Mindfulness meditation helps women but not men, first study suggests


Mindfulness does not help men, a new study has shown
Mindfulness does not help men, a new study has shown 

Mindfulness does not help men, the first study to look at the gender divide in meditation suggests.

Although recent research has shown that mindfulness meditation, the practice of directing attention to present sensations and feelings, can be beneficial, nobody has checked whether the results were the same for both sexes.

But when Brown University broke down results they found a clear difference for men and women. While practising significantly helped women overcome a downcast mood, it actually made men feel slightly worse than before they began.

 “That was the surprising part,”said Dr Willoughby Britton, assistant professor of psychiatry and human behaviour and of behavioural and social sciences.

“I wouldn’t be surprised if this is a widespread phenomenon that researchers hadn’t bothered to investigate.”

Students meditate in the lab component of their coursework
Students meditate in the lab component of their coursework

The study followed 41 male and 36 female students over the course of a full, 12-week academic class on mindfulness traditions which included three one hour-long meditation labs a week.

Over that time the average student had engaged in more than 41 hours of meditation in class and outside.

But while women’s moods improved by an average of 11.6 points over the trial, the average mood of men got slightly worse.

The researchers believe that the traditional way in which men and women deal with emotional distress could be behind the disparity.

“The mechanisms are highly speculative at this point, but stereotypically, women ruminate and men distract,” added Dr Briton.

“So for people that tend to be willing to confront or expose themselves or turn toward the difficult, mindfulness is made for improving that. For people who have been largely turning their attention away from the difficult, to suddenly bring all their attention to their difficulties can be somewhat counterproductive.

 “While facing one’s difficulties and feeling one’s emotions may seem to be universally beneficial, it does not take into account that there may be different cultural expectations for men and women around emotionality.”

Dr Brown said since conducting the study she has found the same gender divide in two other published studies, and will shortly publish new details on her findings.

Source: Frontiers in Psychology.

Tapeworm Drug Effective at Treating MRSA


With the ever persistent threat of bacterial drug-resistance looming like a carrion bird waiting for a meal, scientists are continually on the hunt for new therapeutics to thwart infections like those caused by methicillin-resistant Staphylococcus aureus (MRSA). Fortuitously, scientists from Brown University have come across two drug compounds that are already in use to treat human tapeworm infections, which they report in a new study show great promise in stopping MRSA infections.

The findings from this study were published recently in PLOS ONE under an article entitled “Repurposing Salicylanilide Anthelmintic Drugs to Combat Drug Resistant Staphylococcus aureus.”

The Brown researchers screened over 600 drugs for effectiveness against MRSA, using an in vivo assay that cultures live nematode worms infected with the drug-resistant bacteria. The investigators found two compounds niclosamide, which is on World Health Organization’s list of essential medicines, and oxyclozanide, a closely related veterinary drug, were effective at suppressing MRSA cultures. Moreover, both drugs were observed to be as effective as the current last-line clinical treatment, vancomycin.

“Since niclosamide is FDA approved and all of the salicylanilide anthelmintic drugs are already out of patent, they are attractive candidates for drug repurposing and warrant further clinical investigation for treating staphylococcal infections,” explained Rajmohan Rajamuthiah, Ph.D. a postdoctoral scholar in the Warren Alpert Medical School of Brown University and first author on the current study.

Dr. Rajamuthiah and his colleagues found that oxyclozanide was more effective at killing MRSA, while niclosamide was more bacteriostatic—effectively suppressing, but not completely eradicating the bacteria. However, the researchers speculate that niclosamide may still provide enough of a kick to keep MRSA at bay while the immune system gets up to speed handling the infection.

While results from the current study are very encouraging and have Dr. Rajamuthiah and his colleagues feeling optimistic, the researchers did point out a caveat that the feel warrants further analysis. Drugs such as oxyclozanide and niclosamide are rapidly cleared by the body and are less effective at diffusing out of the bloodstream and into peripheral tissues, where some MRSA infections could reside.

“The low level of systemic circulation coupled with the rapid elimination profile of niclosamide suggests the necessity for further testing of the potential of niclosamide and oxyclozanide for treating systemic infections,” wrote the scientists. “Further studies should include the evaluation of these compounds in systemic and localized infection models in rodents.”

However, the flipside of the rapid clearance scenario is that drugs may impart very limited toxicity to patients. In order to determine the actual effects of these drugs in mammals, the researchers have planned a series of experiments in rodents to determine the two compounds efficacy and overall toxicity, when used to treat MRSA infections.

“The relatively mild toxicity of oxyclozanide is encouraging based on in vitro tests,” stated Dr. Rajamuthiah. “Since it has never been tested in humans and since it belongs to the same structural family as niclosamide, our findings give strong impetus to using oxyclozanide for further investigations.”

Are Alzheimer’s and diabetes the same disease?


HAVING type 2 diabetes may mean you are already on the path to Alzheimer’s. This startling claim comes from a study linking the two diseases more intimately than ever before. There is some good news: the same research also offers a way to reverse memory problems associated with diabetes – albeit in rats – which may hint at a new treatment for Alzheimer’s.

“Perhaps you should use Alzheimer’s drugs at the diabetes stage to prevent cognitive impairment in the first place,” says Ewan McNay from the University at Albany in New York.

Alzheimer’s cost the US $130 billion in 2011 alone. One of the biggest risk factors is having type 2 diabetes. This kind of diabetes occurs when liver, muscle and fat cells stop responding efficiently to insulin, the hormone that tells them to absorb glucose from the blood. The illness is usually triggered by eating too many sugary and high-fat foods that cause insulin to spike, desensitising cells to its presence. As well as causing obesity, insulin resistance can also lead to cognitive problems such as memory loss and confusion.

Are brain changes associated with Alzheimer's (green) reversible? <i>(Image: Medical Body Scans/Jessica Wilson/Photo Researchers/SPL)</i>

In 2005, a study by Susanne de la Monte’s group at Brown University in Providence, Rhode Island, identified a reason why people with type 2 diabetes had a higher risk of developing Alzheimer’s. In this kind of dementia, the hippocampus, a part of the brain involved in learning and memory, seemed to be insensitive to insulin. Not only could your liver, muscle and fat cells be “diabetic” but so it seemed, could your brain.

Feeding animals a diet designed to give them type 2 diabetes leaves their brains riddled with insoluble plaques of a protein called beta-amyloid – one of the calling cards of Alzheimer’s. We also know that insulin plays a key role in memory. Taken together, the findings suggest that Alzheimer’s might be caused by a type of brain diabetes.

If that is the case, the memory problems that often accompany type 2 diabetes may in fact be early-stage Alzheimer’s rather than mere cognitive decline.

Although there is no definitive consensus on the exact causes of Alzheimer’s, we do know that brains get clogged with beta-amyloid plaques. One idea gaining ground is that it is not the plaques themselves that cause the symptoms, but their precursors – small, soluble clumps of beta-amyloid called oligomersMovie Camera. The insoluble plaques could actually be the brain’s way of trying to isolate the toxic oligomers.

To investigate whether beta-amyloid might also be a cause of cognitive decline in type 2 diabetes, McNay, Danielle Osborne and their colleagues fed 20 rats a high-fat diet to give them type 2 diabetes. These rats, and another 20 on a healthy diet, were then trained to associate a dark cage with an electric shock. Whenever the rats were returned to this dark cage, they froze in fear – measuring how long they stayed still is a standard way of inferring how good their memory is.

Memory boost

As expected, the diabetic rats had weaker memories than the healthy ones – they froze in the dark for less than half the time of their healthy counterparts. To figure out whether this was due to the beta-amyloid plaques or the soluble precursors, Pete Tessier at the Rensselaer Polytechnic Institute in Troy, New York, engineered fragments of antibodies that disrupt the action of one or the other.

When the plaque-disrupting antibodies were injected into diabetic rats, no change was seen. However, after receiving antibodies specific for oligomers, they froze for just as long as the healthy rats. “The cognitive deficit brought on by their diabetes is entirely reversed,” says McNay.

Until now, the standard explanation for the cognitive decline associated with type 2 diabetes is that it is a result of insulin signalling gone awry. One effect is to reduce the hippocampus’s ability to transport energy, or glucose, to neurons during a cognitive task. The fact that amyloid builds up in the brains of diabetic animals – and also in people, was seen as an unhappy consequence of insulin imbalance.

These experiments suggest oligomers are actually to blame. Previous work from other groups has shown that the same enzymes break down both insulin and beta-amyloid oligomers – and that the oligomers prevent insulin binding to its receptors in the hippocampus. So when there is too much insulin around – as there is in someone with type 2 diabetes – those enzymes are working flat out to break it down. This preferential treatment of insulin leaves the oligomers to form clumps, which then keep insulin from its receptors, causing a vicious spiral of impaired brain insulin signalling coupled with cognitive decline.

“We think that our treatment soaked up the amyloid oligomers, so that they could no longer block insulin from binding to its receptors,” says McNay, who presented the preliminary data at the Society for Neuroscience meeting in San Diego earlier this month. “Everyone thinks of amyloid build-up as a consequence of the events that cause cognitive impairment in diabetes, but we’re saying it’s actually a cause.” It means, he says, that the cognitive decline seen in type 2 diabetes may be thought of as early-stage Alzheimer’s.

It’s a bold claim, and if correct, one with big implications. Given that the number of people with type 2 diabetes is expected to jump from 382 million now to 592 million by 2035, we might expect to see a similar trajectory for associated Alzheimer’s (New Scientist, 1 September 2012). If beta-amyloid build-up can be stopped in people with type 2 diabetes and their cognitive impairment reversed – perhaps many of them will never progress to Alzheimer’s.

For the last few years, organisations like the UK’s Alzheimer’s Society have been backing clinical trials to look for diabetes drugs that may have an effect on Alzheimer’s patients. “We’re saying that this may be not the only way to think about it,” says McNay.

The next step is to repeat the work, and if the results are corroborated, start looking for a drug that would do the same thing as the group’s modified antibodies, without having to inject the drug directly into the hippocampus. It will also be necessary to work out just how much amyloid the brain can safely do without, since low levels are important for memory formation.

“The work opens the door to inoculating the most at risk group, people with type 2 diabetes,” says Tres Thompson of the University of Texas at Dallas. There have been plenty of failed attempts to use antibodies to relieve Alzheimer’s in the past. “But these were all in people with advanced stages of the disease. Vaccinating people much earlier could give better results.”

Some researchers are still wary of focusing on beta-amyloid when 20 years of working on a treatment for that particular aspect of the disease has come to nothing. “I think it’s brilliant work – he’s using new techniques that seem to be working, but it’s still very beta-centric,” says Olivier Thibault at the University of Kentucky in Lexington. He cautiously agrees that McNay’s data do seem to suggest a causative link between beta-amyloid and impaired insulin signalling but says the group needs to factor in the effect of ageing – both diabetes and Alzheimer’s become more likely as we grow older.

Jessica Smith, spokeswoman for the UK Alzheimer’s Society in London welcomes the work. “We need to tease out the difference between those with type 2 diabetes who develop Alzheimer’s and those who don’t. If people were developing the signs earlier than we thought, then perhaps we can intervene earlier, rather than waiting until they have full clinical Alzheimer’s.”

Of course, there is another solution to staving off type 2 diabetes and any consequential Alzheimer’s that requires no drugs at all. “Go to the gym and eat fewer twinkies,” says McNay.

Mission to Mars moon could be a sample-return twofer.


The study helps to confirm the idea that the surface of Phobos contains tons of dust, soil, and rock blown off the Martian surface by large projectile impacts. Phobos’ orbital path plows through occasional plumes of Martian debris, meaning the tiny moon has been gathering Martian castoffs for millions of years. That means a sample-return mission planned by the Russian space agency could sample two celestial bodies for the price of one. “The mission is scheduled to be flown early in the next decade, so the question is not academic,” said James Head, professor of geological sciences and an author on the study. “This work shows that samples from Mars can indeed be found in the soil of Phobos, and how their concentration might change with depth. That will be critical in the design of the drills other equipment.”

https://i2.wp.com/cdn.physorg.com/newman/gfx/news/2013/missiontomar.jpg

The research appears in the latest issue of Space and Planetary Science.

The Russian mission will be the ‘s second attempt to return a sample from Phobos. Head was a participating scientist on the first try, which launched in 2011, but an engine failure felled the spacecraft before it could leave Earth orbit. The next attempt is scheduled to launch in 2020 or shortly thereafter.

This new research grew out of preparation for the original mission, which would still be en route to Phobos had it not encountered problems. Scientists had long assumed Phobos likely contained Martian bits, but Russian mission planners wanted to know just how much might be there and where it might be found. They turned to Head and Ken Ramsley, a visiting researcher in Brown‘s planetary geosciences group.

To answer those questions, Ramsley and Head started with a model based on our own Moon to estimate how much of Phobos’ regolith (loose rock and dust on the surface) would come from projectiles. They then used gravitational and orbital data to determine what proportion of that projectile material came from Mars.

“When an impactor hits Mars, only a certain of proportion of ejecta will have enough velocity to reach the altitude of Phobos, and Phobos’ orbital path intersects only a certain proportion of that,” Ramsley said. “So we can crunch those numbers and find out what proportion of material on the surface of Phobos comes from Mars.”

According to those calculations, the regolith on Phobos should contain Martian material at a rate of about 250 parts per million. The Martian bits should be distributed fairly evenly across the surface, mostly in the upper layers of regolith, the researchers showed.

“Only recently—in the last several 100 million years or so—has Phobos orbited so close to Mars,” Ramsley said. “In the distant past it orbited much higher up. So that’s why you’re going to see probably 10 to 100 times higher concentration in the upper regolith as opposed to deeper down.”

And while 250 parts per million doesn’t sound like a lot, the possibility of returning even a little Martian material to Earth gets planetary scientists excited. It’s a nice bonus for a mission primarily aimed at learning more about Phobos, a mysterious little rock in its own right.

Scientists are still not sure where it came from. Is it a chunk of Mars that was knocked off by an impact early in Martian history, or is it an asteroid snared in Mars’s orbit? There are also questions about whether its interior might hold significant amounts of water.

“Phobos has really low density,” Head said. “Is that low density due to ice in its interior or is it due to Phobos being completely fragmented, like a loose rubble pile? We don’t know.”

Toddler brain scan language insight.


Regions of the brain that show leftward asymmetry of myelin
The left hand side of the brain has more myelin

The brain has a critical window for language development between the ages of two and four, brain scans suggest.

Environmental influences have their biggest impact before the age of four, as the brain’s wiring develops to process new words, say UK and US scientists.

The research in The Journal of Neuroscience suggests disorders causing language delay should be tackled early.

It also explains why young children are good at learning two languages.

The scientists, based at King’s College London, and Brown University, Rhode Island, studied 108 children with normal brain development between the ages of one and six.

“Start Quote

Our work seems to indicate that brain circuits associated with language are more flexible before the age of 4, early intervention for children with delayed language attainment should be initiated before this critical age”

Dr Jonathan O’Muircheartaigh King’s College London

They used brain scans to look at myelin – the insulation that develops from birth within the circuitry of the brain.

To their surprise, they found the distribution of myelin is fixed from the age of four, suggesting the brain is most plastic in very early life.

Any environmental influences on brain development will be strongest in infanthood, they predict.

This explains why immersing children in a bilingual environment before the age of four gives them the best chance of becoming fluent in both languages, the research suggests.

It also suggests that there is a critical time during development when environmental influence on cognitive skills may be greatest.

Dr Jonathan O’Muircheartaigh, from King’s College London, led the study.

He told the BBC: “Since our work seems to indicate that brain circuits associated with language are more flexible before the age of four, early intervention for children with delayed language attainment should be initiated before this critical age.

“This may be relevant to many developmental disorders, such as autism, since delayed language is a common early trait.”

Growing vocabulary

Early childhood is a time when language skills develop very rapidly.

Babies have a vocabulary of up to 50 words at 12 months but by the age of six this has expanded to about 5,000 words.

Language skills are localised in the frontal areas of the left-hand side of the brain.

The researchers therefore expected more myelin to develop in the left-hand side of the brain, as the children learned more language.

In fact, they found it remained constant, but had a stronger influence on language ability before the age of four, suggesting there is a crucial window for interventions in developmental disorders.

“This work is important as it is the first to investigate the relationship between brain structure and language across early childhood and demonstrate how this relationship changes with age,” said Dr Sean Deoni from Brown University, a co-researcher on the study.

“This is important since language is commonly altered or delayed in many developmental disorders, such as autism.”

Commenting on the study, Prof Dorothy Bishop of the department of Developmental Neuropsychology at the University of Oxford said the research added important new information about early development of connections in brain regions important for cognitive functions.

“There is suggestive evidence of links with language development but it is too early to be confident about functional implications of the findings,” she said.

“Ideally we would need a longitudinal study following children over time to track how structural brain changes relate to language function.”

The study was funded by the National Institutes for Mental Health (US) and the Wellcome Trust (UK).

Frequent Acid Reflux Associated with Throat Cancers.


Gastric reflux is a risk factor for cancers of the pharynx and larynx, and the use of antacids seems to lower that risk, according to an observational study in Cancer Epidemiology, Biomarkers and Prevention.

In a multicenter collaboration, researchers matched some 630 cases of laryngopharyngeal squamous cell carcinomas with twice the number of controls without cancer. Analyses were adjusted for demographics, smoking history, and HPV16 seropositivity.

Among patients who were not heavy smokers or drinkers, a history of self-reported frequent heartburn was significantly associated with throat cancers relative to those without heartburn (odds ratio, 1.78). Use of antacids for heartburn was associated with a lower risk (OR, 0.59). However, there was no such inverse association seen with the use of proton-pump inhibitors or histamine H2 receptor antagonists — possibly due to confounding from increased disease severity leading to their use.

 

The authors speculate that acid reflux may cause cancers by, for example, inducing chronic inflammation or activating signaling pathways of cellular proliferation.

Source: Cancer Epidemiology, Biomarkers and Prevention

GI Bleeds: Benefits of Conservative Transfusion Strategy Seem Confirmed .


A conservative transfusion strategy for acute upper gastrointestinal bleeding appears to confer a greater survival benefit than liberal treatment, according to a New England Journal of Medicine study.

Investigators randomized some 900 patients either to a conservative strategy (transfusion when hemoglobin fell below 7 g/dL) or to a liberal strategy (transfusion when hemoglobin fell below 9). About half those treated conservatively received transfusions, as opposed to 85% of those assigned to the liberal strategy.

Those on conservative treatment showed a 45% relative risk reduction in all-cause mortality at 45 days (absolute mortality, 5% vs. 9% on liberal treatment). Similarly, further bleeding was less frequent on conservative treatment, as was the rate of adverse events. However, patients with severe cirrhosis (Child-Pugh class C) did not show a survival benefit.

An editorialist, noting that the findings “justify current recommendations,” concludes that “most patients with upper gastrointestinal bleeding, with or without portal hypertension, should have blood transfusions withheld until the hemoglobin level drops below 7.”

Source: NEJM

Alzheimer’s May be Caused by Poor Diet.


The cause of the debilitating, and fatal, brain disease Alzheimer’s is conventionally said to be a mystery.

While we know that certain diseases, like type 2 diabetes, are definitively connected to the foods you eat, Alzheimer’s is generally thought to strike without warning or reason.

That is, until recently.

Now, a growing body of research suggests there may be a powerful connection between the foods you eat and your risk of Alzheimer’s disease and dementia, via similar pathways that cause type 2 diabetes.

Some have even re-named Alzheimer’s as “type 3 diabetes.”

Can You Eat Your Way to Alzheimer’s?

In a recent animal study, researchers from Brown University in Providence, Rhode Island were able to induce many of the characteristic brain changes seen with Alzheimer’s disease (disorientation, confusion, inability to learn and remember) by interfering with insulin signaling in their brains.1

Faulty insulin (and leptin, another hormone) signaling is an underlying cause of insulin resistance, which, of course, typically leads to type 2 diabetes. However, while insulin is usually associated with its role in keeping your blood sugar levels in a healthy range, it also plays a role in brain signaling. When researchers disrupted the proper signaling of insulin in the brain, it resulted in dementia.

What does this have to do with your diet?

Everything, as over-consumption of sugars and grains is what ultimately causes your body to be incapable of “hearing” the proper signals from insulin and leptin, leaving you insulin resistant in both body and brain.

Alzheimer’s disease was tentatively dubbed “type 3 diabetes” in early 2005 when researchers learned that the pancreas is not the only organ that produces insulin. Your brain also produces insulin, and this brain insulin is necessary for the survival of your brain cells.

If You Have Diabetes, Your Risk of Alzheimer’s Increases Dramatically

Diabetes is linked to a 65 percent increased risk of developing Alzheimer’s,2 which may be due, in part, because insulin resistance and/or diabetes appear to accelerate the development of plaque in your brain, which is a hallmark of Alzheimer’s.3 Separate research has found that impaired insulin response was associated with a 30 percent higher risk of Alzheimer’s disease,4 and overall dementia and cognitive risks were associated with high fasting serum insulin, insulin resistance, impaired insulin secretion and glucose intolerance.

A drop in insulin production in your brain may contribute to the degeneration of your brain cells, mainly by depriving them of glucose, and studies have found that people with lower levels of insulin and insulin receptors in their brain often have Alzheimer’s disease (people with type 2 diabetes often wind up with low levels of insulin in their brains as well). As explained in New Scientist, which highlighted this latest research:5

“This new focus [on the Alzheimer’s/diabetes/insulin connection] follows a growing recognition of insulin’s role in the brain. Until recently, the hormone was typecast as a regulator of blood sugar, giving the cue for muscles, liver and fat cells to extract sugar from the blood and either use it for energy or store it as fat. We now know that it is a master multitasker: it helps neurons, particularly in the hippocampus and frontal lobe, take up glucose for energy, and it also regulates neurotransmitters, like acetylcholine, which are crucial for memory and learning.

What’s more, it encourages plasticity – the process through which neurons change shape, make new connections and strengthen others. And it is important for the function and growth of blood vessels, which supply the brain with oxygen and glucose.

As a result, reducing the level of insulin in the brain can immediately impair cognition. Spatial memory, in particular, seems to suffer when you block insulin uptake in the hippocampus… Conversely, a boost of insulin seems to improve its functioning.

…this role in the brain ‘makes evolutionary sense,’ since it would help us to remember the location of a food source. As our ancestors gorged on berries in the savannah, for instance, the spike in glucose and the subsequent rush of insulin would signal ‘remember this, it’s important,’ causing the brain to crystallise the memory.

But as we know from type 2 diabetes, processes that evolved to help us meet the challenges of prehistory can easily backfire in the modern world.

When people frequently gorge on fatty, sugary food, their insulin spikes repeatedly until it sticks at a higher level. Muscle, liver and fat cells then stop responding to the hormone, meaning they don’t mop up glucose and fat in the blood. As a result, the pancreas desperately works overtime to make more insulin to control the glucose – and levels of the two molecules skyrocket.

…The pancreas can’t keep up with the demand indefinitely, however, and as time passes people with type 2 diabetes often end up with abnormally low levels of insulin.”

Alzheimer’s Might be “Brain Diabetes”

It’s becoming increasingly clear that the same pathological process that leads to insulin resistance and type 2 diabetes may also hold true for your brain. As you over-indulge on sugar and grains, your brain becomes overwhelmed by the consistently high levels of insulin and eventually shuts down its insulin signaling, leading to impairments in your thinking and memory abilities, and eventually causing permanent brain damage.

You may already know I have become passionate about warning of the dangers of fructose. There is NO question in my mind that regularly consuming more than 25 grams of fructose per day will dramatically increase your risk of dementia and Alzheimer’s disease. Consuming too much fructose will inevitably wreak havoc on your body’s ability to regulate proper insulin levels.

Although fructose is relatively “low glycemic” on the front end, it reduces the affinity for insulin for its receptor leading to chronic insulin resistance and elevated blood sugar on the back end. So, while you may not notice a steep increase in blood sugar immediately following fructose consumption, it is likely changing your entire endocrine system’s ability to function properly behind the scenes.

Additionally, fructose has other modes of neurotoxicity, including causing damage to the circulatory system upon which the health of your nervous system depends, as well as profoundly changing your brain’s craving mechanism, often resulting in excessive hunger and subsequent consumption of additional empty carbohydrate-based calories.

In one study from UCLA, researchers found that rats fed a fructose-rich and omega-3 fat deficient diet (similar to what is consumed by many Americans) developed both insulin resistance and impaired brain function in just six weeks.6

Plus, when your liver is busy processing fructose (which your liver turns into fat), it severely hampers its ability to make cholesterol, an essential building block of your brain crucial to its health. This is yet another important facet that explains how and why excessive fructose consumption is so detrimental to your health.

Since the average American is exceeding this recommendation by 300% this is a pervasive and serious issue. I view significantly reducing fructose consumption as the MOST important step you can take to lower your risk of Alzheimer’s disease.

More Tips for Avoiding Alzheimer’s Disease

The beauty of following my newly revised Nutrition Plan is that it helps treat and prevent all chronic degenerative diseases, from the common ones like heart disease, cancer, diabetes, obesity and Alzheimer’s to the ones you have never heard of or can’t even pronounce. So please read the Plan as soon as you can. It is divided into three helpful sections, Beginner, Intermediate and Advanced to help you start at the right level.

The plan is the first step in addressing Alzheimer’s disease, which is currently at epidemic proportions, with 5.4 million Americans – including one in eight people aged 65 and over – living with the disease.7 By 2050, this is expected to jump to 16 million, and in the next 20 years it is projected that Alzheimer’s will affect one in four Americans.

In spite of how common memory loss is among Westerners, it is NOT a “normal” part of aging. While even mild “senior moments” may be caused by the same brain lesions associated with Alzheimer’s disease and other forms of dementia, these cognitive changes are by no means inevitable! People who experience very little decline in their cognitive function up until their deaths have been found (post-mortem) to be free of brain lesions, showing that it’s entirely possible to prevent the damage from occurring in the first place… and one of the best ways to do this is by leading a healthy lifestyle.

  • Fructose. As mentioned, most everyone will benefit from keeping their total fructose consumed to below 25 grams per day.
  • Improve Magnesium Levels. There is some exciting preliminary research strongly suggesting a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Unfortunately most magnesium supplements do not pass the blood brain levels, but a new one, magnesium threonate, appears to and holds some promise for the future for treating this condition.
  • Optimize your vitamin D levels with safe sun exposure. Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed.8 Researchers believe that optimal vitamin D levels may enhance the amount of important chemicals in your brain and protect brain cells by increasing the effectiveness of the glial cells in nursing damaged neurons back to health.

Vitamin D may also exert some of its beneficial effects on Alzheimer’s through its anti-inflammatory and immune-boosting properties. Sufficient vitamin D is imperative for proper functioning of your immune system to combat inflammation that is also associated with Alzheimer’s.

  • Keep your fasting insulin levels below 3. This is indirectly related to fructose, as it will clearly lead to insulin resistance. However other sugars (sucrose is 50% fructose by weight), grains and lack of exercise are also important factors.
  • Vitamin B12: According to a small Finnish study recently published in the journal Neurology,9 people who consume foods rich in B12 may reduce their risk of Alzheimer’s in their later years. For each unit increase in the marker of vitamin B12 (holotranscobalamin) the risk of developing Alzheimer’s was reduced by 2 percent. Very high doses of B vitamins have also been found to treat Alzheimer’s disease and reduce memory loss.
  • Eat a nutritious diet, rich in folate, such as the one described in my nutrition plan. Vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day.
  • High-quality animal-based omega-3 fats, such as krill oil. (I recommend avoiding most fish because, although fish is naturally high in omega-3, most fish are now severely contaminated with mercury.) High intake of the omega-3 fats EPA and DHA help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression, and lowering your risk of developing the disorder.
  • Avoid and remove mercury from your body. Dental amalgam fillings, which are 50% mercury by weight, are one of the major sources of heavy metal toxicity, however you should be healthy prior to having them removed. Once you have adjusted to following the diet described in my optimized nutrition plan, you can follow the mercury detox protocol and then find a biological dentist to have your amalgams removed.
  • Avoid aluminum, such as antiperspirants, non-stick cookware, vaccine adjuvants, etc.
  • Exercise regularly. It’s been suggested that exercise can trigger a change in the way the amyloid precursor protein is metabolized,10 thus, slowing down the onset and progression of Alzheimer’s. Exercise also increases levels of the protein PGC-1alpha. Research has also shown that people with Alzheimer’s have less PGC-1alpha in their brains11 and cells that contain more of the protein produce less of the toxic amyloid protein associated with Alzheimer’s. I would strongly recommend reviewing the Peak Fitness Technique for my specific recommendations.
  • Avoid flu vaccinations as most contain both mercury and aluminum, well-known neurotoxic and immunotoxic agents.
  • Eat plenty of blueberries. Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against Alzheimer’s and other neurological diseases.
  • Challenge your mind daily. Mental stimulation, especially learning something new, such as learning to play an instrument or a new language, is associated with a decreased risk of Alzheimer’s. Researchers suspect that mental challenge helps to build up your brain, making it less susceptible to the lesions associated with Alzheimer’s disease.
  • Avoid anticholinergic and statin drugs. Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of coenzyme Q10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.

Source: Dr. Mercola