Who are Low Germans and why do they matter to public health?

The best part of my job is that I’m always learning something new. Recently, I was employed by a health department inOntarioto do some lit reviews and one of the topics concerned “Low Germans”, more formally referred to as those who are Low-German-speaking. Of course I knew a bit about Mennonites and the Amish (the … Continue reading »

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A relook at the Milgram obedience experiment: are we all capable of being Nazis?

If you ever took first year psychology – or read any popular psychology – then you’re probably familiar with the obedience studies conducted by Stanley Milgram at Yale in the early 1960s. Inspired in part by the horrors of the Holocaust, Milgram wanted to assess whether some nationalities are more willing than others to obey … Continue reading »

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Is healthcare biased against men? The case of PSA testing

My husband has a cadre of male friends that I refer to as his “pub buddies.” They’re great guys and range from retired professionals to tradesmen. Little moss grows on any of them. Lately, hubby came home with the message that he and his pub buddies had decided that the policy about PSA testing in … Continue reading »

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As Kenny Rogers said, you’ve got to know when to hold ’em, know when to fold ‘em

I’ve been writing a fair bit about motivation and different strategies that have been proposed for helping people stay on track. But there’s another side to the issue that is often overlooked: knowing when to give up. As Kenny Rogers sang, you’ve got to know when to hold ‘em and keep trying but you also … Continue reading »

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It’s not what you think – when health stats are twisted

Years ago, I worked for a health charity that sent out fundraising letters with a message on the envelope proclaiming “One out of every two people who open this envelope with die from [insert disease]!”  The folklore was that it even became a joke on late-night US television, as in “who would want to open … Continue reading »

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Who are Low Germans and why do they matter to public health? A relook at the Milgram obedience experiment: are we all capable of being Nazis? Is healthcare biased against men? The case of PSA testing As Kenny Rogers said, you’ve got to know when to hold ’em, know when to fold ‘em It’s not what you think – when health stats are twisted

Nov
22

Who are Low Germans and why do they matter to public health?

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The best part of my job is that I’m always learning something new. Recently, I was employed by a health department inOntarioto do some lit reviews and one of the topics concerned “Low Germans”, more formally referred to as those who are Low-German-speaking. Of course I knew a bit about Mennonites and the Amish (the Amish being found primarily in theUS) but what was of interest here were Low-German families fromMexico. Mexican Mennonites?

We need to start with a bit of history. Mennonites are a German-speaking people who came toCanadain the mid-1800s and because of religious beliefs prefer to remain separate from mainstream society. (In actual fact, there’s a wide diversity within Mennonite culture in the extent to which they retain traditional ways and accept or reject technology.) During and immediately after World War I, both their language and their refusal to serve in the military resulted in a lot of pressure and tension on Mennonite communities inCanada. By the 1920s, significant numbers emigrated toMexicoand other Latin American countries, particularly after the provincial government took steps to secularize education. However, for many,Mexicodid not turn out to be much of a haven and many were left landless and struggling economically. To earn and save enough money to buy land or repay debts, some families have returned to parts ofCanadaand theUS(for example, there’s appreciable numbers of them inKansas). They typically gravitate to rural areas – parts of the country which are already facing significant public health challenges. Moreover, families are not totally settled but may make frequent trips back toMexico. This disrupts employment, schooling, and health care.

There are a lot of stressors for these families. Relatives in Mexicomay feel deserted or betrayed, while Mennonite communities in Canadaor the USmay be less than welcoming. Education is limited: many children start helping in the fields as early as five or six years of age. Children are “God-sent” and families are large. Men are the “undisputed head of the household” and spousal abuse, alcoholism, child abuse or other family issues are typically swept under the carpet. Given all of these external and internal stressors, it’s not surprising that depression and anxiety are common; in a study conducted in Elgin Country, focus groups among the women founded that many of the men turn to alcohol, creating both financial and emotional problems for families.1

Language barriers, transience, low education, poverty and cultural barriers make health care difficult. Women are not necessarily told about “the facts of life” or birth control, receive prenatal or post-natal care, or have the means to ensure their children receive well-baby visits, vaccinations or dental care. Even if they want or need services, how can they access them when they have no transportation, don’t speak the same language as healthcare providers, and are tied to the home by child-rearing duties?

According to a report prepared by Wellington-Dufferin-Guelph Public Health Unit2, girls typically finish school at Grade 8 or 9. After that some may work in a bakery or store for a while but most are expected to remain in the home helping their mothers until they marry. This remind you of anything? Like the FLDS or Irish Travellers?

According to the World Health Organization, key sociocultural elements that negatively impact on women’s health include, among other things, a) an exclusive focus on women’s roles as wives and mothers and b) reduced or limited access to education and paid employment opportunities. 3 Repeatedly it has been shown that one of the best ways to improve the health of women and children is to improve women’s access to education and, as a result, information and economic opportunities.

Meanwhile, public health organizations in Canadaand the USare struggling to develop programs and processes for effectively reaching this Low German population. In Kansas, for example, the state Department of Health trains local Health Promoters – trusted and respected community members who establish links between health providers and the community members and provide informal health education, case management and interpretation.4 That’s probably only one of several options. It will be interesting to see what emerges as I continue to review the literature.

Take-away message/bottom line

There are many sub-cultures around us that may be invisible to mainstream society and which require tailored approaches for health and social services.

1 Armstrong D, Coleman B. Health Care Needs of Mennonite Women Living inElginCounty.ElginSt. Thomas Health Unit, March 2001

2 Bennett J. Low-German-Speaking Mennonites fromMexico: A Review of the Cultural Impact on Health inWellingtonCounty. Wellington-Dufferin-Guelph Public Health, December 2010.

3 Women and Health, Today’s Evidence, Tomorrow’s Agenda. 2009; World Health Organization, Geneva. http://whqlibdoc.who.int/publications/2009/9789241563857_eng.pdf 

4 Guenther T, Treaster C. Kansas’ Low German Mennonites’: Meeting the Challenge of An Emerging Farmworker Population.Kansas Statewide Farmworker Health Program,Kansas Department of Health and Environment

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Nov
07

A relook at the Milgram obedience experiment: are we all capable of being Nazis?

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If you ever took first year psychology – or read any popular psychology – then you’re probably familiar with the obedience studies conducted by Stanley Milgram at Yale in the early 1960s. Inspired in part by the horrors of the Holocaust, Milgram wanted to assess whether some nationalities are more willing than others to obey authority figures. He designed an experiment in which participants were told by a lab-coated authority figure to administer a memory test to a learner – and to give progressively-severe electric shocks if the learner made a mistake. The learner was not only in a separate room from the “teacher” (who was actually the experimental subject) but was actually only acting to be shocked.

The way I, and I think most people, remember the experiment is that it showed that ordinary people were willing to inflict severe and even lethal levels of electric shock when ordered to do so by an authority figure. It was a chilling reflection of the Holocaust: under the right conditions, any of us could be cold-hearted killers. But a review of the experiment and of Milgram’s broader body of research in this month’s Scientific American Mind suggests that this capsule summary may be misleading.1

To begin with, authors Stephen Reicher and S. Alexander Haslam, point out that even in the original experiment, not everyone followed orders: in fact, 35% of subjects quit or refused to continue. (Personally I don’t remember that from Psych 101 – I assumed everyone complied.) Footage of the experiment showed that many of the participants visibly agonized over what to do.  As Reicher and Haslam describe it, “They argue with the experimenter. They reflect the learner’s concerns back to him. They search for reassurance and justification.” Many felt trapped between their duties to the experimenter and the experiment – which had been described to them as a worthy attempt to advance science – and the pleas of the “learner.”

Although this is the study most of us remember, in actual fact Milgram conducted a number of subsequent studies in which he looked at the influence of various factors. He found that when the subjects sat in the same room as the learner and saw the effects of the “shocks” the percentage who complied fell to 40%. It fell even further if the person had to press the learner’s hand onto an electric plate to deliver the shock. It also plummeted (to less than 20%) when two other “participants” (who were also actors) refused to participate. Finally, no-one went up to the “lethal dose” if the learner asked for the shocks, when the “authority figure” was the person being shocked, or when two authority figures gave conflicting instructions.

Looking at the research, Reicher and Haslam conclude that the issue is not that followers lose their moral compasses so much as they choose particular authorities to guide them through the dilemmas of making difficult decisions. Which authority figures do we chose? Some research suggests our choices are guided by the extent to which we identify with that person and his or her goals. So we need to be careful who we choose as our “moral authority.” But even so, it doesn’t mean we necessarily turn off our own moral compass – or our responsibility.

Take-away message/bottom line

Re-assessment of Milgram’s original study in 1961 suggests that the common interpretation that people are blindly obedience to authority may not be correct; the situation may be much more complex.

1 Reicher S, Haslam SA. Culture of shock. Scientific American Brain 2011 22(5): 57-61

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Oct
31

Is healthcare biased against men? The case of PSA testing

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My husband has a cadre of male friends that I refer to as his “pub buddies.” They’re great guys and range from retired professionals to tradesmen. Little moss grows on any of them.

Lately, hubby came home with the message that he and his pub buddies had decided that the policy about PSA testing in Ontariois sexist and reflects a societal bias against men. After all, he says, mammography and Pap smears are paid for through public health insurance but PSA is not.  

Let’s look at this. PSA testing is a blood test for something called prostate specific antigen. PSA levels are typically low in men but a number of conditions – both benign and cancerous – can increase it. Prostate cancer and benign conditions such as inflammation of the prostate (prostatitis) and enlargement of the prostate (benign prostatic hyperplasia) increase in frequency with age.

It is the position of some organizations that all men over 40 have a PSA to establish a baseline value and men over 50 consider annual or semiannual PSA monitoring. PSA testing for screening purposes (i.e., in a man with no evidence or diagnosis of prostate cancer) is covered by public health insurance in Saskatchewan, Manitoba, New Brunswick, Nova Scotia, Newfoundland, PEI, the North West Territories, Yukon and Nunvaut. But in British Columbia, Alberta, Quebec and Ontario, the cost is only covered if there is a diagnosis, clinical signs of prostate cancer and/or other indicators of risk such as family history, own health history or race (there are differences between the provinces).

Why isn’t PSA testing routinely covered as a screening tool in all provinces? Well, the problem stems from the evidence on its effectiveness. A Cochrane Collaboration Review of the research literature found screening did not significantly reduce prostate-cancer specific mortality.1 Moreover, PSA testing didn’t do very well when they looked at the balance between benefits and risks. Benefits of screening may take up to 10 years to occur, so screening was unlikely to be helpful for men with a life expectancy less than 10-15 years (i.e., elderly men). Meanwhile, you need to consider the draw-backs or potential risk of screening.

The main problem with screening is the high rate of false-positive results. According to the Cochrane review, up to 76% of positive PSA tests are false.1 In other words, up to three-quarters of men who get a “positive” PSA test result don’t have prostate cancer. But because of their test result, they may be exposed to the risk of additional, often invasive, tests such as biopsies. To say nothing of the worry and stress of being told you may have cancer. According to the US National Cancer Institute, “most men with an elevated PSA test result turn out not to have cancer; only 25 to 35 percent of men who have a biopsy due to an elevated PSA level actually has prostate cancer” (emphasis in the original). 2

In addition, a certain proportion of tests may be false-negatives: the PSA level is in the normal range even through prostate cancer is actually present. A false-negative could lull a man into a false sense of security and encourage him to ignore warning symptoms.

If you want to learn more, the October 27, 2011, issue of New England Journal of Medicine has three editorials on the topic in response to the recent US Preventive Services Task Force recommendations (www.nejm.org). FYI, the Task Force recommended against routine PSA-based screening.

The issue is complicated and I think it’s the uncertainty in the science rather than overt sexism that is behind the current patchwork nature of PSA reimbursement across Canada. But I can certainly appreciate that on the surface – yes, it does look like men are being treated differently than women.  However, I think the pub buddies need to appreciate that you can’t just order a PSA – it’s supposed to be accompanied with the dreaded digital rectal exam. Obviously, better screening tools could be helpful and that’s something only research can give us.

Take-away message/bottom line

There are significant issues with PSA testing which may help to explain why it is not routinely covered as a screening tool in all provinces. What is needed is something only research will be able to give us – a more accurate screening tool.

1 Ilic D, O’Connor D, Green S. Wilt TJ. Screening for prostate cancer. Cochrane Database of Systematic Reviews. Last assessed as up-to-date: June 10, 2009. http://www2.cochrane.org/reviews/en/ab004720.html

2 National Cancer Institute at the National Institute of Health. Prostate-Specific Antigen (PSA) Test. http://www.cancer.gov/cancertopics/factsheet/detection/PSA

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Oct
24

As Kenny Rogers said, you’ve got to know when to hold ’em, know when to fold ‘em

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I’ve been writing a fair bit about motivation and different strategies that have been proposed for helping people stay on track. But there’s another side to the issue that is often overlooked: knowing when to give up. As Kenny Rogers sang, you’ve got to know when to hold ‘em and keep trying but you also have to know when it’s a lost cause and you should disengage.

As described by psychologist Charles Carver and Michel Sheier,1 there’s no simple, linear relationship between goals and effort. Intentions can tell us where to direct our efforts (whether we want to approach a positive goal or avoid a negative goal) but emotions shape the intensity of our motivation. Those emotions can be influenced by our basic personality (whether we’re an optimist or pessimist), past experiences (perceived self-efficacy) and how things are going. If it’s an approach goal, such as losing weight, then when we see we’re making progress we feel happy, eager and excited. But when things start to go bad, we may experience anger. That anger may help us stay on track and maybe even intensify our efforts. But too much failure and we’re likely to end up feel depressed, sad or beaten. Those feelings are associated with giving up.

In our society, we tend to think of giving up as a bad thing. But there are many situations in which giving up is actually a good and healthy thing. Not every kid in Timbits Hockey has the natural ability to make it to the NHL, just as not every woman can look like Angelina Jolie. We’ve all known people who have pursued goals to the point of damaging their families (e.g., the guy who persists in an unrealistic dream of becoming a golf pro) or well-being (e.g., someone addicted to booze, alcohol, gambling or sex). Sometimes, walking away is actually the smart and sane thing to do.

What shapes our ability to let go? Carver and Sheier point out that goals such as perfecting your golf game are often inputs into how you define yourself (e.g., as being athletic or successful). The key to disengagement without despair is finding some other way to support that definition or vision of yourself.  Sometimes, this can be accomplishing by scaling back from a lofty goal to something more realistic (e.g., abandoning dreams of competing on the PGA and focusing instead on winning local amateur tournaments). Other times, it may involve shifting from one activity to another. That could mean shifting your attention to something you already do (e.g., from golf to curling); other times it may mean stepping outside of your existing framework and developing new goals.

We live in a society that glorifies stories of success through perseverance and vilifies giving up. It’s especially acute when it comes to behaviours that we see as socially unacceptable, such as addictions, being overweight or, for the Tea Party types, poverty. “Try, try again,” we admonish, “Never say never,” “Quitters are never winners and winners never quit,” and so on and so on. But not only is it important to “know when to fold ‘em” but to “quit when you’re ahead,” and to “stop beating a dead horse.”

Take-away message/bottom line

To live a healthy life, we need to know when to persist at something and when to disengage and direct our energies elsewhere.

1 Carver CS, Scheier MF. Engagement, Disengagement, Coping, and Catastrophe. IN Handbook of Competence and Motivation, Elliot AJ, Dweck CS, eds. 2005;New York:Guilford Press. pp 527-547

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Oct
19

It’s not what you think – when health stats are twisted

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Years ago, I worked for a health charity that sent out fundraising letters with a message on the envelope proclaiming “One out of every two people who open this envelope with die from [insert disease]!”  The folklore was that it even became a joke on late-night US television, as in “who would want to open the envelope if this is what will happen?”  

At the time, I tried to get through to the TPTB at the organization that this was a distortion of the facts. At that time, about 48% of Canadian deaths had the disease in question listed on the death certificate. That means that almost half of Canadians who died in any one year were considered to have died from that disease. That doesn’t mean that half of the entire Canadian population of that time would die from the disease – there’s a difference between all Canadians and those Canadians who die in any one year.

Two decades later and the organization in question is still making this sort of claim (although the numbers have shifted). And I still see it as inaccurate and a personal pet peeve.

The problem with the claim is that it confuses two different populations: all Canadians and that sub-set of the population that dies in any one year. There are not the same, primarily because not all people have the same risk of dying in any one year. Children have a much lower risk of dying than adults and men typically have a higher risk than women. The following chart is taken from an article published by Bandolier (a really great site) and shows annual risk of death by age and gender in the UK. The pattern is similar in most western countries.

 
Figure 1: Annual risk of death by age and sex in the UK 1

 

So you can see the lovely J-shaped curve and the epidemiologic issue. In any one year, a male between the ages of 25-34 has a risk of 1 in 1,215 of dying, while a female in that age group has a risk of 1 in 2,488. In comparison, a male between the ages of 75 to 84 has a 1 in 15 risk of dying and a female 1 in 21. Big difference. So the people dying in any one year are not representative of the general population: they are a sub-set of the population that is strongly skewed to the older age groups.

The other thing to consider is cause of death. Let’s look here at the top three causes of death for Canadians at different ages: 2

  • Under 1 years of age: congenital abnormalities, short gestation, maternal complications of pregnancy
  • 1 to 14 years: accidents, cancer, congenital abnormalities
  • 15 to 24 years years: accidents, suicide, and a tie for third place between cancer and homicide
  • 25 to 34 years: accidents, suicide, cancer
  • 35 to 44 years: cancer, accidents, suicide
  • 45-54 years: cancer, heart disease, accidents
  • 55 to 64 years: cancer, heart disease, accidents
  • 65 to 74 ears: cancer, heart disease, chronic lower respiratory disease
  • 75 to 84 years: cancer, heart disease, stroke
  • 85 and over: heart disease, cancer, stroke

The point of this is that younger people have a much lower risk of dying and, more importantly, when they do die, they typically die from different things than older people. Again, a stat developed by looking at deaths (“1 in 3 deaths are due to x”) is not transferrable to the general population (“1 in 3 Canadians will die from x”).

Of course, what we’re actually talking about here is the gap between statistics and marketing. For marketing and fundraising purposes, health charities and other organizations need simple messages that are supposed to be strong and – let’s face it – scary. A message like “1 in 3 Canadians who die will die from our disease” is considered too complicated and obtuse for mass communication. I get that – I don’t like it, but I get it.

Take-away message/bottom line

In trying to create marketing messages, health statistics can sometimes be mis-interpreted. The risk of dying from any one cause differs widely among the general population by age and gender.

1 Risk of death by age and sex. Bandolier “Evidence based thinking about health care” http://www.medicine.ox.ac.uk/bandolier/booth/Risk/dyingage.html

2 Statistics Canada. Leading Causes of Death in Canada, 2007. Table 3 Ranking and number of deaths for the 10 leading causes by age group, Canada, 2007.  http://www.statcan.gc.ca/pub/84-215-x/2010001/table-tableau/tbl003-eng.htm

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Oct
11

Women and heart disease – time to stop blaming menopause?

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For a long time, it’s been argued, women’s risk of heart disease is relatively low until menopause, at which point it begins to increase dramatically. However, new analysis is challenging this paradigm.

In an article published in BMJ (British Medical Journal),1 researchers at John Hopkins and the University of Alabama looked at ischemic heart disease mortality data from England, Wales and the US. They concluded that in women, heart disease mortality increased exponentially with age – period. They found no evidence of any acceleration or jump in mortality at menopause. Among men, risk increased rapidly during young adulthood and then slowed down somewhat. But at no point does the mortality rate among women match that of men; even after menopause male mortality rates are higher than those of women.

The authors compared the pattern of mortality of three different birth cohorts: people born between 1914-25, 1926-35 and 1936-45. Presumably, factors that could impact on CVD mortality, such as medical treatment and lifestyle and environmental risk factors (including smoking rates, prenatal nutrition, diet, etc.) would vary between the three cohorts. And yet, the same mortality patterns emerged across all three. That’s pretty convincing.

The authors conclude that the early and rapid acceleration in male heart disease mortality may have misled people to think that women’s heart disease risk was linked to the effects of menopause. In other words, because acceleration of risk in women occurs later than it does in men, it happens to coincide with the time that most women become menopausal. As a result, we assumed the two were linked. You’re not alone if you’ve heard that “after menopause” there are increased rates in women of many CVD risk factors, such as high blood pressure, blood glucose, and high cholesterol. But in actual fact, there is some evidence that at least some of these risk factors may increase because of age rather than menopause. For others, such as cholesterol, the relationships between age, lipids and menopause appears to be complex.2

Why is this important? For one thing, the authors of the BMJ article point out that it means we’ve been sending out a misguided health promotion message. We’ve been saying that women pretty well don’t have to worry until after menopause, whereas what we should be focusing upon is lifetime risk. Second, I think anything that helps to relieve the stigma of menopause is a good thing. Right now, women are viewing menopause as something akin to the Black Death. It’s not the end of good health, youth or sexuality – it’s just a part of the natural aging process.

In case you’re interested, the authors of the BMJ article speculate that the root cause of the patterns they observed in CVD mortality involves telomeres. A telomere is like that plastic tip on the end of your shoelaces, except it’s found at the ends of a chromosome. Its job is to protect the end of the chromosome from deteriorating or from fusing with neighbouring chromosomes. Each time a chromosome reproduces itself, the telomere is shortened a bit. Over time, the telomere becomes too short to do its job and the chromosome loses its ability to reproduce. The good news is that this is a mechanism that helps to prevent cancer (which is a form of uncontrolled cell reproduction). The bad news is that when cells stop reproducing, we start to age.

In the case of heart disease, what we may be seeing is the result of cumulative insults to the blood vessels. Some of these insults may be from things we do (e.g., smoking), whereas others may be genetic or just part of the natural physiology of the body (e.g., turbulent blood flow at places where the blood vessels turn or twist). When we’re young, the body’s natural defenses are able to respond to these insults and repair any damage. But over time, as the telomeres wear down, the body loses its ability to respond and vascular injuries and damage begin to take their toll.

According to the authors, there’s evidence that the telomere loss per age-year is slightly (but not significantly) greater in men than women but age-adjusted telomere length substantially shorter in men. This difference, they say, is equivalent to the telomere-shortening process occurring 7.6 age-years sooner in men compared to women. In other words, men get the short end of the stick, telomere-speaking. As a result, they develop heart disease earlier than women.

Warning, Will Robinson! Just because there’s a correlation between the time lines of telomere shortening and CVD mortality, doesn’t mean it’s been proven that one causes the other. The authors only analyzed mortality data: they didn’t measure any telomeres. So their explanation that telomere length, rather than menopause, is the reason for the mortality curve they found in women is a hypothesis, not a fact.

Take-away message/bottom line

New research suggests that age, not menopause, is responsible for the increase in heart disease witnessed in women age 55+.

1  Vaidya D et al. Ageing, menopause, and ischaemic heart disease mortality in England, Wales, and the United States: modeling study of national mortality data. BMJ 2001;343.d5170

2 Bittner V. Menopause, age, and cardiovascular risk, a complex relationship. J Am Coll Cardiol 2009;54:2374-5

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Oct
03

The lay epidemiology of heart disease or why bad things happen to good people

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Recently, I was reading some interesting articles on “lay epidemiology” – how the general public understands the incidence of disease. 1, 2  In this case, the disease was heart disease, specifically cardiac deaths.  As the authors point out, the health community has spent a lot of time, money and effort educating people that cardiovascular mortality is determined by modifiable behaviours such as smoking, inactivity, and poor diets.  And to a large extent, the education has been effective.  Ask people and they can readily recite the modifiable risk factors for cardiovascular disease. And yet, there’s still a gap between knowledge and actual behaviour. So what gives?  Are people in denial, foolhardy, or just plain stupid?

As it turns out, when you sit down and listen to people, it emerges that they are actually quite rational. They understand the idea of behavioural risk factors and can easily identify people who fall into the “high risk” category (typically, those who are overweight, out of shape, or highly stressed). But their own experiences have shown them that risk factors aren’t the only forces at work. Almost everyone knows of, or knows someone who knows, the seemingly “healthy” person who did “everything right” and yet died at a young age from heart disease. They also know lots of people who have done “everything wrong” and yet lived to a ripe old age. The only way of reconciling the concept of risk factors with the reality of what they’ve seen is to add another concept: that of luck, fate or destiny. In other words, although people may increase or decrease their risk by their behaviours, their ability to change their fate is limited. If “your number is up” then even the best of behaviours won’t save you. The tenants of prevention are fallible; they can’t explain the “unwarranted longevity” of people who routinely make unhealthy choices or the “unwarranted deaths” of those who make healthy ones. Risks work only up to a point, and then random fate takes over. The lay epidemiology of heart disease is dichotomous.

As described by Davison et al, this dichotomous lay epidemiology is in many respects a reflection of our health promotion strategies. The essence of the population approach to heart disease prevention is to reduce the risk of as many people as possible, if not all people. But risk is determined by identifying characteristics (risk factors) that can distinguish between low and high risk of a disease. Risk is a concept rooted in the group and not the individual. Only a relatively small proportion of people fall into the highest risk groups; if everyone fell into the high risk group, the factor would not be helpful in determining risk.  As a result, the majority of people fall into the medium or even low risk groups. In the case of heart disease, the outcome is that most fatal heart attacks happen to people outside the high risk group.

Wow, you say, how does that happen? Let’s work through a hypothetical situation and I’ll keep it as simple as possible.  You screen 100 people and 25 fall into your high-risk category of having high blood pressure. Of the high risk group, 60% have a heart attack in the following five years (an unrealistically high rate, but this is just an illustration). That works out to about 15 deaths. Of the 75 people in your medium- to low-risk group (i.e., those without high blood pressure), the death rate is only a measly 25% — less than half that of the high risk group. But 25% of 75 works out to roughly 19 people, 4 more than in the high risk group. Can you now see the problem?

In a classic article published in 1981, Gregory Rose called this the prevention paradox. You ask people to change their behaviour to theoretically reduce their heart health risk but many of them wouldn’t have had a heart attack anyway (or at least a premature heart attack). You can’t predict which individuals may benefit from making changes. So you ask entire population to change their evil ways even though you can’t predict who will benefit and who won’t. Given this reality, it’s not surprising that lay epidemiology views death as a bit of a crap shoot. In many respects, it is.

Take-away message/bottom line

The general public is not being irrational when its explanation of cardiovascular death incudes an element of luck or fate; the prevention paradox means it’s impossible to tell who may benefit from health promotion interventions.

1  Davison C, Smith GD, Frankel S. Lay epidemiology and the prevention paradox: the implications of coronary candidacy for health education. Sociology of Health & Illness. 1991;13(1):1-19.

2 Davison C, Frankel S, Smith GD. The limits of lifestyle: re-assessing ‘fatalism’ in the popular culture of illness prevention. Soc Sci Med. 1992;34(6):675-85.

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Sep
26

Motivation – time to accept the new paradigm?

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A number of books are now out there showing that the idea that positive reinforcement (e.g., a bonus or commission) is actually a bad idea.  But unfortunately, as predicted in Thomas Kuhn’s The Structure of Scientific Revolutions, it’s been hard to get rid of the old paradigm.  Schools, businesses and families around the world continue to operate under the old and misguided concept that you can bribe or reward employees or kids into acting the way you want.  Well, you can in the short term but it’s unlikely you’ll be happy with the ultimate results. Why? Because what you end up with are individuals who lack internal (intrinsic) motivation and so are going through the motions in order to get the reward but apt to take short-cuts to get it.

In his book Drive (Riverhead Books, 2009) Daniel H. Pink quotes research showing that rewards not only reduce intrinsic motivation – but are addictive. Like drugs, rewards give an initial buzz – but one that fades. A $5 reward is great the first time you get it, but after the thrill dies away you want another – and this time it has to be even bigger to give you the same sensation.

Pink describes research using MRI technology in which the brain functioning of healthy volunteers was monitored during a game involving the prospect of either winning or losing money. When participants knew there was a chance of winning money, a part of the brain called the nucleus accumbens received a burst of dopamine. This is the same physiologic process that occurs in drug addiction. But as the dopamine dissipates, so does the feeling.

Pink argues that the fact that rewards mimic the physiology of addiction is disturbing if what we really want are healthy, motivated employees or kids. Furthermore, he goes on to ask whether this process can perhaps explain why so many reward programs for health behaviours backfire. For example, a program that pays people to not smoke may, Pink suggests, simply replace one dopamine-fueled addictive behaviour (smoking) with another (reward seeking). That works in the short term but when the reward is no longer sufficient to trigger the dopamine release or is even stopped, then you’ve got an addict in search of a drug of choice. Which for many people means going back to smoking, while some may replace it with food. 

The data on using rewards for health behaviours appears to support Pink’s predictions. So far, studies have shown that rewards can trigger people to make changes like quitting smoking, exercising, or losing weight – but only in the short term.  When the rewards end, the relapse rate can be high. 

Take-away message/bottom line

It’s time to shift from the old paradigm of motivation based on rewards and punishments, to one rooted in the psychology of self-determination theory.

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Sep
18

Can we “end” the two primary causes of mortality – heart disease and cancer?

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Recently, there’s been a spate of campaigns promising to “end” cancer, or at least certain types of cancer.  I’m not naming any names here. I mean, I understand why organizations are making these sorts of claims – they want and need some sort of dramatic claim to galvanize donors and volunteers. The more flamboyant the better, some PR firm probably told them. But the fact of the matter is that claims of this type are just – well, to be honest – silly.

First of all, diseases such as cancer and heart disease have multiple causes and risk factors, including genetics, ethnicity, socioeconomic status and spontaneous gene mutations. In the case of coronary heart disease (just one form of heart disease), the consensus is that there is “no clear etiology” and numerous risk factors. 1 How in the world can you control or prevent all possible causes of such diverse and complex diseases? 

Well, what about lifestyle changes to prevent diseases?  Wikipedia quotes a report by the World Cancer Research Fund that estimated that 38% of breast cancer cases in the US are preventable through lifestyle modification (reducing alcohol intake, increasing physical activity levels and maintaining a healthy weight).2  That’s good but leaves 62% up for grabs. The fact of the matter is that breast cancer is, to quote Wikipedia, “strongly related to age with only 5% of all breast cancers occurring in women under 40 years.” 2 And heart diseases? As the World Heart Federation puts it, “Simply getting old is a risk factor for cardiovascular disease; risk of stroke doubles every decade after age 55.”3 So unless we’re going to resort to some sort of Logan’s Run future, I think we’re stuck with a world with both cancer and cardiovascular disease as the major causes of mortality. The only way it could change would be if we were to have huge epidemics so the major causes of death would become (once again) communicable diseases. But is that an alternative anyone would like to see?

Given this PR-driven hyperbole, it was refreshing to see the announcement of the USgovernment’s Million Heart initiative. 4 The campaign is based on the calculation that more than 2 million American die of heart attack or stroke each year, and the goal is to prevent 1 million of these deaths over the next five years. It’s not claiming to be able to wipe out heart disease or stroke – just to prevent 250,000 deaths per year.  So it’s reasonable but the 1 million figure still gives it PR flash.

Take-away message/bottom line

Unless we want to go back to the good ol’ days of epidemics of typhoid, scarlet fever, smallpox and bubonic plaque, complex diseases that increase with age, such as most forms of cardiovascular disease and cancer, are probably going to stay with the human race. 

1  Coronary disease.. Wikipedia. http://en.wikipedia.org/wiki/Coronary_heart_disease

2  Breast cancer. Wikipedia. http://en.wikipedia.org/wiki/Breast_cancer

3 Cardiovascular disease risk factors. World Heart Federation. http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors/

 

4 Frieden TR, Berwick DM. The “Million Hearts” initiative – preventing heart attacks and strokes. NEJM September 13, 2011. http://www.nejm.org/doi/full/10.1056/NEJMp1110421?query=featured_home

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Sep
11

Is it time to move beyond ‘fight club’ analogies?

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In light of Jack Layton’s death from cancer, there was an op-ed article in the Globe and Mail about the problems and limitations of the common practice of using fight analogies when talking about disease.1  The author, Carly Weeks, makes the point that equating illness with a war, battle or fight with an enemy diminishes our understanding of the challenges and complexities of living with a serious illness. By talking about “a battle against cancer” (or ALS or MS, or whatever), there’s the subtle inference that people who “lose” didn’t fight “hard enough.” People are artificially divided into “winners” – “survivors” being a common lexicon – or “losers.” 

She also quotes a British writer who has multiple myeloma (a cancer of the bone marrow) who feels the emphasis on the patient’s “bravery” and “courage” implies that if you die – if you don’t “conquer your cancer” – “there’s something wrong with you, some weakness or flaw.”  Christopher Hitchens, who has esophageal cancer, has also gone public with his dislike of the “battle” analogy.

It’s a problem that we as a society need to recognize.  Sometimes, no matter what you do, you can’t stop a disease process.  A positive attitude is great and will undoubtedly support a better quality of life, but we shouldn’t act like patients are responsible for their own prognosis. They aren’t. They can do everything they are capable of to help themselves and to live as well and fully as possible, but the responsibility – and the blame – doesn’t lie with them.

The use of the ‘fight club’ analogies extends far beyond cancer. We talk about people ‘battling’ mental illness, heart disease, MS, AIDS, etc., etc. But it’s not like people have a choice or there’s any sort of level playing field. It’s not a test of anyone’s courage or determination – it’s a disease.

About 30 years ago, my father had a severe stroke that left him paralyzed on one side and aphasic. Around the same time, a TV movie was made about Patricia Neal’s stroke and recovery. I remember my mother hating that movie. She hated it because it inferred that Neal recovered because of her hard work and determination. It inferred that if you just worked hard enough, you too could make a full recovery. But the fact of the matter is that although my father worked as hard as possible at his rehabilitation (my mother attended some of his rehab sessions and was impressed and saddened by how hard he tried), his brain damage was so extensive that he could never hope to make a recovery like Neal’s. The “fight hard enough and you can triumph” scenario can be a cruel mirage.

It’s interesting to see the comments on Weeks’ article on the Globe and Mail website. Overall, they are positive – particularly among those who have been touched by cancer. A small minority thinks it’s nitpicking, political correctness run amok or even offensive. Needless to say, I don’t agree with the minority. Language matters – it influences our interpretation of the world and thus shapes our reality.

Take-away message/bottom line

Current common analogies or clichés can have unfortunate influences on our perceptions and expectations.

1 Weeks, C. Jack Layton didn’t lose a fight: he died of cancer. The Globe and Mail. August 22, 2011.  http://www.theglobeandmail.com/life/health/new-health/conditions/cancer/jack-layton-didnt-lose-a-fight-he-died-of-cancer/article2137736/

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