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

The article documents how most psychologists fail to provide empirically proven treatment approaches and instead use methods which are often ineffective. The truth is there is very little evidence for most of the types of therapy commonly performed in private practices by psychologists and by Masters level therapists. If you are shopping for the most effective types of therapy you need to find a practitioner who is skilled at cognitive behavioral therapy (CBT) which is one of the few psychotherapy approaches that has been proven to work on a variety of problems.

Another interesting article in Newsweek about evidence-based treatment discussed bulimia. Here’s the summary:

So the bottom line is this:

1. Most psychologists who don’t practice Cognitive Behavioral Therapy (CBT) are just winging it, using treatments that haven’t been shown to work by scientific studies. It’s as if you went to a regular physician and got treatment with leaches!

2. Many psychologists claim to use CBT but haven’t really trained in the use of CBT, or have taken a weekend workshop. Unless they prescribe weekly homework that involves writing down thoughts, and learning skills to analyze and change your thoughts, then they aren’t really doing CBT, and I recommend you find someone else.

3. If you have an anxiety disorder, depression, bulimia, or obsessive compulsive disorder, and haven’t been offered CBT, then you are not receiving state of the art treatment.

Copyright © 2009 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

The key behaviors that were associated with longevity were not smoking, keeping a healthy weight, controlling blood pressure, getting regular exercise, and preventing diabetes.

The results?

“There was no less chronic illness among survivors than among those who died before 90. But after controlling for other variables, smokers had double the risk of death before 90 compared with nonsmokers, those with diabetes increased their risk of death by 86 percent, obese men by 44 percent, and those with high blood pressure by 28 percent. Compared with men who never exercised, those who did reduced their risk of death by 20 percent to 30 percent, depending on how often and how vigorously they worked out.”

So there you have it. First stop smoking, or don’t start. Second, control your weight and eating patterns to avoid Type 2 diabetes. Third, lose weight so that you are not obese. Control your blood pressure, and exercise, and you’ve got longevity nailed. What is interesting is that although smoking is a completely independent risk factor, the other four are highly related to something called Syndrome X, a metabolic syndrome that is associated with high levels of blood sugar and insulin production, which leads to weight gain, hypertension, and pre-diabetes. Exercise leads to weight loss, and independently reduces the tendency to Syndrome X.And it’s not too late. Since the study only looked at these five behaviors after age 72, even change that occurs late in life can greatly extend and improve life.

Unfortunately, since the study only included men, we can’t really generalize the results to women, but it is likely that the same principles apply.

And now, I have to go take a swim…

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.)

But what about the truly profound and serious decisions of life?  What about something as serious as suicide?  Can it be that even such a grave decision is affected by seemingly small external factors?

The New York Times Magazine recently published a fascinating article “The Urge to End It All“, which addressed this very issue.  I highly recommend you read the entire article.

First, some numbers.  (I love numbers).  The current suicide rate is 11 victims per 100,000 people, the same as it was in 1965.  In 2005, about 32,000 Americans committed suicide, which is two times the numbers who were killed by homicide.

For many years the traditional view of suicide was that it reflects mental illness — depression, bipolar illness, psychosis, schizophrenia, or other mental illnesses.  This view assumed that the method of suicide was not important; it was the underlying mental illness that mattered.

But something happened in Britain in the 1960s and 1970s that set this model on its head.  It’s called the “British Coal Gas Story” and it goes like this:

For many years people in Britain heated their homes and stoves with coal gas.  This was very cheap, but the unburned gas had very high levels of carbon monoxide, and a leak or an opened valve could kill people in just a few minutes in a closed space.  This made it a popular method of suicide — “sticking one’s head in the oven” killed 2500 Britons a year by the late 1950s — half of all suicides in Britain!

Then the government phased out the use of coal gas, replacing it with natural gas, so that by the early 1970s almost no coal gas was used.  During this time Britain’s suicide rate dropped by a third, and has remained at that level since.

How can we understand this?  If suicide is the act of an ill mind, why didn’t those who could no longer use coal gas find another means? Why did the suicide rate in Britain drop by a third when the option of coal gas was no longer available?
The answer turns conventional wisdom about suicide on its head. Conventional wisdom is that people plan out suicides carefully, and so convenience of method shouldn’t matter. But actually it appears that often suicide is an impulsive act, and when you make it less convenient, people are less likely to complete the act.

Another example of this is found in the Golden Gate Bridge.  For years this gorgeous bridge has been a popular suicide point, where nearly 2000 people have ended their lives.  There have been many debates about erecting suicide barriers on the bridge, but most opponents say “they will just find another way.”

But Richard Seiden, professor at University of California Berkeley, collected data that addresses this issue.  What he did was to get a list of all potential jumpers who were stopped from committing suicide between 1937 in 1971, 515 people in all.  He then pulled their death certificate records to see how many had gone on to kill themselves later.  What would you guess was the percentage of these people who tried to jump off the Golden Gate Bridge and who later killed themselves?  50%?  75%?  25%?

Actually it was only 6%!  Even allowing that some accidents might have been suicides, the number only went up to 10%.  Although higher than the general population, it still means that for 90% of these would-be jumpers, they got past whatever was bothering them, and went on to live full lives.

Richard Seiden got some great stories out of this study.  One of the things he found was that would-be suicides tend to get very fixated on a particular method.  They tend to only have a Plan A, with no Plan B. As he says, “At the risk of stating the obvious,” Seiden said, “people who attempt suicide aren’t thinking clearly. They might have a Plan A, but there’s no Plan B. They get fixated. They don’t say, ‘Well, I can’t jump, so now I’m going to go shoot myself.”

One example he cites was a man who was grabbed on the east side of the bridge after pedestrians noticed him looking upset.  The problem was that he had picked out a spot on the west side of the bridge that he wanted to jump from, but there were six lanes of traffic between the two sides, and he was afraid of getting hit by a car on his way over!

As Seiden said, “Crazy, huh? But he recognized it.  When he told me the story, we both laughed about it.”

Another great example is from two bridges in Northwest Washington.  The Ellington Bridge and the Taft Bridge both span Rock Creek, and both have about a 125 foot drop into the gorge below.  For some reason the Ellington has always been famous as Washington’s “suicide bridge”.  About four people on average jumped from the Ellington Bridge each year as compared to slightly less than two people from the Taft.

In 1985, after a rash of suicides from the Ellington, a suicide barrier was erected on the Ellington Bridge, but not the Taft Bridge.  Opponents countered with the same argument, that if stopped from jumping from the Ellington, people would simply jump from the Taft.

But they were wrong.  Five years after the Ellington suicide barrier went up a study showed that while all suicides were eliminated from the Ellington, the rate at the Taft barely changed, inching up from 1.7 to 2.0 deaths per year.  What’s even more interesting is that the total number of jumping suicides in Washington dropped by 50%, or the exact percentage the Ellington had previously accounted for. So people stopped from jumping from the Ellington did not jump from other locations.

Coming back to our model that small external factors can have large influences on behavior, you might wonder why the Ellington was the suicide bridge instead of the Taft.  It turns out that the height of the railing was what made the difference. The concrete railing on the Taft was chest high, while the concrete railing on the Ellington (before the barrier) was just above the belt line.  One required a bit more effort and a bit more time to get over and this tended to reduce the impulsive action of jumping.

Which brings us to guns. Although guns account for less than 1% of all American suicide attempts, because they are so lethal, they account for 54% of successful suicides.  In 2005 that meant 17,000 deaths.  It turns out there when you compare states with high rates of gun ownership to states with low rates of gun ownership; you find that there is a direct correlation between the rate of gun ownership and the rate of gun suicide.  This is not surprising.

What is more surprising is that in the states with low gun ownership, the rates of non-gun suicide are the same as those states with high gun ownership.  So the lack of availability of guns does not encourage people to find other means of harming themselves.  Studies show that the total suicide rate in high gun ownership states is double that of in low gun ownership states.  So the Supreme Court, in their recent ruling regarding Washington, D.C.’s ban on handguns, may have missed the more important data when they focused on homicide rates.  From these studies scientists conclude that a 10% reduction in firearm ownership would result in a 2.5% reduction in the overall suicide rate.

I am not anti-gun. I like shooting, and if I were a hunter, would probably own a rifle.  But this is why I don’t own a gun, and this is why I don’t recommend that most people own a gun.  All of us are potentially subject to dark moments of the soul, and the research detailed in this New York Times article suggests that the more barriers and impediments there are to impulsively harming ourselves, the less likely we are to try.  If you do own guns, at least try to create barriers and delays such as keeping the guns locked up in a gun safe, keeping ammunition separate from the guns, or even not keeping ammunition in the home where guns reside.  Not only does this protect you from those dark moments of the soul but it may also protect someone you love, your spouse, or your child.

Again, I highly recommend a careful reading of the original article, as it has much other information that is useful and interesting.

In answering the question of the title, I have to say that reading this article convinced me that we should build a suicide barrier for the Golden Gate Bridge. Yes, it would lower the beauty of this gorgeous bridge, at least for pedestrians, but I have to believe that saving another 2000 lives trumps a pretty walk across the Bay.

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.)

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.)