How Inactivity Harms Your Health

I came across this nifty diagram showing how being inactive contributes to illness. Get moving to stay healthy! When you don't move you gain weight, especially around the middle. White blood cells from your immune system move into the fat around your organs. This ignites inflammation everywhere in your body, which leads to insulin resistance and more weight gain, and ultimately diabetes. This raises your risk for heart disease, high blood pressure and stroke. This inflammation also leads to brain issues like dementia, Parkinsons and Alzheimers. Also increased is your risk for cancer. It is worth saying again. Get moving to protect your health!

Omega-3 fatty acids, vitamin D may control brain serotonin, affecting behavior and psychiatric disorders.

In a previous paper published last year, authors Patrick and Ames discussed the implications of their finding that vitamin D regulates the conversion of the essential amino acid tryptophan into serotonin, and how this may influence the development of autism, particularly in developing children with poor vitamin D status.

Here they discuss the relevance of these micronutrients for neuropsychiatric illness. Serotonin affects a wide-range of cognitive functions and behaviors including mood, decision-making, social behavior, impulsive behavior, and even plays a role in social decision-making by keeping in check aggressive social responses or impulsive behavior.

Many clinical disorders, such as autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), bipolar disorder, schizophrenia, and depression share as a unifying attribute low brain serotonin. "In this paper we explain how serotonin is a critical modulator of executive function, impulse control, sensory gating, and pro-social behavior," says Dr. Patrick. "We link serotonin production and function to vitamin D and omega-3 fatty acids, suggesting one way these important micronutrients help the brain function and affect the way we behave."

Eicosapentaenoic acid (EPA) increases serotonin release from presynaptic neurons by reducing inflammatory signaling molecules in the brain known as E2 series prostaglandins, which inhibit serotonin release and suggests how inflammation may negatively impact serotonin in the brain. EPA, however, is not the only omega-3 that plays a role in the serotonin pathway. Docosahexaenoic acid (DHA) also influences the action of various serotonin receptors by making them more accessible to serotonin by increasing cell membrane fluidity in postsynaptic neurons.

Their paper illuminates the mechanistic links that explain why low vitamin D, which is mostly produced by the skin when exposed to sun, and marine omega-3 deficiencies interacts with genetic pathways, such as the serotonin pathway, that are important for brain development, social cognition, and decision-making, and how these gene-

micronutrient interactions may influence neuropsychiatric outcomes. "Vitamin D, which is converted to a steroid hormone that controls about 1,000 genes, many in the brain, is a major deficiency in the US and omega-3 fatty acid deficiencies are very common because people don't eat enough fish," said Dr. Ames.

This publication suggests that optimizing intakes of vitamin D, EPA, and DHA would optimize brain serotonin concentrations and function, possibly preventing and ameliorating some of the symptoms associated with these disorders without side effects.
Rhonda P. Patrick And Bruce N. Ames. Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar, schizophrenia, and impulsive behavior. FASEB Journal, February 2015

High HDL Cholesterol Levels Associated With Reduced Alzheimer’s Risk

High levels of high-density lipoprotein (HDL), also known as “good” cholesterol, appear to be associated with a reduced risk for Alzheimer’s disease in older adults.

”Dyslipidemia [high total cholesterol and triglycerides] and late-onset Alzheimer’s disease are highly frequent in western societies,” the authors write as background information in the article. “More than 50 percent of the U.S. adult population has high cholesterol. About 1 percent of people age 65 to 69 years develop Alzheimer’s disease, and the prevalence increases to more than 60 percent for people older than 95 years.”

Christiane Reitz and colleagues studied 1,130 older adults to examine the association of blood lipid (fat) levels with Alzheimer’s disease. The study included a random sampling of Medicare recipients 65 or older residing in northern Manhattan, with no history of dementia or cognitive impairment. The researchers defined higher levels of HDL cholesterol as 55 milligrams per deciliter or more.

To determine this association, data were collected from medical, neurological and neuropsychological evaluations. Additionally, the authors assigned a diagnosis of “probable” Alzheimer’s disease when onset of dementia could not be explained by any other disorder. A diagnosis of “possible” Alzheimer’s disease was made when the most likely cause of dementia was Alzheimer’s disease but there were other disorders that could contribute to the dementia, such as stroke or Parkinson disease.

During the course of follow-up, there were 101 new cases of Alzheimer’s disease, of which 89 were probable and 12 were possible. The mean (average) age of individuals at the onset of probable and possible Alzheimer’s disease was 83 years, and compared with people who were not diagnosed with incident Alzheimer’s disease, those who did develop dementia were more often Hispanic and had a higher prevalence of diabetes at the start of the study. Higher plasma levels of HDL cholesterol were associated with a decreased risk of both probable and possible Alzheimer’s disease, even after adjusting for vascular risk factors and lipid-lowering treatments. Although higher plasma total cholesterol, non-HDL cholesterol and LDL cholesterol levels also were associated with decreased risks of probable and possible Alzheimer’s disease, these associations became non-significant after adjusting for vascular risk factors and lipid-lowering treatments.

“In this study, higher levels of HDL cholesterol were associated with a decreased risk of both probable and possible Alzheimer’s disease,” the authors conclude. “An important consideration in the interpretation of the results is that it was conducted in an urban multiethnic elderly community with a high prevalence of risk factors for mortality and dementia. Thus, our results may not be generalizeable to cohorts with younger individuals or to cohorts with participants with a lower morbidity [disease] burden.”

Arch Neurol. 2010;67(12):1491-1497. doi:10.1001/archneurol.2010.297.

Inflammation Resolution the Key to Preventing or Reversing Alzheimer's disease Suggests Compelling New Study

Supplementation with omega-3 fatty acids could help to prevent and even reverse the progression of Alzheimer’s disease. 

The connection is resolving inflammation. The beneficial fats may come to the affected person’s rescue by stimulating newly identified ‘resolution pathways’ in the brain, according to research outlining an ‘entirely new’ approach to the condition.

The new study, published in the journal Alzheimer’s & Dementia, demonstrates a new approach to dementia and Alzheimer’s disease – suggesting that omega-3 fatty acid derivatives stimulate the uptake of amyloid-beta proteins. The proteins are the alleged culprits in the deteriorating health of brains affected by this dreadful disease. They apparently kill brain cells and form Alzheimer's disease hallmark plaques.

Led by Professor Marianne Schultzberg from the Karolinska Institute, Sweden, the team behind the research revealed that normal inflammatory processes should ultimately lead to tissue repair in a process known as restoration. However, with Alzheimer's disease this normal process is interrupted – meaning that rather than repair and restore tissue, debris from dead cells and other microorganisms fails to be cleared away, and instead accumulates in the brain, wreaking havoc.

"Our hypothesis is that stimulation of resolution of inflammation in Alzheimer's disease may result in reduced neuronal death in the brain, and in turn have a beneficial effect in disease progression and cognition,” explained Schultzberg.

“This is an entirely new approach and provides the opportunity to develop new treatment principles for Alzheimer's disease," she said.

The Swedish team found protective compounds formed in the brain from omega-3 fatty acids help to induce the resolution process and stimulate the uptake or clearing away of amyloid-beta proteins that have been linked to the progression of Alzheimer's disease through the development of plaques.

The team will now try to prove the hypothesis by using animal models to see if omega-3 fatty acids can prevent memory loss and further loss of brain cells.

In the study, Dr Schultberg and her group examined cerebrospinal fluid from 15 patients with Alzheimer's disease, 20 patients with mild cognitive impairment and 21 control subjects. They also analyzed brain tissue from 10 Alzheimer's patients and 10 control subjects.

Schultzberg and her team looked for the presence, and comparative levels of several inflammatory molecules and receptors involved in the resolution pathway – including specialised pro-resolving mediators (SPMs), receptors, biosynthetic enzyme, and downstream effectors - in postmortem hippocampal tissue from AD patients and non-AD subjects.

SPMs were also measured in cerebrospinal fluid (CSF).

The team found that SPMs and SPM receptors were detected in the human brain – indicating the resolution pathway does exist in the brain. They also found that levels of the SPM lipoxin A₄ (LXA₄) were reduced in AD patients, both in the CSF and hippocampus.

In addition, an enzyme involved in LXA₄ synthesis and two SPM receptors were elevated in AD brains, said the team, while LXA₄ and RvD1 levels in CSF correlated with Mini-Mental State Examination (MMSE) scores.

As a result, the team concluded that the resolution pathway exists in the brain, adding that the alterations identified in the study “strongly suggest” a dysfunction of this pathway in Alzheimer’s disease.

They added that treatment with SPMs, or alternatively, by stimulating the resolution pathway – such as might occur with omega-3 fatty acid supplementation – “is suggested as a new and promising therapy in neurodegenerative disorders such as Alzheimer’s disease.”

Source

High Carb Diet Bad For Elderly Cognitive Function

Just say no!

Seniors who follow a high-carbohydrate diet are nearly four times as likely to develop mild cognitive impairment, especially if their food intake is high in sugar, researchers from the Mayo Clinic report in the Journal of Alzheimer's Disease. They also found that seniors whose diets are high in protein and fat are less likely to develop cognitive impairment.

The researchers found that:

      

    The highest carbohydrate eaters had a 1.9 times higher risk of mild cognitive impairment than the participants who ate the fewest carbs.

             

   The highest sugar consumers had a 1.5 times higher risk of cognitive impairment compared to the lowest consumers.           

    

   The participants with the highest fat intake had a 42% lower risk of developing cognitive impairment compared to the lowest fat eaters.

            

   The highest protein consumers had a 21% lower chance of developing dementia compared to the lowest consumers of protein.

      

   When taking into account fat and protein intake, the highest carb eaters had a 3.6 times higher chance of developing mild cognitive impairment.

"Relative Intake of Macronutrients Impacts Risk of Mild Cognitive Impairment or Dementia"
Rosebud O. Roberts et al
Journal of Alzheimer's Disease, October 2012. 10.3233/JAD-2012-120862

Poor Glucose Control Raises Risk of Dementia and Alzheimer's

Getting your blood sugar under control appears to have far reaching effects according to a new study coming out of Japan. The study links glucose regulation with dementia and prediabetes and diabetes with dementia, vascular dementia and Alzheimer’s Disease. In the population group studied poor glucose control accounted for one in six cases of dementia and one in five cases of Alzheimer’s.

Diabetes patients were 74% more likely to develop dementia of any type over 15 years of follow-up after adjustment for other confounding factors.

And Alzheimer's disease developed 2.05-fold more often in those with diabetes than in those with normal glucose tolerance.

Most interesting, though, was the strong risk prediction of postload glucose levels during the oral glucose tolerance test, mimicking how meals are metabolized.

Higher two-hour postload glucose levels correlated with greater risk of developing dementia, Alzheimer's disease, and vascular dementia.

After adjustment for age, sex, hypertension, electrocardiogram abnormalities, body mass index, waist-to-hip ratio, total cholesterol, prior stroke, education, smoking, alcohol intake, and physical activity in the multivariate analysis:

Two-hour postload glucose levels of 7.8 to 11.0 mmol/L predicted 50% elevated risk of all-cause dementia and 87% elevated likelihood of Alzheimer's disease.

Two-hour postload glucose levels above 11.0 mmol/L predicted 2.47-fold higher risk of all-cause dementia and 3.42-fold elevated Alzheimer's risk and 2.66-fold elevated vascular dementia risk (P=0.01).

Those findings suggested "that postprandial glucose regulation is critical to prevent future dementia.

Hyperglycemia itself may have an impact on the brain through atherosclerosis, oxidative stress and accumulation of advanced protein glycation, and changes in insulin metabolism yielding distorted amyloid metabolism.

One important tool to reduce high after meal blood sugar levels is the glycemic index. Foods that are low are better than foods that are high.

Have a look at how the foods you eat frequently score on the index here.

http://www.glycemicindex.com/

Ohara T, et al "Glucose tolerance status and risk of dementia in the community: The Hisayama Study" Neurology 2011; 77: 1126–1134.

Suffer From Brain fatigue? Get Off of That Couch!

Scientists have long understood that regular exercise increases the number of organelles called mitochondria in muscle cells. Mitochondria produce energy, Thus one of the positive physical effects of exercise is increased strength or endurance. Exercise also works in the brain to reduce depression and boost memory. Now we may know why.
Exercise doesn’t just boost cellular powerhouses, (mitochondria) in muscles—it increases their population in brain cells too. Thus exercise increases the number of mitochondria in the brain just as it increases mitochondria in muscles. The benefits? Better exercise endurance by energizing the brain and having it be more resistant to fatigue. A boost in brain mitochondria play a supporting role for reducing the impact of mental disorders. Exercise may prove to be a potential treatment for psychiatric disorders, genetic disorders, and neurodegenerative diseases.


Jennifer L. Steiner, E. Angela Murphy, Jamie L. Mcclellan, Martin D. Carmichael, J. Mark Davis. Exercise Training Increases Mitochondrial Biogenesis in the Brain.American Journal of Physiology -- Regulatory, Integrative, and Comparative Physiology, 2011

Inherited Alzheimer's May be Detected 20 Years before the Onset of Dementia.

It soon may be possible for doctors to identify persons who have Alzheimer’s decades before dementia is present, allowing earlier intervention to protect the brain. This breakthrough in identification methods was reported on July 20 at the Alzheimer’s Association International Conference on Alzheimer’s Disease in Paris. The new insights come from an ongoing study: the Dominantly Inherited Alzheimer’s Network (DIAN), an international study of inherited forms of Alzheimer’s.

Based on what is seen in the study group, brain chemistry changes can be detected up to 20 years before the expected age of detectable symptoms.  The Alzheimer’s-related changes can be specifically targeted for prevention trials in patients with inherited forms of Alzheimer’s.

The doctors are looking specifically at the value of disease indicators from cerebrospinal fluid analyses. DIAN researchers are studying members of families who have mutations in one of three genes: amyloid precursor protein, presenilin 1 or presenilin 2. Participants with these mutations are certain to develop Alzheimer’s disease early, with symptoms beginning in their 50s, 40s, or, in some rare cases, 30s.

Participants who carry the mutations but are still asymptomatic have significantly lower levels of amyloid beta and higher levels of tau protein in their cerebrospinal fluid than participants without the mutations.

Amyloid beta normally is cleared from the brain and into the spinal fluid. Scientists theorize that decreases in spinal fluid levels of amyloid beta reflect a buildup of this sticky protein fragment in the brain, where it forms Alzheimer’s plaques. Tau protein is a structural component of central nervous system cells. Its increase in cerebrospinal fluid is thought to be a byproduct of damage to brain cells.


DIAN is supported by funding from the National Institute on Aging. One hopes that our contentious political climate will not result in a loss of funding for this important work.

National Institutes of Health Article Here

Lifestyle factors that are protective against amyloid and tau accumulation in the brain include fish and fish oil consumption, it is especially important to get adequate DHA which is specifically protective against the increases of amyloid.

Get cold sores? Treat them quickly!

Researchers Link Herpes to Alzheimer’s Disease; “Cold Sores” Connected to Cognitive Decline.

Researchers recommend people treat a cold sore as quickly as possible to minimize the amount of time the virus is actively traveling through a person’s nervous system. The faster a cold sore is treated, the faster the HSV1 returns to a dormant stage.

How prevalent is this virus? In developed countries such as the U.S., approximately 20 percent of children are infected with HSV1 prior to the age of five. By the second and third decades of life, as much as 60 percent of the population is infected, and late-in-life infection rate reaches 85 percent.

Here's the journal article:

Herpes Simplex Virus Dances with Amyloid Precursor Protein while Exiting the Cell.

Read it here.

Zovirax or acyclovir is an antiviral drug that slows the growth and spread of the herpes virus so that the body can fight off the infection. Zovirax contains an active antiviral ingredient called acyclovir. Acyclovir stops the herpes virus from spreading from one host cell to other normal cells. Acyclovir converts itself into a more active agent inside the infected cells of the body. Then, it blocks the action of an enzyme called DNA polymerase which copies the herpes virus’ genetic material from RNA to DNA. By blocking DNA polymerase, Zovirax prevents the multiplication and growth of the herpes virus. This allows the body to treat the existing outbreak and relieve the pain caused by cold sores.