I was intrigued. Discovering a gene that caused late onset Alzheimer’s would be a major scientific breakthrough, perhaps leading to effective new treatments. So I read the article carefully.

To summarize the findings, a United States research team looked at the entire genome of 2269 people who had late onset Alzheimer’s and 3107 people who did not. They were looking for differences in the genome.

In the people who had late onset Alzheimer’s, 9% had a variation in the gene MTHFD1L, which lives on chromosome 6. Of those who did not have late-onset Alzheimer’s 5% had this variant.

So is this an important finding? The article suggested it was. But I think this is a prime example of bad science reporting. For instance, they went on to say that this particular gene is involved with the metabolism of folate, which influences levels of homocysteine. It’s a known fact that levels of homocysteine can affect heart disease and Alzheimer’s. So is it the gene, or is it the level of homocysteine?

The main reason why I consider this an example of stupid science reporting is that the difference is trivial. Let me give you an example of a better way to report this. The researchers could have instead reported that among people with late-onset Alzheimer’s, 91% of them had no gene changes, and then among people without late onset Alzheimer’s 95% of them had normal genes. But this doesn’t sound very impressive, and calls into question whether measurement errors would account for the differences.

So this very expensive genome test yields absolutely no predictive value in terms of who will develop Alzheimer’s and who will not. There is a known genetic variant, called APOE, which lives on chromosome 19. Forty percent of those who develop late-onset Alzheimer’s have this gene, while only 25 to 30% of the general population has it. So even this gene, which has a much stronger association with Alzheimer’s, isn’t a particularly useful clinical test.

The other reason this is an example of stupid science is that basically this is a negative finding. To scan the entire human genome looking for differences between normal elderly people and elderly people with Alzheimer’s, and discover only a subtle and tiny difference, must’ve been a huge disappointment for the researchers. If I had been the journal editor reviewing this study, I doubt I would’ve published it. Imagine a similar study of an antidepressant, which found that in the antidepressant group, 9% of people got better, and in the placebo group 5% got better. I doubt this would get published.

Interestingly enough, the study hasn’t been published yet, but is being presented as a paper at the April 14 session of the American Academy of Neurology conference in Toronto. This is another clue to reading scientific research. If it hasn’t been published in a peer-reviewed scientific journal, be very skeptical of the research. Good research usually gets published in top journals, and research that is more dubious often is presented at conferences but never published. It’s much easier to get a paper accepted for a conference than in a science journal.

It’s also important when reading media coverage of scientific research to read beyond the headlines, and to look at the actual numbers that are being reported. If they are very small numbers, or very small differences, be very skeptical of whether they mean anything at all.

As quoted in the article, “While lots of genetic variants have been singled out as possible contributors to Alzheimer’s, the findings often can’t be replicated or repeated, leaving researchers unsure if the results are a coincidence or actually important,” said Dr. Ron Petersen, director of the Mayo Alzheimer’s disease research Center in Rochester, Minnesota.

So to summarize, to be a savvy consumer of media coverage of scientific research:

1. Be skeptical of media reports of scientific research that hasn’t been published in top scientific journals. Good research gets published in peer-reviewed journals, which means that other scientists skeptically read the article before it’s published.

2. Read below the headlines and look for actual numbers that are reported, and apply common sense to these numbers. If the differences are very small in absolute numbers, it often means that the research has very little clinical usefulness. Even if the differences are large in terms of percentages, this doesn’t necessarily mean that they are useful findings.

An example would be a finding that drinking a particular type of bourbon increases a very rare type of brain tumor from one in 2,000,00 to three in 2 million. If this was reported in percentage terms the headline would say drinking this bourbon raises the risk of brain tumor by 300%, which would definitely put me and many other people off from drinking bourbon. (By the way, this is a completely fictitious example.) But if you compare the risk to something that people do every day such as driving, and revealed the driving is 1000 times more risky than drinking this type of bourbon, it paints the research in a very different light.

3. Be very skeptical of research that has not been reproduced or replicated by other scientists. There’s a long history in science of findings that cannot be reproduced or replicated by other scientists, and therefore don’t hold up as valid research findings.

4. On the web, be very skeptical of research that’s presented on sites that sell products. Unfortunately a common strategy for selling products, particularly vitamin supplements, is to present pseudoscientific research that supports the use of the supplement. In general, any site that sells a product cannot be relied on for objective information about that product. It’s much better to go to primarily information sites like Web M.D., or the Mayo Clinic site, or one can go directly to the original scientific articles (in some cases), by using PubMed.

So be a smart consumer of science, so that you can tell the difference between smart science and stupid science.

Copyright © 2010 Andrew Gottlieb, Ph.D. /The Psychology Lounge/TPL Productions

• “bupropion SR (sustained release; Zyban, GlaxoSmithKline), 150 mg twice daily for 1 week before a target quit date and 8 weeks after the quit date;
• nicotine lozenge (2 or 4 mg) for 12 weeks after the quit date;
• nicotine patch (24-hour, 21, 14, and 7 mg titrated down during 8 weeks after quitting;
• nicotine patch plus nicotine lozenge;
• bupropion SR plus nicotine lozenge; or
• placebo (1 matched to each of the 5 treatments).”

Everyone received six 10- to 20-minute individual counseling sessions, with the first 2 sessions scheduled before quitting.

What were the results?

Three treatments worked better than placebo during the immediate quit period: the patch, bupropion plus lozenge, and patch plus lozenge.

At six months, only one treatment was effective; the nicotine patch plus nicotine lozenge. The exact numbers , as confirmed by carbon monoxide tests, were: “40.1% for the patch plus lozenge, 34.4% for the patch alone, 33.5% for the lozenge alone, 33.2% for bupropion plus lozenge, 31.8% for bupropion alone, and 22.2% for placebo.”

So we see that the combined nicotine substitution therapy worked best, followed closely by either nicotine substitute alone. Zyban or Welbutrin (bupropion) was a bust, no more effective than the simple nicotine lozenge. The only advantage to Zyban would be if one prefers not to use nicotine substitutes.

Now I mentioned that they omitted one drug treatment, which is the drug Chantix (varenicline). This is probably because the drug is a nicotine receptor blocker, so wouldn’t have made sense to combine with nicotine substitutes. Also, there have been some disturbing case reports of people having severe depressive reactions to Chantrix.

Of course, there was one glaring omission that any card-carrying psychologist would spot in a moment–the lack of a behavior therapy component. Giving 6 ten minute sessions is hardly therapy. I would have liked to see true smoking cessation behavior therapy combined with the drug treatments.

So, if you’re trying to quit smoking, combine nicotine patches with nicotine lozenges, sold in any pharmacy. If you do, you have a 40 percent chance of succeeding at 6 months.

Now I am off to have a cigarette….just kidding.

Study: http://cme.medscape.com/viewarticle/712074_print

Copyright © 2009/2010 Andrew Gottlieb, Ph.D. /The Psychology Lounge/TPL Productions

More in a continuing series about one of my favorite topics, something we all do every day, and spend roughly a third of our lives doing…sleep!

Since we are in the middle of the common cold season, this post will be particularly relevant.

It turns out, grandma was right. Getting good sleep really does prevent colds. This supports a favorite belief of mine—that I don’t believe in the germ theory of illness.  Read on and you will see why I liked the referenced article.

Researchers at a variety of universities collaborated and did a clever study looking at sleep and its effects on susceptibility to the common cold. First they had their 153 subjects, healthy men and women between 21 and 55, report their sleep duration and efficiency for 2 weeks. (Efficiency is what percent of the time you are actually sleeping while in bed.) Next, these diabolical researchers sprayed cold virus up the noses of all the subjects (in quarantine), and watched what happened over the next 5 days.

The results were very interesting. Those subjects who slept less than 7 hours were almost 3 times more likely to develop a cold than those who slept 8 hours or more. In addition, those whose sleep was less than 92% efficient were 5.5 times more likely to develop a cold than those with 98% or more sleep efficiency. Interestingly, how rested subjects reported feeling after sleep was not associated with colds.  The lead author of the study concluded, “The longer you sleep, the better off you are, the less susceptible you are to colds.”

Now I promised that I would report evidence that this study bolsters my theory that germs don’t really matter that much. Remember the researchers sprayed virus up everyone’s noses. After five days, the virus had infected 135 of 153 people, or 88% of the people, but only 54 people (35%) got sick. What this suggests is that even among the people who were infected with cold virus, 60% stayed healthy, while 40% got sick. And the ones who got sick were much more likely to have reported less and lower quality sleep in the two weeks before infection. 

This is very relevant for everyday life, since much of the time we can’t really avoid exposure to common germs like colds and flu. If good sleep protects us even when infected with such germs, then it may be the key to staying healthy.

What is truly fascinating about this study is the precise immune regulation showed by those who got infected, but stayed healthy. To understand this let me digress for a moment with a short primer on the common cold. Most people think cold symptoms are caused by cold virus. This is wrong. Actually, cold symptoms are caused by our bodies’ immune reaction to the cold virus. Our bodies produce germ fighting proteins called cytokines, and when our bodies make too much, we get the congestion and runny nose symptoms. If our bodies make just the right amounts of cytokines, we fight the virus without feeling sick.

So getting 8 or more hours of sleep a night may allow your body to fine tune an immune response, and make just the perfect amount of germ fighting proteins.

Another interesting finding is the relationship of sleep efficiency and illness. Sleep efficiency was an even more powerful predictor of getting sick than total sleep. (Of course, this might reflect an overall difference in sleep quality. Those who sleep deeply may tune up their immune systems better, and they are likely to spend most of their time in bed asleep.)

But assuming that increasing sleep efficiency is useful, then those people who take a long time to fall asleep, and who sleep fitfully may benefit from spending less time in bed, and working on sleeping more of the time they are in bed. On the other hand, those who fall asleep as soon as their head hits the pillow, and who are sleep like logs, would probably benefit from spending a little more time in bed, since they are not getting enough sleep.

So there you have it. Sleep 8 hours or more, try to sleep well, and you can lower your odds of getting a cold greatly. Even if you are exposed to the virus, if you have good sleep quality, you probably won’t get sick. So much for the simple germ theory! I suspect that this applies to all infectious diseases. So getting good quality and quantity in sleep may be one of the most important health behaviors for staying well.

It’s late, and I’m off to bed now…..zzzzzzzzzzzzzzz.

Copyright © 2009 The Psychology Lounge/TPL Productions/Andrew Gottlieb

It’s been a while since I wrote, and some of that is that I’ve been trying to get to bed earlier, and get a more consistent 8 hours of sleep. Since I last wrote, I saw an interesting factoid from an interview with Daniel Kripke, who is the co-director of the Scripps Clinic Sleep Center in La Jolla, California. In this interview, he talked about research he did on more than 1 million Americans that correlated sleep and mortality. There were some surprising findings, which have been corroborated by similar studies in other countries.

The results showed that those who slept between 6.5 and 7.5 hours a night lived the longest. And that those who slept more than 8 hours a night or less than 6.5 hours a night don’t live as long. This is interesting in that most previous writing I have seen suggests that sleeping more is good for you, but these data don’t support that.

Another good point he made was that when people try to get too much sleep, because they think the normal amount is 8 or 9 hours, they may unintentionally develop insomnia. Staying in bed longer than you can sleep will result in wakefulness, and anxiety about not being able to sleep. So for those of you who only can sleep 6.5 or 7 hours, just get up, it won’t hurt your health. In fact, restricting the time in bed is a more effective treatment for insomnia than sleeping pills, according to Kripke.

What we don’t know is which direction the causality runs in this association. Does the amount of sleep you get create your health status, or is it a reflection of underlying health? Do sicker people sleep too little or too much? Or does sleeping too little or too much make you sicker? No one knows for now, so I wouldn’t necessarily rush to change your sleep habits based on this study. But if you are sleeping in the 6.5 to 7.5 hour range, you can relax and not worry about it (especially late at night!)

Now I’ve got to stay up a little longer, so I don’t get too much sleep tonight…

Copyright © 2008 The Psychology Lounge/TPL Productions

Was Grandma Right?

It’s been too long since I last wrote, but I’ve been catching up on my sleep. Why will become relevant after you read this article.

Sleep is something we mostly take for granted as part of our daily lives, much like eating and showering. But why do we sleep? What does sleep do for our minds and our bodies? What happens if we don’t sleep, or if we don’t sleep enough?

For those of you who are interested in these questions, I’d highly recommend that you read the transcript of The Science of Sleep, an excellent piece by 60 Minutes that aired on March 16, 2008. Not only did I learn many interesting facts about sleep, I learned about my own health and how sleep affects it. More on that later.

Why do we sleep? After all, from a survival point of view, sleep is not really a good thing, in the sense that we are unconscious and helpless during sleep. So for sleep to have evolved, then it must serve some vital functions. (I should point out though, that sleep might have survival advantages, since if early humans slept in caves and other sheltered places, sleep would have kept them out of the reaches of nocturnal predators. The folks who didn’t sleep much, and who wandered around all night, probably got eaten!)

One clue of how important sleep is in studies done in the 1980’s with rats. When rats were prevented from sleeping (did they use disco music to keep them awake?) they died after 5 days! Sleep seems to be as important to rats as food.

Let me present a quick primer on sleep. When we sleep, we actually go through multiple cycles of different stages of sleep. These stages are stages 1-4 of non REM (NREM) sleep, and stage 5 which is REM (rapid eye movement) sleep. The key stages are Stage 4, or Delta Sleep, and Stage 5, REM sleep. Stage 4 Delta sleep is the deep restorative sleep where our bodies get rebuilt and restored. Stage 5 REM sleep is when we dream, and it appears that our minds get restored during REM sleep. Typically the whole cycle takes about 100 minutes, and we have 3 or 4 of them each night.

Sleep may play an important role in enhancing memory. One study found that when people learned a new skill in the afternoon, and then were tested after a night of sleep, they did 20-30 percent better than those who were tested after twelve hours, but with no sleep in between the learning and testing. This is fascinating, and jibes with a trick I learned in graduate school. When I would study statistics, I’d always review my notes right before going to sleep. The next morning, the memories of those notes were imprinted magically in my mind.

Sleep also plays a critical role in stabilizing mood. One experiment tested people who were sleep deprived by showing them disturbing images within an fMRI scanner, to look at their brain activation. They found the sleep deprived subjects had a disconnect between the brain’s emotional center (the amygdala) and the part of the brain that controls rational thought (the frontal lobe). So they couldn’t control their emotional reactions. They looked more like psychiatric patients. Of course we all know that sleep deprivation makes us cranky and short-tempered, this explains why.

Another important function of sleep is physical rejuvenation. It appears that Stage 4 sleep is essential here. In the 60 Minutes piece they show an experiment where a young man named Jonathan is deprived of only Stage 4 sleep. Each time his brain waves show Stage 4 sleep, loud sounds are played to bring him out of deep sleep. He gets a normal amount of sleep, but a reduced amount of Stage 4 sleep. After 4 nights of this regimen, this 19 year old is starting to look physically like a 70 year old. His body becomes no longer able to metabolize sugar effectively, putting him temporarily at increased risk for Type 2 diabetes.

Other studies confirm this. After just a few nights of partial sleep deprivation, young healthy people show a metabolic change that is similar to what happens as people develop Type 2 diabetes. They no longer metabolize sugar effectively. They deposit more fat. The hormone leptin, which controls appetite, seems to drop, and they want to eat more.

This is truly astonishing. If relatively short term sleep deprivation can cause such a profound shift in the body’s sugar metabolism, then this may be the key to unlock one of the great medical mysteries of the 20^th century: Why obesity has increased so rapidly since 1980? Could it be that the obesity epidemic is really a sleep deprivation epidemic? Could it be so simple? Not junk food, television, lack of exercise, and all of those things that people talk about? Could grandma have been right?

Here’s the clue.

In 1960 a survey of a million Americans showed an average of 8.0 hours of sleep per night. Today similar studies show we are only getting 6.7 hours a night. That’s a drop of 16.25% in less than a generation. And teenagers are the most sleep deprived of all, since they require 9-10 hours of sleep, and most get less than 7 hours of sleep, thanks to ridiculously early school start times. Teenagers may be lacking between 22 percent and 30 percent of their needed sleep.

So we have a plausible explanation for why everyone, even children and teenagers, is getting fatter. Sleep deprivation causes shifts in metabolism, creating a pre-diabetic state, and lowering level of the satiety hormone leptin, which causes us to eat more, and store more fat. Add sugary or high carbohydrate foods, and we get even fatter. Add inactivity, and we get even fatter. The damage begins early, perhaps in early teenage years.

So if we want to lose weight, then the old saw of a healthy diet and plenty of exercise may be wrong. The proper advice is probably lots of sleep, a reasonably healthy diet, and a little exercise. Or since exercise improves sleep quality, sleep, exercise, and diet. Without adequate sleep, diet and exercise are doomed to failure, since even young people may unintentionally be turning their bodies pre-diabetic, which makes it very hard not to gain fat.

So that’s why I haven’t written. After a lifetime of staying up late, and cheating sleep, I’m starting to try to get a solid 8 hours of sleep a night. Already I’ve lost a few pounds, even though I haven’t been exercising much. The other advantage of going to bed earlier is that when you are sleeping you are not eating.

So try it. Get 8 or 8 1/2 hours of sleep a night. And make sure your teenagers get 9 or 10 hours a night. No more websurfing or TV late at night. And write me and let me know if your weight drops as a result.

Now I’ve got to stop writing and go to sleep…

Copyright © 2008 The Psychology Lounge/TPL Productions

All Rights reserved (Any web links must credit this site, and must include a link back to this site.)

A fascinating idea is how to protect your brain using simple nutrients. Can we protect our brains from depression, Alzheimer’s, even stroke using simple nutrients or over the counter supplements?

The Wall Street Journal just published an interesting article about using fish oil to treat or prevent a variety of illnesses. They even summarize the findings with recommended doses of fish oil. For instance, to prevent heart disease, they recommend one gram of EPA or more per day. For optimum brain health, take one half gram of DHA or more. Even Rheumatoid arthritis may respond to 2 grams or more of fish oil.

Fish oil contains omega-3 fatty acids, of which there are two main ones; EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid). Repeat after me if you want to really impress your physician: “eye-coh-sah-pent-ah-eh-no-ick  acid” and “doh-coh-sah-hex-ah-eh-no-ick acid”. Now you see why articles always say EPA and DHA!

There is a very interesting tie in with DHA and Alzheimer’s disease, as explained by an article on medicinenet.com.  It turns out that people with Alzheimer’s disease (AD) tend to have low levels of a brain protein called LR11, and about 15% of those with AD have a gene mutation that reduces LR11. LR11 works to clear the brain of amyloid proteins, which are implicated in the production of beta-amyloid plaque that clogs the neurons of those with AD.  Scientists tested DHA in rodents and in cultures of brain cells, and found that DHA causes higher production of LR11.

So should you be taking fish oil capsules, and how many, and which brand? I’d say if you eat oily fish like salmon 3 times a week or more, don’t worry about it. But for the rest of us (all of us?) it may make sense to add fish oil capsules to our vitamin regimen. A 1999 Italian study found that adding 3 capsules a day reduces the incidence of sudden cardiac death by 45%! The subjects in this study mostly also took baby aspirin, which may work to increase the effects of fish oil.

I’d certainly talk to your doctor about it. Be sure to print out the Wall Street Journal article, which demonstrates that there were few if any side effects. Some doctors think taking fish oil will make you bleed more easily, but studies of very high doses haven’t found this. In fact, the main side effect is belching fish smells, but I have found this is dependent on the brand and type of capsules you take.

Here’s a quick rundown on what to look for in fish oil capsules. First of all, they vary as to how much of the essential ingredients they contain. Most capsules contain 1 gram of oil, but much less Omega-3 fatty acids EPA and DHA. Some contain as little as 200mg. of the Omega-3’s, which means you have to eat  a LOT of capsules to get much EPA or DHA. Often the bottles will mislead you by citing the amount per serving, and when you look more carefully you will see that one serving is 3 or 4 capsules!

So you want as high a concentration of EPA and DHA as possible. You also want fish oil that has been molecularly distilled to remove any possible contaminants such as pesticides, dioxin, etc.

Although I rarely make product recommendations, I heartily recommend Trader Joe’s Fish Oil capsules. Priced at $7.99 for a bottle of 100 capsules, these capsules are molecularly distilled, and contain 300 mg. of EPA, and 200 mg. of DHA per capsule. That means that 2 capsules make up 1 gram of Omega-3’s.  So it is easy to take 1 or 2 grams of Omega-3’s per day, at an affordable cost. These compare favorably with much more expensive brands of omega-3 capsules.  Another trick is to store these in the refrigerator, so the oil doesn’t turn, and occasionally break open a capsule and smell it. Although it may have a slightly fishy smell, it should smell rancid or strong.

So there you have it, a simple way to reduce heart disease, autoimmune disease and inflammation, and improve brain health. Cost? About $0.16  per day for 2 capsules.

As always, as I am not a physician, and certainly not your physician, talk to your doctor and do your own research before consuming more than a capsule a day of fish oil.

Copyright 2008 The Psychology Lounge/ TPL Productions 

All Rights reserved (Any web links must credit this site, and must include a link back to this site)

Today’s New York Times has a fascinating article about current research in Alzheimer’s called Finding Alzheimer’s Before a Mind Fails. It is simultaneously encouraging and deeply disturbing.

The encouraging part is that researchers are discovering ways to examine patients that can find evidence of Alzheimer’s many years before the disease manifests itself in symptoms. A radioactive dye call Pittsburgh Compound B (PIB) is injected into the patient. This dye attaches itself to amyloid plaques in the brain, and then these can be seen by using a Positron Emission Tomography (PET) scan.  Studies using PIB have found the astonishing fact that amyloid plaques are found in 20-25 percent of people over 65 who appear normal! If the amyloid hypothesis is accurate, then many of these people will go on to develop Alzheimer’s disease.  Using PIB testing we could predict more accurately who will develop the disease, and perhaps develop prevention methods much like we give statins to heart patients who have plaques in their arteries. This is encouraging.

Someday in the future hopefully we will be tested for early signs of Alzheimer’s disease in our 40’s, and those who at risk given medications that will prevent it, just like we do for heart disease now. This would make aging much less scary.

Current Facts About Alzheimer’s disease

But the current facts about Alzheimer’s are less encouraging. It is the sixth more common cause of death by disease in the U.S. Five million people over 65 have Alzheimer’s disease. Estimates suggest that perhaps as many as 16 millions will have the disease by 2050, which is a staggering number that would bankrupt the health care system. (Of course, this assumes that in 43 years we have made no progress in the treatment and prevention of Alzheimer’s disease, which is absurd.)

Costs are already staggering–$148 billion dollars per year, and are increasing every year. Why? Here’s the dark truth. Alzheimer’s disease is a disease of the elderly. Almost 40 percent of those who live past 85 will eventually develop Alzheimer’s disease. The problem is that medical improvements are curing the diseases that used to kill us well before 85. One of the reasons Social Security starts at age 65 is that until recently, most people didn’t live much past the age of 65. Now as we defeat cancer and heart disease, and people stop killing themselves with diet and smoking, we are living into our 80’s and 90’s.  And getting Alzheimer’s disease.

What is Alzheimer’s disease?

Let’s talk a little more about what Alzheimer’s disease really is. Everyone worries about Alzheimer’s disease as they age. But some forgetfulness is completely normal. (We hope.) There is a old joke about Alzheimer’s disease which actually is a useful rule of thumb, it’s not a big deal if you forget where you put the car keys, as long as you can remember what keys are for. It is significant changes in memory and problem solving that are more worrisome.

When does Alzheimer’s disease begin?

This is a mystery currently. Conventional wisdom says that Alzheimer’s disease may begin a few years before symptoms appear, but some scientists question this. Because the brain has a lot of spare capacity, it may take years of deterioration before we lose enough brain function to notice. This may explain one of the common findings that the more highly educated (and probably more intelligent) develop Alzheimer’s disease as  a lower rate. They may have more spare capacity. If you start off with an IQ of 150, and lose a third of your brain functioning, you end up with an IQ of 100, and can still function. Start at IQ 100, lose 1/3, and you now are functionally retarded with an IQ of 66, and you won’t be able to live independently.

One scientist, Dr. Richard Mayeux, who is a professor at Columbia University, says, “I think there’s a very long phase where people aren’t themselves.”

“If Dr. Mayeux asks family members when a patient’s memory problem began, they almost always say it started a year and a half before. If he then asks when was the last time they thought the patient’s memory was perfectly normal, many reply that the patient never really had a great memory.” (New York Times)

This is interesting and disturbing stuff. Other research finds that people who later develop Alzheimer’s disease showed lower intelligence scores even early in life, suggesting that perhaps Alzheimer’s disease is a genetic disorder that affects the brain in subtle way even early in life. If this is true, then the data on highly educated people may have been interpreted in a backwards way—instead of higher education preventing Alzheimer’s disease, it may be that Alzheimer’s disease prevents higher education!

Treatment of Alzheimer’s disease

Currently there are drugs that address the symptoms of Alzheimer’s disease, but no drugs that address or slow the underlying disease progress. The good news is that there are numerous studies attempting to find drugs that will actually address the underlying disease process in Alzheimer’s disease. The bad news is that no one really knows exactly what that underlying disease process is.

There are two finding from examining the brains of those with Alzheimer’s disease. The first is that they show plaques of beta amyloid between the nerve cells of the brain. The second is that the brains show tangles inside nerve cells made of a protein called tau. This damaged tau kills the nerve cells because they no longer get nutrients.  Both these are well-established facts, but no one knows what is the relationship between beta amyloid and tau, and how much each contributes to Alzheimer’s disease.

What Society Should Do About Alzheimer’s disease?

So what can we as a society do about Alzheimer’s disease? My grandfather used to say, “Everyone dies, so it’s just a matter of how you die.” By choosing to treat or prevent heart disease and cancer, are we choosing to die from Alzheimer’s disease?   This is a scary thought.  It’s clearly worse to outlive your mind than to outlive your body. And Alzheimer’s disease puts huge burdens on society and caretakers. Maybe we should start a campaign to encourage cigarette smoking in the elderly! (Or motorcycle riding, but this might make the roads a bit dicey.) 

More seriously, we are in the unfortunate window of time where we have successfully improved longevity without really addressing this core disease of longer life, Alzheimer’s disease.  Society desperately needs to find an Alzheimer’s disease cure or preventative treatment. Without this we will as a society incur great costs and individual suffering. I believe that this should become a top priority of private and government research spending. First we need better basic research to find out what the disease process of Alzheimer’s disease looks like. Then we can develop effective drugs to block or reverse that disease process.

In the meantime, all we can do is not worry too much, since stress may damage the brain. Eat healthy, exercise, maybe take some anti-oxidant vitamins, and hope that science can solve this puzzle so we can get old without losing our brain function.   

As for me, I aspire to these not-so famous words of the comedian Will Shriner, “I want to die in my sleep like my grandfather… Not screaming and yelling like the passengers in his car.”

Copyright 2007 The Psychology Lounge/ TPL Productions, All Rights Reserved

For those readers curious about the mechanisms by which emotional stress affects brain function, I found an interesting piece of research about the physical mechanisms for how chronic stress can induce brain changes that could lead to cognitive impairment.

Scientists at Salk Institute for Biological Studies subjected mice to mild chronic stress for two weeks. What they found was fascinating. First some background on the physiology of Alzheimer’s disease. As the article explains:

“Alzheimer’s disease is defined by the accumulation of amyloid plaques and neurofibrillary tangles. While plaques accumulate outside of brain cells, tangles litter the inside of neurons. They consist of a modified form of the tau protein, which–in its unmodified form–helps to stabilize the intracellular network of microtubules. In Alzheimer’s disease, as well as various other neurodegenerative conditions, phosphate groups are attached to tau. As a result, tau looses its grip on the microtubules, and starts to collapse into insoluble protein fibers, which ultimately cause cell death.”

So basically, when phosphate attaches the the tau molecules, it causes them to change from helpful molecules to damaging the neurons.

The mice research found that the brain-damaging effects of negative emotions are relayed through the two known corticotropin-releasing factor receptors, CRFR1 and CRFR2, which are part of the body’s central stress mediation system.

So what does this all mean? It suggests that we have to protect our brains from stress, particularly chronic stress. Occasional stress doesn’t cause problems, but daily chronic stress does. The mice only showed permanent brain changes after 2 weeks of daily stress.

So stress management through cognitive behavioral therapy (CBT) or other means is not just a nice comfort option, but may be essential if you want your brain to last. Emotional pain doesn’t just cause emotional damage, it also damages the brain.

Perhaps scientists will be able to develop drugs that change CRF1 and CRF2 levels, but in the meantime, better take up that yoga, meditation, relaxation exercise, or CBT stress management program!

Copyright 2007 The Psychology Lounge/TPL Productions

So you’ve been putting off getting therapy, even though most of the time you feel anxious and upset? Well, a new study suggests that you may be putting your brain in danger.

Researchers at Rush University Medical Center in Chicago, Illinois, followed more than 1200 men and women who were 65 and older, average age of about 76. At the beginning of the study they made sure that none of them had mild cognitive impairment (MCI), and measured their emotional distress using a simple 6 item scale of neuroticism. Items such as 1) “Are you the type of person whose feelings are easily hurt?”; 2) “Are you the type of person who is rather nervous?”; and 3) “Are you the type of person who is a worrier?” make up this scale.

At the beginning of the study the average score was about 15 on this emotional distress scale. Patients were followed up for up to 12 years. About 38% developed MCI during the study. Those in the top 10% of emotional distress at the beginning of the study were about 40% more likely to develop MCI.

What is interesting is this relationship held even after researchers statistically removed the effects of depressive symptoms at the beginning of the study. So the results were from emotional distress, not from depression. The risk for MCI increased by 2% for every 1 point increase on the distress scale. This is a pretty strong correlation.

So what does this mean? I think what it means is that chronic emotional upset is hard on the brain. It makes sense, since emotional stress raises stress hormones such as cortisol, which we know can damage the brain, especially the hippocampus, which controls memory. What we don’t know is whether this study was picking up some early brain changes in the elderly, changes which correlate with both emotional distress AND a tendency to develop MCI. A better study would look at younger people, and see if emotional distress in those aged 40 or 50 leads to the development of MCI in later life.

Since about a third of those with MCI will develop Alzheimer’s Disease, any reductions in the prevalence of MCI would be tremendously beneficial to society. Perhaps psychotherapy should be mandatory for all those over 65!

What can you do to lower your brain risk? First of all, honestly evaluate whether you suffer chronic emotional stress. Ask yourself if most of the time you feel calm and happy, or upset and worried and stressed. Also ask your close friends and/or family what they think. If you are someone who suffers chronic stress, then get help. A cognitive behavioral psychologist can teach you good stress management skills, and may help break lifelong patterns of emotional stress. Another good option is to learn mindfulness meditation and yoga and practice them daily. These are known to reduce psychological distress.

Whatever you do, don’t take it lightly if you are in long term distress. Your brain wants you to be mellow!

Copyright 2007 The Psychology Lounge/TPL Productions

Even pure psychological stress can affect fertility. Here’s the biological mechanism. A few hours before ovulation, the pituitary gland sends out luteinizing hormone (LH), which tells the ovaries to release an egg. But if you are experiencing psychological stress such as a fight with your husband, or a dressing down from your boss, or a kid having a tantrum, then your LH will be suppressed, disrupting ovulation.

Even mild stress may have a big effect. One study of monkeys found that moving monkeys to a new cage, combined with a little less food and 1 hour on treadmill caused 70 percent of the monkeys to have irregular menstruation! So don’t skip that meal and take a long run when stressed, or you’ll greatly lower you odds of getting pregnant.

What’s worse is that IVF treatment itself may lead to large amounts of psychological stress. One fertility expert found that 40 percent of women in infertility treatment had all of the symptoms of an anxiety disorder or depression: sleep disturbances, difficulty concentrating, and irritability. So if stress lowers fertility, and fertility treatment increases stress, then fertility treatment may actually harm fertility!

But cognitive behavioral therapy may improve the situation. Alice Domar and colleagues at Harvard found that a 10 week cognitive behavioral group therapy program improved the success of fertility treatment from 20 percent to 55 percent in the women who participated in the group therapy. So what can we learn from this research?

1. A woman’s body is wise. It will respond to behavioral and psychological stressors by lowering fertility. Anything that resembles stress, even hard exercise, will trigger physical responses that lower fertility.
2. At critical points such as several hours before ovulation, even normal stressors can disrupt the ovulation process. And in stress-prone or perfectionist or angry women, the likelihood of experiencing stress during these critical hours is very high. Thus for women who are experiencing difficulty getting pregnant and who by personality are “stressy” (you know who you are!) cognitive behavioral therapy (CBT) will be helpful in learning to manage and lower stress.
3. Infertility treatment is by its nature stressful, and this leads to a paradox; infertility treatment may lower fertility if it increases stress. It may be helpful to evaluate stress levels in women undergoing IVF and if stress is high, intervene with CBT group or individual therapy.
4. The ultimate in infertility treatment may be what I recommended to my friend Jill, who had tried many cycles of IVF to no avail. I told her, “You’re young, why don’t you and your husband stop trying to get pregnant, and just have sex for fun, and enjoy life for a few years. If nothing happens then you can adopt.” She was pregnant within the year, and now has two lovely children. A good long relaxing vacation with no schedule, no hard exercise, healthy food, and no stress may be the best fertility treatment available, and even if it doesn’t work, at least you’ve gotten a great vacation!
5. Finally, what this research shows us is how linked our minds and bodies are. Changing thoughts and feelings and behaviors changes our bodies, and fertility is just one example of this.

Copyright 2007 The Psychology Lounge/TPL Productions