"That will be us someday!" It's the sweet wish of a young couples when they spy older couples on the street, in restaurants, on the dance floor who still seem to be in love.
But the other side of that wish is this: love may have no expiration date, but all people do. Death of a partner is most likely to happen in old age, more likely to happen to older women, and is often considered to be one of the most traumatic events a person can experience. This sort of loss, or bereavement, is often related to Major Depressive Disorder (clinical depression). The most recent version of the Diagnostic and Statistical Manual (DSM-V) removed the "bereavement exclusion": thus a grieving person who exhibits the symptoms of depression may receive that diagnosis even though these symptoms are a normative response to loss of a loved one. Fried, Bockting, Arjadi, Borsboom, Amshoff, Cramer, Epskamp, Tuerlinckx, Carr, and Streoebe (2015) note that we often assume bereavement causes a person to have depression, and depression produces symptoms. This is called the "Common Cause Hypothesis" because all symptoms are thought to come from one situation: depression. However, the authors caution us that this hypothesis may not be appropriate because there are thousands of symptoms that depressed people may have, these may contradict each other (e.g.; some depressed people eat too much while other depressed people don't feel like eating at all), and risk factors, such as suicide, may vary depending on the constellation of symptoms that an individual exhibits. Instead, Fried et al. (2015) encourage us to consider a Network model. From this view, bereavement would cause symptoms, and these symptoms would create situations, such as depression. These symptoms could also interact with (influence) each other to produce such situations. To test these two viewpoints, the authors used data on depression symptoms from the Changing Lives of Older Couples (CLOC) study. First, they compared the scores on a depression test from 241 widowed seniors (from Follow-Up 1) to 274, age- and gender-matched, married seniors (from Follow-Ups 1-3). The majority of the participants were female and senior citizens. When these individuals joined the CLOC study there was no difference in their reported depression symptoms, but in the follow-up interviews, six months after the death of a spouse the bereaved seniors demonstrated slightly more of these symptoms compared to the seniors who were still married. In fact, 84 of the widowed seniors exceeded the criteria for Major Depressive Disorder by endorsing at least six symptoms. The most commons symptoms were: feeling lonely; feeling sad; feeling depressed; having trouble motivating themselves; problems sleeping; problems eating. Then Fried et al. (2015) applied complicated statistical models to see if the Common Cause or the Network frameworks would best explain the relationship between bereavement, depression, and depression symptoms. For the Common Cause model to be supported these six symptoms should be better predicted by Depression; instead four of these symptoms were better predicted by loss itself (bereavement) lending support to the Network model. Further investigation revealed that bereavement was especially linked to one symptom, feeling lonely. These results caution us to think more broadly about depression and spousal loss in older age, especially for older women. Instead of assuming that bereavement causes depression, it may be that bereavement causes a set of symptoms including loneliness. In turn, it could be that this loneliness is what eventually leads a person to experience Major Depressive Disorder. As this week's meme suggests, true love may last forever: into old age and even when the person we love is gone. With love still in our hearts but now suddenly on our own, it is easy to see how loneliness could set in. And that is a depressing thought.
You never thought this would happen. As a teenager it was drilled into your head that having sex without using birth control would surely result in a pregnancy. Now you are an adult, you want to have a baby, and it is not happening. So what do you do? You probably talk with a doctor and maybe she suggests some infertility treatments. One of the cheaper interventions is Artificial Insemination: injecting sperm into the uterus during ovulation. This costs on average $865, although the price can vary considerably. Other interventions like In Vitro Fertilization (embryos are created from sperm and egg and then inserted into the uterus) cost an average of $8,158, with additional expenses up to $5,000 for the medication used to increase egg production prior to each treatment. Because there is no guarantee of pregnancy, these procedures may need to be repeated many times before it occurs, if it occurs at all. With yearly college tuition costing $9,000 - $30,000 it is possible to spend more trying to create your child than to educate your child.
Insurance lightens this burden for some but not everyone has health insurance or insurance policies that cover infertility treatments. As of 2016 only 15 states in the U.S. require that infertility treatments are covered by private insurance; and even in those states there are exceptions based on a woman's place of employment and the specific insurance plans offered through that workplace. In some states insurance companies' definitions of infertility (failure to conceive after a year of unprotected heterosexual sexual intercourse) also unfairly deny lesbian women coverage. Blanchfield and Patterson (2015) raised further concerns about access to infertility help and insurance coverage. They evaluated data from thousands of women who participated in the 2002, then in the 2006-2013 waves of the National Survey of Family Growth (NSFG) to determine if racial minority women (non-White) and sexual minority women (lesbian women and women who report sexual attractions that are not exclusively heterosexual) have the same access to "fertility assistance" and insurance coverage as women in related majority groups. From 2002 to the most recent wave in 2013, about twice as many White women compared to racial minority women reported getting medical assistance for pregnancy. Heterosexual women were also more likely to receive this help compared to sexual minority women. However, regardless of race or sexual orientation, women who received help reported getting the same forms of assistance, including advice, testing, fertility drugs, and Artificial Insemination. Private health insurance coverage varied by race and sexual orientation with White heterosexual women being most likely to have this financial help. In 2002, this comparative lack of insurance and related lower income failed to explain racial and sexual minority women's lower rate of medical assistance for pregnancy: even when these women could pay for these services they were less likely to receive them. However, from 2006-2013, lack of insurance coverage was enough to completely explain the persistent lower level of medical assistance for sexual minority women's infertility. In other words, if sexual minority women can pay for the treatments they are now just as likely to receive them as heterosexual women. On the other hand, even from 2006-2013 lower income and lack of insurance could only account for part of the persistent lower level of medical assistance for racial minority women's infertility. This means that even when non-White women have the means to pay they do not always get these interventions. This is particularly disturbing as White, Black, and Hispanic women have approximately the same rate of infertility (11%) and these groups represented more than 90% of the women surveyed in the NSFG. Thus with equal means to pay, these groups should have reported equal experience with medical assistance. Blanchfield and Patterson (2015) offer three possible explanations for this racial discrepancy. First, racial minority women may not have the "social support" that White women have when they are faced with infertility: if your friends and family don't suggest talking to a doctor then you are less likely to do so. Second, for Black women in particular, our nation's history of abusing Black citizens for medical testing (see for example: U.S. Military in WWII; the Tuskegee Study; Henrietta Lacks) may make them more cautious about involving the medical community in their personal lives. Finally, although it is unethical and illegal, stereotypes and prejudices about racial minority fertility may bias doctors away from discussing infertility with women from these groups. This is something that we must try to change. Along with the emotional and financial devastation that often accompanies infertility, a woman should not have to fear or be denied the chance to talk with her doctor about this condition. FURTHER READING: You can access the Blanchfield and Patterson (2015) article online or through your local college library. Resolve: The National Infertility Association offers facts and information about support groups for individuals and couples coping with infertility. The Broken Brown Egg is a blog about Black women and infertility; it also includes links to useful resources.
When negative stress affects our well-being, we sometimes feel like we are losing our minds...
But when in the lifespan does this really happen? When do we lose our brains? Until age two we experience rapid growth of brain cells, or neurons. Around that age, rarely used neurons and unneeded connections between neurons (synapses) are reduced. Past research by Hedman, van Haren, Schnack, Kahn, and Hulshoff (2012) suggests that childhood is a time of brain growth, with more neurons being produced. Starting around age thirteen and continuing through adolescence we see brain volume loss as pruning reoccurs so that our brains can be more efficient. Most of young adulthood sees little change in brain volume, but starting at age 35, MRI scans demonstrate a yearly loss of about 0.2% of brain volume. This loss accelerates in older age: in our sixties this increases to a loss of about 0.5% of brain volume every year; this acceleration is often given as one of many explanations for other normal declines associated with aging. To examine in detail the brain volume loss during the transition to midlife, Guo, Isohanni, Miettunen, Jääskeläinen, Kiviniemi, Nikklinen, Remes, Huhtaniska, Veijola, Jones, and Murray (2016) examined MRI scans of 43 men and 23 women as they aged from their 30s (33-35 years) to their 40s (42-44 years). The participants in this longitudinal study were part of the Northern Finland 1966 Birth Cohort so they should have had similar experiences in their lives as they grew up at the same time. The researchers' goals were to measure overall brain volume at both ages, to identify the locations of any loss as observed in the second MRI performed when the participants were in their 40s, and to clarify any sex differences that emerged. Total brain volume decline was higher than predicted by past research: on average men lost 3.21% and women lost 4.03%. This sex difference was very small but it reached statistical significance, meaning that the difference was unlikely to be due to chance. The location of loss also showed a sex difference. After taking into account percentage of total brain loss, Guo et al. found that men lost most of their neurons in the midline areas (specifically: bilateral precentral gyri; bilateral paracingulate gyri; and bilateral supplementary motor cortices). Most of these areas relate to motor skills and one may be involved in decoding certain emotions. Women's loss was more spread out with most of it occurring in the outer brain (specifically: bilateral frontal parietal; temporal lobe; occipital cortex; cerebellum). These areas relate to language, motor skills, sensory interpretation, vision and visual memories, and emotion association. Guo et al. did not make guesses beyond a quick mention of hormones as to what caused the sex differences in overall brain loss or the sex differences in loss locations. They also speculated that these differences may translate into differences in midlife men's and women's health or behavior, yet they did not offer any examples. That leaves us all free to speculate. One bit of demographic information that caught my eye was that the researchers coded participants on "parental leave" as working full-time, because it meant that the participants usually worked full-time but were absent from that work to take care of a newborn child. This made me think about other research related to brain volume and parenting. For example, when women are pregnant their brain volumes can shrink an average 4% and not return to normal volume until about six months after birth. First, that makes the 4.03% decline found in Guo et al.'s female participants sound less ominous: this sort of decline is a normal experience for many women in young adulthood. Second, although most Finnish women in the 1980s usually started having babies at age 29, is it possible that some of the 23 women in this study gave birth just before the second MRI scan? Or is the location of brain loss during pregnancy similar to the location of women's brain loss in the transition to middle age?
Starting in the 80s, Finland offered parental leave to fathers as well as mothers. So it is possible that some of the male participants may have also identified themselves as being on parental leave. However, we know that fathers and mothers often take on different roles in parenting. For example, women are more likely to report that they get up to feed or care for babies in the middle of the night; mothers report more sleep loss than fathers even as children grow older. Poor sleep is associated with brain volume loss in the frontal, temporal, and parietal lobes. Different parental roles and related sleep loss may contribute to women's additional 1% of brain loss; brain volume loss related to poor sleep and brain volume loss related to women's transition to midlife are located in similar areas. In the end we do not know what is causing these declines or sex differences, and even if we did, at this point we cannot know if these are related to any changes in men's and women's behavior or health as they age. The one thing you can know for sure is that if you are middle aged, pregnant, a new mother, or are sleep-deprived, you ARE losing your mind. FURTHER READING: The Guo et al. (2016) article can be accessed online or through your local college library. Loss of brain cells does not always relate to loss of cognitive functioning. Read an APA Monitor on Psychology article by Melissa Phillips on the strengths of the middle-aged mind. Childhood trauma can also reduce brain volume. Read a report on trauma's effects on brain development from the Child Welfare Information Gateway (U.S. Dept. of Health and Human Services). BONUS: Watch a video from Brown University on Synaptic Pruning:
When I was growing up, all the girls read Are you There God? It's Me Margaret., by Judy Blume. Its main character, Margaret, looks forward to developing breasts and getting her first menstrual period. When these finally occur she feels triumphant! More recently, Hello Flo advertisements also portray puberty as something that girls desire: they are upset if menstruation doesn't start quickly enough. Of course, fiction writing and advertisements may not reflect the full story of girls' puberty as witnessed by these memes:
Keenan, Culbert, Grimm, Hipwell, and Stepp (2014) investigated the relationship between African-American and European-American girls' pubertal timing (what age things happen), pubertal tempo (how much time passes between stages of puberty; how long puberty lasts), and depression symptoms. Their sample was part of the longitudinal Pittsburgh Girls Study, so it was large (more than 2,000 girls of diverse backgrounds), data were collected at age 10 and then each year for up to a decade, and the participants were more likely to come from low-income homes. Each year the girls completed a depression inventory; their caregivers (mostly mothers) completed the same depression inventory about their daughters. From this Keenan et al. could learn how many depression symptoms were common at each age and see how they related to the other variables of ethnicity and puberty. Overall, depression symptoms were highest at age 10 and declined at various rates after that. Even so, across the decade the girls reported that only one or two symptoms on average. The authors maintained that even "minor depression" like this can put individuals at risk for other problems. The girls provided data on pubertal timing and tempo by matching themselves to standard pictures that portrayed different stages of breast and pubic hair development, and by indicating if they had gotten their first period. One of these scales was also completed by the caregivers in reference to their daughters' development. The results replicated past research in that the earliest maturing girls (early pubertal timing for breast and pubic hair development) reported more depression symptoms at age 10 than later maturing girls (late pubertal timing). A new finding was that girls who were late to develop breasts (late pubertal timing) and also had a slow pubertal tempo (change progressed slowly) also reported more depression symptoms. There was no effect on depression related to the development of pubic hair and pubertal tempo. Similar to past research, African-American girls reported slightly higher depression symptoms. For example, at age 10 African-American girls reported one extra depression symptom compared to European-American girls. Likewise, African-American girls demonstrated earlier pubertal timing: pubic hair development occurred almost nine months earlier and breast development began about eleven months earlier than what was reported by European-American girls. Keenan et al. added to the literature by suggesting a trend: African-American girls demonstrated a little slower pubertal tempo, meaning that they took just ever so slightly longer to pass through the stages of puberty compared to the European-American girls. This trend requires further investigation in future research. New and most importantly, the relationship between depression, ethnicity, and pubertal timing was significant. The ethnic difference in depression symptoms at age 10 (their peak) was reduced up to 32% when pubertal timing was factored in. Pubertal tempo did not have a similar effect. Thus, a considerable portion of the ethnic difference in depression can be explained by African-American girls' earlier entry into puberty compared to European-American girls. In explaining their findings Keenan et al. suggested that sex hormones might be to blame for at least some of the low level depression seen in preteen girls. Girls with an earlier pubertal timing have higher levels of sex hormones like estrogen compared to girls who have not yet begun pubertal development. This biological argument would, at least in part, explain African-American girls' slightly higher rates of depression.
On the other hand, the authors predicted that a slow pubertal tempo would also predict higher levels of depression because it would mean exposure to high levels of hormones for an extended period of time. In this study, only for girls with later breast development (which implies lower hormone levels) did slow pubertal tempo predict slightly higher depression symptoms. As well, slow pubertal tempo did not explain any of the differences in depression between African- and European-American girls. So hormones cannot be the only explanation for girls' depression symptoms during puberty.
One possibility is that girls receive feedback based on their development that makes them self-conscious. Increases in estrogen cause weight gain so an early maturing girl may feel overweight compared to other girls. Breast development, a sign of puberty that is visible to others, may be desired to attract dating partners - so later maturing girls (especially those with a slow tempo) might be embarrassed by smaller breasts (but not care about lacking pubic hair, a trait that is not socially visible). Conversely, early breast development may bring with it unwanted sexual attention and comments that are uncomfortable for a young girl to navigate. It is also possible that early development of breasts and early menarche may lead parents to treat girls differently: for example, fathers may be less affectionate with their daughters once puberty begins. Parents, fearing sexual experimentation, sexually transmitted infections, teen pregnancy, or sexual assault may also impose new limits on what an early maturing girl can wear, where she can go, and whom she can be with. These sorts of social factors could also explain some of the low level depression seen in preteen girls. FURTHER READING: The Keenan et al. (2014) article is available online and through your local college library. Parents are not the only ones who may regulate girls bodies once puberty begins. Read an article in The Atlantic magazine by Li Zhou: "The Sexism of School Dress Codes." Starting at puberty, girls and women are twice as likely as boys and men to suffer from depression. This also means that depression symptoms might be missed in males because we are not expecting them to be depressed. Counselor and writer, Michael Gurian, explains some possible symptoms to look for in boys:
The late American artist and televised painting teacher, Bob Ross, was best known for his positive attitude summed up by his classic saying, "we don't make mistakes, we just have happy accidents." Because of this cheery outlook he has been much loved and often parodied in our culture:
If Bob Ross was creative, would he be likely to think aggressive memes like this one were funny? Was Bob Ross creative because he was so positive or because he was a complex person (he was also a Master Sergeant in the United States Air Force, a rescuer of injured squirrels in Muncie, Indiana, the father of three boys from two marriages, a painter of - as he often said - "happy trees"). Chang, Chen, Hsu, Chan, and Chang (2015) were interested in a similar question: does a person's style of humor relate to that person's level of creativity? To answer this, they conducted a large study (1,252 participants) with Chinese 13-year-olds living in Taiwan. The measures that they used were translated into Chinese and were chosen because they worked in cross-cultural settings (meaning that the nationality of the participants should not be an issue that will influence the results). The teenagers competed a Humor Styles Questionnaire and a cluster analysis of their answers placed them into groups. Similar to past research, four styles emerged: 1) Positive Humor: joking about yourself in a positive way (showing off) or joking about others in a positive way to show that you like them. 2) Negative Humor: joking about yourself in a negative way (putting yourself down) or joking about others in a negative way to be aggressive. For example, implying that nobody will date you! 3) General Humor: joking in both positive and negative ways about yourself and about others. In this case humor can be used to both befriend and to be aggressive at times. 4) Humor Deniers: below average use of any type of humor. Among other measures, the participants took a modified figure drawing test of creative thinking. Each teenager received a piece of paper with 27 versions of the Chinese character for "Human" printed on it. They were asked to doodle upon each symbol to create drawings that incorporated that shape. The drawings were rated on: Fluency (how many of the 27 versions were drawn upon in ten minutes); Flexibility (the number of categories in the drawings' themes); Originality (how novel the drawings were compared to others); and Elaboration (the number of details in the drawings). The most robust results strongly supported a theory of creativity: Intrapersonal Variability. In this perspective, "...individuals who hold opposing or conflicting traits...[or have] complex personalities..." are more creative (p. 307). The teenagers whose main humor style was General, or full of contradictions and complexity, scored noticeably higher than the other students on all four ratings of creativity. On the other hand, one comparison did seem to support an alternate theory: the Positivity Perspective suggests that positive humor is linked to more creative thinking. Only in the ratings of Elaboration did participants with Positive Humor outscore the participants with Negative Humor. If we accept that Bob Ross was a creative man, the most prominent results of this study support that his complex personality and conflicting life experiences may have increased that creativity. Chang et al. explain that creativity may be enhanced when people are able to accept their inner conflicts (self-integration) or when their complex personalities allow them to be psychologically flexible in their thinking. At the same time, the Elaboration finding implies that Bob Ross' attention to detail in his paintings may have been, at least in part, related to his positive outlook on life. The Positivity Perspective assumes that using positive humor is associated with being in a positive mood, which is assumed to allow one to be more creative, or in this case, to embellish creative acts. Although Bob Ross' humor clearly included positivity, his life experiences may have led him to embrace a General Humor style, which in turn may have fostered his creativity. In that case Bob Ross would probably find this week's meme funny, even though its humor is aggressive. Further Reading: The Chang et al. (2015) article can be accessed through your local college library. Watch a talk by Dr. Robert Provine, a psychologist and neuroscientist, on laughter. Read a press release from the Association for Psychological Science about a research study by Vohs, Redden, and Rahinel (2013) that links a messy work environment to increased creativity. BONUS: Feel the positivity! Feel the creativity! The Public Broadcasting Service (PBS) Digital Studios created a really amazing musical remix of Bob Ross using manipulated clips from his television program.
This week in the United States we will celebrate Thanksgiving. In addition to feelings of gratitude, family gatherings can also stir up heated arguments about political issues and other differences between family members. Today's meme suggests that the neurotransmitter found in turkey meat, the centerpiece of most Thanksgiving feasts, may be an antidote to this problem:
Tryptophan naturally occurs in turkey meat and other common foods (including beans for vegetarians). Its presence in the brain has been linked to an increase in Serotonin, another neurotransmitter associated with positive mood and decreased aggression. Could eating Tryptophan-rich foods decrease fighting? An experiment with non-human subjects suggests that a touch of Tryptophan might help. Walz, Stertz, Fijtman, dos Santos, and de Almeida (2013) divided male mice into five groups: four groups received a dose of Tryptophan that was 1%, 2%, 3%, or 10% of 30 ml of a carrier liquid; the last group was the control group so they did not get any Tryptophan in their liquid. Immediately after dosing, the mice were individually exposed to an intruder: a stranger male mouse. This encounter lasted for five minutes as the test mouse's behaviors were recorded. This experience occurred eight times for all male mice from the five groups. When the animals' reactions were coded across these trials, Walz et al. found that the mice dosed with a 1% and 2% Tryptophan solution were less likely than the control group to aggressively bite or to threaten the stranger mouse from the side. The other doses did not show a significant reduction in these aggressive behaviors, and none of the doses was related to changes in non-aggressive behaviors, such as activity levels or grooming. At a low dose, Tryptophan is speculated to raise Serotonin levels enough to take the edge off this stressful experience; at larger doses it may be that Serotonin rises so high that it sends a feedback signal to the mouse's body to decrease Serotonin production thereby undoing any good effect of supplementation. The authors concluded, "...that low doses of [Tryptophan] are able to reduce aggressive behavior in male mice....Tryptophan supplementation may be an alternative treatment for aggression in groups that exhibit such behavior" (p. 400). Of course, we can't be sure that the same dose of Tryptophan (especially if it is combined with cranberry sauce, mashed potatoes, and stuffing) would have the same effect on humans or that it would diminish verbal aggression as it did physical aggression. Walz et al. encouraged further research: "To control aggressiveness, a person's diet may be an important factor" (p. 397). Until then, when discussions get heated at your next family gathering, try changing the subject to something that everyone can agree on. Until we know the details about Tryptophan we will apparently have to rely on Adele.
Further Reading: The Walz et al. (2013) article is available online and the Psychology and Neuroscience journal article can be accessed through your local college library. People used to think that the Tryptophan in turkey was responsible for that sleepy feeling so many of us have after the big meal. Find out what is more likely to blame in this Live Science piece by Tanya Lewis. Why do family celebrations so often turn into family fights? Read Olga Khazan's article in The Atlantic: "Why families fight during the holidays."
One of my students asked me if I make the memes that I use in this blog: the answer is "no" - truly, I am too busy grading papers. Fortunately there are a lot of memes floating around social media. Most of the time I start with a meme and then do a literature search to find recent research on that topic. Other times, like this week, I find a great article then search Google Images for a meme to match. Sometimes I stumble upon the perfect combination and reach article/meme perfection:
Would it be mean to trick a hurting person into thinking that a piece of candy is actually a tablet of pain reliever? The answer would be, "yes" if the act of swallowing that orange Skittle would have no effect on her headache - but what if it helped just as much as a real Advil? Faasse, Martin, Grey, Gamble, and Petrie (2015) conducted a simple experiment to answer a similar question. They recruited 87 New Zealander university students (83% female) who frequently suffered from headaches. The students were each given four identical-looking tablets: two were labeled "Nurofen," a brand name for Ibuprofen - like Advil in the United States, and the other two were labeled "Generic Ibuprofen." Thus, each of them believed that he or she received two brand name pills and two generic pain-relief pills. However, the researchers had tricked them with some mild deception! For each participant one of the tablets labeled "Nurofen" was actually a placebo (a sugar pill) containing no medicine - much like a Skittle; likewise, one of the tablets labeled "Generic Ibuprofen" was also a placebo. The remaining two tablets were always identical doses (400 mg) of Ibuprofen; there was no difference beyond how they were labeled. This was a within-subjects experiment because all participants experienced all of the possible versions of the tablet: placebo labeled Nurofen; Ibuprofen labeled Nurofen; placebo labeled Generic; Ibuprofen labeled Generic. The participants were instructed to use the tablets for their next four headaches, and the order of the pills was dictated by the researchers for counter-balancing. Each time the participants got headaches they had to rate the intensity of their pain, take the designated tablet, wait one hour, and then rate the intensity of any remaining pain and note any side effects. As you would expect, the overall results showed that Ibuprofen did a better job than the placebo at resolving headache pain. What was more interesting to Faasse et al. was that placebo and Ibuprofen tablets labeled Nurofen were rated equally well on pain relief. In this case, the Placebo Effect was clear: just believing that you took brand name Ibuprofen was enough to cure your pain as well as the real medicine would! Alternatively, when participants took the tablets labeled "Generic Ibuprofen," pain relief was much higher from the actual Ibuprofen than from the placebo. Again participants' beliefs influenced their experiences: in this case a mistrust of off-brand medicines overcame the Placebo Effect. Side effect data followed a similar trend: when participants believed that they were taking "Generic Ibuprofen" they reported more side effects from the placebo tablets than from the actual Ibuprofen (that really could produce side effects)! When placebos produce negative effects this is call the Nocebo Effect. This Nocebo Effect was limited to the Generic labeled tablets. No difference in side effects was seen between the placebo and Ibuprofen when they were labeled Nurofen, so a mistrust of off-brand medicine encouraged the Nocebo Effect. Faasse et al.'s experiment would suggest that orange Skittles stored an old Advil bottle would probably fix your sister's headache just as well as actual medicine! On the other hand, if she saw the Skittles come out of a store brand (generic) bottle she might be complaining an hour later: her head would still hurt and the "pills" you gave her are upsetting her stomach. Of course, the side effects of tricking your sister would be far worse than a headache, so please don't try this at home. Further Reading: The Faasse et al. (2015) article is available online or can be obtained through your local college library. Curious about the placebo effect in medicine? Get two perspectives from an article in the New England Journal of Medicine by Drs. Ted Kaptchuk and Franklin Miller, and from a TED talk by Dr. Lissa Rankin. Orange Skittles resemble Advil: similarities between candy and medicine can lead to accidental poisoning of children. Play the Pill vs Candy game from California Poison Control. Can you tell the difference between a sweet treat and a pharmaceutical? BONUS: Our suspicion of generic brands extends to other products as well. Watch some of the Buzzfeed crew attempt to tell the difference between off-brand and brand name cereals.
