Traumatic Brain Injury and Accelerated Alzheimer’s

This is the Medscape Neurology Minute. I am Dr. Alan Jacobs. There are thought to be epidemiologic and pathophysiologic links between traumatic brain injury (TBI) and Alzheimer disease. Amyloid plaques have been found in the brains of up to 30% of patients who died at any age in the acute phase of a TBI. Now, researchers from the University of Cambridge, England, have published a study in JAMA Neurology [1] in which they performed PET using Pittsburgh Compound B (PiB), a marker of brain amyloid deposition in 15 patients with TBI and 11 healthy control individuals. The patients with TBI were recruited after a maximum of 1 year after injury. They validated their findings using autopsy-acquired brain tissue from 16 TBI victims and 17 patients with nonneurologic causes of death. The results showed that compared with the controls, the patients with TBI showed significantly increased PiB binding throughout the cortical gray matter and the striatum. In the autopsy tissue samples, they found PiB binding in the neocortical gray matter in the same regions where amyloid deposition was demonstrated by immunohistochemistry, thus validating the specificity of the PiB signal to amyloid. The investigators concluded that the use of PiB PET for amyloid imaging following TBI provides the potential for understanding the pathophysiology of TBI, for characterizing the mechanistic drivers of disease progression or suboptimal recovery in the subacute phase of TBI, and for identifying patients at high risk for accelerated Alzheimer disease and for evaluating the potential of antiamyloid therapy. This has been the Medscape Neurology Minute. I’m Dr. Alan Jacobs.

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By Dr. Alan Jacobs –

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Alzheimer’s Is Expensive, Deadly and Growing. So Where’s the Research Money?


Sitting before a mostly absent Senate committee in February, actor Seth Rogen sought to draw attention to an as yet incurable disease that is quietly killing millions of Americans and, perhaps worse, reducing their final years to a harrowing ordeal for both them and their families. He had come to Washington, D.C., to talk about Alzheimer’s.

Rogen, known more for his vulgar comedy and stoner persona than his activism, had a personal reason for testifying. In 2006, his mother-in-law was diagnosed with early-onset Alzheimer’s at 55. At first he thought this meant a future of lost keys and mismatched shoes. A few years later, the family faced “the real, ugly truth of the disease,” Rogen testified. “After forgetting who she and her loved ones were, my mother-in-law, a teacher for 35 years, then forgot how to speak, feed herself, dress herself and go to the bathroom herself—all by the age of 60.”

An estimated 5.2 million Americans have Alzheimer’s, and there is no treatment that prevents, slows, stops or reverses it. If doctors don’t find a cure, the future is grim: By 2025, the number of people age 65 and older with Alzheimer’s is expected to grow by 40 percent to 7.1 million Americans, according to the Alzheimer’s Association‘s 2014 Alzheimer’s Disease Facts and Figures report. Americans are living longer than ever before, many well into their 80s and 90s. With advanced age the number one risk factor for Alzheimer’s, there could be as many as 16 million Americans with Alzheimer’s in 2050, costing $1.2 trillion in health care, long-term care and hospice care.

“The situation is so dire that it caused me, a lazy, self-involved, generally self-medicated man-child, to start an entire charity organization,” Rogen told the few senators who had bothered to show up, referring to Hilarity for Charity, which raises money to support Alzheimer’s research and help families.

“Americans whisper the word Alzheimer’s because their government whispers the word Alzheimer’s,” he added. Later, Rogen blasted the absent senators,tweeting, “Not sure why only two senators were at the hearing. Very symbolic of how the government views Alzheimer’s. Seems to be a low priority.”


“The epidemic is upon us,” says Dr. John Trojanowski, co-director of the Center for Neurodegenerative Disease Research and director of the Institute on Aging, both at the University of Pennsylvania School of Medicine. “It’s a very difficult thing to say to a patient that there’s nothing we have for you, but that is the honest response. There are no disease-modifying therapies for Alzheimer’s.”

Alzheimer’s is one of the costliest chronic diseases to the country. Total costs of caring for Americans with Alzheimer’s and other dementias is expected to reach $214 billion this year, with Medicare and Medicaid covering $150 billion and out-of-pocket expenses reaching $36 billion.

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By Abigail Jones –

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Anesthesia, Surgery May Double Dementia Risk

Anesthesia and surgery significantly increase the risk for dementia, new research suggests.

A large population-based study conducted by investigators at the Neurological Institute in Taipei Veterans General Hospital, in Taipei City, Republic of China, showed that the risk of developing dementia nearly doubled within 3 to 7 years of anesthesia and surgery. In addition, the average time to dementia diagnosis was shorter in patients who had anesthesia and surgery compared with their counterparts who did not undergo these procedures.

The study adds to “growing concerns that anesthetic agents may have neurodegenerative complications,” study investigator Jong-Ling Fuh, MD, of the Neurological Institute, told Medscape Medical News.

“In vitro and animal studies showed that inhaled anesthetic drugs can promote amyloid beta oligomerization and impair memory. However, it remains controversial whether anesthesia and surgery contribute to the development of dementia in human studies,” she said.

“This population-based study provides statistically sound evidence for the association of dementia with anesthesia and surgery. Our findings support the view that patients who undergo anesthesia and surgery may be at increased risk of dementia.”

“Although we do not know how to mitigate the risk of dementia after anesthesia and surgery at this point, physicians and surgeons should be more vigilant about the possible development of long-term cognitive decline postoperatively in patients who have undergone anesthesia and surgery,” Dr. Fuh added.

The study was published in the March issue of the British Journal of Psychiatry.

Need for More Research

Using the Taiwan National Health Insurance Research Database, Dr. Fuh and colleagues extracted the records of 24,901 patients aged 50 years and older who underwent anesthesia for surgery between 2004 and 2007, and a control group of 110,972 randomly selected individuals matched for age and sex. They excluded anyone with a history of cancer, dementia, Parkinsonism, stroke, or brain operations.

During 3 to 7 years of follow-up, 661 patients in the anesthesia group (2.65%) and 1539 in the control group (1.39%) were diagnosed with dementia. Alzheimer’s disease accounted for the majority of these cases.

Dementia occurred sooner in the anesthesia group (mean 907 days) than in the control group (mean, 1104 days; P < .0001).

After adjusting for hypertension, hyperlipidemia, depression, and Charlson index, patients who underwent anesthesia and surgery had an estimated 1.99-fold increased risk of developing dementia (95% confidence interval [CI], 1.81 – 2.17; P < .001). The risk for dementia after anesthesia was increased similarly in men and women.

The risk was greatest with regional anesthesia (adjusted hazard ratio [HR], 1.80; 95% CI, 1.57 – 2.07), followed by intravenous/intramuscular anesthesia (HR, 1.60; 95% CI, 1.11 – 2.30) and general anesthesia (HR, 1.46; 95% CI, 1.28 – 1.68).

Of the 8 types of surgery, 5 were associated with an increased risk for dementia (dermatologic, musculoskeletal, genitourinary, digestive, and eye surgery). Ear, nose, and throat (ENT), respiratory, and cardiovascular surgery was not associated with increased dementia risk.

Dr. Fuh said “caution must be exercised in asserting causality between development of dementia and anesthesia-associated neurotoxicity. More clinical studies are needed to investigate the association and causality between anesthesia with surgery and subsequent dementia.”

Red Flags and Caveats

Commenting on the findings for Medscape Medical News, Roderic G. Eckenhoff, MD, professor and vice-chair of research, Department of Anesthesia and Critical Care, University of Pennsylvania in Philadelphia, who was not involved in the study, said that sometimes surgery is necessary, but in cases of elective surgery, patients may want to think twice.

However, he cautioned that the study has some “big red flags” and said this “is an area in need of further clarification.”

“If it’s surgery, is it the actual surgery, or the anesthesia, or is it the stress of being in the hospital? It’s probably all those things combined, but it’s probably the surgical procedure itself that causes the largest risk, at least that’s what we believe,” Dr. Eckenhoff said.

“This is a good additional study, and its real strength is its size,” Dr. Eckenhoff said.

“Even when corrected for comorbidity, they found a significant effect of having had surgery in the past and risk for dementia. The level of risk is about consistent with some of the other studies performed,” he noted.

What’s “very concerning,” he said, is that the demographics and comorbidity are “significantly different” in the surgery group and the control group, “although they did try to correct for that.”

Still, “a big red flag and qualifier with this study is that the patients needing surgery are in fact different than the patients who don’t need surgery. It may be those differences and not the fact that they had surgery itself that account for the difference in propensity for getting dementia,” Dr. Eckenhoff said.

“I think in the end we are going to find that there are small populations of people that are more vulnerable to another insult like surgery and who go downhill more quickly afterwards. The challenge is to figure out who those people are, and that’s going to require really good biomarkers,” said Dr. Eckenhoff.

The study was supported by Taipei Veterans General Hospital and other noncommercial entities. The authors have disclosed no relevant financial relationships.

Br J Psychiatry. 2014;204:188-193. Abstract

By Megan Brooks –

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New study ranks Alzheimer’s as third-leading cause of death, after heart disease and cancer

Alzheimer’s disease likely plays a much larger role in the deaths of older Americans than is reported, according to a new study that says the disease may be the third-leading cause of death in the United States.

The Centers for Disease Control and Prevention lists Alzheimer’s as the sixth-leading cause of death, far below heart disease and cancer. But the new report, published Wednesday in the medical journal of the American Academy of Neurology, suggests that the current system of relying on death certificates for causes misses the complexity of dying for many older people and underestimates the impact of Alzheimer’s.


While the CDC attributed about 84,000 deaths in 2010 to Alzheimer’s, the report estimated that number to be 503,400 among people 75 and older. That puts it in a close third place, behind heart disease and cancer, and well above chronic lung disease, stroke and accidents, which rank third, fourth and fifth.

Alzheimer’s is somewhat of a sleeping giant compared with other leading killers that have received more funding over the years. While deaths from these diseases have been going down thanks to better treatment and prevention, the number of people suffering from Alzheimer’s is quickly rising and the disease is always fatal.

More than 5 million people in the United States are estimated to have Alzheimer’s. With the aging of the baby-boom generation, this number is expected to nearly triple by 2050 if there are no significant medical breakthroughs, according to the Alzheimer’s Association.

The disease cost the nation $210 billion last year; that rate is expected to rise to $1.2 trillion by 2050.

“Scientists told us we need $2 billion a year over the coming 10 years” to see significant advancement in treatment and prevention, said Keith Fargo, director of Scientific Programs and Outreach at the Alzheimer’s Association. Funding by the National Institutes of Health for Alzheimer’s in 2012 was about $500 million, far below funding for heart disease and cancers. The estimated funding in 2013 was $484 million.

“We would like to see a response that is commensurate with the problem,” Fargo said. “Alzheimer’s disease is a serious disease and it needs to be taken seriously, and if we have the right kind of investment as a country, then we will be able to make strides similar to what we’ve made in heart disease, HIV and cancer.”

For the study, researchers at Rush Alzheimer’s Disease Center in Chicago followed 2,566 people 65 and older for an average of eight years, testing them annually for Alzheimer’s-type dementia and observing the risk of death in those who did and did not receive a clinical diagnosis of the disease.

But death certificates for many with Alzheimer’s often listed a more immediate reason for death, leading to a severe underreporting of the disease as an underlying cause, said Bryan James, the report’s lead author and an epidemiologist at the center. The study was funded by the National Institute on Aging and the Illinois Department of Public Health.

“Death certificates may not be the best way to measure how many people die from something that takes up to 10 years” to break down a person’s system, he said, adding that the disease leaves people more vulnerable to dying from infections and other problems. “We’re not saying they didn’t die of those things; we’re just saying, ‘Well, what put them in the hospital with that condition?’ ”

For example, if Alzheimer’s compromises one’s ability to swallow and results in food repeatedly going down the windpipe, that can leave a person more vulnerable to dying of pneumonia, he said.

“Trying to identify a single cause of death in elderly people is often not reflective of the real situation,” James said.

The idea that Alzheimer’s causes many more deaths is not new among experts, but the scope of the undercount is striking, said Dallas Anderson, science administrator for population studies of Alzheimer’s at the National Institute on Aging.

“Anybody who has somewhat of a knowledge of the disease registration system in the U.S. would not be surprised that there was an undercount; the surprising thing is how much of an undercount,” he said, adding that while earlier studies have had similar findings, this is the first peer-reviewed study to produce them.

“It’s shocking,” he said, “and it’ll be interesting to see how it plays out. . . . It would be nice if we could actually improve our death registration system.”

President Obama’s budget for fiscal 2015 included $100 million for an initiative to map the human brain to better understand diseases including Alzheimer’s.

But many in the field think Alzheimer’s should receive more funding.

“The disease is still very underfunded in comparison to other diseases,” James said. “Cancer has about 10 times the amount of funding, and only about three times as many people have cancer.”

Alzheimer’s is not always taken as seriously as other diseases, which may contribute to the historical lack of funding, Fargo said. “There are many people who still think of Alzheimer’s disease as just a memory problem — you forgot where you left your keys. But currently, Alzheimer’s is a universally fatal brain disease that has kind of fallen by the radar.”

By , The Washington Post

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Elevated Serum Pesticide Levels and Risk for Alzheimer Disease

Jason R. Richardson, PhD1,2; Ananya Roy, ScD2; Stuart L. Shalat, ScD1,2; Richard T. von Stein, PhD2; Muhammad M. Hossain, PhD1,2; Brian Buckley, PhD2; Marla Gearing, PhD4; Allan I. Levey, MD, PhD3; Dwight C. German, PhD5


Importance  The causes of late-onset Alzheimer disease (AD) are not yet understood but likely include a combination of genetic, environmental, and lifestyle factors. Limited epidemiological studies suggest that occupational pesticide exposures are associated with AD. Previously, we reported that serum levels of dichlorodiphenyldichloroethylene (DDE), the metabolite of the pesticide dichlorodiphenyltrichloroethane (DDT), were elevated in a small number of patients with AD (n=20).

Objective  To evaluate the association between serum levels of DDE and AD and whether the apolipoprotein E (APOE) genotype modifies the association.

Design, Setting, and Participants  A case-control study consisting of existing samples from patients with AD and control participants from the Emory University Alzheimer’s Disease Research Center and the University of Texas Southwestern Medical School’s Alzheimer’s Disease Center. Serum levels of DDE were measured in 79 control and 86 AD cases.

Main Outcomes and Measures  Serum DDE levels, AD diagnosis, severity of AD measured by the Mini-Mental State Examination score, and interaction with APOE4 status.

Results  Levels of DDE were 3.8-fold higher in the serum of those with AD (mean [SEM], 2.64 [0.35] ng/mg cholesterol) when compared with control participants (mean [SEM], 0.69 [0.1] ng/mg cholesterol; P < .001). The highest tertile of DDE levels was associated with an odds ratio of 4.18 for increased risk for AD (95% CI, 2.54-5.82; P < .001) and lower Mini-Mental State Examination scores (−1.605; range, −3.095 to −0.114; P < .0001). The Mini-Mental State Examination scores in the highest tertile of DDE were −1.753 points lower in the subpopulation carrying an APOE ε4 allele compared with those carrying an APOE ε3 allele (P interaction = .04). Serum levels of DDE were highly correlated with brain levels of DDE (ρ = 0.95). Exposure of human neuroblastoma cells to DDT or DDE increased levels of amyloid precursor protein.

Conclusions and Relevance  Elevated serum DDE levels are associated with an increased risk for AD and carriers of an APOE4 ε4 allele may be more susceptible to the effects of DDE. Both DDT and DDE increase amyloid precursor protein levels, providing mechanistic plausibility for the association of DDE exposure with AD. Identifying people who have elevated levels of DDE and carry an APOE ε4 allele may lead to early identification of some cases of AD.

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By JAMA Neurology

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Blood test predicts Alzheimer’s disease

(CNN) — In a first-of-its-kind study, researchers have developed a blood test for Alzheimer’s disease that predicts with astonishing accuracy whether a healthy person will develop the disease.

Though much work still needs to be done, it is hoped the test will someday be available in doctors’ offices, since the only methods for predicting Alzheimer’s right now, such as PET scans and spinal taps, are expensive, impractical, often unreliable and sometimes risky.

This is a potential game-changer,” said Dr. Howard Federoff, senior author of the report and a neurologist at Georgetown University Medical Center. “My level of enthusiasm is very high.”

The study was published in Nature Medicine.

‘We were surprised’

In the beginning, the researchers knew they wanted to find a blood test to detect Alzheimer’s but didn’t know what specifically to look for. Should they examine patients’ DNA? Their RNA? Or should they look for the byproducts of DNA and RNA, such as fats and proteins?

They decided to start with fats, since it was the easiest and least expensive. They drew blood from hundreds of healthy people over age 70 living near Rochester, New York, and Irvine, California. Five years later, 28 of the seniors had developed Alzheimer’s disease or the mild cognitive problems that usually precede it.

Scouring more than 100 fats, or lipids, for what might set this group apart, they found that these 28 seniors had low levels of 10 particular lipids, compared with healthy seniors.

To confirm their findings, the researchers then looked at the blood of 54 other patients who had Alzheimer’s or mild cognitive impairment. This group also had low levels of the lipids.

Overall, the blood test predicted who would get Alzheimer’s or mild cognitive impairment with over 90% accuracy.

“We were surprised,” said Mark Mapstone, a neuropsychologist at the University of Rochester Medical Center and lead author of the study. “But it turns out that it appears we were looking in the right place.”

Alzheimer’s risk before symptoms: Do you want to know?

The ‘holy grail’

The beauty of this test, Mapstone says, is that it caught Alzheimer’s before the patient even had symptoms, suggesting that the disease process begins long before people’s memories start failing. He says that perhaps the lipid levels started decreasing at the same time as brain cells started dying.

He and his team plan to try out this test in people in their 40s and 50s. If that works, he says, that would be the “holy grail,” because then researchers could try experimental drugs and treatments in a group that’s almost sure to get the disease. That would speed research along immensely.

Plus, people could get a heads up that they were probably destined to get Alzheimer’s. Although some people might not want to know that they’re destined for a horrible disease, others might be grateful for the warning.

Federoff said he would want to know whether he was on his way to getting the disease, even though there’s nothing he could do about it. He might want to take a family trip he’d been thinking about or might want to appoint a successor at work.

“I would make sure that things that are important to me get done,” he said.

But, Federoff added, others might not want to know they were about to get a devastating disease they were powerless to stop.

“I think it’s a very personal decision,” Federoff said. “It would have to be thought through on multiple dimensions. Patients and their families would have to be counseled.”

Next steps

Other research teams are looking at other possible tests for Alzheimer’s. The need for a screening test of some kind for Alzheimer’s has never been greater: A report released last weeksays the disease claims the lives of perhaps a half a million Americans, making it nearly as deadly as heart disease and cancer.

If any of these tests work out — and that’s still an if — it would take years to make it to doctors’ offices, since the test would need to be validated by other labs and with larger groups of people. Thee test developed by the Georgetown and Rochester researchers, for example, was used mainly in white people, and it might not work as well with other groups.

Heather Snyder, a spokeswoman for the Alzheimer’s Association, said the study was well done but much work is still needed.

“It’s an interesting paper. It’s an intriguing study. But it is very preliminary,” she said.

Overwhelming burden, cost of Alzheimer’s to triple, report says

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Brain Food: What to Avoid

Medscape’s 2-part Brain Food slideshow series looked at how what we eat can benefit the brain. From salmon cutting stroke risk to coffee curbing depression, the data are copious. But the past couple of years have seen countless studies also looking at how certain foods and dietary patterns can impair neurologic and psychiatric function.


Based primarily on Medscape Medical News coverage and expert opinion, this slideshow examines recent data on what foods we should potentially avoid in the interest of preserving our cognitive capacities, and fending off — or at least slowing — diseases of the brain.

Click on the link to see the full slideshow:

By Medscape

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Alzheimer’s, Parkinson’s groups team up for research

Three organizations will combine their efforts to look at common factors involved in diseases of Alzheimer’s and Parkinson’s.


Although people with the memory loss of Alzheimer’s disease and the physical problems of Parkinson’s disease look very different, a growing body of research suggests that their biological damage is quite similar.

To better understand those similarities — and why some people end up with one condition versus the other — three foundations that support research into the diseases are joining forces.

The Michael J. Fox Foundation for Parkinson’s Research, the Alzheimer’s Association and The W. Garfield Weston Foundation of Canada announced Wednesday that they will offer joint research grants to help unpack the similarities and differences between these degenerative diseases, which together affect 6 million Americans.

The biology of the two diseases look “much more similar than they do clinically and much more similar than we thought,” said Todd Sherer, CEO of the Michael J. Fox Foundation, named for the actor who launched it after being diagnosed with the disease.

Both diseases are caused by a buildup of proteins in the brain, and both show symptoms years if not decades after the disease process has begun. Inflammation is known to play a role in both. And in both conditions, there are medications that can improve symptoms, but none that affects the course of disease.

The hope is that by collaborating on research, scientists will gain insights that will lead to early diagnostics and better, more targeted treatments for both diseases, said Heather Snyder, director of medical and scientific relations for the Alzheimer’s Association.

Alzheimer’s is characterized

by memory loss, personality change, and a declining ability to plan or perform the functions of daily life. It usually strikes people in their 70s or 80s, though genetic mutations can lead to earlier onset. Striking more women than men, it is eventually fatal, with death often taking a decade or more.

Parkinson’s generally strikes earlier — usually in the 50s or 60s — is more likely to be diagnosed in men, and causes motor problems like tremors, rigidity and slowness, though it can also affect cognition, mood and sleep.

One recent study of people who had died from Alzheimer’s showed a buildup of proteins that are the hallmark of Parkinson’s, suggesting a closer connection between the two conditions than has been commonly appreciated.

It makes sense to collaborate now, Snyder and Sherer said, to take advantage of new, large data sets and biological sample collections in both diseases — t

he Parkinson’s Progression Markers Initiative and the Alzheimer’s Disease Neuroimaging Initiative.

“We have an incredible opportunity in these two diseases because of these large-scale studies,” Sherer said. “You now have this chance to fundamentally test hypotheses across the two diseases because the information and biological material exist, ready to go.”

Researchers can begin applying for the Biomarkers Across Neurodegenerative Disease grant funding as soon as Thursday.


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Culinary Culprits: Foods That May Harm the Brain

For all the attention paid to the negative effects poor dietary choices have on the body, the effects of diet on the brain are largely unexplored. However, emerging research is providing new insights to support the suggestion that food can have a profound influence on mental health and cognition.

From sugar and carbohydrates to fats and even, according to one controversial theory, whole grains, the list of dietary choices having potentially negative effects on the brain is growing by leaps and bounds.

And although the big caveat for the bulk of evidence is that most studies show an association with but not necessarily causation of mental health and cognitive deficits, many clinicians report seeing first-hand improvement in patients’ mental health outcomes with the tweaking of a diet to eliminate some of the most notorious culinary culprits.

“While we don’t want to send the message to patients that all they have to do is change their diet and their severe depression will be cured, I can say that I have absolutely seen dietary changes work to improve outcomes for a lot of patients, and there are a lot of reports of that,” said Drew Ramsey, MD, an assistant clinical professor of psychiatry at Columbia University College of Physicians and Surgeons in New York City.

Dr. Ramsey, the author of The Happiness Diet: A Nutritional Prescription for a Sharp Brain, Balanced Mood, and Lean, Energized Body (Rodale, 2011) and Fifty Shades of Kale (HarperWave, 2013), asserts that the role of diet, so strongly emphasized in general practice, is simply too commonly overlooked in mental health practice.

“If someone has a severe mental illness, it is very important to talk to them about diet,” he toldMedscape Medical News. For example, he said, if a patient has certain nutrient deficiencies, it will be difficult for any medications to help until such deficiencies are treated.

“Yet I know clinicians who simply never talk to their patients about food because they’re not taught to discuss the topic,” he added.

“But certainly that will change over the next decade with the data that’s coming out, including epidemiological data showing a clear signal that the risk of depression increases when you eat a diet of highly processed modern food.”

“Junk Food”

In some of the strongest data along these lines, researchers led by Felice Jacka, PhD, of Deakin University, in Melbourne, Australia, have conducted a series of studies showing a poor diet to be associated with cognitive deficits.

In one longitudinal study of 2054 Australian adolescents, a diet consisting of “junk food,” ranging from chips, chocolates, and sweets to pizza and soda, was associated with a worsening of mental health status during a 2-year period ( PLoS One, published online September 21, 2011).

Another study of more than 23,020 women and children in the Norwegian Mother and Child Cohort Study showed that high consumption of junk foods during pregnancy and during the first 5 years of life predicted externalizing problems, such as aggression, hyperactivity, or tantrums, among children, independent of other confounding factors and of the childhood diet.

Children with unhealthy diets postnatally also were found to have had greater problems with externalizing as well as internalizing problems, such as worrying, sadness, and anxiety ( J Am Acad Child Adolesc Psychiatry, published online August 17, 2013).

And in a third study of 5731 adult and older men and women, the research team found a lower risk for depression among participants with better-quality diets, and increased anxiety was observed with a higher intake of processed and unhealthy foods ( Psychosomatic Medicine, 2011:73;483-490 ).

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Dairy foods and risk of stroke: A meta-analysis of prospective cohort studies


Background and aims

Epidemiological studies evaluating the association of dairy foods with risk of stroke have produced inconsistent results. We conducted a meta-analysis to summarize the evidence from prospective cohort studies regarding the association between dairy foods and risk of stroke.

Methods and results

Pertinent studies were identified by searching Embase (1950–November, 2013), Web of Knowledge (1950–November, 2013) and Pubmed (1945–November, 2013). Random-effect model was used to combine the results. Dose–response relationship was assessed by restricted cubic spline. Eighteen separate results from fifteen prospective cohort studies, with 28 138 stroke events among 764 635 participants, were included. Total dairy [relative risk (95% CI): 0.88 (0.82–0.94)], low-fat dairy [0.91 (0.85–0.97)], fermented milk [0.80 (0.71–0.89)] and cheese [0.94 (0.89–0.995)] were significantly associated with reduced risk of stroke, but whole/high-fat dairy, nonfermented milk, butter and cream were not significantly associated with risk of stroke. Stronger association was found for stroke mortality than incidence, and for studies conducted in Asia than Europe, while the association did not differ significantly by sex. Limited data did not find any significant association with either ischemic or hemorrhagic stroke. A non-linear dose–response relationship (P = 2.80*10−13) between milk and risk of stroke was found, and the relative risk of stroke was 0.88 (0.86–0.91), 0.82 (0.79–0.86), 0.83 (0.79–0.86), 0.85 (0.81–0.89), 0.86 (0.82–0.91), 0.91 (0.84–0.98) and 0.94 (0.86–1.02) for 100, 200, 300, 400, 500, 600 and 700 ml/day of milk, respectively.


Dairy foods might be inversely associated with the risk of stroke.


To read the full study:

By The NMCD (Nutrition, Metabolism, & Cardiovascular Deseases)

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