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Your Mental Health


For years, the placebo effect has baffled doctors and scientists. People taking inactive medications really do get better to a certain extent and there has been much questioning as to why this happens and exactly what triggers the power of the placebo.

Placebos are used in virtually all clinical research. New medications are tested against inactive ones to ensure the medicine is truly helping people get better. Study volunteers do not know whether they are receiving the fake medicine or the real one and in order for the new drug to be deemed effective, it has to be shown to work better than the placebo.

Although it may seem as though the group taking the real medicine would stick out very obviously from those taking the fake drug, many people do experience significant improvement just taking the placebo.

Until fairly recently, this was deemed to be almost entirely a psychological effect. When we believe we are getting better, our body tricks us into feeling a bit better.

Some research over the past few years has finally quantified a mind-body connection showing our physiology does indeed react to placebo.

One study of Parkinson’s disease patients completed out of UBC found the placebo effect was maximized when study volunteers were told they had a good chance of getting the real treatment instead of a sugar pill but were still kept somewhat unsure.

In this study of placebo, all volunteers received inactive medication. Equal numbers were told they had a 25, 50, 75 or 100 percent chance of getting real medicine. Those who were told they had a 75 percent chance of getting the active drugs experienced the most significant improvement.

It seems the hope of real treatment coupled with uncertainty stimulated the brain’s reward system and their brains produced significant amounts of dopamine – a chemical key to reward that is also lacking in the brains of Parkinson’s sufferers.

No dopamine response occurred in those given placebo after being told they had only a 25 or 50 percent response and interestingly, no response occurred for those told they had a 100 percent chance of real medicine either.

These findings showed that a person’s expectations directly regulate the power of the placebo by stimulating the brain’s reaction.

More research into different conditions including chronic pain, depression and others are needed to see whether this effect would be the same. In Parkinson’s disease, the brain’s reward system is abnormal, so there are questions remaining about whether some response might happen at lower expectations in those with normal reward systems.

This study was somewhat similar to another one completed in the US a few years ago where healthy volunteers were given painful stimuli and told they were receiving medicine to ease their pain.

In this case, the volunteers’ brains released endorphins to block pain receptors when they were told they were receiving medication.

Although it is interesting and valuable to learn how the placebo response works as it may be a useful tool to augment effective treatment, it is dangerous to assume replacing active medication with placebo would yield long term results. In cases of serious, chronic or life-threatening illness, the person may feel better but still die sooner if not using an effective treatment.

Generally, placebo effect does not last indefinitely. In psychiatry placebo effects are generally short-lived and do not eliminate all symptoms or lead to lasting improvement in a person’s ability to function.


Obesity gene affects brain function

We all know it’s not good for us to gain too much weight. Health consequences such as diabetes, high blood pressure, heart disease and stroke are very well documented and warnings abound. Some evidence also shows that obesity could be linked to negative mental health outcomes as well.
Research identified a link between a fairly common gene variant associated with obesity and less brain volume in certain areas.
The gene variant is known as the FTO gene and almost half of people with European or African heritage carry it. For those who do, it predisposes to weight gain. Individuals with one copy of the gene weigh an average of four and a half pounds more than those without it and people with two copies weigh about nine pounds more than those without. This gene is also expressed in the brain and since some studies have linked higher body mass index with brain volume loss, a group of researchers at the University of California wanted to study whether the gene itself might be associated with brain volumn deficits.
Researchers examined 206 cognitively healthy people between the ages of 70 and 90 who had already been genotyped for a study attempting to identify factors that resist dementia as the brain ages. Results were published in 2010 in Proceedings of the National Academy of Science.  Although the study subjects were comparable in age, education and general health, it was noted that 128 had either one or two copies of the FTO gene while 78 did not. A relatively new MRI technique was used to map brain volume and those with the FTO gene variant had an average of eight percent less tissue in the frontal lobes of their brains. Similarly, FTO carriers had roughly 12 percent less tissue in the occipital lobes of their brains when compared to those without the gene variant.
Even if the FTO gene variant may lead to a reduction in brain volume in some areas of the brain, the question remains whether this has any real-life implications for those individuals.
More research is needed to fully understand the complex relationship, but the authors of this study feel the lower brain volumes may lead to difficulty with executive functioning – a set of brain processes involved in planning, abstract thinking rule acquisition, initiating appropriate actions and inhibiting inappropriate actions, and selecting relevant sensory information.
This hypothesis is made because poor executive function has been linked to frontal lobe deficits in the past and because in general obese individuals are known to have poorer executive function than average. Another possibility is that the FTO gene variant may set the stage for dementia in later life. Other studies have shown obesity as a risk factor for dementia and Alzheimer’s Disease so more research will have to determine whether this particular gene variant is harmful in that respect.
Research into different age groups will also help to further understand the relationship between the presence of this ‘obesity gene’ and brain volume or functional problems.

Depression and smoking often linked

If you suffer from depression, odds are good that you have also smoked at some point in your life. Unfortunately, those with depression also seem to have a much harder time kicking the habit than smokers who are not depressed.

It has long been known there is some relationship between depression and smoking and one US survey shows the two are more closely linked than we knew.

The survey conducted by the US Center for Disease Control’s National Center for Health Statistics showed a strong relationship between smoking and depression. In a national health and nutrition survey called “Depression and Smoking in the US Household Population Aged 20 and Over 2005-2008”, smoking rates were significantly elevated in every age and gender group.

For example, 49 percent of depressed men aged 20-39 smoked compared with 34 percent of non-depressed men in that age range. Among women in that age category, 50 percent of those with depression smoked compared with only 21 percent of those without depression.

More than 60 percent of adults with depression had smoked at some point in life whereas in those without depression only 43 percent of those aged 20-39 had ever smoked and 53 percent of those aged 55 and over.

Heavy smoking is also more common among depressed adults with 28 percent smoking more than a pack a day – almost twice the rate of adult smokers without depression.

Not only are depressed people more likely to smoke and more likely to smoke a lot, but they also seem to have a harder time quitting. In the 20-39 age group of depressed people who had ever smoked, 17 percent had quit compared to 36 percent of non-depressed people in the same age group. Among adults over age 55 who had ever smoked, 57 percent of those with depression had quit smoking compared with 75 percent of those without depression.

This indicates that individuals with depression who also smoke are likely to need a lot of help quitting.

If you are a smoker and also experience depression, don’t be afraid to ask your doctor for help. You will probably have an easier time butting out if you adequately treat your depression and also work on a smoking cessation program with encouragement from someone you trust.

The use of bupropion/Wellbutin/Zyban makes sense in this situation. This medication is both an effective antidepressant and an effective smoking cessation agent. In BC, this medication is covered by Pharmacare only if it is prescribed for depression. This requires a Special Authority form to be completed by the prescribing doctor. If it is prescribed for smoking cessation alone it is not covered.


Importance of Alzheimer's treatment

Canada’s population is aging. This is not news, but seems to be a fact our politicians overlook in setting long term policy and priorities for our country.

An area where we need to be particularly proactive is in healthcare. I have written at various times about the looming healthcare crisis getting even worse over the next couple of decades when baby boomers will enter old age.

Alzheimer’s disease is one example of a healthcare issue that will soon become critical if we don’t place a higher priority on finding a treatment that can offer some modification to the course of the illness by delaying its onset or slowing its progression significantly.

One European study announced the global cost of dementia may exceed $604 billion this year with that figure doubling every 20 years. Seventy percent of that cost is being spent in North America and Western Europe.

Clearly, we need a strategy for dealing with what is coming.

A report put out by the American Alzheimer’s Association earlier this year referred to Alzheimer’s disease as an unfolding natural disaster to which their federal government has sent a token response and for which there is no real plan. I believe the situation is no different here in Canada.

In their study, the Alzheimer’s Association did an economic analysis based on projections of the number of Americans expected to get Alzheimer’s over the next four decades and what it will cost to treat them.

With numbers of patients rising as the population ages and the life expectancy continuing to climb, there will be more people living with Alzheimer’s disease and also living longer with it. Obviously, costs to society in terms of personal and family suffering as well as financial strain will climb dramatically too.

The report made hypothetical projections for what may happen if we were to have a breakthrough in treatment research over the next five years and found if a treatment were discovered that could delay the onset of the disease for five years, it could reduce the number of patients and overall expense by roughly 40 percent.

Another projection was done for a hypothetical treatment that would truly slow disease progression and this also showed a potential 20 percent reduction in cost as well as a large reduction in the number of patients dealing with severe symptoms.

Of course, these were simply hypothetical scenarios and we don’t know if either is possible, but what is certain is that more research into novel treatment approaches is needed. I have written before about a grim study showing the inadequate nature of all the current treatments for Alzheimer’s disease.

Our governments need to step up their support of ongoing research in this field or we will all pay a very high price in the coming years.

At Okanagan Clinical Trials, we have an ongoing study of an investigative treatment for Alzheimer’s Disease. To learn if you may be eligible, contact our office.

Read more Mental Health articles


About the author...

Paul Latimer has over 25 years experience in clinical practice, research and administration. After obtaining his medical degree from Queen's University in Kingston, Ontario, he did psychiatric training at Queen's, Oxford and Temple Universities. After his residency he did a doctorate in medical science at McMaster University where he was also a Medical Research Council of Canada Scholar. Since 1983 he has been practicing psychiatry in Kelowna, BC where he has held many administrative positions and has done numerous clinical trials. He has published many scientific papers and one book on the psychophysiology of the functional bowel disorders. He is an avid photographer, skier and outdoorsman.


The views expressed are strictly those of the author and not necessarily those of Castanet. Castanet presents its columns "as is" and does not warrant the contents.

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