimer’s Disease

The possibility that Alzheimer’s disease (AD) has a microbial aetiology has been proposed by several researchers. Here, we provide evidence that tissue from the central nervous system (CNS) of AD patients contain fungal cells and hyphae. Fungal material can be detected both intra- and extracellularly using specific antibodies against several fungi. Different brain regions including external frontal cortex, cerebellar hemisphere, entorhinal cortex/hippocampus and choroid plexus contain fungal material, which is absent in brain tissue from control individuals. Analysis of brain sections from ten additional AD patients reveals that all are infected with fungi. Fungal infection is also observed in blood vessels, which may explain the vascular pathology frequently detected in AD patients. Sequencing of fungal DNA extracted from frozen CNS samples identifies several fungal species. Collectively, our findings provide compelling evidence for the existence of fungal infection in the CNS from AD patients, but not in control individuals.  ...continue reading "Fungal Infections Involved in Alzheimer’s Disease?"

Another study providing evidence that the Mediterranean diet is good for the brain. In elderly dementia-free adults (mean age 80 years) - those that generally followed a Mediterranean diet (higher adherence) had a larger brain volume than those not following the Mediterranean diet, as well as more total gray and white matter volume.The difference between the groups is equal to about 5 years of aging.

Having "higher adherence to the Mediterranean diet" in the study meant higher consumption of healthy foods or lower consumption of unhealthy foods. The Mediterranean diet stresses a  high intake of vegetables, legumes, fruits, whole grains, fish, olive oil, and low intake of saturated fatty acids, dairy products, meat, and poultry; and mild to moderate amounts of alcohol. Specifically: Higher fish intake (at least 3 to 5 oz. weekly) and lower meat intake (no more than 3.5 oz. daily) correlated with greater total gray matter volume. Higher fish intake was also associated with "greater mean cortical thickness". From Medical Xpress:

Mediterranean diet may keep your mind healthier in old age

In news that sounds a bit like it came straight from a sci-fi thriller, researchers say that eating too much meat might shrink your brain. On the flip sid e, however, eating healthy foods from the so-called Mediterranean diet may help your brain stay in good shape as you get older, the new study suggests. The researchers said that people over 65 who ate more fish, vegetables, fruit, grains and olive oil had a larger brain volume than a similar group who didn't follow a Mediterranean diet.

"It was encouraging to see that the more you adhere to this Mediterranean diet, the more protection you get against brain atrophy [shrinkage]," said study author Yian Gu, an assistant professor of neuropsychology at Columbia University in New York City. .... But Gu noted that her study's observational findings cannot prove a definitive cause-and-effect relationship between diet and brain volume. The study was only designed to find an association.

Previous research has linked the Mediterranean diet to a lower risk of Alzheimer's disease, the study said. The diet stresses the consumption of vegetables, legumes (beans, peas and lentils), fruits, cereals, fish and monounsaturated fats such as olive oil, the study authors said. The eating plan also includes a low intake of meat, poultry, saturated fats and dairy products, as well as mild to moderate amounts of alcohol, according to the researchers.

For the study, Gu and her colleagues split 674 adults into two groups based on how closely their diets aligned with the Mediterranean diet. Their average age was 80 years. All participants underwent MRI scans of their brains to measure total brain volume and thickness. They also completed questionnaires about their food choices and eating patterns.

The researchers found that brain volumes of those who didn't follow a Mediterranean diet were smaller than those who did. The difference was minor in overall size—equated to about five years of aging, the study authors said. But, more specifically, the investigators found that eating more fish and less meat was associated with even less brain shrinkage. Using the study findings, Gu contended that eating at least 3 to 5 ounces of fish weekly, or no more than 3.5 ounces of meat each day, could protect the brain from shrinkage. She acknowledged that study participants may have inaccurately recalled their food consumption habits in the questionnaires used.

Over and over studies find that a person's diet is linked to health and diseases, and now a study finds that an unhealthy diet is linked to shrinkage of the brain, specifically the volume of the left hippocampus. The biggest effects on the hippocampus are found with both greater consumption of an unhealthy diet and lower consumption of a healthy diet.  The hippocampus is a brain structure associated with both learning and memory, as well as mood regulation, and is specifically implicated in depression. In dementia and Alzheimer's disease, the hippocampus is one of the first regions of the brain to suffer damage.

So....you want to protect your hippocampus from shrinkage. The researchers themselves  suggest that the effects may be reversible, and suggest "dietary interventions to promote hippocampal health". Once again, a healthy diet means lots of plant-based foods (for example, a Mediterranean based diet with lots of fruits, vegetables, legumes, nuts, berries, seeds), and decreasing a Western-style diet with highly processed foods, low fiber, lots of meat, fat,  and refined sugars. From Medscape:

Unhealthy Diet May Shrink the Brain

Consumption of an unhealthy Western diet characterized by meat, hamburgers, chips, and soft drinks, may reduce the volume of the left hippocampus, whereas a healthy diet of fresh vegetables and fish may increase hippocampal volume. In a study of more than 250 individuals, investigators found that during a period of 4 years, there was a difference of more than 200 cubic millimeters in hippocampal volume between individuals who ate a healthy diet and those who consumed an unhealthy diet.  ...continue reading "Shrink Your Brain With An Unhealthy Diet"

New research has found that low vitamin D levels among older adults is associated with accelerated cognitive decline and impaired performance (particularly in areas of memory and executive function). The next research in this area will have to look at whether vitamin D supplementation will change (slow down) the decline. Please note that it is widely accepted that an average daily intake of 1000 IU  of D3 daily is safe. The best source of  vitamin D is sunlight. From Science Daily:

Low vitamin D among elderly associated with decline in cognition, dementia

Vitamin D insufficiency among the elderly is highly correlated with accelerated cognitive decline and impaired performance, particularly in domains such as memory loss that are associated with Alzheimer's disease and dementia, researchers with the UC Davis Alzheimer's Disease Center and Rutgers University have found. The effect is "substantial," with individuals with low vitamin D declining at a rate three times faster than those with adequate vitamin D levels

The researchers said their findings amplify the importance of identifying vitamin D insufficiency among the elderly, particularly high-risk groups such as African-Americans and Hispanics, who are less able to absorb the nutrient from its most plentiful source: sunshine. Among those groups and other darker-skinned individuals, low vitamin D should be considered a risk factor for dementia, they said. "Independent of race or ethnicity, baseline cognitive abilities and a host of other risk factors, vitamin D insufficiency was associated with significantly faster declines in both episodic memory and executive function performance," said Joshua Miller...

The large, longitudinal study was conducted in nearly 400 racially and ethnically diverse men and women in Northern California participating in longitudinal research at the Alzheimer's Disease Center in Sacramento, Calif. Fifty percent of participants were Caucasian and 50 percent were African-American or Hispanic. The participants had a mean age of 76 and were either cognitively normal, had mild cognitive impairment, or dementia.The participants' serum vitamin D status was measured at the beginning of the study.... Overall, 26 percent were deficient and 35 percent were insufficient. Among Caucasians, 54 percent had low vitamin D, compared with 70 percent of African-Americans and Hispanics.

Over five years of follow-up, vitamin D deficient individuals experienced cognitive declines that were two-to-three times faster than those with adequate serum vitamin D levels. In other words it took only two years for the deficient individuals to decline as much as their counterparts with adequate Vitamin D declined during the five-year follow-up period.

Exposing the skin to sunlight is the major source of vitamin D. Racial and some ethnic minorities are at greater risk of low vitamin D because the higher concentration of melanin that makes their skin darker -- and protects against skin cancer in sunny climates -- also inhibits synthesis of vitamin D. Diet is the other major source of vitamin D. Dietary vitamin D is obtained particularly through dairy consumption. The intake of dairy products is especially low among minority groups, with only 6.5 percent of African-Americans and 11 percent of Mexican-Americans nationwide consuming the recommended three daily servings of dairy products, the study says.