Archive for the ‘OLD AGE CONDITIONS’ Category


Sunday, March 1st, 2015


Human life expectancy: myth and reality

When we talk about human life expectancy, we have to take a close look at how we’re measuring it – and this is where things can get confusing.

What most of us refer to as ‘average life expectancy’ is actually ‘life expectancy at birth’.What most of us refer to as ‘average life expectancy’ is actually ‘life expectancy at birth’. It’s based on the average number of years a newborn baby can expect to live in a specific society at a particular point in history, assuming living conditions will remain roughly the same for the duration of that life. Unfortunately, this isn’t a terribly efficient way to measure and compare adult longevity. It’s based on the average number of years a newborn baby can expect to live in a specific society at a particular point in history, assuming living conditions will remain roughly the same for the duration of that life. Unfortunately, this isn’t a terribly efficient way to measure and compare adult longevity. Why? Because one of the most influential factors in life expectancy at birth is the infant (and child) mortality rate. For our ancestors (whether 200 or 2000 years ago), this figure was much higher than it is today, which had the effect of skewing ‘average life expectancy’ rates downward quite dramatically in previous eras.

To say that ‘the life expectancy of our prehistoric ancestors was only 37’ doesn’t mean that the average person in those times only made it to age 37. Many of them would have lived to 60 or 70, but extremely high infant/child mortality rates seriously dropped the average age of longevity.

So the common modern perception that we’re living nearly twice as long as people did in the not-too-distant past isn’t accurate at all. What these statistics show instead is that a lot more of us today are now surviving into adulthood, thereby increasing our ‘average lifespans’ in a big wayAccording to the US National Centre for Health Statistics, life expectancy for American men was 45.6 years in 1907 but rose to 75.5 years by 2007 – an astounding increase of 30 years within one century! What made the major difference, however, was infant mortality – a rate of around 10% in 1907, but only 0.68% in 2007. Infant mortality reduction wasn’t the only factor in this extraordinary increase of course, but it was the defining one.

So the common modern perception that we’re living nearly twice as long as people did in the not-too-distant past isn’t accurate at all. What these statistics show instead is that a lot more of us today are now surviving into adulthood, thereby increasing our ‘average lifespans’ in a big way. Interestingly, if you look at the age of the oldest-living people from around 1960 (between 110 and 115 years of age), you’ll find that it’s virtually identical to the ages of the longevity record-holders of today – so maximum lifespans really haven’t changed at all in over half a century.

The age of medical miracles

Latest figures show that life expectancy in Australia is 79.9 years for men and 84.3 years for women1, which puts us among the top 10 countries in the world for both male and female longevity2 according to WHO World Health Statistics (2014).

There’s no doubt that medical advancements in the past century have played a huge part in improving life expectancy rates in Australia. Our understanding of the causes of diseases has progressed mightily, which in turn has led to major victories in the battle against illness and age-related ailments. Medical science has put a big dent in many of the diseases that once led to premature death.There’s no doubt that medical advancements in the past century have played a huge part in improving life expectancy rates in Australia. Our understanding of the causes of diseases has progressed mightily, which in turn has led to major victories in the battle against illness and age-related ailments. Medical science has put a big dent in many of the diseases that once led to premature death.

Looking back to the beginning of the 19th century, the primary causes of premature death were diseases like typhoid, scarlet fever, smallpox and rheumatic fever. Modern vaccination programs, antibiotics and a better understanding of medical science have made these diseases far less of a threat today.

Historically, here are some of the most important medical breakthroughs that have contributed to increased human longevity:

  • Vaccines
    Vaccination has had a profound effect in preventing the spread of a number of once-dreaded diseases including polio, diphtheria, whooping cough and tetanus. The first successful vaccine was developed in 1798 (for smallpox). Smallpox was once rightly considered one of the world’s most dangerous diseases, but it was declared officially eradicated by the World Health Organisation in 1979, thanks to a comprehensive global vaccination program.
  • Penicillin
    The surge in life expectancy in the 20th century owes a lot to the discovery of penicillin in 1928. This was the first of the antibiotics, and it had a massive impact in the prevention of deaths from bacterial infections due to staphylococci, streptococci and similar scourges. Deaths from tuberculosis also plummeted and cases of infections after surgery fell to all-time lows. Antibiotics still play a major role in the fight against infection today.
  • Pasteur’s Germ Theory
    For most of us, the name Louis Pasteur is mainly associated with pasteurised milk. Pasteur did a lot more than make milk safer to drink, however – he was the clever fellow who discovered that germs were the cause of many common diseases. Before his discovery, there were all sorts of dubious theories about what caused disease, which meant that many of the popular treatments of the day were either ineffective or even harmful to patients. It’s no exaggeration to say that Pasteur’s research into the role played by viruses and bacteria in disease causation marked the birth of modern medical science.
  • Anaesthesia
    Another of the reasons post-surgery life expectancy has increased so much in the past century is because of major advances in the science of anaesthesia. Long gone are the days when anaesthesia consisted of a quick dose of whiskey followed by a hard piece of rubber to bite down on!
  • Insulin
    For diabetics, the discovery of insulin and other advances in the control of blood sugar levels has meant vastly improved life expectancy rates for those who suffer from this disease.


Of course, these are just a few of the breakthroughs that have played a starring role in helping humans live longer. Others include X-rays, DNA research, blood-thinning agents, high blood pressure medications and cholesterol-lowering drugs.

Medical advancements have become such a normal part of our everyday lives that we now tend to take them for granted. Australian snakebite statistics present a classic example. Anyone who watches Animal Planet knows that 19 of the 23 deadliest snakes on earth are found Down Under, and that we’re the only continent where venomous snake species outnumber non-venomous varieties. Every year around 2000 people are bitten by snakes in this country, so you would naturally assume the potent combination of lots of deadly snakes and plenty of bites would translate to a fairly high death rate. But the statistics tell a completely different story: on average, only 3 or 4 people die from snakebite in Australia each year3.

This extremely low fatality rate is due to the increased availability and effectiveness of antivenins and the introduction of much improved first aid techniques. As recently as the 1960s, some outdoor survival manuals were still advocating cutting a cross shape into the bite site with your penknife, sucking out the venom and then applying a tourniquet – methods considered not only ineffectual but downright dangerous today (the modern technique involves a pressure bandage and immobilisation).

And now for the bad news

It’s clear that recent generations have done a great job of eliminating or at least seriously reducing many of the factors that once resulted in lower life expectancies. Poor sanitation practices have been replaced with a better understanding of hygiene (doctors didn’t adopt the practice of washing their hands before surgery until the mid-1800s). The quality of training for medical personnel has improved out of sight, along with health technology. Guesswork about the causes and best treatments of illnesses has been replaced with scientific fact (people once believed malaria was caused by breathing ‘bad vapours’ and that bloodletting was a handy cure for just about everything). Cutting edge stem cell research, new medications, space-age treatments and superior aged care are all playing a part in ensuring that people today have every chance of living to a ripe old age.

Unfortunately, just as we celebrate our successes in conquering many of the major health issues of yesterday, we find ourselves confronted with a whole new set of health and environmental challenges in the 21st century.

According to the World Health Organisation, the 3 major causes of premature death in 2014 were coronary heart disease, stroke and lower respiratory infections (such as pneumonia). We may have thrashed smallpox and diphtheria, learned how to tackle gangrene and put the bite on bubonic plague, but we’ve supplanted these gains with a whole new set of ‘lifestyle diseases’, many of which are caused by nothing more than physical inactivity, poor diet and unhealthy lifestyle choices.According to the World Health Organisation, the 3 major causes of premature death in 2014 were coronary heart disease, stroke and lower respiratory infections (such as pneumonia). We may have thrashed smallpox and diphtheria, learned how to tackle gangrene and put the bite on bubonic plague, but we’ve supplanted these gains with a whole new set of ‘lifestyle diseases’, many of which are caused by nothing more than physical inactivity, poor diet and unhealthy lifestyle choices.

The human race is now fatter than ever before – and this has all happened very quickly. Obesity rates in Australia have doubled in the past 20 years, and if current trends continue, 83% of Aussie men and 75% of Aussie women over the age of 20 will be overweight or obese by 2025 – not to mention about a third of all 5-19 year olds. This equates to roughly 17 million obese/overweight Australians within the next 15 years4.

These days we sit more, move less and eat a lot of processed and adulterated foods that previous generations would scarcely recognise as food at all. In an increasingly urbanised society, the family vegetable garden, chicken coop and milking shed are long gone. In their place are ‘diet’ soft drinks with no nutritional value (but plenty of ‘interesting’ chemical ingredients) and takeaway foods overloaded with harmful fats and excessive sugar.


And while the number of smokers in Australia has been steadily decreasing since 19905 (great news), diabetes is on the rise and is now the fastest growing chronic disease in Australia (and the 6th-highest cause of disease death in this country overall), with one person being diagnosed every 5 minutes6.

21st century afflictions like obesity, heart disease and stress-related illnesses are sure to put a damper on any optimistic predictions of soaring life expectancies in the near future. Global cancer cases are also on the rise, up 20% in just the past decade7, with a fair chunk of this increase attributed to lack of exercise, excessive alcohol and tobacco consumption, poor dietary habits and other lifestyle-driven factors. We’re working longer hours, sleeping less and being bombarded with conflicting marketing messages about exactly what is ‘healthy’.

Be careful what you wish for

The other obvious question is this: even if we could live to be 150, would we really want to? By stretching out the human lifespan, age-related health issues would expand: Alzheimer’s, dementia, coronary heart disease, arthritis, osteoporosis, Parkinson’s, cancer, eye problems and much more; incidents of broken bones and head injuries from falls would soar. Many of us like to think of increased human longevity as a wondrous possibility symbolising our ingenuity, but there are negative aspects to consider as well.

So, could we really live to be 150? At the moment, such a prospect is pure conjecture – there is no scientific evidence to suggest it will ever happen.


Henry Sapiecha


Thursday, July 4th, 2013



NEW YORK | Wed Jul 3, 2013 4:06pm EDT


(Reuters Health) – People who spend a lot of time reading, writing and otherwise seeking and processing new information lose their thinking and memory skills more slowly as they age, a new study suggests.



Researchers found being “cognitively active” both early and later in life was tied to better performance on memory tests among people in their 80s.


That was still the case once they autopsied participants’ brains after they died and accounted for changes that signal cognitive problems, such as early Alzheimer’s disease.


“There’s been a real controversy about why a cognitively active lifestyle is associated with (a lower risk of) cognitive decline,” said Robert Wilson, who led the study at Rush University Medical Center in Chicago


“One theory has been that cognitive inactivity is simply a consequence of the underlying disease, rather than a true risk factor,” he told Reuters Health.


But the new study, Wilson said, suggests the link is not explained by people who have more diseased brains being less active in old age.


He and his colleagues asked more than 1,600 older adults starting in 1997 about how often they went to the library, wrote letters and sought information as a child and young adult and more recently. Then they gave participants a thinking and memory test every year and tracked their progress.


The new study included 294 of those participants who died at an average age of 89 and underwent a brain autopsy to look for cognition-related changes.


They had each taken an average of six annual cognitive tests during the study, which showed that 102 developed dementia and 51 developed mild cognitive impairment.


On a scale of 1 to 5 measuring how often a person engaged in cognitively stimulating activities, with 1 being the least frequent, the average participant scored a 3.2 for late-life cognitive activity and a 3.1 for early-life activity.


Compared to people with average late-life cognitive activity, thinking and memory skills declined 48 percent faster among those with infrequent activity and 32 percent slower among those who were the most cognitively active.


Likewise, the study team found cognition declined 42 percent faster for participants who rarely read and wrote early in life than for the average person, and 32 percent slower for the very cognitively active.


“This confirms that the effect of cognitive activity is over and above anything having to do with pathology,” said Charles Hall, who has studied the effects of mental activity at the Albert Einstein College of Medicine in Bronx, New York.


“We’ve been thinking for a long time that there’s not going to be any harm from cognitive activity and there might be some good, and this is more confirmation of that,” Hall, who wasn’t involved in the new research, told Reuters Health.



The study, published Wednesday in Neurology, doesn’t prove that being mentally active wards off cognitive decline. But Wilson said he thinks it “moves us closer to that.”


“We do think a cognitively active lifestyle is good for your cognitive health and brain health in old age,” he said.


But keeping mentally busy shouldn’t be a chore, he added. Wilson said photography, quilting and book clubs may all keep people’s minds working.


He recommended that people choose something stimulating and challenging that they enjoy and can keep doing as they age.


Prashanthi Vemuri of the Mayo Clinic in Rochester, Minnesota, who co-wrote an editorial accompanying the new study, also told Reuters Health the type of mental activity doesn’t seem to matter as much as just being active in general. And it’s never too late to start, she noted.


“Just keeping mentally stimulated is very important,” Vemuri said.


SOURCE: Neurology, online July 3, 2013.


Henry Sapiecha

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Thursday, May 23rd, 2013

Alzheimer’s disease can now be cured in mice-Are humans next?

Although no one is announcing a cure for Alzheimer’s disease just yet, research recently conducted at the University of Southern California does at least offer a glimmer of hope. Using drugs known as TSPO (translocator protein) ligands, scientists there have successfully halted and even reversed the effects of Alzheimer’s in mice.


The mice, all of which were male, had been genetically engineered to develop the disease. The drugs were tested on both 7-month-old young adult mice and 24-month-old elderly mice. Because the TSPO ligands increase production of steroid hormones, it was important that the animals’ existing testosterone levels be kept low before beginning the treatment. While this had already occurred naturally with the older mice as a result of aging, the younger ones had to be castrated in order to bring their levels down.

After receiving once-a-week treatments for four weeks, all of the mice showed improvements. This was particularly noteworthy with the older mice, as their Alzheimer’s had become quite severe. After the four treatments, however, they showed “significant lowering of Alzheimer’s-related pathology and improvements in memory behavior.”

It’s already known that TSPO ligands help protect nerve cells by reducing inflammation, and that they increase the production of neuroactive hormones in the brain. The scientists now plan on determining which factor plays more of a part in the success with the mice, then developing new TSPO ligands designed around those findings.

“From the optimistic perspective, our data provide very promising findings with tangible potential benefits for both the prevention and treatment of Alzheimer’s,” said lead scientist Prof. Christian Pike. “On the pessimistic side, research scientists have developed many interventions that cured Alzheimer’s in mice but have failed to show significant benefits in humans. A critical direction we are currently pursuing is successfully translating these findings into humans.”

A paper on the research was recently published in The Journal of Neuroscience

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Henry Sapiecha

Alzheimers is most times mis-diagnosed as the doctor explains in this video

Sunday, December 23rd, 2012

Alzheimers is not dignosed well

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Sourced & published by Henry Sapiecha


Sunday, March 4th, 2012

Protiens effect on alzheimers patients condition

There have been many reports on numerous different approaches by scientists looking to tackle Alzheimer’s disease. While some, such as the anticancer drug bexarotene and a compound known as J147, show great promise, there is still no approved treatment to slow the disease’s progression. The latest promising candidate for a treatment comes from Canada’s Simon Fraser University (SFU), where a team has concluded that ensuring that sugar levels in a brain protein known as tau are maintained could slow or prevent the fatal disease.

Tau proteins are abundant in neurons of the central nervous system where they stabilize microtubules, which act like highways inside cells that allow intracellular transport. Earlier research has shown that defective tau proteins can lead to Alzheimer’s disease and that linkage of sugar molecules to proteins like tau is essential in cells.

Previous research has also shown a naturally occurring enzyme known as O-GlcNAcase robs tau of these essential sugar molecules, resulting in an Alzheimer brain having clumps of tau have almost none of this sugar attached to them. This clumping is an early sign of the disease and the number of clumps correlates with its severity.

Using a chemically-created inhibitor called Thiamet-G, SFU chemistry professor David Vocadlo and his colleagues have been able to stop O-GlcNAcase from depleting tau proteins of sugar molecules. The researchers found that mice given a daily dose of Thiamet-G in their drinking water had fewer clumps of tau and maintained healthier brains.

“A lot of effort is needed to tackle this disease and different approaches should be pursued to maximize the chance of successfully fighting it,” said Vocadlo. “In the short term, we need to develop better inhibitors of the enzyme and test them in mice. Once we have better inhibitors, they can be clinically tested.”

The team’s paper, “Increasing O-GlcNAc slows neurodegeneration and stabilizes tau against aggregation,” is published in the journal Nature Chemical Biology.

Source: Simon Fraser University

Sourced & published by Henry Sapiecha


Sunday, March 27th, 2011

Let them eat fish & fat

Older folk who suffer from depression don’t need a drug, a hug, or a room in an senior’s home.

Just let them eat their fatty meats and fish by the bucketload!

A fresh study proves again what’s been said all along — the best way to get your groove back is to put fat back on the menu.

It’s true at any age, but the latest study looks at seniors: Iranian researchers recruited 66 who suffered from moderate to somewhat more severe depression, then gave them either a placebo or a 1-gram fish oil supplement containing 300 mg each of DHA and EPA.

That’s not a lot — you can and should get more — but the new study shows it’s a pretty good start, because the patients who got the supplement saw more relief from their depression as measured by a standardized 15-question survey than those given the placebo.

Side note: Anyone who can diagnose a serious mental disorder in 15 questions is full of it, and I don’t mean fish oil.

But that’s an argument for another day.

In any case, none of this surprises me — and if you’re a longtime reader, it won’t surprise you either. The only real surprise here is that researchers think this is still worth studying.

It’s not.

The verdict was in long ago — fish oil, cod liver oil, omega-3 fatty acids or whatever other name you want to sell it under is essential to the human brain at any age… and the shift away from these fats in the diet has been disastrous.

Don’t expect a mea culpa from the mainstream on this any time soon — they’re still pushing bunny chow despite the fact that it hasn’t made anyone thinner, happier or healthier.

Save your own noggin — enjoy your fats, and take a quality omega-3 supplement.


Sunday, March 27th, 2011

Pink power can save your brain

Algae pigment chases dementia marker

Big Pharma’s going to hate this — and that means I love it already: One of the tiniest and most humble creatures on the planet could hold the key to preventing Alzheimer’s disease.

It’s an algae called Haematococcus pluvialis, and it sits literally at the bottom of the food chain.

Because of its pink pigment, which comes from the antioxidant astaxanthin, anything that eats this algae also turns pink… as do the creatures that eat those creatures, and so on.

Think shrimp, salmon and flamingos.

But to explain how it works, I’m going to have to take you from the bottom of the food chain to the brink of cutting-edge science, where researchers have been investigating a compound called phospholipid hydroperoxides.

It’s called PLOOH for short, but don’t snicker at the name — this stuff is deadly serious: It builds up in the red blood cells of dementia patients.

Now, Japanese researchers say astaxanthin can actually flush all that extra PLOOH right out of your system (OK, you can snicker a little).

In a double-blind experiment, 30 healthy volunteers between the ages of 50 and 69 years old were given either a placebo or 6 or 12 mg of astaxanthin a day for 12 weeks.

While the placebo patients had no change in PLOOH, those given the astaxanthin saw their levels plunge by between 40 and 50 percent, with those who took the higher dose getting the biggest benefit, according to the study in BMJ.

Since dementia can take so many years before it manifests, it may be decades before anyone can say for certain whether astaxanthin will stop it.

But there’s no reason to wait — because by then, it might be too late for you. And besides, there’s enough research on its other benefits that I’ve already been calling this stuff “the alpha antioxidant.”

And with 500 times the antioxidant power of vitamin E, it’s easy to see why.

Studies have found that astaxanthin can protect everything from your heart to your eyes — and since it’s sat at the bottom of the food chain for millions of years, you might sat it’s been time-tested by Mother Nature herself.

You can’t beat that kind of lab work!

Age-Related Macular Degeneration: the leading cause of blindness in the aging population
· Alzheimer’s and Parkinson’s Diseases: two of the most important neurodegenerative diseases
· Cholesterol Disease: ameliorates the effects of LDL, the “bad” cholesterol
· Inflammatory, chronic viral and autoimmune diseases
· Dyspepsia
· Semen fertility improvement
· Muscle function
· Sunburn from UV light
· Normalization of cardiac rhythm
· Anti-hypertension agent
· Stress management
· Benign Prostatic Hyperplasia (BPH)
· Stroke: repairs damage caused by lack of oxygen.

A demand for natural ASTAXANTHIN is now emerging in the fast-growing, multi-billion dollar nutraceutical market; in particular, increasing evidence suggests that ASTAXANTHIN was shown to be a much more powerful antioxidant than vitamins C and E, or than other carotenoids such as beta-carotene, lycopene, lutein and zeaxanthin, among others.
The enhanced activity of ASTAXANTHIN may stem from its molecular structure. ASTAXANTHIN belongs to the xanthophyll group of carotenoids, or the oxygenated carotenoids (see other members of the group in Fig. 1). The hydroxyl and keto functional groups (see Fig. 1) present in the ending ionone ring of ASTAXANTHIN may be responsible for its uniquely powerful antioxidant activity and for its ability to span the membrane bilayers as a direct result of its more polar configuration relative to other carotenoids (3,1014). Carotenoids with polar end groups like ASTAXANTHIN span the lipid membrane bilayer with their end groups located near the hydrophobic-hydrophilic interface, where free-radical attack first occurs.


Monday, December 27th, 2010


Alzheimer’s disease and high levels of triglycerides and total cholesterol are very much common in western societies.  It is said that, in the United States alone, greater than 50 percent of its adult population has high cholesterol levels.  Approximately 1 percent of individuals aging between 65 to 69 years acquire Alzheimer’s disease.  For people who are older than 95 years old, the prevalence is increased by more than 60 percent.

Dyslipidemia:  Up Close

Increased levels of cholesterol present a variety of health hazards to the affected person.  This predisposes one to a multitude of illness, some of which are often fatal.  High cholesterol levels are tough on the blood vessels, especially on the arteries.  This may lead to the accumulation of fatty deposits within the walls and linings of the arteries which could seriously impede blood flow.  The blood flow in the specific area of the artery where fatty deposits have accumulated becomes sluggish.  This prompts the heart to pump harder in order to make sure that blood reaches the vital organs.  This doubles the heart effort, putting more workload to one of the most important organs in the body. As a result of the cascade of events, the dangers are foreseen:  high blood pressure, the possibility of embolism, stroke, heart attack, atherosclerosis, peripheral vascular disease, kidney failure, heart failure and many more.  These are reason enough for you to make sure that essential steps are done in order to prevent the onset of dyslipidemia.

Shedding a Light on Alzheimer’s Disease

According to a report released by the Alzheimer’s Disease International (ADI), an association composed of 73 Alzheimer’s organization, 5.3 million Americans are afflicted with Alzheimer’s disease and approximately 500,000 new cases will be diagnosed by 2010.  The economic impact is devastating – Alzheimer’s disease severely affects the person’s quality of life as it causes the loss of normal cognitive functioning such as reasoning, remembering and thinking.  It is a progressive and irreversible disease that slowly destroys thinking skills and memory, and will eventually hinder the patient’s ability to perform even the most simple task.

Scientists are currently hard at work try to pinpoint the exact mechanism that causes Alzheimer’s disease, and why majority of the affected individuals are the elderly.  Because the cause is unknown, treatment also remains out of reach.

Associating Dyslipidemia and Alzheimer’s disease

A report published in the December issue of one of the JAMA/Archives journals, Archives of Neurology, stated that high amounts of high-density lipoprotein (HDL), commonly known as the “good” form of cholesterol, seem to be linked to a lowered risk of Alzheimer’s disease in elderly adults.

Dr. Christiane Reitz, Ph.D and her colleagues enrolled 1,130 elderly individuals in order for the researchers to examine the link between Alzheimer’s disease and the levels of fat present in the blood.  A random sampling of old adults with ages 65 and older and who are residents of Northern Manhattan was conducted.  The other criteria for inclusion include being a Medicare recipient and having no history of cognitive impairment or dementia.  The researchers’ definition of high cholesterol levels was at 55 milligrams per decilitre, or more.

In order to determine the link between HDL levels and Alzheimer’s disease, data were gathered from neuropsychological, neurological and medical evaluations.  Furthermore, the researchers assigned the following diagnosis based on the cause of dementia:

  • “Probable” Alzheimer’s disease – dementia onset could not be further explained by other disorders
  • “Possible” Alzheimer’s disease – the cause of dementia is mostly likely Alzheimer’s disease but other disorders are present which could contribute to the development of dementia, such as Parkinson’s disease or stroke.

For the duration of the follow-up period, 101 subjects were diagnosed with new cases of Alzheimer’s disease – 12 were possible, and 89 belonged to the probable category.  Average age of possible and probable onset of Alzheimer’s disease was 83 years.  It was found that Hispanic subjects as well as those who had higher incidence of diabetes at the beginning of the study have been shown to have developed dementia.  Moreover, for subjects who had higher levels of HDL in their plasma (55 mg/dl or higher), there was a decreased risk of developing both possible and probable Alzheimer’s disease, even after adjustments on lipid-lowering treatments and vascular risk factors were made.

Other Natural Means to Prevent Alzheimer’s Disease

  • The American Journal of Medicine has published a study indicating that people who consume at least three servings of vegetable and fruit juices each week have a 76 percent reduction in their risk of Alzheimer’s disease as compared to people who consume less than one serving each week.  However, for people who have problems with their blood sugar levels and because some fruits contain high sugar levels, vegetable juices are more recommended. Eating raw vegetables, with the absence of a juicer, can also help.Examples of vegetables and fruits include cherries, plums, raisins, blueberries, apples, red bell peppers, spinach and eggplant.
  • The regular intake of foods rich in Omega-3 Fatty Acids, especially docosahexaenoic acid (DHA),  can also help slow Alzheimer’s disease progression.  This is according to the results of a study which was published in the Journal of Neuroscience. Omega-3 fatty acids helps build and maintain the healthy state of the nervous system – the main system affected in Alzheimer’s disease.Excellent food sources include salmon, flax seeds, purslane, seaweeds, walnuts and cod liver oil.
  • The National Institutes of Health said that some aluminum compounds have been linked to the neurological damage featured in Alzheimer’s disease. Although it is impossible to totally avoid being exposed to aluminum because we may never know that the air we breathe, the water we drink and the food on our table may be contaminated, still, it is important to know the most common sources of aluminum exposure such as antiperspirants; over-the-counter drugs like buffered aspirin and antacids; and processed cheese.
  • Doing mentally-stimulating activities is a perfect way to exercise your brain cells. Adopt hobbies that will force you to think – go for the crossword puzzles in the morning paper, learn a new language, memorize a new poem, catch up with current events.  This will not only reduce your risk of Alzheimer’s disease, but it will also help you feel more in-touch, alert and enthusiastic.
  • Sourced & published by Henry Sapiecha


Sunday, August 8th, 2010

Low vitamin D linked to Alzheimer’s and Parkinson’s disease

So you’ve listened to mainstream and now you don’t even know what the sun looks like anymore.

Well, I’ve got some bad news for you — because if, like most people, you’re deficient in the sunshine vitamin, you’re also at risk for life-robbing diseases like Parkinson’s and Alzheimer’s.

One new study out of England’s University of Exeter found that seniors with the lowest levels of D had a dramatically higher risk of dementia warning signs.

Researchers followed 858 seniors for six years, and found that those with less than 25 nanomoles of D per liter of blood were 60 percent more likely to experience general cognitive decline, and 31 percent more likely to start losing their abilities to plan, organize and prioritize.

That’s a road you don’t want to go down — because it ends in a nursing home, where you think every orderly is a long-dead relative and you can’t tell noon from midnight anymore.

But what’s truly bizarre about this new study in the Archives of Internal Medicine is the accompanying editorial, which is straight out of the Dark Ages. In it, Dr. Andrew Grey of the University of Auckland in New Zealand urges people NOT to take a D supplement. He also writes that most people shouldn’t even bother to have their D levels measured.

Paging Dr. Grey, there’s a reality check for you on line one: Ignorance isn’t bliss!

I wonder if this guy even bothers reading these journals. Let me help him out here, because a second new study finds that high levels of D can help save you from Parkinson’s disease.

The study in the Archives of Neurology looked at the D levels of 3,173 Finns between the ages of 50 and 79, and found that those with the most had a 65 percent lower risk of Parkinson’s than those with the least.

Meanwhile, a new report in Endocrine Today says it’s now clear beyond all doubt that vitamin D is needed by the immune, pancreas, cardiovascular, muscle and brain systems.

That’s in addition to all the other well-established benefits of vitamin D, which can help everything from your bones to your longevity. Low levels of vitamin D have also been linked to diabetes, multiple sclerosis, autism and schizophrenia

Sortced & published by Henry Sapiecha


Tuesday, July 27th, 2010

Protein could battle Alzheimer’s disease

NEW YORK (UPI) — U.S. researchers say they are looking at a new approach to treating Alzheimer’s disease with a protein thought to extend lifespan in laboratory animals.

Scientists at the Massachusetts Institute of Technology said that in mice prone to developing Alzheimer’s, activating a protein called sirtuin suppressed the disease and destroying the protein made the disease much worse, The New York Times reported.

The finding raises the hope that Alzheimer’s, and possibly other neurodegenerative diseases like Parkinson’s and Huntington’s, could be treated with drugs that activate sirtuin, researchers say.

“We think it is a scientifically compelling story that ties the sirtuins to the biology of Alzheimer’s disease,” said Dr. Dennis J. Selkoe, an Alzheimer’s expert at Harvard Medical School who was not a part of the study.

Drugs that activate sirtuin already exist, including resveratrol, a minor ingredient of red wine and other foods.

One drug company, Sirtris, is in preclinical trials with sirtuin-activating drugs.

“We think it has very significant potential in neurodegenerative diseases,” Sirtris Chief Executive Officer George P. Vlasuk said.

Copyright 2010 by United Press International

Sourced & published by Henry Sapiecha