Dementia Risk Tied to Blood Sugar Level, Even With No Diabetes

A joint Group Health-University of Washington (UW) study in the New England Journal of Medicine has found that higher blood sugar levels are associated with higher dementia risk, even among people who do not have diabetes.

Blood sugar levels averaged over a five-year period were associated with rising risks for developing dementia, in this report about more than 2,000 Group Health patients age 65 and older in the Adult Changes in Thought (ACT) study.

For example, in people without diabetes, risk for dementia was 18 percent higher for people with an average glucose level of 115 milligrams per deciliter compared to those with an average glucose level of 100 mg/dl. And in people with diabetes, whose blood sugar levels are generally higher, dementia risk was 40 percent higher for people with an average glucose level of 190 mg/dl compared to those with an average glucose level of 160 mg/dl.

"The most interesting finding was that every incrementally higher glucose level was associated with a higher risk of dementia in people who did not have diabetes," said first author Paul K. Crane, MD, MPH, an associate professor of medicine at the UW School of Medicine, adjunct associate professor of health services at the UW School of Public Health, and affiliate investigator at Group Health Research Institute.

"There was no threshold value for lower glucose values where risk leveled off."
"One major strength of this research is that it is based on the ACT study, a longitudinal cohort study, where we follow people for many years as they lead their lives," said senior author Eric B. Larson, MD, MPH, a senior investigator at Group Health Research Institute who also has appointments at the UW Schools of Medicine and Public Health. "We combine information from people's research visits every other year with data from their visits to Group Health providers whenever they receive care. And this gave us an average of 17 blood sugar measurements per person: very rich data."

These measurements included blood glucose (some fasting, some not) and glycated hemoglobin (also known as HbA1c). Blood sugar levels rise and fall in peaks and valleys throughout each day, but glycated hemoglobin doesn't vary as much over short intervals. R. Walker, MS

R. Hubbard, PhD Combining glucose and glycated hemoglobin measures into a composite measure required special statistical techniques, which Drs. Crane and Larson's co-authors Rod Walker, MS, a biostatistician, and Rebecca Hubbard, PhD, an associate investigator, both from Group Health Research Institute, had developed. (Dr. Hubbard is also an affiliate assistant professor of biostatistics at the UW School of Public Health.) These sophisticated statistical models required specialized data on the relationships between glycated hemoglobin and glucose levels, and they used data generated by co-author David M. Nathan, MD, a professor of medicine at Harvard Medical School and director of the Diabetes Center at Massachusetts General Hospital.

So should people try to eat less sugar -- or foods with a lower "glycemic index"? Not necessarily, Dr. Crane said: "Your body turns your food into glucose, so your blood sugar levels depend not only on what you eat but also on your individual metabolism: how your body handles your food." But he does suggest that taking walks couldn't hurt: The ACT study has previously linked physical activity to later onset and reduced risk of dementia, including Alzheimer's disease.

Furthermore, Dr. Crane emphasized that these results come from an observational study: "What we found was that people with higher levels of glucose had a higher risk of dementia, on average, than did people with lower levels of glucose," he said. "While that is interesting and important, we have no data to suggest that people who make changes to lower their glucose improve their dementia risk. Those data would have to come from future studies with different study designs."

Breastfeeding proven to lower risk of Alzheimer's in moms.

As more research becomes available, it is increasingly clear that breastfeeding children provides infinitely more long-term health benefits to both baby and mom. Now, a new study shows that mothers who breast feed run a lower risk of developing Alzheimer's disease later in life.

The research  indicates the link may have something to do with key biological effects of breastfeeding. Scientists also found that breastfeeding for longer periods of time decreased overall risk.

Previous studies have established that breastfeeding can reduce a mother's risk of other diseases but until now little has been done to examine the impact of breastfeeding duration on Alzheimer's risk.

Biological changes could be responsible for the additional protection

Researchers from the University of Cambridge's Department of Biological Anthropology conducted the study using data gathered from a relatively small group of 81 women. But, they said, the correlation between breastfeeding and Alzheimer's was especially consistent and significant, though it was much less common in women who had a history of dementia in their family.

The findings could lead to new ways to combat what is being called a global Alzheimer's epidemic. Also, researchers note that the study could offer some indications as to why some people are more susceptible to developing the disease than others.

The study argues that there may be a number of biological reasons for the connection between Alzheimer's and breastfeeding. One theory is that breastfeeding deprives the body of the hormone, progesterone, compensating for high levels of progesterone which are produced during pregnancy.

Researchers note that progesterone is known to have a desensitizing effect on the brain's oestrogen receptors; it may also play a role in protecting the brain against Alzheimer's, they add.

Still another possibility: Breastfeeding boosts a woman's glucose tolerance by restoring her sensitivity to insulin following pregnancy, which in and of itself "induces a natural state of insulin resistance and Alzheimer's is characterized by a resistance to insulin in the brain," the Telegraph reported.

"Women who spent more time pregnant without a compensatory phase of breastfeeding therefore may have more impaired glucose tolerance, which is consistent with our observation that those women have an increased risk of Alzheimer's disease," Dr. Molly Fox, who led the study, said.

"Alzheimer's is the world's most common cognitive disorder and it already affects 35.6 million people. In the future, we expect it to spread most in low and middle-income countries. So it is vital that we develop low-cost, large-scale strategies to protect people against this devastating disease," she said.

Prior research has established that breastfeeding can lower a mum's risk of other diseases and a possible link between breastfeeding and cognitive decline later in life. But until now, little work has taken place on the effect on Alzheimer's of the length of time women breastfeed for.

More research is warranted, but so far, it's promising

The 81 women involved in the study were between 70 and 100 years old. Fox, along with Prof. Carlo Berzuini and Prof. Leslie Knapp interviewed the women; they discovered that "women who breastfed were less likely to have developed the disease and the threat fell still further for those with a longer history of breastfeeding," Cambridge said, in a press release.

Researchers said the link between breastfeeding and Alzheimer's was not affected by other factors such as the drinking and smoking history of the women, education history, age or other variables.

The university said its researchers hope the study will lead to more research into the relationship between the risk of Alzheimer's and the reproductive history of women.

Alzheimer's Progression

New research seeks to delineate just how Alzheimer's disease unfolds in the human brain.

Biological changes may happen earlier than scientists had previously thought, according to a new disease model. This suggests that early signs of risk could potentially become treatment targets long before symptoms of Alzheimer's begin to appear, the researchers said. "We're getting a better idea of what is happening during the asymptomatic [symptomless] phases of the disease," said Dean Hartley, director of science initiatives at the Alzheimer's Association, who was not involved with the new research.

The scientists behind the new research identified distinct but overlapping phases in the course of Alzheimer's disease, each detectable by biological "markers" showing physical changes in the brain. They also have refined their model to distinguish between these "biomarkers" of Alzheimer's disease and those of normal aging.

In the first phase of Alzheimer's, brain markers signaling changes in beta-amyloid protein show up first, the model suggests. Beta-amyloid plaques are protein pieces from the fatty membrane surrounding nerve cells that clump together, contributing to nerve dysfunction.

In the second phase of the disease, signs of degeneration and death of brain cells occur.

Symptoms of dementia are seen in the third phase of Alzheimer's disease, according to the new model.

The refined model should help researchers design better research, guide the selection of study participants, suggest the ideal time to begin treatment and help measure the impact of treatment, said Dr. Clifford Jack Jr.

In addition to beta-amyloid proteins, "tau" - another protein - also plays a role in Alzheimer's, creating what are called "neurofibrillary tangles." Jack said the changes in the brain created by tau seem to occur first, but amyloid aggregation, or clumping, accelerates the changes in tau and causes it to spread.

The central message is that tau and beta-amyloid plaque interact with each other in a synergistic way, said Jack, a professor of radiology and a neuroradiologist at the Mayo Clinic College of Medicine, in Rochester, Minn.

Alzheimer's disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. Symptoms typically appear after age 60, and about 5 million Americans may have the disease, according to the U.S. National Institute on Aging.

How could the model spark new ideas for treating Alzheimer's disease? "What really makes sense probably is a combined therapeutic approach where you target a point or points in tau and in the amyloid pathways simultaneously," Jack explained.

Just as people often take statins -- drugs that lower cholesterol -- to reduce their risk of heart disease, it could someday be possible that those at risk for Alzheimer's could take medication to help prevent it, Jack said. He envisions a "cocktail" or combination of drugs that could target different points in the molecular pathways of the disease, administered at an early age, depending on a person's risk for Alzheimer's disease.

The Alzheimer's Association's Hartley said he's excited about the revised model. "It suggests that some of the treatments we're using may be too late in the progression of the disease."

Two related studies were also scheduled for presentation at the meeting. Dr. Victor Villemagne at the University of Melbourne, in Australia, and colleagues followed about 200 people with and without signs of Alzheimer's disease over four years to estimate when beta-amyloid levels tend to become abnormal. The scientists concluded that Alzheimer's disease is a slow process, likely extending for more than 20 years.

The other study, led by Daniela Bertens at VU University Medical Center, in Amsterdam, Holland, provided more evidence that abnormal beta-amyloid is what triggers the development of Alzheimer's disease. The research included about 300 people with abnormal beta-amyloid, and followed them over four years, testing their cerebrospinal fluid for diagnostic signs of the disease.

Common Blood Pressure Drugs May Help Slow Dementia

Older adults with dementia who use certain blood pressure medications may have a slower rate of mental decline, new research suggests. The study found that dementia patients on particular ACE inhibitors showed a somewhat slower decline in memory and other mental skills than patients not on the drugs. And dementia patients who were newly started on the drugs had, on average, a small improvement in the first six months.

The drugs linked to the benefit are known as centrally acting ACE inhibitors, which means they cross from the blood into the brain.

However, the findings do not mean that people with dementia should be started on those ACE inhibitors, according to a neurologist who was not involved with the research. The study was not a clinical trial set up to test the effects of ACE inhibitors, noted Dr. Gayatri Devi, of Lenox Hill Hospital in New York City. Instead, she said, it was an "observational" study, where researchers followed more than 350 older adults with Alzheimer's or other forms of dementia -- about one-quarter of whom happened to be on ACE inhibitors. Those types of studies cannot prove that a drug is the reason for a particular benefit. "And there are past studies that have contradicted this one, and have not shown a benefit of ACE inhibitors," Devi said. On the other hand, the findings support the "larger message" that better cardiovascular health -- including controlling blood pressure and cholesterol levels -- can benefit the brain as well, she said.

Previous studies have linked better blood pressure control -- and various classes of blood pressure drugs -- to both a lower risk of developing dementia and a slower progression of the disease. Currently, no treatments exist to prevent or modify dementia. "The blood pressure medication that's best for you is the one that most effectively controls your blood pressure," Devi said. "People respond differently to the different classes of blood pressure drugs." The study included 361 dementia patients, average age 77, who completed standard tests of memory, planning and other mental abilities. Of those, 85 were already on a centrally acting ACE inhibitor, and 30 more started on one during the study period. On average, test scores declined by 1.8 points every six months among patients who were already on ACE inhibitors. That compared with 2.1 points for patients not on the drugs. Among patients who newly started an ACE inhibitor, test scores typically rose 1.2 points in the first six months -- which was as long as that group was followed. The rest of the study patients were tracked for about a year-and-a-half.

Those are small differences in test scores. But if they persisted over years, that could add up to a significant difference in dementia patients' rate of decline, said Dr. William Molloy, one of the researchers on the study. Clinical trials are needed to confirm whether certain ACE inhibitors do, in fact, slow down dementia, according to Molloy, a professor of gerontology and rehabilitation at University College Cork in Ireland. He said he does not think the benefit linked to ACE inhibitors is explained by better blood pressure control. There is animal research showing that ACE inhibitors that cross into the brain may have a stronger effect on brain functioning than ACE inhibitors that do not breach the blood-brain barrier. One possibility, Molloy said, is that the drugs reduce inflammation in the brain. But another expert not involved in the study urged caution. "I don't think these findings should be used in any clinical decision-making," said Dr. Jacobo Mintzer, chair of the Alzheimer's Foundation of America's medical advisory board. "This study supports the general concept that controlling blood pressure and other cardiovascular risk factors could have an effect" on dementia progression, said Mintzer, of Roper St. Francis Healthcare in Charleston, S.C. But he agreed with Devi that the specific medication you take for high blood pressure should be the one -- or ones -- that best rein in your numbers.

Cinnamon beats Alzheimers

The miracle spice cinnamon is the scented bark of a tropical evergreen tree, native to India and Sri Lanka. Cinnamon comes from an evergreen tree in Southeast Asia and is cultivated widely in Vietnam, China, Burma, and Laos for its bark and the oil processed from the bark. Once upon a time in ancient Rome, cinnamon was worth more than silver.

Cinnamon is harvested from the inner bark of the tree branches after scraping off the corky outer layer and then drying the bark. As it dries, the bark curls up into quills which are then cut into sticks to be ground into the spice form. Full of calcium and fiber, cinnamon is one of the oldest known spices, it is mentioned in the Bible and was used in ancient Egypt as medicine, beverage flavoring and an embalming agent.

According to traditional Chinese medicine, cinnamon helps improve the body's "fire."

Cinnamon - Not just a spice!

Professor Daniel Fung, an expert in food science at Kansas State University, says cinnamon contains a compound that has the ability to kill bacteria. "If cinnamon can knock out E.coli 0157:H7, one of the most virulent food-borne microorganisms that exists today, it will certainly have antimicrobial effects on other common food-borne bacteria such as Salmonella and Campylobacter."

Now researchers from Tel Aviv University found that extracts from cinnamon bark inhibit the toxic amyloid polypeptide oligomers and fibrils that have been found in Alzheimer's Disease (AD) brain plaque formations. In animal models of Alzheimer's, cinnamon reduced s-amyloid plaques associated with the pathology of AD. Reduction of these proteins can improve mental cognition. In one model, cinnamon extract resolved AD associate reduced longevity, helped recover locomotion defects and completely abolished tetrameric species of plaque in the brain.

Other benefits of cinnamon are: anti-microbial actions, blood sugar balancing, improving colon health, boosting brain function. Cinnamaldehyde in cinnamon has been well researched for its effects on blood platelets which help the blood clot to stop bleeding. Platelets can also cause strokes if they clump together too much. Cinnamon has been shown to help prevent this deadly clumping. Cinnamon will stop vomiting and relieve feelings of nausea. Cinnamon also helps slow tumor growth while inhibiting inflammatory markers connected to cellular proliferation.

In a recent study, people reduced their blood sugar levels by as much as 29 percent with cinnamon in just 40 days. That's with NO drugs, NO diet changes - just plain old cinnamon!

Study volunteers who took a cinnamon extract showed significant decreases in fasting blood glucose and increases in lean muscle mass compared with the placebo group. Pre and post study analysis of the extract group revealed a statistically significant decrease in body fat and blood pressure.

Research found that cinnamon can have favorable effects on brain function. Participants in a study chewed cinnamon gum or even just smelled the sweet spice. Cognitive tests revealed that subjects who used cinnamon had better memory functions and could process information more quickly.

What kind and how much

Which is best: Ceylon cinnamon, Saigon cinnamon, cinnamomum zeylanicum or regular grocery store variety cinnamon? Interestingly, the grocery store variety known as cinnamomum cassia works the best in most research studies and clinical trials.

Drink cinnamon in tea or sprinkle a little cinnamon on your toast, cereal, oatmeal, or sliced apples. It not only tastes good, it lowers your blood sugar!

Taking two 500 mg capsules of cinnamon a day will help good cholesterol levels and taking two capsules with each meal can make a big difference in blood sugar and insulin levels for diabetics.

Alzheimer’s Aggression

Alzheimer’s aggression most often flares up during the later stages of Alzheimer’s disease. The person may become easily agitated, angry, and abusive - often for no apparent reason. The person may curse, hurl insults, and scream. Though verbal assaults are more common than physical assaults, a person with Alzheimer’s disease may throw things or resist care by pushing and hitting.

Why Does Alzheimer’s Aggression Occur? - No one knows for sure why Alzheimer’s patients become aggressive. Aggression may be a symptom of Alzheimer’s disease itself. It may also be a reaction to actions of others or to the environment around the person with Alzheimer’s disease.

Understand the Triggers of Alzheimer’s Aggression - Alzheimer’s aggression can flare up without warning. There may not be an obvious cause. However, often there are triggers that caregivers can look for. By knowing the triggers, you may be able to lower the frustration level of the person with Alzheimer’s disease. This can reduce the number of aggressive outbursts. Here are some common triggers of Alzheimer’s aggression:

Discomfort caused by lack of sleep, side effects from medication, or pain that the person is not able to describe
The surrounding environment, such as loud noises, busyness around the person, or clutter
Confusion caused by being asked too many questions at once, trying to understand complex instructions, or feeling the stress of caregivers

Tips to Reduce Alzheimer’s Aggression - Once you understand the triggers for Alzheimer’s aggression, you can take steps to prevent it. Try these suggestions:

• Anticipate situations in which the person with Alzheimer’s may be uncomfortable, overstimulated, or confused.
• Avoid asking too many questions at once, giving overly complicated instructions, and speaking negatively. That way, you are less likely to confuse and agitate the person you are caring for.
• Limit the amount of loud noises, frenetic movement, and clutter.
• Don’t contradict. Those with Alzheimer’s disease see a different reality than you do. Rather than challenge that reality, sit and listen. Ask questions about it.
• Focus on the past. Alzheimer’s affects short-term memory. It’s often easier and less stressful for someone with Alzheimer’s disease to recall and talk about distant memories than it is for them to remember what they watched on TV the night before.
• Use memory cues. As the disease progresses, remembering to do and how to do everyday tasks like brushing your teeth or getting dressed becomes more difficult. Reminder notes placed in key locations can help prevent frustration.

Caregiver Stress and Alzheimer’s Aggression - It’s not easy to care for a person with Alzheimer’s disease. The burden of round-the-clock care takes an emotional toll. Add to it the frustration and sadness of watching a loved one deteriorate. It’s not surprising that caregivers may feel isolated and depressed. Left unrelieved, these feelings can lead to abusive behavior toward the person with Alzheimer’s disease, from insults to physical injury.

If you are a caregiver, do yourself and the person you care for a favor. Seek help for yourself if you notice signs of depression, anxiety, sleeplessness, exhaustion, or irritability. Taking care of yourself will help you take better care of others.

Mechanism of Alzheimer's Therapy

Gammagard™ IVIg is a therapy that has been investigated for treatment of Alzheimer's. Despite small clinical studies that have reported efficacy of the approach, the mechanism of action is poorly understood.
The UK researchers set out to investigate the mechanism by which the treatment may act in the brain to lower amyloid deposition (amyloid deposits being a key pathology in Alzheimer's).

To conduct their investigation, researchers introduced IVIg directly into the brains of mice which carry a human gene causing them to develop amyloid plaques. They found that IVIg lowers amyloid deposits in the brains of the mice over the course of seven days. Their data suggest that the modulation of inflammation in the brain by IVIg is a key event that leads to the reduction in amyloid deposition.

The scientists hypothesize that the IVIg acts as an immune modulator, and this immune modulation is responsible for the reductions in amyloid pathology.

The data suggests that modulating the immune response in the brain may help ameliorate the Alzheimer's pathology. Researchers are currently investigating other ways to produce the same modulation of the immune response because the access of IVIg to the brain when administered peripherally is very limited.