TIME diabetes

Having The Right Kind of Fat Can Protect Against Diabetes, Study Says

Brown tissue, also known as brown fat
Brown tissue, also known as brown fat Getty Images

People with more "brown fat" were better able to keep blood sugar under control and burn off fat stores

Not all fat is created equal, it seems. When we’re born, we have larger amounts of brown fat, so-called because it contains more dark mitochondria, the cell’s energy factories that pull in glucose and use it as fuel to drive cellular functions. Like a hard-working battery, however, brown fat releases heat as it performs its functions, which is helpful to keep newborn infants warm but gets less useful for adults as we’re better able to regulate our body temperature. So as we get older, this brown fat is gradually lost.

But in a report published in the journal Diabetes, scientists led by Labros Sidossis, professor of internal medicine at University of Texas Medical Branch at Galveston, found for the first time that adults who retained more amounts of brown fat were better able to keep blood sugar under control and burn off fat stores. Previous studies have linked brown fat to better weight control, but these results also hint that the tissue may be important for managing diabetes.

MORE: How Now, Brown Fat? Scientists Are Onto a New Way to Lose Weight

The researchers measured the brown fat in a small group of healthy men and also tracked how much energy they used while resting, how well they metabolized glucose, and their sensitivity to insulin, which breaks down and controls blood sugar. Because brown fat tends to be activated under cold temperatures, the scientists also measured these factors after the men sat at room temperature, and again after they sat at 65 degrees to 70 degrees F for five to eight hours.

The men who had higher amounts of brown fat – about 70g on average – increased their metabolic rate by 15%, meaning they burned more calories when they were exposed to slightly cooler temperatures, compared to the men with little or no brown fat. That alone, says Sidossis, contributed to burning 300 more calories for these men.

Those with higher brown fat were also able to break down more sugar, leading to less of it in their blood, something that hasn’t been shown before in human studies. If the subjects sat in the cooler room for 24 hours, the researchers found, that would lead to a reduction of 25g of sugar in the blood thanks to their brown fat alone. “That’s significant because if you consider people who have diabetes, they only have about 2g to 3g more sugar in the blood,” says Sidossis.

MORE: Study: Scientists Find a Way to Trigger Fat-Burning Fat

Interest in brown fat has exploded in recent years, and investigators found that adults retain more brown fat than previously thought, on either side of the base of the neck. Activating this fat store has become a popular area of research; so far, cold temperatures are the only reliable way to stimulate it, but others are exploring ways to transform white fat into brown fat. As of yet, experts haven’t found a reliable way to turn brown fat on or off in a reliable and metabolically useful way. Genetics may determine how much brown fat people are born with, but if early research is validated, it may also be possible to modify that amount, either with drugs or by transforming white fat.

MORE: Turn Down the Thermostat, Drop a Few Pounds?

If the results of the current study are confirmed, the need to do so might become more urgent. “Our data suggest that brown fat may function as both anti-obesity and anti-diabetic tissue in humans,” says Sidossis. “And that makes it a therapeutic target in the battle against obesity and chronic disease. Anything that helps in this area, we need to pursue and make sure that if there is potential there, we exploit it.”

TIME Mental Illness

Schizophrenia Linked to 108 Genes

In a groundbreaking study, researchers reveal a host of new genes involved in schizophrenia, making it possible to develop desperately needed treatments

It took 80,000 genetic samples, seven years and the work of 300 scientists from around the world, but scientists now have the most complete dossier on schizophrenia ever.

In an historic paper published in the journal Nature, the Schizophrenia Working Group of the Psychiatric Genomics Consortium identified 108 new regions on the genome linked to the psychiatric disorder, which is associated with hallucinations and psychotic episodes and affects about 1% of people worldwide.

The genetic clues are the most dramatic hints that experts have gotten so far about what causes that mental illness. Schizophrenia has had a rocky history in the psychiatric community, with some doctors early on not even recognizing it as a disorder, and others debating whether its origins were biological or caused by traumatic events or other experiences. Now, by comparing the genomes of people with and without the disorder, it’s clear that at least some of the psychotic symptoms can be traced to changes in the genes.

“For the first time, we are starting to see the underlying biological basis of the disease, and that can lay the foundation for understanding the disorder, and eventually developing treatments,” said Eric Lander, founding director of the Broad Institute of MIT and Harvard, where about one third of the DNA samples were sequenced.

MORE: Older Fathers Linked to Kids’ Autism and Schizophrenia Risk

The study used genome wide association, a technique that sequences the genomes of affected and unaffected individuals, and then compares where they differ. Those DNA differences may be hints about why people develop schizophrenia in the first place, and therefore lead to new drugs or treatments.

The 108 genetic regions aren’t all located in specific genes, nor is it known yet if this is what actually causes schizophrenia. But, like evidence at a crime scene, they may point to certain molecular pathways that are responsible for the mental illness. It’s already known that some of the identified regions, for example, are involved in how adaptable or plastic the brain is, and in regulating the immune system, a connection that experts have previously not investigated before. Other genes may also reveal new ways to potentially treat the disease, a significant improvement over the existing therapies, which only address one brain system, involving dopamine. “Thorazine was approved in 1954 as the first anti-psychotic medication, and every antipsychotic since then has relied on the same fundamental mechanism of action,” Steve Hyman, director of the Broad Institute’s Stanley Center for Psychiatric Research and professor of stem cell and regenerative biology at Harvard University said. “And their efficacy has plateaued since the 1960s.”

MORE: Most Common Psychiatric Disorders Share Genetic Roots

Having a greater suite of potential areas of inquiry, the researchers hope, will attract pharmaceutical companies back to the field of mental illness. “We now have more than 100 genes pointing to distinct pathways – calcium channels, glutamate, the immune system – this is concrete stuff, and it means that the pharmaceutical companies who left [this area of drug development] because they didn’t have anything concrete to work on, are beginning to get their toes in the water, and are thinking of jumping back in the water,” says Lander.

The genetic windfall can also help scientists piece together how genetic changes may work in tandem to cause symptoms of psychoses. They warn that these advances, and new treatments, may not come in the next year, but they may be able to provide better answers to questions about which drugs may work better in which patients, and in finding ways to detect and hold off symptoms of schizophrenia earlier, before they become debilitating. All of the genetic information released in the paper will be deposited in a public database for researchers to access and advance the understanding of the disorder.

TIME Diet/Nutrition

Yogurt Could Lower Your Blood Pressure: New Study

The latest study links certain probiotics with better blood pressure control

Bacteria aren’t the first allies we turn to for staying healthy – there are enough strains that can cause serious illness, after all – but there’s growing evidence that certain strains of the bugs can actually be good for your health, and may even relieve symptoms of inflammatory conditions, allergies and possibly even obesity.

In the latest report on these microbial allies, researchers add one more possible benefit of probiotics – the live concoctions of bacteria contained in foods like yogurt. In an analysis of nine studies that looked at probiotic use and blood pressure, the report in the journal Hypertension found that people using probiotics tend to have lower blood pressure compared to those who didn’t eat them. The effects seemed to be stronger among those with higher blood pressure to begin with, and among those consuming multiple probiotic strains and in higher doses.

What do bacteria have to do with blood pressure? The researchers say that the micro-organisms could be helping to address hypertension in a variety of ways, from lowering cholesterol levels, which can contribute to less fatty buildup in the vessels and therefore reduce the chances of developing hypertension, to controlling blood sugar and keeping the enzymes and proteins that control blood flow and fluid volumes in check.

The results aren’t exactly a prescription for treating hypertension — at least not yet. But they raise the interesting possibility of incorporating a probiotic regimen into blood pressure management. The study authors admit, however, that more questions still need to be answered, such as which micro-organisms might be associated with the strongest effect on blood pressure, as well as which combinations of bacterial strains work best. The formulation of the probiotic may also be important, they say – in the studies they reviewed, participants consumed probiotics primarily from yogurt, but also from cheese, sour milk and supplements (liquid or capsules). Hitting the right threshold of microbes also seems to be important, and figuring out that volume is also essential before any advice about using probiotics to lower blood pressure is given.

TIME HIV

Researchers Find New Way to Kick Out HIV From Infected Cells

Scanning electron micrograph of HIV-1
Scanning electron micrograph of HIV-1 Getty Images

The technique addresses the problem of hidden reservoirs of HIV in the body, and could herald a new way of battling the viral infection

Once HIV invades the body, it doesn’t want to leave. Every strategy that scientists have developed or are developing so far to fight the virus – from powerful anti-HIV drugs to promising vaccines that target it – suffers from the same weakness. None can ferret out every last virus in the body, and HIV has a tendency to hide out, remaining inert for years, until it flares up again to cause disease.

None, that is, until now. Kamel Khalili, director of the Comprehensive NeuroAIDS Center at Temple University School of Medicine, and his colleagues took advantage of a new gene editing technique to splice the virus out of the cells they infected – essentially returning them to their pre-infection state. The strategy relies on detecting and binding HIV-related genetic material, and therefore represents the first anti-HIV platform that could find even the dormant virus sequestered in immune cells.

MORE: Treatment as Prevention: How the New Way to Control HIV Came to Be

Even more encouraging, they also used the system to arm healthy cells from getting infected in the first place, by building genetic blockades that bounced off HIV’s genetic material. “It’s what we call a sterilizing cure,” says Khalili.

His work was done on human cells infected with HIV in cell culture, but, he believes the results are robust enough to move into animal trials and eventually into testing the idea in human patients.

The key to the strategy is the gene editing technique known as CRISPR, a way of precisely cutting DNA at pre-specified locations. CRISPR acts as a customizable pair of molecular scissors that can be programmed to find certain sequences of DNA and then, using an enzyme, make cuts at those locations. Because HIV is a retrovirus, its genetic material comes in the form of RNA; the virus co-opts a host cell’s genetic machinery to transform that RNA into DNA, which it then inserts into the cell’s genome. HIV’s genes, which it needs to survive, then get churned out by the cell.

MORE: David Ho: The Man Who Could Beat AIDS

Khalili designed a CRISPR that recognized the beginning and end of HIV’s DNA contribution, and then watched as the enzyme snipped out HIV from the cell’s genome. “I’ve been working with HIV almost since day 1 [of the epidemic] and we have developed a number of molecules that can suppress transcription or diminish replication of the virus. But I have never seen this level or eradication,” he says. “When you remove the viral genes from the chromosomes, basically you convert the cells to their pre-infection state.”

The advantage of the system lies in the fact that CRISPR can recognize viral genes wherever they are – in infected cells that are actively dividing, and in infected cells in which the virus is dormant. Current drug-based strategies can only target cells that are actively dividing and releasing more HIV, which is why they often lead to periods of undetectable virus but then cause levels of HIV to rise again. That’s the case with the Mississippi baby, who was born HIV positive and given powerful anti-HIV drugs hours after birth and appeared to be functionally cured of HIV when the virus couldn’t be detected for nearly four years, but then returned.

MORE: Rethinking HIV: After Five Years of Debate, a New Push for Prevention

Khalili admits that more work needs to be done to validate the strategy, and ensure that it’s safe. But it’s the start, he says, of a potential strategy for eradicating the virus from infected individuals. That may involve excising the virus as well as bombarding it with anti-HIV drugs. “We can get into cells, eradicate the viral genome, and that’s it,” he says.

TIME sexual abuse

Childhood Sexual Abuse Raises Heart Disease Risk In Adulthood

Researchers link early sexual abuse to greater risk of developing blocked heart arteries

Sexual and physical abuse during childhood can have long term effects on both mental and physical health, and previous studies have linked childhood sexual abuse to a greater risk of heart attack and other heart events—but it has been unclear exactly why. New research published Thursday in the journal Stroke adds to the case, showing thatwhether or not women had other risk factors for heart problems, a history of childhood sexual abuse remained a strong potential contributor to their atherosclerosis.

“What was a surprise was that when we controlled for [heart disease] risk factors, such as smoking and obesity, the association didn’t go away. We just couldn’t get rid of the association,” says Rebecca Thurston, director of the Womens’ Biobehavioral Health Laboratory at the University of Pittsburgh, who led the research with a team of colleagues.

MORE: Viewpoint: Why a Mandatory Child Abuse Reporting Law Could Backfire

More than 1,000 middle-aged women of various ethnic backgrounds from across the U.S. had yearly clinical exams beginning in 1996 for 12 years. At the end of the study, they also answered questions about sexual and physical abuse and had an ultrasound of their carotid arteries. About a quarter of the women reported being sexually abused as a child, and a similar percentage reported the experience as an adult.

When Thurston compared the women’s answers to their ultrasound, she found that those who reported childhood sexual abuse showed higher rates of plaque buildup in their arteries. They also had hearts and vessels that looked about two to three years older than those of women who hadn’t been abused.

MORE: Psychological Abuse: More Common, as Harmful as Other Child Maltreatment

Thurston’s findings suggest that whether or not the women had other risk factors for heart problems, their history of childhood sexual abuse remained a strong potential contributor to their atherosclerosis.

Thurston plans to continue the work by studying women who have had heart events – in this study, only women without heart disease were included – to see if the correlation still holds. She also wants to better understand how the early abuse affects women in later life. There is some evidence that traumatic experiences may change the stress response system in lasting, and possibly permanent ways.

While none of the women had signs of heart disease at the start of the study, Thurston says the results hint that physicians should be considering childhood experience, particularly traumatic ones, as part of comprehensive heart care for women. If the results are validated, then they might lead to ways of intervening with stress reduction or other psychological techniques to hopefully slow down the hardening of the arteries and lower their risk of heart disease.

TIME Breast Cancer

Removing Both Breasts May Not Improve Survival From Breast Cancer

The latest study adds support to the data suggesting that in some cases, less may be more in treating breast cancer

Researchers at the University of Minnesota confirm that when it comes to treating some forms of breast cancer, drastic surgery to remove breast tissue may not help in improving survival from the disease.

Reporting in the Journal of the National Cancer Institute, the scientists describe a model for calculating life expectancy based on recent rates of recurrent cancers among women with stage 1 or stage 2 disease. Although previous studies found that among women diagnosed with breast cancer in one breast, removing the other breast can lower risk of breast cancer in that breast by up to 90%, few studies have documented whether that also translated into greater survival of breast cancer, which can recur in other organs.

According to the researchers’ model, the overall difference in survival at 20 years after diagnosis for both women who had their opposing, unaffected breast removed and those who did not, was less than 1%.

The data confirm recent findings from a study of women with metastatic disease, which also showed that women who received additional surgery to remove lymph nodes and their breasts did not survive any longer than those who were treated with chemotherapy only. As TIME wrote about that study,

Researchers from Tata Memorial Hospital in Mumbai, India, recruited 305 women between 2005 and 2013, all of whom had metastatic breast cancer and had responded to six cycles of chemotherapy. The women were split into two groups. One group of 173 women received additional surgery and radiation treatment, and 177 did not. The women who received surgery had partial or total removal of their breasts and lymph nodes followed by radiotherapy.

After just over two and a half years, the scientists found no overall difference in survival between the two groups; in fact, there was a slight, but not significantly significant, increase in risk of death for the women undergoing surgery and radiation. The lack of difference remained strong even after the scientific team adjusted for the types of breast cancer the women had, and the extent to which their cancer had spread to other organs. The findings should provide more confidence to both doctors and patients who choose not to go under the knife or receive radiation in an effort to prolong their lives, since the evidence suggests that the added measures don’t provide significant benefit, and may only expose the women to more complications.

In the current study, the researchers note that survival is only one factor that women may take into account when debating whether to remove an unaffected breast. In an accompanying editorial, other researchers echoed the distinction, saying that quality of life and peace of mind factors may be important reasons for supporting the continued use of prophylactic mastectomy surgery.

TIME heart

Pigs Can Grow Their Own Pacemakers

And the scientists say that the technique, which involves cutting edge reprogramming of cells, may be tested in people soon

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Pacemakers are remarkable devices that save the lives of 300,000 people in the U.S. each year. They essentially take over for failing hearts, but since the devices require invasive surgery to implant in the heart, researchers have been looking for less invasive approaches to keeping the heart ticking. And now, reporting in the journal Science Translational Medicine, Dr. Eduardo Marban, director of the Cedars-Sinai Heart Institute, has a lead—thanks to pigs.

“We were able for the first time to create a biological pacemaker using minimally invasive methods, and show that the new pacemaker cells suffice to support the demands of daily life,” he said. “When the pigs exercised, the hearts beat faster. When they were at rest, their hearts slowed down.”

He and his colleagues say that a single gene can transform existing heart cells to take over the function of ailing pacemaker cells in the heart, The group tested their theory in mice, and were encouraged enough by the results to predict that human trials may be as close as three years away.

MORE: A ‘Vaccine’ for Heart Disease Could Mean No Pills, Lettuce or a Gym

Marban has been working for more than a decade to find a better way to keep pacemaker patients’ hearts pumping at the right rate. In particular, he was focused on the 2% of them who need to go on antibiotics to treat an infection—because the devices are foreign objects implanted into the body, infections are possible—and in the interim have their pacemakers removed to be cleaned. During that time, these patients receive a temporary pacing device connected to a catheter, but the catheter itself may be an additional source of infection and make the antibiotic treatment less effective.

MORE: Single Gene Responsible for Group of Heart Disease Risk Factors

In Marban’s experiment, he simply loaded deactivated cold viruses, which are able to easily infect cells, with a gene—called TBX18—that is active during fetal development but later shuts off. Earlier studies showed that simply bathing cells in TBX triggered normal heart cells to start morphing into the ones that keep hearts working. That’s exactly what happened in the seven pigs whose hearts were injected with the gene. A small proportion of their normal heart cells, the size of a peppercorn, were transformed into electrically pulsing cells and essentially took over the pacemaker function of the pigs’ hearts.

Dr. Eugenio Cingolani, director of the cardiogenetics-familial arrhythmia clinic at Cedars Sinai and a co-author of the paper, said that while encouraging, more studies on the efficacy of the genetic reprogramming process, as well as a more in-depth analysis of the potential adverse effects are needed.

But the findings represent a promising first step toward a potentially new technique for treating certain life-threatening conditions.

“This development heralds a new era in gene therapy, where genes are used not only to correct deficiency disorders but to convert one cell to another to treat disease,” said Marban. “Now that we and others are hot on the trail of developing therapeutics based on this principle of cell reprogramming, I anticipate that the flood gates will open and people will look for genes of interest to do whatever they want in particular organs or tissues of interest.”

At the very least, he believes that a hardware-free, biological pacemaker based on the technique could become reality.

TIME

5 Groundbreaking Trials Are Testing Ways to Prevent Alzheimer’s

Researchers are testing some promising drug candidates to halt Alzheimer’s dementia – even before symptoms start

At the Alzheimer’s Association International Conference in Copenhagen, scientists described five trials that taking the unprecedented step of testing drugs that may prevent the onset of the neurodegenerative disease in people not yet experiencing cognitive decline.

The participants in the trial are all at high risk of developing Alzheimer’s either because they carry two copies of the ApoE4 gene, which is associated with a strong chance of developing the disease, or a genetic mutation that triggers the condition much earlier in life, during the 40s.

Most will be testing drugs that target amyloid, the protein that builds up in abnormal amounts in the brains of Alzheimer’s patients and triggers other damaging changes that affect memory and cognitive functions. While other scientists reported some encouraging data on the effectiveness of diet, exercise, social support and controlling heart-related risk factors—see our piece about the lifestyle changes that prevented the disease—most experts believe that the best way to prevent Alzheimer’s may involve a combination of such lifestyle approaches with an effective drug.

Here’s the latest information on the five trials.

1. Dominantly Inherited Alzheimer Network Trial (DIAN TU)

Who is enrolled: People with a genetic mutation for Alzheimer’s disease or those who don’t know their genetic status but have a parent or sibling with Alzheimer’s-related mutations

When they should enroll: when they are cognitively normal or have mild cognitive impairment

Drugs tested: Two experimental drugs, gantenerumab and solanezumab, both of which are antibodies designed to bind to amyloid and prevent it from forming brain-damaging plaques

2. Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Study (A4)

Who is enrolled: People aged 65 to 85 years with normal thinking and memory

When they should enroll: Any time they become age eligible

Drugs tested: Solanezumab, an experimental anti-amyloid compound

3. TOMMORROW

Who is enrolled: Healthy seniors

When they should enroll: When they are cognitively normal or have mild cognitive impairment

Drugs tested: The trial will first pilot a screening test for two genes to see if it can accurately predict risk of mild cognitive impairment. The next phase of the trial will test an experimental compound designed to delay symptoms of mild cognitive impairment and Alzheimer’s disease in people without symptoms.

4. Alzheimer’s Prevention Initiative Autosomal Dominant Alzheimer’s Disease Treatment Trial

Who is enrolled: 300 people from a family in Columbia affected by a genetic predisposition to developing Alzheimer’s disease early in life

When they should enroll: Before symptoms begin

Drug tested: Anti-amyloid antibody crenezumab

5. Alzheimer’s Prevention Initiative APOE4 Treatment Trial

Who is enrolled: people with two copies of APOE4, who are at high risk of developing Alzheimer’s disease

When they should enroll: Before cognitive symptoms of Alzheimer’s begin

Drugs tested: An immunotherapy that prompts the body’s immune system to produce antibodies against amyloid protein, and a beta-secretase inhibitor that blocks the production of certain forms of amyloid.

TIME Cancer

Breast-Cancer Drug Has a Surprising New Application, Study Finds

An early study shows that gel-based tamoxifen may be as effective as the oral drug, and have fewer side effects

Tamoxifen is a mainstay of breast cancer treatments: it blocks the effects of the female hormone estrogen on the breast, inhibiting estrogen’s tendency to encourage breast tissue to grow uncontrollably. Now, Dr. Seema Khan, professor of surgery at Northwestern University Feinberg School of Medicine, reports in Clinical Cancer Research that putting the drug in a gel, and applying it directly to the breast tissue, where it needs to work, may have merit.

Doctors generally prescribe tamoxifen for women diagnosed with early breast cancer, including very early-stage ductal carcinoma in situ (DCIS), to prevent recurrent growths. But the drug has also been linked to an increased risk of stroke, blood clots and cancers in other tissues, including the uterus. That’s why more women, including those who have not yet had cancer but are at high risk for the disease could benefit from the drug but are reluctant to take it.

MORE: Why Mammograms Are Less Effective Among Breast Cancer Survivors

Dr. Khan’s study was small—only 26 women—but it provides proof that the principle of applying tamoxifen directly on the breast may be worth investigating. All of the women were diagnosed with DCIS, which generally does not spread. But 30% of DCIS can recur even after surgery and proper treatment, so most women are prescribed tamoxifen. In the current study, about half of the women in the study were randomly assigned to take the oral form of the drug, while the other half were given doses of a tamoxifen gel to apply directly to the breast tissue for six to 10 weeks before their surgery. Khan analyzed the breast tissue after surgery to study markers for tumor growth, and conducted blood tests for levels of tamoxifen metabolites as well.

At the end of the study, the women in both groups showed similar decreases in tumor-related proteins, but blood levels of tamoxifen were five times lower among the women using the gel than those taking the oral pill. That, says Dr. Khan, suggests that the major side effects of the drug, which occur in the blood and other reproductive organs, may be largely avoided if women use the gel.

MORE: High-Tech 3D Mammograms Probably Saved This Woman’s Life

“Our study showed that applying the drug through the breast skin leads to high concentrations in the breast and low concentrations in the rest of the body,” she says. “The biological effect on the breast is consistent with the benefit of oral tamoxifen, so for that reason, we hope that this kind of approach would make preventive medication more acceptable to women with non-invasive breast cancer and how may be at high risk of developing breast cancer.”

Dr. Khan says that the breast may be uniquely designed for such transdermal therapy, since it is essentially an appendage of the skin, with its own internal lymphatic circulation. That may keep things applied to the breast skin within the breast tissue, and could explain the higher concentrations of tamoxifen metabolites she and her team found after the gel applications.

Still, she says that the small number of participants in the study means more research is needed to confirm the results. Right now, the gel version is not available. The company that provided the experimental doses for the study stopped making that formulation, so Dr. Khan is studying a related, similar metabolite called endoxifen that may have similar cancer-fighting effects on breast tissue.

If the strategy proves effective, it’s possible that cancer treatments, or at least breast cancer treatments, may become useful in preventing cancer as well, as more women at high risk who have yet to be diagnosed with the disease take advantage of them. Applying a gel with relatively few side effects may help more women to eliminate small tumors before they have a chance to grow. And if other types of drugs can be used on the skin as well, that could significantly broaden the therapies available to women looking for ways to prevent the disease.

“For high-risk women who need better prevention strategies, delivering the drug to the breast is a very desirable solution,” says Dr. Khan.

TIME Brain

To Prevent Alzheimer’s, Diet and Exercise Are Effective, Large Study Shows

In a groundbreaking study that looked at how diet, exercise and other non-drug interventions affect cognitive decline, researchers see some hope for relatively easy dementia-fighting strategies

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No one believes that a disease as complicated as Alzheimer’s can be warded off by an apple a day or by faithfully hitting the weight room. But a breakthrough study presented Sunday at the Alzheimer’s Association International Conference shows that after just two years, people who underwent lifestyle interventions showed improvements in their mental functions, including in memory, executive function and speed tests of their cognitive skills.

Dr. Miia Kivipelto from the Karolinska Institute in Sweden knew that several studies have linked some lifestyle behaviors, such as exercise and a healthy diet, as well as being more socially active, to less cognitive decline and stronger scores on memory and organizational tests. But it wasn’t clear whether people who ate better, exercised more and had more friends also shared something else in common that could explain their ability to slow down dementia symptoms.

So Kivipelto conducted one of the first studies to randomly assign 1,260 older individuals at high risk of developing Alzheimer’s to a lifestyle intervention or to normal health care, to see if the behaviors linked to better brain health actually helped to stave off intellectual decline. “We were surprised that were able to see a clear difference already after two years,” says Kivipelto. She was especially pleased to see the effect since the control group also received adequate and appropriate health care. “We thought that two years may not be enough, but the multi-domain approach seems to be an effective way of doing something to protect memory.”

MORE: New Understanding on Understanding Alzheimer’s

All of the participants, part of the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) study, had some risk factor for developing dementia, including their age, education, and poor heart-health profile. Half were randomly assigned to get an intensive lifestyle makeover, with both group and individual nutrition advice, an exercise trainer, and a nurse or physician who made sure they took their medications. In addition, these volunteers benefited from a social support system. The other half received appropriate health care, but not at the intensive level the intervention group did, and without the social support of their fellow participants.

MORE: New Criteria May Change Alzheimer’s Diagnosis

After just two years, the group that group that got the lifestyle makeover were in much better shape.

MORE: Study: Brain Scans Help Predict Alzheimer’s Disease Early

She and her team plan to continue following up with the participants in another seven years, to see if the effect remains. But she is aware that sticking with a lifestyle plan like the one in the study is a challenge, and says that any such program needs to incorporate ways of keeping patients motivated to comply. That’s why social support may be an important part of any such plan; in this study, for example, if participants missed exercise sessions, others called to find out why they were absent, cementing a pact to adhere to the new behaviors.

Kivipelto also recognizes that genetic factors can play a role in cognitive decline and risk of memory loss, but she says there may be a role for lifestyle interventions in helping people who may be at high risk of developing dementia or Alzheimer’s disease—before their symptoms start.

“These findings show that prevention is possible, and that it may be good to start early,” she says. “With so many negative trials for Alzheimer’s drugs reported lately, it’s good that we may have something that everyone can do now to lower their risk.”

 

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