Posts Tagged ‘Research’

Researchers have found that the insulin signaling pathways in worms have a direct bearing on their lifespan. This research is particularly interesting because humans and worms share very similar insulin signaling pathways.

Over a decade ago, the first part of this research led to some positive news as researchers found that certain mutations involved in the insulin pathways can greatly extend lifespan in worms.

“In the early 90s, we discovered mutations that could double the normal life span of worms,” Kenyon said. Those mutations effected insulin signals. Specifically, a mutation in a gene known as daf-2 slowed aging and doubled life span. That longer life depended on another “FOXO transcription factor” called DAF-16 and the heat shock factor HSF-1.

Unfortunately, the recent results show that adding sugar to the worm diet has the opposite effect.

By adding just a small amount of glucose to C. elegans usual fare of straight bacteria, they found the worms lose about 20 percent of their usual life span. They trace the effect to insulin signals, which can block other life-extending molecular players.

Here is the technical aspect of the results:

In fact, glucose makes no difference to the life span of worms that lack DAF-16 or HSF-1, they show. Glucose also completely prevents the life-extending benefits that would otherwise come with mutations in the daf-2 gene.Ultimately, worms fed a steady diet containing glucose show a reduction in aquaporin channels that transport glycerol, one of the ingredients in the process by which the body produces its own glucose. “If there is not enough glucose, the body makes it with glycerol,” Kenyon explained. That glycerol has to first get where it needs to go, which it does via the aquaporin channels.

There are a few ways in which the result from studying worms affects us as humans.

A diet with a low glycemic index seems like a safe bet for now. One of the scientists was alarmed enough with the data to make serious changes to her diet:

As an aside, Kenyon says she read up on low-carb diets and changed her eating habits immediately — cutting out essentially all starches and desserts — after making the initial discovery in worms. The discovery was made several years ago, but had not been reported in a peer-reviewed journal until now.

Another area of concern is medicine. Current drugs may be offering treatment which carry as of yet unknown long term side effects. Fortunately, as is the case with anti-depressant medication, science is continually advancing to make our lives better and this research will undoubtedly result in better life saving medicines.

She says the findings may also have implications for drugs now in development for the treatment of diabetes, which are meant to block glucose production by inhibiting glycerol channels. The new findings “raise a flag” that glycerol channels might be doing something else, she says, and that drugs designed to block them might have a downside.

A long term study recently found a connection between consuming two servings of diet soda daily and a significant decline in kidney function. How do different types of artificial sugars factor into these results? Is there any connection between these two studies?

Aging in humans is far more complex than in worms.

“Although we do not fully understand the mechanism by which glucose shortens the life span of C. elegans, the fact that the two mammalian aquaporin glycerol-transporting channels are downregulated by insulin raises the possibility that glucose may have a life-span-shortening effect in humans, and, conversely, that a diet with a low glycemic index may extend human life span,” the researchers write. Kenyon also points to recent studies that have linked particular FOXO variants to longevity in several human populations, making the pathway the first with clear effects on human aging.

Glucose and the insulin signaling pathways are probably just one piece in a complex puzzle explaining the aging process. With every piece of the puzzle that gets illuminated and understood we come one step closer to allowing science an opportunity to stop aging.

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A surefire way to suck the romance out of any kiss is to envision it as free shipping for germs. Recent research by British scientists sheds light on why that is actually a good thing.

Writing in the journal Medical Hypotheses, researcher Dr Colin Hendrie from the University of Leeds said: ‘Female inoculation with a specific male’s cytomegalovirus is most efficiently achieved through mouth-to-mouth contact and saliva exchange, particularly where the flow of saliva is from the male to the typically shorter female.’

Cytomegalovirus is likely to be only one of many germs which take advantage of kissing as a transfer system and which can confer benefits rather than harm to the recipient.

Cytomegalovirus, which lurks in saliva, normally causes no problems. But it can be extremely dangerous if caught while pregnant and can kill unborn babies or cause birth defects.

These can include problems ranging from deafness to cerebral palsy.

Kissing, over the course of several months and increasing in intensity, transfers small amounts of the virus each time. The result is a built up immunity to the virus, thereby cutting the risk of infection and potential damage to the fetus tremendously. Previous research had hypothesized that kissing was important because it conveyed fitness information about the individual through saliva. Given this new data and given that there are many other methods for determining fitness, kissing is not likely to have evolved as a means of determining fitness from an evolutionary perspective.

Dr Hendrie said: ‘Information concerning body tone, smell, reproductive condition, disease state and, of course, personal physical and oral hygiene can all be gained solely from close physical proximity.’

‘The small amount of additional information from kissing is an unlikely pressure for its development.’

People have subconsciously understood for a long time that germs can be transferred via kissing, hence that use of copious amounts of alcohol when strangers kiss. Clearly, it is being used as an antiseptic.

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Here is a “dog bites man” story from researchers at Columbia University Medical Center and Massachusetts General Hospital.

It is no secret that anabolic steroids have all sorts of nasty side effects.

Anabolic steroids can cause many adverse effects. Most of these side effects are dose-dependent, the most common being elevated blood pressure, especially in those with pre-existing hypertension, and harmful changes in cholesterol levels: some steroids cause an increase in LDL cholesterol and a decrease in HDL cholesterol. Anabolic steroids have been shown to alter fasting blood sugar and glucose tolerance tests. Anabolic steroids such as testosterone also increase the risk of cardiovascular disease or coronary artery disease. Acne is fairly common among anabolic steroid users, mostly due to stimulation of the sebaceous glands by increased testosterone levels. Conversion of testosterone to dihydrotestosterone (DHT) can accelerate the rate of premature baldness for males who are genetically predisposed, but testosterone itself can produce baldness in females.

There is a whole bunch more (we left out some of the nastier bits) where that came from. Now we can include damage to kidneys as a side effect of abusing anabolic steroids too. In fact, the damage incurred is worse than what is seen in the kidneys of morbidly obese individuals.

The investigators studied a group of 10 bodybuilders who used steroids for many years and developed protein leakage into the urine and severe reductions in kidney function. Kidney tests revealed that nine of the ten bodybuilders developed a condition called focal segmental glomerulosclerosis, a type of scarring within the kidneys. This disease typically occurs when the kidneys are overworked. The kidney damage in the bodybuilders has similarities to that seen in morbidly obese patients, but appears to be even more severe.

However, some good news also comes from this study:

When the bodybuilders discontinued steroid use their kidney abnormalities improved, with the exception of one individual with advanced kidney disease who developed end-stage kidney failure and required dialysis. Also, one of the bodybuilders started taking steroids again and suffered a relapse of severe kidney dysfunction.

If stopped in time, kidney function can improve enough for daily functioning. Kidneys in particular are so vulnerable to the effects of anabolic steroids because they are affected both directly and indirectly:

The researchers propose that extreme increases in muscle mass require the kidneys to increase their filtration rate, placing harmful levels of stress on these organs. It’s also likely that steroids have direct toxic effects on the kidneys. “Athletes who use anabolic steroids and the doctors caring for them need to be aware of the potentially serious risks to the kidney,” said Dr. Herlitz.

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Gene therapy has been successfully used to restore vision in patients suffering from a rare genetic disorder. The nature of this disorder means that the therapy is much more successful in children than adults.

Leber’s congenital amaurosis (LCA) causes sight to deteriorate beginning at birth and and resulting in complete blindness before the age of forty.

Children born with one form, LCA2, have defects in a gene called RPE65 that helps the retina’s light-sensing cells make rhodopsin, a pigment needed to absorb light. Without rhodopsin, the photoreceptor cells gradually die.

Gene therapy works by using a modified virus as a delivery system to get specific genes into specific areas. (Take a look at our article Is Chronic Fatigue Syndrome Caused By A Virus? for some background about how viruses work explained in plain English). Researchers first tested the therapy on dogs and found they could partially restore sight by using a virus loaded with the RPE65 gene. Then the researchers conducted a limited study on six young adult humans, which also resulted in sight improvements.

But the Penn researchers knew from their studies in animals that children should improve even more because they have more intact retinal tissue than adults do. Today in an online paper in The Lancet, their team and collaborators in Europe report full study results for three of the adults they treated earlier and nine more patients, including four children ages 8 to 11. The children gained more light sensitivity than the adults did–their light sensitivity increased as much as four orders of magnitude, versus one–and they made far fewer mistakes in an obstacle course.

This is one of those good news/bad news stories.

The bad news:

  • Older individuals with this disorder have lost more tissue, and therefore the therapy can be significantly less effective.
  • This therapy only applies to blindness caused by a specific defective gene, and will not benefit someone suffering from any other type of blindness.

Now, the good news:

  • Gene therapy sounds great in theory but has had few successes in real life applications. The success of this study will serve as boost to continue research into gene therapy.
  • Other vision diseases are caused by genetic defects. In the near future it may be possible to do a simple blood test to determine which defective gene a child has and then apply the appropriate therapy to prevent a loss of vision from occurring in the first place.

There is a lot of excitement in the air because of the successful results. Take a look here to see a video of one of the patients, Cory Haas, breezing through an obstacle course a mere three months after therapy.

The LCA2 trials are a rare success for the field of gene therapy, which has also cured children with the immune disorder known as bubble boy disease. And they should pave the way for treating more vision disorders. “It’s an incredible launching pad to be able to target other diseases,” says Penn gene therapy researcher Jean Bennett, who led the study.

Showing that the LCA2 gene therapy treatment works best in children is “a big step” for inherited blindness, says geneticist Frans Cremers of Radboud University Nijmegen Medical Center in the Netherlands, who wrote an accompanying commentary in The Lancet. He notes that eight other vision diseases, including retinitis pigmentosa, have now been treated in mice and are ready to be tested in people. The challenge, he says, will be to expand genetic testing of people with blindness so as to find enough eligible patients for clinical trials of these rare disorders.

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Eva Redei, the David Lawrence Stein Professor of Psychiatry at Northwestern’s Feinberg School has published new research which explains why antidepressants don’t work for so many people.

There are two prevailing theories about the causes of depression. One is that depression can be caused by stressful life events and the second is that depression results from an imbalance in neurotransmitters. However, medications based on those theories are treating effects, not causes.

Most animal models that are used by scientists to test antidepressants are based on the hypothesis that stress causes depression. “They stress the animals and look at their behavior,” she said. “Then they manipulate the animals’ behavior with drugs and say, ‘OK, these are going to be good anti-depressants.’ But they are not treating depression; they are treating stress.”

That is one key reason why current antidepressants aren’t doing a great job, Redei noted. She is now looking at the genes that differ in the depressed rat to narrow down targets for drug development.

She said another reason current antidepressants are often ineffective is that they aim to boost neurotransmitters based on the popular molecular explanation of depression, which is that it’s the result of decreased levels of the neurotransmitters serotonin, norepinephrine and dopamine. But that’s wrong, Redei said.

Redei examined the genes involved in both stress and depression. Of the 254 genes related to stress and the 1275 genes related to depression there is an overlap of only 5 genes.

“This overlap is insignificant, a very small percentage,” Redei said. “This finding is clear evidence that at least in an animal model, chronic stress does not cause the same molecular changes as depression does.”

If current medications are only treating effects then research should be focused on finding and treating the causes.

In the second part of the study, Redei found strong indications that depression actually begins further up in the chain of events in the brain. The biochemical events that ultimately result in depression actually start in the development and functioning of neurons.

“The medications have been focusing on the effect, not the cause,” she said. “That’s why it takes so long for them to work and why they aren’t effective for so many people.”

Her animal model of depression did not show dramatic differences in the levels of genes controlling neurotransmitters functions. “If depression was related to neurotransmitter activity, we would have seen that,” she said.

Unfortunately, although we now know those theories are wrong, we still do not have a theory that is right.

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Eat, Drink & Be Merry

We recently discussed the apparent contradiction between the facts that America is fatter than ever and people are living longer than ever. BMI is the determining factor in declaring Americans overweight.

However, the theory which says America should be suffering health problems and increased mortality because of increased obesity is quite wrong.

So why are death rates dropping and people living longer? Something must be wrong with the model — it’s pretty hard to quarrel with the data as being inadequate. Certainly the increased incidence of obesity should have produced something by this time (it started 30 years ago).

In case you have been living in a cave or something, there are several serious flaws with the BMI which make it unsuitable for determining health. A new German study by Matthias Lenz of the Faculty of Mathematics, Computer Science, and Natural Sciences of the University of Hamburg and his co-authors present these and other results in the current issue of Deutsches Ärtzeblatt International:

The Süddeutsche Zeitung published an advance notice of the report (http://www.sueddeutsche.de/gesundheit/140/489526/text/), which shows that overweight does not increase death rates, although obesity does increase them by 20%. As people grow older, obesity makes less and less difference.

For coronary heart disease, overweight increases risk by about 20% and obesity increases it by about 50%. On the other hand, a larger BMI is associated with a lower risk of bone and hip fracture.

In relation to cancer, the overall death rate among extremely obese men (BMI above 40) is no higher than among those of normal weight. Men who are overweight even have a 7% lower death rate. No significant association was found in women.

According to the authors’ analysis, overall mortality is unchanged by overweight, but increased by 20% by obesity, while extreme obesity raises it by up to 200%.

Futurepundit raises a few interesting points:

What I’m expecting: Genetic testing might show us what our relative risks are for a large variety of diseases and this knowledge could push us toward different ideal weights depending on which diseases we have the greater risks for. Also, some people are probably genetically better adapted to carrying more weight.

Note that you have other options for slowing bone decay aside from carrying more weight around. Exercise, better food, and a combination of vitamin D and vitamin K might cut bone fracture risks with age.

Weight studies are problematic because weight can vary due to muscle mass as well (albeit less often). Also, people can lose weight during the early stages of an illness before they even know they are sick. How well did the researchers adjust for these factors?

According to the CDC:

BMI is a fairly reliable indicator of body fatness for most people.

In light of this new study, will the CDC change it stance on using BMI data as a way of reliably gauging the health of Americans?

If the BMI chart is based on an illogical formula concocted over 200 years ago and can only give a general assessment of obesity in a population while failing on an individual level, why is it still in use by the government?

The answer is because government loves to create problems for which it is the solution. Pay close attention to what is happening here because this is a pattern that repeats over and over again.

We would not bet on it because it is not the first time nanny staters in the government have used bogus data to justify their agendas regardless of scientific truth, nor will it be the last. Rather than letting those busybodies get you down, learn how to eat your way to happiness. Being drunk and gassy is one recent formula for living a long life, although can easily be a life of bachelorhood if you are not careful to find the right wine/broccoli balance.

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A major question rested heavily on the minds of certain people in the scientific community: can you taste carbonation?

One way to answer that question would be to consume a carbonated beverage in an environment which prevents the bubbles from bursting.

Ryba added that the taste of carbonation is quite deceptive. “When people drink soft drinks, they think that they are detecting the bubbles bursting on their tongue,” he said. “But if you drink a carbonated drink in a pressure chamber, which prevents the bubbles from bursting, it turns out the sensation is actually the same. What people taste when they detect the fizz and tingle on their tongue is a combination of the activation of the taste receptor and the somatosensory cells. That’s what gives carbonation its characteristic sensation.”

Perhaps some of you are interested in a little bit of history. What on Earth prompted people to indulge in fizzy beverages? Hint: it predates Coca-Cola.

In 1767, chemist Joseph Priestley stood in his laboratory one day with an idea to help English mariners stay healthy on long ocean voyages. He infused water with carbon dioxide to create an effervescent liquid that mimicked the finest mineral waters consumed at European health spas. Priestley’s man-made tonic, which he urged his benefactors to test aboard His Majesty’s ships, never prevented a scurvy outbreak. But, as the decades passed, his carbonated water became popular in cities and towns for its enjoyable taste and later as the main ingredient of sodas, sparkling wines, and all variety of carbonated drinks.

Other research has been conducted on our sense of taste for sweet, sour, salty, bitter and savory. Jayaram Chandrashekar, Ph.D., David Yarmolinsky Ph.D. and Lars von Buchholtz, Ph.D. teamed up to find the source responsible for detecting the taste of carbonation.

Here is the science of what they found:

Carbonic anhydrase 4, or CA-IV, is one of a family of enzymes that catalyzes the conversion carbon dioxide to carbonic acid, which rapidly ionizes to release a proton (acid ion) and a bicarbonate ion (weak base). By so doing, carbonic anhydrases help to provide cells and tissues with a buffer that helps prevent excessive changes in pH, a measure of acidity.

The scientists found that if they eliminated CA-IV from the sour-sensing cells or inhibited the enzyme’s activity, they severely reduced a mouse’s sense of taste for carbon dioxide. Thus CA-IV activity provides the primary signal detected by the taste system. As CA-IV is expressed on the surface of sour cells, Chandrashekar and co-workers concluded that the enzyme is ideally poised to generate an acid stimulus for detection by these cells when presented with carbon dioxide.

They worked with mice, which have a sense of taste similar to human. The question remains, why do mammals taste carbonation at all?

The scientists are still not sure if carbon dioxide detection itself serves an important role or is just a consequence of the presence of CA-IV on the surface of the sour cells, where it may be located to help maintain the pH balance in taste buds. As Ryba says, “That question remains very much open and is a good one to pursue in the future.”

Thanks to their hard work you can rest assured it is not merely your imagination.

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As with many scientific discoveries, there is an interesting back story here.

The story begins with a biologist, Robert Silverman of the Cleveland Clinic Foundation in Ohio, investigating if prostate cancer is caused by a virus.

Actually, the story begins a bit earlier than that. Scientists have known that viruses can cause cancer since the early 20th century.

In 1909 Peyton Rous discovered that a virus could cause sarcomas in chickens. For discovering the Rous Sarcoma Virus, Dr. Rous was awarded the Nobel Prize in 1966. This discovery led directly to the discovery of cellular oncogenes (genes that cause cancer) by Bishop and Varmus, which also was rewarded with a Nobel Prize.

Subsequently, numerous other human cancers have been associated with viral infections. The most important of these is Burkitt’s lymphoma. Burkitt’s lymphoma comes in three varieties: one form is endemic to sub-Saharan Africa and is most likely caused in large part by infection with a virus called Epstein-Barr Virus (EBV, which also causes mono), one form is sporadic (as opposed to endemic), and one form is associated with immunodeficiencies such as AIDS. The endemic form of Burkitt’s lymphoma typically causes a large, painful jaw mass, while the sporadic form more commonly involved the intestines. Interestingly, another name for EBV is Human Herpesvirus-4 (HHV-4). EBV, or HHV-4, also causes nasopharyngeal carcinoma in southeast Asia (and elsewhere). It is clear that there is a real connection between viruses and cancer.

Now back to Robert Silverman, who discovered a new retrovirus called XMRV.

The retrovirus was very similar to MLV, a group of viruses that can cause cancer and neurological and immunological diseases in mice. Silverman found XMRV in a subset of prostate tumours, and more recent research found a stronger correlation between XMRV and aggressive prostate tumours.

We should pause for a moment and explain the difference between a virus and a retrovirus. A virus is a very simple organism – basically a protein shell containing a little DNA. Viruses need to find hosts because they lack the tools to multiply on their own.

Cells also contain DNA, but cells (especially those of complex organisms such as humans) have ridiculous amounts of DNA. Most of the instructions in DNA used by cells on a daily basis are for creating proteins. Since mistakes are most likely to occur proportionally to how often DNA is copied, a system using RNA minimizes copying by only duplicating the specific section of DNA needed to build a specific protein. RNA is slightly different than DNA on a molecular level, so cellular machinery can respond to it but not to DNA. A cell which needs a particular protein manufactured goes through the following (simplified) steps:

  1. A portion of DNA is translated into RNA.
  2. RNA is sent to the endoplasmic reticulum.
  3. The specified protein is built.

A standard virus hijacks the cell’s machinery by inserting DNA, which gets translated into RNA, which is then made into the specified protein; only in that case the protein is the virus.

Retroviruses are more insidious. They contain RNA rather than DNA. When a retrovirus attacks a cell, the RNA gets translated into DNA, which then gets incorporated into the cell’s own genome. Rather than hijacking the cellular machinery for their own nefarious plans, they Borg the cell. From then on, every time the cell multiplies it is bringing the virus along with it. Our genome is littered with scars from ancient battles with retroviruses which may have fundamentally shaped us into what we are today.

Alright, enough with the interruptions already.

Judy Mikovits of the Whittemore Peterson Institute for Neuro-Immune Disease in Reno, Nevada, asked Silverman to see if there was a connection to chronic fatigue syndrome.

Mikovits asked Silverman to analyze the blood samples of 101 CFS patients and 218 healthy controls. The authors detected XMRV DNA in the immune cells of 67% of the CFS patients but in only 3.7% of healthy controls. The authors also showed that the virus was able to spread from infected immune cells to cultured prostate cancer cells and that the virus’s DNA sequence was more than 99% similar to the sequence of the virus associated with prostate cancer. The findings were published in Science.

So far, although the results are encouraging, there has only been one pilot study completed. The magic which makes science work is verification and duplication of results.

William Reeves, principal investigator for the Centers for Disease Control and Prevention (CDC)’s CFS public health research programme, says the findings are “unexpected and surprising” and that it is “almost unheard of to find an association of this magnitude between an infectious agent and a well-defined chronic disease, much less an illness like CFS”.

But Reeves is cautious. “Until the work is independently verified, the report represents a single pilot study,” he says. According to Reeves, the CDC is already trying to replicate these findings. He also notes that CFS is a heterogeneous disease and likely arises from a combination of many factors.

The Wall Street Journal has a heartbreaking example of the suffering caused by CFS:

Ms. Whittemore-Goad says she was a regular school girl, playing sports and involved in school activities, until the age of 10, when she became ill with a monolike virus that she couldn’t shake. She said doctors first told her parents that the illness was psychological, that she had school phobia and was under stress from her parents. “We kept searching for an answer,” says Ms. Whittemore-Goad, who says lymph nodes in her groin were so painful that her brothers and sisters used to have to carry her upstairs. She was diagnosed at age 12 with chronic-fatigue syndrome.

Over the years, doctors have treated her symptoms, like intense headaches and severe pain, but the illness persists. She has had her gallbladder, spleen, and appendix removed because they became infected. She tried an experimental drug that she says gave her relief for years, but she then started experiencing side effects and had to stop taking it. Recently the illness has become worse; she began suffering seizures and can no longer drive.

Go read the whole thing.

If this virus is the cause of CFS, diagnosis and detection can be done with a simple blood test. Antiretroviral therapies designed in the fight against HIV are under investigation as a potential cure. The story is not yet over but we remain hopeful that this breakthrough represents the real deal for sufferers of CFS.

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It has been known for a long time that there is a connection between dense breast tissue and an increased risk of developing breast cancer, but only recently have researchers begun to understand why.

Breast tissue is composed of several different types of cells which create different structures. There is the epithelium, consisting of duct cells and milk glands, the stroma, which is the connective tissue for the epithelial cells, and fat.

The 60 women who participated in the Mayo Clinic study were healthy with no history of breast cancer. Their breast tissue was biopsied to determine the difference in cellular composition between dense and non-dense tissue.

Results are now available from more than half of the participants who donated biopsy tissue. Dr. Ghosh found that areas of density contained much more epithelium (6 percent) and stroma (64 percent) and much less fat (30 percent), compared to non-dense tissue that contained less than 1 percent epithelium, about 20 percent stroma, and almost 80 percent fat. “This shows us that both the epithelium and stroma contribute to density, and suggests that the large difference in stroma content in dense breast tissue may play a significant role in breast cancer risk,” Dr. Ghosh says.

Another study took these results a step further:

In a second study, researchers also found that dense breast tissue has more aromatase enzyme than non-dense tissue. This is significant because aromatase helps convert androgen hormones into estrogen, and estrogen is important in breast cancer development, says that study’s lead investigator, Celine Vachon, Ph.D.

“If aromatase is differentially expressed in dense and non-dense breast tissue, this could provide one mechanism by which density may increase breast cancer risk,” Dr. Vachon says.

The researchers have found some strong links thus far, but they are recruiting more women for a second study to validate their findings.

“These are initial findings from one of the first attempts to study breast density at the level of healthy tissue. It doesn’t explain everything yet, but is providing really valuable insights,” says Dr. Ghosh, who established the patient resource for both studies.

Drs. Ghosh and Vachon are finishing their analysis of the initial 60 volunteers, and they are also enrolling more participants in order to validate and expand their findings. “No one knows why density increases breast cancer risk, but we are attempting to connect the dots,” Dr. Vachon says.

October is National Breast Cancer Awareness Month.

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The article we published recently, Smoking Bans Reduce Heart Attacks: Lying By Omission, was posted for discussion on LinkedIn. Since the discussion and comments are only viewable to members of the Cornell network, we cannot address any issues which are being raised directly on LinkedIn.

A member of the network forwarded some of the comments to us and we will address them here. Please take a moment to register and comment on our site if you would like to join in the discussion. We are willing to answer your questions but we have to know the questions exist in the first place.

Since a few commenters made multiple points and because there is overlap on some of the issues raised, we will first post the comments in full and then address the individual points.

Vernon C.:

Do you deny that smoking causes heart and lung disease? Do you deny that we, as a society, pay higher health insurance premiums when there is a higher incidence of disease? Then why is it questionable for society to limit smoking by any method it chooses in order to reduce our costs?

Bonnie F.:

The article is focusing on the smoking issue and the specific way in which scientific data about secondhand smoke has been manipulated to promote indoor smoking bans. The larger point seems to be that letting public officials with pretty fundamentalist agendas get away with lying to the public about the science in order to get laws passed is setting a bad precedent.

Steve K.:

And this makes the public officials different from the ‘I had no idea nicotine was addictive’ Tobacco CEOs in WHAT way? Secondhand smoke is DISGUSTING. I do not CARE what the science says, it is DISGUSTING, and I have absolutely no problem with smoking being banned EVERYWHERE.It is also a public health risk, and if the health issues are not enough for you, look at the fire statistics. The only likely supporters of smoking are people in the tobacco business and firefighters – depending on whose numbers you want to use, tobacco is responsible for 40% to 80% of house fires.. which keeps them employed.

Mark C.:

A implies B, and I believe B, so A must be true. This fallacy is the foundation of public support for bogus science. People like the conclusions so they accept any rationale that comes their way. They really don’t care if the science is bogus, so long as the conclusion is what they want to hear.

But, just because A is bogus, doesn’t mean B is false. Matter of fact it is easier to get bogus A’s accepted when B is true.

Eric S.:

Hi there. Tobacco is a known carcinogen. I would anticipate that, since the smoking bans have only recently gone into effect, it’s a bit soon to be able to trace benefits to reduction in disease from second hand smoke. Are you aware of any studies that measure the reduction in carcinogenic material that occurs by retention/conversion in the smoker’s lungs and blood stream?

Please be careful about charging fraud in the discussion of the health effects of tobacco ingestion (smoke, chew, etc.) when the obscene fraud practiced by the tobacco companies and their allied state representatives has been well documented.

Marc M.:

>>The larger point seems to be that letting public officials with pretty fundamentalist agendas get away with lying to the public about the science in order to get laws passed is setting a bad precedent.<<

I don’t even know where to start with this comment, but let me start by saying I live in Texas, a state well known for folks with fundamentalist agenda’s lying to the public about science to get laws passed, albeit in quite a different manner than you might be thinking. That said, Mark makes an excellent point that notwithstanding the possible misinterpretation of allegedly bogus science (where the general scientific consensus is fairly consistent in favor of anti-smoking activists, however), there is still an extremely strong case in favor of indoor smoking bans on just the yuck factor, amongst other reasons.

And it is interesting that the 3 Monkeys also repeat the mantra about the alleged economic catastrophe that would occur with indoor smoking bans, which has repeatedly been show to be bogus (including in several places here in Texas!).

And Steve, firefighters are never in favor of things that actually start fires. I wold rather take my training and sit on my rear in the fire station than make a fire – fires are tragedies in terms of both potential for lives lost AND for the loss of personal history and memories when it is damaged by smoke, water and fire.

Steve K.:

Re: Fire prevention – what I was trying to convey is that I have never heard of a fire department advocating a ban on indoor or unenclosed flame sources. (maybe someone has done so, but I have not heard of it) There must be commerical fire suppression systems that could be installed over gas stoves. Beyond that, ban all unenclosed flame sources, and if a fire is found to have been started by an unenclosed flame source, send the person responsible a bill for the full cost of fighting the fire.
Fires started by cigarettes are NOT accidents, they are acts of stupidity. Why should firefighters have to risk their lives to put out such fires? How many fewer firefighters would a community need if cigarettes were simply banned?

Marc M.:

Steve, you were on the hill about the same time (OK, a few years earlier, but not much) as I was – don’t you remember the ban of candles in campus residence halls? And that was back in the 80’s.

Gas stoves are relatively contained flames and there are codes which govern the installation of such objects – only in commercial occupancies are there rules requiring fire suppression systems. These codes are promulgated for fire prevention reasons and supported by the fire service through the NFPA and other organizations.

Re: fires started by cigarettes – the problem with a fire is that you don’t always know what caused the fire before you put it out – often you don’t know what started it. They get put out, then we determine cause. But there would probably be little decrease in the number of firefighters required because staffing and deployment patterns are governed by time and distance more than by actual numbers of events. Plus, most fire departments now are actually EMS delivery system that provide fire suppression as an ancillary service, so decreases in numbers would impact those services more than the fire suppression services.

And no doubt fires caused by cigarettes are acts of stupidity (or drunkenness, actually, but that may be the same thing).

Here is a distillation of the points raised above, and the answers:

  • Tobacco smoking is a major cause of house fires and indoor smoking even at home should be banned.

Factually incorrect. According to the CDC and the NFPA, cooking fires are the number one cause (40%) of house fires. However, it is worth noting that although under 12% of fires (4% of fires originate in the living room, family room, or den; 8% in the bedroom) can be attributed to smoking, it is responsible for more (25%) of the fatalities.

It seems likely that many of the people who were involved in fatal fires with smoking as a cause were impaired by alcohol at the time. By logical extension, we should advocate a ban on drinking alcohol at home. We are sure an intrepid researcher can unearth a strong connection between drinking at home and all sorts of preventable physical and property damage.

We pay for the fire department through taxes and we are required by law to have fire insurance. On on unrelated note, health insurance should be like fire insurance – covering catastrophes, not routine medical expenses.

  • Big Tobacco lied about the extent of the dangers associated with their products, therefore claiming that there is fraud involved in research supporting indoor smoking bans is probably a lie supported by Big Tobacco.

Even if Big Tobacco were directly funding research showing how data is being manipulated to support indoor smoking bans, it in no way changes the fact that data is being manipulated. Aside from the lack of direct funding from Big Tobacco, those sources arguing for an examination of the underlying research have been proven right by the original research.

The primary justification for curtailing the freedom of businesses to choose to allow their customers to smoke indoors and for customers to choose to support such businesses is based on the health risks posed to the employees by the secondhand smoke. According to the Surgeon General’s report the actual correlation between secondhand smoke (aka ETS, Environmental Tobacco Smoke) and things like cardiovascular disease, ischemic heart disease, and arrhythmic heart failure or coronary arrest mortality is low enough to be attributable to statistical noise.

Here’s a bit of perspective: the highest risk ratio is for cardiovascular disease, at 1.25. The risk ratio of dying from a traffic accident (for women) on Friday the 13th is 1.38 according to research published in the American Journal of Psychiatry. Therefore it is safe to bet that traffic will be light on November 13th, 2009 because all our female readers will have opted to take the bus or train to work instead.

  • Many people simply find tobacco “yucky” and therefore it should be banned anywhere it may come into contact with others. Also, smoking is really bad for you.

Smoking tobacco is bad for you and there is no great controversy in saying so. However, it is not the issue we are dealing with here. To reiterate: the issue is that the science shows no ill effects from secondhand smoke, therefore the justification for banning smoking indoors in the name of protecting employees is nonexistent.

The “yucky” argument is flat out childish and sophomoric. Try to defend against it when used as an argument against something you like, which other people abhor.

  • People making out on TV is “yucky” and against my religious values, therefore it should be banned from being broadcast.

There is no law forcing anyone to own a television, watch particular shows, or derive spiritual sustenance from it. Turn it off, change the channel, or don’t buy a TV in the first place since broadcasters are providing their audience with what they want. You can affect change by not being part of the audience.

  • Small dog breeds are ankle biting terrorists and should be banned. They are a menace to everyone with ankles, and creating something called a “dog” which can get its butt whooped by a 10 lb. house cat is an affront to the basic dignity afforded to every living creature.

No law forces anyone to buy a small dog or hang out at the dog park. In the rare instance you are bitten by one, call the police and file a report.

Now we would like you to imagine that an individual with such a view was in a position of power – say as mayor of Big Major City – and used some shady statistics to justify banning certain breeds of small dogs. Due to the importance of Big Major City, many other cities followed suit and banned those breeds as well. Then a report is issued citing selected cities in which banning those small dogs improved quality of life. In fact, the report is so positive that the mayor of Big Major City and others begin pushing to expand on the success of the original ban by extending it to include all dogs.

All that, because some nutter thinks dogs are “yucky”.

  • The reports indicating an economic decline after smoking bans were put into effect are false and misleading.

We came across research which clearly showed an economic decline as a result of indoor smoking bans. To argue otherwise you must show a flaw in the research or provide some other source of data to back up that claim.

Absent a smoking ban, how can someone who finds secondhand smoke “yucky” go about creating change? By choosing with whom you do business. Whether it is a restaurant, bar, or bowling alley, by choosing to direct your business to places with a smoke free environment your actions are causing them to be more successful and thereby encouraging more of that type of business.

The fact that many nightlife places were environments which encouraged smoking shows that the majority of people voted with their hard earned money to keep those places thriving. It means that many of the people who participated in nightlife either liked having a cigarette with their drink or did not mind that others did. To argue that bars and clubs did not suffer economically after smoking bans were put into effect is to ignore the huge support they were receiving from locals and to ignore that people respond to incentives. Furthermore, if only a small percentage of nightlife participants are non-smokers and/or cannot tolerate secondhand smoke, where are all the extra people coming from to replace the smokers who choose to stay at home?

Freedom is what is at stake here. Smoking is dangerous and bad for you, but so are many other things. The indoor smoking bans in effect are the result of the minority imposing their views and beliefs on the majority by lying. The economics show that the majority of the public impacted by ban were against it.

Exit question: If the indoor smoking ban cannot be justified based on science, are supporters of the ban essentially guilty of “we’re just trying to do what’s best for you” paternalism? If that is true, what can citizens do to prevent something like this from happening in the future?

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If you have never heard of electrosurgery before, here is some background information:

Electrosurgery is the application of a high-frequency electric current to biological tissue as a means to cut, coagulate, desiccate, or fulgurate tissue. […] Its benefits include the ability to make precise cuts with limited blood loss. Electrosurgical devices are frequently used during surgical operations helping to prevent blood loss in hospital operating rooms or in outpatient procedures.

In electrosurgical procedures, the tissue is heated by an electric current. Although electrical devices may be used for the cauterization of tissue in some applications, electrosurgery is usually used to refer to a quite different method than electrocautery. The latter uses heat conduction from a probe heated by a direct current (much in the manner of a soldering iron), whereas electrosurgery uses alternating current to directly heat the tissue itself.

The main reason surgeons use electrosurgical tools is to minimize blood loss. A team of German and Hungarian researchers decided to adapt one such electroscalpel by attaching a pump to suck up tiny particles of tissue which get vaporized during cutting.

In electrosurgery, tissue is locally exposed to high-frequency electrical current in order to guide a cut, remove tissue, or halt bleeding. The tissue being treated becomes very hot and is partially vaporized. The electrical current also generates electrically charged molecules during the vaporization. The team of scientists from the University of Giessen, the Budapest firm Massprom, Semmelweis University, and the National Research Institute for Radiobiology and Radiohygiene, also in Budapest, made use of this process for their new method called rapid evaporation ionization mass spectrometry, or REIMS. They equipped an electrosurgical instrument with a special pump that sucks the vaporized cell components up through a tube and introduces the charged molecules into a mass spectrometer.

Once it was shown that obtaining the tissue was feasible, they were fortunate to discover that the different types of tissue are rapidly and easily distinguished by a mass spectrometer.

It turns out that mainly lipids, the components of cell membranes, are registered by the mass spectrometer. “Different tissue types demonstrate characteristic differences in their lipid composition,” explains Takáts. “Tumor tissue also differs from healthy tissue.” The scientists were able to develop a special algorithm to unambiguously identify and differentiate between types of tissue.

“Tissue analysis with REIMS, including data analysis, requires only fractions of a second,” according to Takáts. “During an operation, the surgeon thus received virtually real-time information about the nature of the tissue as he was cutting it.” This opens new vistas for cancer surgery in particular: the method helps to precisely localize the tumor during surgery and to delimit it from the surrounding healthy tissue. REIMS also provides information about whether the carcinoma is in an early or advanced stage.

We hope this technique becomes widely available as soon as possible.

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Two studies were recently published which showed a correlation between a community adopting a smoking ban and a subsequent reduction in heart attack rates. The results are based on aggregated data from several other studies. Unfortunately, we do not have access to the original reports so we cannot question their methodology directly.

Report #1:

The research — which incorporated data from a total of 24 studies of smoking bans across the country — found at least a 17 percent reduction in heart attacks one year after the bans had been enacted.

Report #2:

The other study, published in the Sept. 21 issue of Circulation, found a 17 percent drop in heart attack rates after one year and about a 36 percent drop three years after smoking restrictions had been enacted.

It incorporated data from 13 studies in the United States, Canada and Europe. Meyers’s research effort analyzed data from 11 studies of 10 public smoking bans in the same geographic regions.

We will examine the motivation for presenting the public with false information by exposing the agenda behind it later. First, we will take a close look at how this type of fraud occurs.

The crime in this case is one of omission. Both studies show impressive results based on data from multiple sources. One of these reports used data from 24 other studies and the other used 13. How many studies have been left out which don’t support their conclusions?

It would be very inconvenient for the authors and proponents of these studies if some communities experienced an increase in heart attacks after a smoking ban was put into effect, and they conveniently left those out of their research. The most conclusive study would be one which examined the data on a national level.

In fact, such a study exists and was published a few months ago.

A new study by researchers from the RAND Corporation, Congressional Budget Office, University of Wisconsin, and Stanford University is the first to examine the relationship between smoking bans and heart attack admissions and mortality trends in the entire nation, using national data. All previous U.S. studies only examined one particular city. In contrast, this study examined data from the Nationwide Inpatient Survey (NIS), which is nationally representative and includes 20% of all non-federal hospital discharges in the United States. The study has been published as Working Paper 14789 of the National Bureau of Economic Research Working Paper Series.

The study came to a completely different conclusion than the ones recently published.

The most important finding of this study is that there are just as many smoking ban communities in which heart attack admissions and mortality have increased in comparison with control communities as there are smoking ban communities in which heart attacks have decreased relative to control communities. The mean difference was found to be zero.

Thus, the study not only fails to find a short-term effect of smoking bans on heart attacks, but it also explains the positive findings of previous studies. What appears to be going on is what is referred to as publication bias.

Another major problem with studies being touted by the media and pushed by anti-tobacco activists is the level of harm attributed to second hand smoke.

Epidemiologists use “relative risk” (RR or Risk Ratio and informally including the similar Odds Ratio computation) as a means for measuring the severity of risk. The U.S. Surgeon General stated the relative risk for secondhand smoke is between 1.20 to 1.30. This is far below the minimum level at which any meaningful risk might be indicated. Both the World Health Organization and the National Cancer Institute have clearly stated that RRs below 2.0 are too low to be relied upon. The same is true of the federal Reference Manual on Scientific Evidence and textbooks such as Breslow and Day’s Statistical Methods in Cancer Research. A report by the independent health consulting firm Littlewood & Fennell characterizes RRs below 2.0 as “dancing on the tiny pinhead of statistical insignificance.”

The Surgeon General’s report went out of its way to make a claim which ran counter to the evidence. It had to be explicitly pointed out after the report’s publication that there is no justification for banning indoor smoking.

The 1992 report Revised Comments on the 1986 Surgeon General’s Report…EPA…and NIOSH states: “Risk estimates below 2.0 or 3.0 are described as ‘weak’ and thus any conclusions drawn from them are unreliable.” The summary of this 47-page document concludes: “…these reports [Surgeon General’s, EPA, and NIOSH] do not provide a defensible basis for regulation of smoking in the workplace.” Comments in the report are supported by 113 references in the scientific literature.

Even with that censure, the Surgeon General’s office continues to be promote nonsense for the anti-tobacco crusade. It is shameful for a governmental organization to promote political agendas using scare tactics which run counter to the scientific data.

The 2006 SG’s report claims 46,000 deaths annually due to heart disease from secondhand smoke. But the American Heart Association website lists the following RRs for ETS: 1.25 for Cardiovascular disease, 1.18 for ischemic heart disease, and 1.13 for arrhythmic heart failure or coronary arrest mortality. None of these suggests credible risk. Death estimates are derived from relative risk. If a RR is meaningless, so are the estimates of deaths based upon it. So the big scary estimate of 46,000 deaths has no validity. It is simply a phony number put out to scare people and panic them into political action. If such death estimates were valid, the new study would not have found that smoking bans have zero effect on heart attack mortality.

The EPA (Environmental Protection Agency) also helped to promote this madness. The Surgeon General’s report relied on data from a 1992 EPA study, which concluded that 3,000 deaths per year are attributable to secondhand smoke.

The U.S. House of Representatives then held a Congressional Investigation of EPA’s findings. It concluded: “EPA could reach that conclusion [3,000 lung cancer deaths] only by ignoring or discounting major studies, and deviating from generally accepted scientific standards.” Further, it found EPA guilty of “conscious misuse of science and the scientific process to achieve a political agenda that could not otherwise be justified.” It also stated: “The agency [EPA] has deliberately abused and manipulated scientific data in order to reach a predetermined, politically motivated result.” (emphasis added.) Over the next seven years, five similar studies (meta-analyses) of secondhand tobacco smoke were performed by other researchers who, unlike EPA, followed correct scientific standards. The RRs of these studies showed a range of 0.98 to 1.03 and an average RR of 1.01, compared to EPA’s RR of 1.19. Levois and Layard performed a meta-analysis of all the original studies utilized by EPA and came up with a RR of 1.00. Furthermore, these studies all had the standard 95% confidence level. The EPA study did not qualify for that. Instead, EPA used a degraded confidence level of only 90 percent, thus doubling the likelihood that its results were mere chance.

The motivation behind this shady business comes from several fronts. The strongest force are the absolutists, the prohibitionists, the fundamentalists who would like tobacco to be eliminated from the face of the Earth. Some of them become politicians and work towards achieving that goal incrementally. Their motivation is “the ends justify the means”. Others are the media and do-gooders who are not intelligent enough or simply too lazy and ignorant to examine the background science and automatically assume people they look up to are working in everyone’s best interests.

A steep price is paid for this stupidity. First, indoor smoking bans cause economic losses. Second, they promote the kind of “save me from myself” paternalism which is a way of expanding the power of government in the name of helping people who cannot handle the responsibility that comes with freedom. There are eerie similarities between those who wish to ban tobacco and the prohibitionist war on drugs.

In case it was not clear until this point, smoking is bad for you, and you should use whatever means necessary to quit. However, it is a legal product and adults should be allowed to enjoy it even without big government nanny approbation. The danger from tyranny is far greater than the dangers of indoor smoking.

Exit question: If the general public knew how much of the science being used to push for banning tobacco was nonsense, would such legislation continue to receive support?

UPDATE: The answers to a few critiques raised by this article can be found here: Where There’s Smoke, There’s Fire.

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Two teams conducting parallel studies each found 2 genetic variants associated with Alzheimer’s disease, one of which was common to both studies. Philippe Amouyel’s team identified variants within CLU and CR1, while Julie Williams and her team also identified CLU and added PICALM to the mix. Combined, these 3 variants represent about 20% of the genetic risk relating to getting the disease.

In other words,

“If we were able to remove the detrimental effects of these genes through treatments, we could reduce the proportion of people developing Alzheimer’s by 20%,” Williams, of Cardiff University in Wales, told a press conference. “In the UK alone this would prevent just under 100,000 people developing the disease. So the significance of these results in truly meaningful.”

Alzheimer’s disease is the stuff of nightmares:

Although the course of Alzheimer’s disease is unique for every individual, there are many common symptoms. The earliest observable symptoms are often mistakenly thought to be ‘age-related’ concerns, or manifestations of stress. In the early stages, the most commonly recognised symptom is memory loss, such as difficulty in remembering recently learned facts. When a doctor or physician has been notified, and AD is suspected, the diagnosis is usually confirmed with behavioural assessments and cognitive tests, often followed by a brain scan if available. As the disease advances, symptoms include confusion, irritability and aggression, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis.

The genomes of over 19,000 patients were analyzed, making the results statistically valid.

One of the new variants is in a gene active at synapses, the junctions between brain cells, and the two others help damp down inflammation in the brain. Inflammation is a known feature of Alzheimer’s, but it is often regarded as a consequence of the disease. Dr. Williams said that the detection of the new variants, which undercut the brain’s efforts to restrain inflammation, suggested inflammation might play a primary role.

Neil Hunt, chief executive of the Alzheimer’s Society agrees that these results can be referred to as a breakthrough and is calling for more research funding.

It is not very often that scientists are prepared to stick their necks out and refer to research results as a “breakthrough”. This is one of those very rare occasions when it is a word that really does fit the bill. The importance of the discovery of three new genes with an association with Alzheimer’s disease in such a short space of time is significant.

Even before this latest development, clinical research was underway investigating different avenues for a cure.

As of 2008 there were more than 400 clinical trials under way to understand and treat Alzheimer’s disease. Over 100 of these studies were in the last phase before commercialization (phase three trials).

Many different investigation approaches coexist. Amyloid beta is a common target, existing many trials which aim to reduce it with different agents such as bapineuzumab, an antibody in phase III for patients in the mild to moderate stage, semagacestat, a γ-secretase inhibitor, MPC-7869, and acc-001, a vaccine to amyloid beta in phase II to be used in the mild stage. However, in a recent study an experimental vaccine was found to have cleared patients of amyloid plaques but did not have any significant effect on their dementia, casting doubt on the utility of such approaches.[2]

Other approaches are neuroprotective agents, like AL-108 (phase II completed); or metal-protein interaction attenuation, as is the case of PBT2 (phase II completed). Finally, there are also many basic investigations trying to increase the knowledge on the origin and mechanisms of the disease that in the future may help to find new treatments.

Faster, please.

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That Magic Slumber Number

Scientists have been saying for years that 8 hours is the magic number needed for a good night’s rest. Most working Americans get less and it has a detrimental effect on health.

Ying-Hui Fu, Ph.D at the University of California, San Francisco along with a team of scientists* found a mother and daughter with a mutated gene (DEC2) which is somehow responsible for their ability to thrive on only 6 hours of sleep.

Scientists are still trying to unravel the mysteries of sleep.

Sleep remains a relatively inscrutable biological phenomenon. Scientists know that it is regulated in large part by two processes: 1) circadian rhythms—genetic, biochemical and physiological mechanisms that wax and wane during a 24 hour period to regulate the timing of sleep, 2) and homeostasis – unknown mechanisms that ensure that the body acquires over time the necessary amount of sleep, nudging it toward sleep when it has been deprived, prompting it out of sleep when it has received enough.

Genetically engineered mice who carried the mutated gene not only were getting less sleep in general, but also had a faster recovery time after a period of sleep deprivation.

The specific function of DEC2 remains elusive.

DEC2 could be involved in modulating “sleep quantity” alone, or it could be mediating both “sleep quantity” and “wakefulness-behavioral drive,” according to Fu. The latter drive, she says, is critical for the procurement of food, shelter, and mates and could be more potent in individuals with this mutation.

*Co-authors of the study are Christopher R. Jones, MD, at the University of Utah; Nobuhiro Fujiki, PhD, and Seiji Nishino, PhD, both of Stanford University; Ying Xu, PhD, and Jimmy Holder, MD, PhD, both at the time of the study in the Fu lab; Bin Guo, PhD, of the University of California, Berkeley; and Moritz J. Rossner, PhD, of the Max-Planck-Institute of Experimental Medicine.

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Use It Or Lose It

Putting your brain to use through years of formal education can serve as a protector against the effects of Alzheimer’s disease. The remarkable effect discovered was not that years of education lower the odds of getting the disease. Instead, researchers discovered that those individuals with more formal education were not showing clinical symptoms of brain deficits compared to other people with Alzheimer’s and without the educational background.

These phenomena are often ascribed to the theoretical concept of cognitive reserve. A high level of cognitive reserve results in a strong individual resilience against symptoms of brain damage; cognitive reserve can therefore be seen as protective against brain damage.

The amount of brain tissue lost was assessed through MRI (Magnetic Resonance Imaging) scans. Somehow, those with the benefit of a formal education showed an equal amount of brain volume lost, yet they were able to function normally.

Human brains are flexible organs, and it’s never too late to give them a workout. Although this study, published in the current issue of the Journal of Alzheimer’s Disease (“Education attenuates the effect of medial temporal lobe atrophy on cognitive function in Alzheimer’s disease: The MIRAGE Study,” Journal of Alzheimer’s Disease, August 2009), used formal education as a convenient guideline, you can get similar benefits by exercising your brain regularly with mentally challenging activities.

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