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Autism quiz T or F

July 2, 2025/in Psychology Questions /by Besttutor

Please answer the following True and False questions and justify your answer (1 paragraph PER question)

1. Autism is more often diagnosed in boys than in girls? _____

2. Autism can be caused by emotional deprivation. _____

3. Autism is on the increase. _____

4. Autism has the same rate of occurrence worldwide _____

5. Autism can be detected before a child is 2 years old _____

6. Autism runs in families ____

7. There is a single gene for autism ____

8. Autism can be caused by the MMR vaccine _____

9. A person with autism can grow out of it _____

10. People with autism all have below average intelligence _____

11. People with autism always prefer being alone _____

12. Adults with autism are not capable of working _____

13. People with autism can’t feel emotions ____

14. People with autism do not easily understand that other people are thinking _____

15. All people with autism display deficits in communication _____

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SOCW-6210-6351-W6-Discussion

July 2, 2025/in Psychology Questions /by Besttutor

DISCUSSION 1:

 

The Aging Process

 

As individuals grow older, they experience biological changes, but how they experience these changes varies considerably. Senescence, or the process of aging, “affects different people, and various parts of the body, at different rates” (Zastrow & Kirst-Ashman, 2016, p. 658).

 

What factors affect the aging process? Why do some individuals appear to age faster than others? In this Discussion you address these questions and consider how, you, as a social worker, might apply your understanding of the aging process to your work with older clients.

 

To prepare for this Discussion, read “Working With the Aging: The Case of Francine” in Social Work Case Studies: Foundation Year.

 

Post a Discussion in which you:

 

o   Apply your understanding of the aging process to Francine’s case. How might Francine’s environment have influenced her aging process? How might you, as Francine’s social worker, apply your knowledge of the aging process to her case?

 

o   Identify an additional strategy you might use to apply your knowledge of the aging process to social work practice with older clients in general. Explain why you would use the strategy.

 

 

Be sure to support your posts with specific references to the resources. If you are using additional articles, be sure to provide full APA-formatted citations for your references

 

References

 

Plummer, S. -B., Makris, S., & Brocksen, S. M. (Eds.). (2014). Social work case studies: Foundation year. Baltimore, MD: Laureate International Universities Publishing. [Vital Source e-reader].

 

Zastrow, C. H., & Kirst-Ashman, K. K. (2016). Understanding human behavior and the social environment (10th ed.). Boston, MA:  Cengage Learning.

 

 

 

Working With the Aging: The Case of Francine

Francine is a 70-year-old, Irish Catholic female. She worked for 40 years as a librarian in an institution of higher education and retired at age 65. Francine has lived alone for the past year, after her partner, Joan, died of cancer. Joan and Francine had been together for 30 years, and while Francine personally identifies as a lesbian, she never came out to her family or to her colleagues. When speaking to all but her closest confidantes, Francine referred to Joan as her “best friend” or her “roommate.” Francine’s bereavement was therefore complicated because she did not feel she could discuss the true nature of her partnership with Joan. She felt that there was little recognition from her family, and even some of her close associates, of the impact and meaning of Joan’s death to Francine. There is a history of alcohol abuse in Francine’s family, and Francine abused alcohol from late adolescence into her mid-30s. However, Francine has been in recovery for several decades. Francine has no known sexual abuse history and no criminal history.

Francine sought counseling with me for several reasons, including an ongoing depressed mood, a lack of pleasure or enjoyment in her life, and loneliness and isolation since Joan’s death. She also reported that she had begun to drink again and that while her drinking was not yet at the level it had been earlier in her life, she was concerned that she could return to a dependence upon alcohol. Francine came to counseling with several considerable strengths, including a capacity to form intimate relationships, a successful work history, a history of having maintained her sobriety in the past for many years, as well as insight into the factors that had contributed to her current difficulties.

During our initial meetings, Francine stated that her goals were to feel less depressed, to reduce or stop drinking, and to feel less isolated. In order to ensure that no medical issues were contributing to her depression symptoms, I referred Francine to her primary care physician for an evaluation. Francine’s physician did not find any medical cause of her symptoms, diagnosing Francine with moderate clinical depression and recommending that Francine begin a course of antidepressant medication. Francine was reluctant to take medication and first wanted to try a course of counseling.

In order to help Francine meet her goal of reducing her depression symptoms, I employed a technique called behavioral activation (BA), which is drawn from principles of cognitive behavioral therapy and helps to reengage people in pleasant physical, social, and recreational activities. We began with a small initial goal of having Francine dedicate at least 5 minutes of each day to an activity she found pleasant or rewarding. Over the following weeks, we increased the time. Francine’s treatment progress was monitored through weekly completion of the Patient Health Questionnaire (PHQ-9) in order to determine whether or not her depressive symptoms were improving.

I helped Francine address her drinking by reconnecting her with effective coping strategies she had used in the past to achieve and maintain her sobriety. These included identifying triggers for the urge to drink and exploring her motivations for both continuing to drink and for stopping her use of alcohol. Francine began attending regular meetings of Alcoholics Anonymous™ (AA) and found several meetings that were specifically for older women and for lesbians. In addition, Francine spoke regularly with a sponsor who helped her to remain abstinent during particularly stressful moments during her reengagement in sobriety.

Finally, in order to address Francine’s goal of feeling less lonely and isolated, we explored potential avenues to increase her social networks. In addition to spending time with her family, friends, and her AA sponsor, Francine began to visit the local lesbian, gay, bisexual, and transgender (LGBT), center for the first time in her life and attended a support group for women who had lost their partners. Francine also began spending time at her local senior center and went there at least three times a week for exercise classes, other recreational activities, and lunch. She also began to do volunteer work at her local library once a week.

Over several months of counseling, Francine stopped drinking; significantly increased her daily involvement in pleasant and rewarding activities, including social and recreational activities; and reported feeling less lonely, despite still missing her partner a great deal. Francine’s scores on the PHQ-9 gradually decreased over time, and after 16 weeks of counseling, Francine reported that she no longer felt she needed the session to move on with her life. In addition, Francine visited her primary care physician, who found upon evaluation that her depression had lifted considerably and that an antidepressant was no longer indicated. By the end of counseling, Francine’s focused work on identifying her depression symptoms and her triggers for drinking equipped her to better recognize when she might need support in the future and to whom she could reach out for help if she needed it.

 

 

 

 

 

Discussion 2: Mental Health Care

 

Mental health care is a primary concern to social workers, who are the main providers of care to populations with mental health diagnoses. The system that provides services to individuals with mental health issues is often criticized for being reactive and only responding when individuals are in crisis. Crisis response is not designed to provide on-going care and is frequently very expensive, especially if hospitalization is involved.

 

Critics suggest a comprehensive plan, which involves preventive services, as well as a continuum of care. However, there are few, if any, effective and efficient program models. Social work expertise and input are vital to implementing effective services. Targeting services to individuals with a diagnosis of mental illness is one strategy. Another approach includes providing an array of services that are also preventative in nature. How might these suggestions address potential policy gaps in caring for individuals such as the family members in the Parker Family case?

 

For this Discussion, review this week’s resources, including the Parker Family video. Then consider the specific challenges or gaps in caring for individuals with a chronic mental illness might present for the mental health system based on the Parker case. Finally, think about how environmental stressors, such as poverty, can aggravate mental illness and make treatment more challenging.

 

·      Post an explanation of the specific challenges or gaps in the mental health care system for the care of individuals with chronic mental illnesses.

 

·      Base your response on the Parker case.

 

·      Then, describe how environmental stressors, such as poverty, can aggravate mental illness and make treatment more challenging.

 

Support your post with specific references to the resources. Be sure to provide full APA citations for your references.

 

 

References

 

Popple, P. R., & Leighninger, L. (2015). The policy-based profession: An introduction to social welfare policy analysis for social workers. (6th ed.). Upper Saddle River, NJ: Pearson Education.

World Health Organization. (2004). Mental health policy and service guidance package: Mental health policy, plans and programmes. Retrieved from http://www.who.int/mental_health/policy/en/policy_plans_revision.pdf

 

Plummer, S. -B., Makris, S., & Brocksen, S. (Eds.). (2014). Sessions: Case histories. Baltimore: MD: Laureate International Universities Publishing. [Vital Source e-reader].

 

 

Parker Family Episode 5 Program Transcript

 

COUNSELOR: So you’ve been hospitalized, let’s see, four times altogether.

 

FEMALE CLIENT: Well actually, I should have only been in the hospital three times.

 

COUNSELOR: Why do you say that?

 

FEMALE SPEAKER: Well, on the third hospital visit they kicked me out before I was ready to leave. They said I was just in there to get away from my mom, but I told them they were wrong. My sister even backed me up on this. But they didn’t care. They just checked me out, and home sweet home I went. I was barely gone like a month and I was back in their monkey house. So technically, for me, hospital visits three and four are the same. I remember going back to that hospital seeing the same docs and nurses, and I just smiled and waved and said, see, I told you so. I mean, we picked up right where we left off.

 

COUNSELOR: What do you mean your sister backed you up?

 

FEMALE CLIENT: Jane, that’s my sister. Jane, she knew how crazy my mom is, so she took pictures of all that mess and all that junk my mom hoards, and she showed them to the social worker in the hospital.

 

COUNSELOR: What happened?

 

FEMALE CLIENT: You know what the social worker said? She said that there was nothing that she can do about it, that her job was to only make sure that patients have a place to go when they leave the hospital. Translation, when you’re out the door, good riddance and good luck. Some policy, huh?

 

 

 

 

 

 

 

Discussion 3: Emerging Issues in Mental Health Care

 

Like so many areas of practice in social work, mental health is dynamic and ever-evolving. Research continues to provide new information about how the brain functions, the role of genetics in mental health, and evidence to support new possibilities for treatment. Keeping up with these developments might seem impossible. However, being aware of and responsive to these developments and incorporating them into both your practice and social policy is essential to changing the lives of individuals and families who live with a mental health diagnosis and the impact it brings to their daily lives.

 

For this Discussion, review this week’s resources. Search the Library and other reputable online sources for emerging issues in the mental health care arena. Think about the issues that are being addressed by social policy and those that are in need of policy advocacy and why that might be the case. Then, consider what social workers can do to ensure that clients/populations receive necessary mental health services. Also, think about the ethical responsibility related to mental health care social workers must uphold in host settings when they encounter conflicts in administration and home values. Finally, search your state government sites for the mental health commitment standards in your state and reflect on the mental health services covered under your state’s Medicaid program.

 

·      Post an explanation of those emerging issues in the mental health care arena that the policymakers address and those that are in need of policy advocacy and why.

 

·      Then, explain what strategies social workers might use to ensure that clients/populations receive necessary mental health services.

 

·      Finally, explain the mental health commitment standards and mental health services in your state. In your explanation, refer to the services covered under your state’s Medicaid program.

 

Support your post with specific references to the resources. Be sure to provide full APA citations for your references.

 

References

 

Popple, P. R., & Leighninger, L. (2015). The policy-based profession: An introduction to social welfare policy analysis for social workers. (6th ed.). Upper Saddle River, NJ: Pearson Education.

World Health Organization. (2004). Mental health policy and service guidance package: Mental health policy, plans and programmes. Retrieved from http://www.who.int/mental_health/policy/en/policy_plans_revision.pdf

 

Plummer, S. -B., Makris, S., & Brocksen, S. (Eds.). (2014). Sessions: Case histories. Baltimore: MD: Laureate International Universities Publishing. [Vital Source e-reader].

 

 

Mental Health America. (n.d.). Retrieved October 10, 2013, from www.mentalhealthamerica.net

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Case study APA Code of Ethics Outline

July 2, 2025/in Psychology Questions /by Besttutor

Okay here is my case study

 

Case Study 10-53: Zena Freeman is a contention between a student and her male teacher (Dr. Macho Mann ) Organizational Psychology course. She goes to her teacher requesting help understanding specific organizational psychology research ideas. Educator Macho Mann remarks his student that women don’t have a place in the course since they are not suited for the field and exclusively decline to answer her questions, yet he kept on criticizing her and the female sex overall. He went ahead about how women are inadmissible for function in the business world and utilized her issues understanding specific ideas as his proof to help this. A way to deal with breaking down this case study would be analyzing why a renowned teacher wants to disparage his student looking for his assistance and clarifying which ethical and moral violations he has supported.

Ethical Conflict was::

 

The main ethical conflict includes the standard of “Human Relations” and the guideline of “Regard for People’s Rights and Dignity.” The standard of human relations incorporates sexual harassment, unfair discrimination, exploitative relationships, and avoiding harm. These were available for Zena’s case. Zena was subjected to unfair discrimination exclusively because she is a girl. She was likewise subjected to a type of sexual harassment. Although there were no immediate sexual references or inappropriate touching, she is sexually harassed by Macho Mann’s attempt to keep her in a subordinate position by exclusion and ridicule (Koocher, 2016). The Respect for People’s Rights and Dignity is described as respecting the dignity and worth of all people, their right to privacy, confidentiality, and self-determination. Be aware of, and respect cultural and role differences, and don’t willingly participate or condone activities of others based on prejudices (“Ethical Principles of Psychologists and Code of Conduct.”, 2017).

INSTRUCTIONS FOR HOMEWORK

in this milestone, apply the APA Code of Ethics to your chosen case study vignette and expand the outline of your final case study analysis paper you began in Milestone Two.

The APA Code of Ethics Principles a. Identify and define all five principles b. Highlight, bold, or summarize all that might apply to your case study vignette’s ethical conflict c. Justify why highlighted or bolded principles apply to your case study vignette’s ethical conflict 6. The APA Code of Ethics Standards a. List and define all ten standards b. Highlight, bold, or summarize all that might apply to your case study vignette’s ethical conflict c. Justify why highlighted or bolded standards apply to your case study vignette’s ethical conflict 7. Statement of Culture and Social Orientations in the Case Study

I posted a sample code of ethic outline paper below

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I already started some of the question

July 2, 2025/in Psychology Questions /by Besttutor

Item Development and Analysis Worksheet

 

 

 

 

 

Student Name:                                                                        Section:   PSYC421-

 

 

 

 

 

PART 1: Writing Multiple Choice Test Items

 

 

 

Develop one multiple choice question that covers content from each of the four chapters listed below.  When writing your sample questions, please keep in mind the specifications regarding item construction discussed in the textbook.  Also, remember the importance of carefully crafted distractor options.  Finally, please limit the number of response options to 4 (1 correct response and 3 distractors), and avoid the options of “all of the above,” none of the above,” or the like.  Be sure to indicate which of the response options is the correct one.

 

 

 

Chapter 3 Multiple Choice Question (2.5 points)

 

An estimate of the relaibility of a speed test is a measure of ?

 

 

 

A) the consistancy of flood

 

B) the consistancy of response

 

C) the consistancy of the response speed

 

D) the consistancy of the response of intensity

 

 

 

 

 

Chapter 4 Multiple Choice Question (2.5 points)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Chapter 5 Multiple Choice Question (2.5 points)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Chapter 6 Multiple Choice Question (2.5 points)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

PART 2: Item Analysis: Item Difficulty Index(Cohen et al., 2013, pg. 263)

 

 

 

A test is only as good as its questions!  When researchers, test constructors, and educators create items for ability or achievement tests, we have a responsibility to evaluate the items and make sure that they are useful and high-quality.  The process that we use to evaluate test items is known as Item Analysis.  When bad items are identified and eliminated from a test, that increases the efficiency, reliability and validity of the entire test!    One way that we can distinguish among good and bad items is with the Item Difficulty Index.

 

 

 

Part 2A: Calculating Item Difficulty

 

 

 

Using the data below, calculate the Item Difficulty Index for the first 6 items onQuiz 1 from a recent section of PSYC101.  For each item, “1” means the item was answered correctly and “0” means it was answered incorrectly. Type your answers in the spaces provided at the bottom of the table. (1 pt. each)

 

PSYC101 Quiz 1 Item Distribution and Total Scores
Examinee Item 1 Item 2 Item 3 Item 4 Item 5 Item 6 Total Score
Andre 1 1 1 1 1 1 16
Allison 1 1 1 1 0 0 7
Heather 1 1 1 1 0 0 10
Corey 1 1 0 1 1 1 17
Christina 0 0 1 1 0 1 3
Jeffrey 0 1 1 1 0 0 11
Shawn 1 1 1 1 0 1 14
Dana 0 0 1 1 0 1 10
Megan 1 1 1 1 0 1 13
David 0 1 1 1 0 1 12
Isabel 0 0 0 1 0 0 4
Lance 1 1 1 1 0 0 9
Aliyah 1 1 1 1 0 1 15
Blaire 0 1 1 1 0 1 12
Gabriel 0 0 1 1 0 0 6
Item
Difficulty
53.333 73.333 86.667 100 13.333 60  

 

 

 

 

 

 

 

 

 

Part 2B: Calculating Optimal Item Difficulty (.5 pt. each)

 

 

 

1.      For a test item with two response options (e.g., true/false), what is the probability of selecting the correct answer by chance?

 

%

 

 

 

2.      Calculate the optimum level of difficulty for a test questions with two response options.

 

%

 

 

 

3.      For a test item with three response options, what is the probability of selecting the correct answer by chance?

 

%

 

 

 

4.      Calculate the optimum level of difficulty for a test questions with three response options.

 

%

 

 

 

5.      For a test item with four response options, what is the probability of selecting the correct answer by chance?

 

%

 

 

 

6.      Calculate the optimum level of difficulty for a test questions with four response options.

 

%

 

 

 

7.      For a test item with five response options, what is the probability of selecting the correct answer by chance?

 

%

 

 

 

8.      Calculate the optimum level of difficulty for a test questions with five response options.

 

%

 

 

 

 

 

PART 3: Item Analysis: Item Discrimination Index(Cohen et al., 2013, pg. 265–266)

 

 

 

Another way that test creators can distinguish between good and bad items is with an analysis called the Discrimination Index.  The discrimination index measures how well an individual test item distinguishes between high scorers and low scores on the test.  An item is considered to be “good” if most of the high scorers get it right, and most of the low scorers get it wrong.

 

 

 

Interpreting the Discrimination Index (d)

 

·         The discrimination index can range from -1.0 to 1.0.

 

·         The closer d is to 1.0, the better the item discriminates between high and low scorers

 

·         The closer d is to 0, the more poorly the item discriminates between high and low scorers.

 

·         An item with a negative discrimination index is considered a “negative discriminator” because more low scorers get the item correct than high scorers.

 

·         A discrimination index of 1.0 means all the high scorers got the item correct and all of the low scorers got it incorrect.

 

·         A discrimination index of -1.0 means all of the low scorers got the item correct and all of the high scorers got it incorrect.

 

·         Items with d’s close to 0 or with negative d’s ought to be eliminated from the test!

 

Calculating the Item Discrimination Index (d)

 

 

 

Calculate the item discrimination index (d) for the 7 hypothetical test items presented below.  Type your answers in the spaces provided at the right of the table (1 pt. each).

 

 

 

Item # U L n d
Item 1 21 17 25  
Item 2 23 7 25  
Item 3 25 0 25  
Item 4 3 24 25  
Item 5 22 3 25  
Item 6 0 25 25  
Item 7 19 6 25  

 

 

 

 

 

Based on your calculations above, answer the following questions (1 pt. each).

 

 

 

1.      Which item discriminates the best?

 

 

 

2.      Which item discriminates most poorly?

 

 

 

3.      Based on your analysis, identify which two items would you choose to eliminate from this test and explain why you would eliminate each.

 

 

 

 

 

Part 4: Item Characteristic Curves (Cohen et al., pg. 268–270)

 

 

 

Another method that test creators can use to assess the usefulness of test items is with Item Characteristic Curves.  Item characteristic curves provide a graphical depiction of examinees’ performance on individual test items.  As indicated in the figure below, Total Test Score is plotted on the x-axis of the curve, while proportion of examinees who got the item correct is plotted on the y-axis

 

 

 

 

 

 

 

 

Using the figure above, provide a written description of how test items A–D discriminate among examinees at various levels of performance.  In your responses, discuss why each item would be considered a “good” or a “bad” item.  EXAMPLE: “This item discriminates well among high scores, but doesn’t discriminate well among low scorers.  So this item would be considered a good item because it discriminates at the highest levels of performance.” (2 pt. each)

 

 

 

Item A:

 

 

 

Item B:

 

 

 

Item C:

 

 

 

Item D:

 

 

 

Item E:

 

 

 

 

 

Part 5: Qualitative Item Analysis (Cohen et al., pg. 272–274)

 

 

 

Qualitative item analysis refers to a set of non-statistical procedures used to gather information about the usefulness of test items.  These analyses typically involve interviews, panel discussions, questionnaires and other forms of verbal exchange with test-takers to explore how individual test items work.

 

 

 

As an online student, you have a very different test-taking experience than residential students.  Based on your readings from Chapter 8, identify 4 topics related to online test taking, and create 4 qualitative questions that you could ask online test-takers to gain an understanding of their experiences with test-taking.  Also, as students at a Christian institution of higher education, course assignments/assessments are supposed to give students an opportunity to integrate course content with their Christian worldview.  Given the topic of faith and learning, create one qualitative question that you could ask test-takers.

 

 

 

 

 

 

 

 

 

Qualitative Item Analysis
Topic (1 pt. each) Sample Question for Test-Takers (1 pt. each)
 

 

 

 
 

 

 

 
 

 

 

 
 

 

 

 
 

 

 

 

 

 

 

 

 

 

 

Assignment Scoring

 

 

 

Part 1 Subtotal:

 

 

 

Part 2 Subtotal:

 

 

 

Part 3 Subtotal:

 

 

 

Part 4 Subtotal:

 

 

 

Part 5 Subtotal:

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Complete Entire Week 3

July 2, 2025/in Psychology Questions /by Besttutor
Qualitative vs. Quantitative Research

PSYCH/610 Version 2

1

Qualitative vs. Quantitative ResearchUse the table below to answer the following:· Define and distinguish between qualitative and quantitative research.· Provide examples of qualitative and quantitative research.· Imagine that you are a researcher interested in identifying the components of ‘giftedness’ in pre-teen children. What quantitative methods might you use to help you better understand the experience of giftedness? What qualitative methods might you use?· What are the advantages and disadvantages of each approach?

 

Definition

Examples

Examples of methods to study ‘giftedness’

Advantages

Disadvantages

Quantitative

Research

 

 

 

 

 

Qualitative

Research

 

 

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Complete Chapter 8

July 2, 2025/in Psychology Questions /by Besttutor

CHAPTER 14 Generalization

LEARNING OBJECTIVES

· Discuss the issues created by generalizing research results to other populations, including potential problems using college students as research participants.

· Discuss issues to consider regarding generalization of research results to other cultures and ethnic groups.

· Describe the potential problem of generalizing to other experimenters and suggest possible solutions.

· Discuss the importance of replications, distinguishing between exact replications and conceptual replications.

· Distinguish between narrative literature reviews and meta-analyses.

Page 292IN THIS CHAPTER, WE WILL CONSIDER THE ISSUE OF GENERALIZATION OF RESEARCH FINDINGS. When a single study is conducted with a particular sample and procedure, can the results then be generalized to other populations of research participants, or to other ways of manipulating or measuring the variables? Recall from  Chapter 4  that internal validity refers to the ability to infer that there is a causal relationship between variables. External validity is the extent to which findings may be generalized.

GENERALIZING TO OTHER POPULATIONS

Even though a researcher may randomly assign participants to experimental conditions, rarely are participants randomly selected from the general population. As we noted in  Chapters 7  and  9 , the individuals who participate in psychological research are usually selected because they are available, and the most available population consists of college students—or more specifically, first- and second-year students enrolled in the introductory psychology course to satisfy a general education requirement. They may also be from a particular college or university, may be volunteers, or may be mostly males or mostly females. So, are our research findings limited to these types of subjects, or can we generalize our findings to a more general population? After considering these issues, we will examine the larger issue of culture and how research findings can be generalized to different cultural groups.

College Students

Smart (1966) found that college students were studied in over 70% of the articles published between 1962 and 1964 in the Journal of Experimental Psychology and the Journal of Abnormal and Social Psychology. Sears (1986) reported similar percentages in 1980 and 1985 in a variety of social psychology journals; Arnett (2008) found that 67% of the articles in the 2007 volume of the Journal of Personality and Social Psychology used college student samples. The potential problem is that such studies use a highly restricted population. Sears points out that most of the students are first-year students and sophomores taking the introductory psychology class. They therefore tend to be young and to possess the characteristics of emerging adults: a sense of self-identity that is still developing, social and political attitudes that are in a state of flux, a high need for peer approval, and unstable peer relationships. They are intelligent with high cognitive abilities. Thus, what we know about “people in general” may actually be limited to a highly select and unusual group. Indeed, Peterson (2001) found that students, as a group, are more homogenous than nonstudent samples. That is, students are more similar to each other than adults are similar to other adults in the general population.

Research by Henry (2008) illustrates how the use of college students may affect the external validity of research on prejudice. In his sample of articles Page 293from 1990 to 2005, an increasing percentage of studies used college students as participants. Further, in looking at the actual results of studies on prejudice that compared college students with adults, he reported a variety of differences among adults and college students. For example, college students were less conservative and rated women and ethnic minorities more favorably.

Volunteers

Researchers usually must ask people to volunteer to participate in their research. At many colleges, introductory psychology students are required either to volunteer for research or to complete an alternative project. If you are studying populations other than college students, you are even more dependent on volunteers—for example, asking people at a homeowners’ association meeting to participate in a study of marital interaction or conducting research on the Internet in which people must go to your web page and then agree to participate in the study, or conducting a telephone survey of county residents to determine health care needs. In all these cases, external validity of the findings may be limited because the data from volunteers may be different from what would be obtained with a more general sample. Some research indicates that volunteers differ in various ways from nonvolunteers. In their comprehensive study on the topic, Rosenthal and Rosnow (1975) reported that volunteers tend to be more highly educated, of a higher socioeconomic status, more in need of approval, and more social.

Further, different kinds of people volunteer for different kinds of experiments. In colleges, there may be a sign-up board with the titles of many studies listed or a web page that manages research participants and volunteer opportunities for the university. Different types of people may be drawn to the study titled “problem solving” than to the one titled “interaction in small groups.” Available evidence indicates that the title does influence who signs up (Hood & Back, 1971; Silverman & Margulis, 1973).

Online Research

Another important consideration arises when asking participants to volunteer for online surveys and experiments. Researchers can find potential participants through online survey design services. Psychologists are increasingly using Amazon Mechanical Turk ( https://www.mturk.com ; Jacquet, 2011), a website for recruiting people to work on many types of tasks including participating in research for a specified payment. This sort of sampling strategy has important implications for external validity. While the online sample is more diverse than the typical college student sample, there are still generalization issues because Internet users represent a unique demographic. The Pew Research Center’s Internet and American Life Project (Pew Internet, 2010) found that living in an urban/suburban area, being college educated, being younger, and having a higher income are all related to reporting more time online. Thus, by asking Page 294for volunteers for an online survey, researchers are sampling from a particular demographic that may not generalize well to the population of interest.

Gender

Sometimes, researchers use only males or only females (or a very disproportionate ratio of males to females) simply because this is convenient or the procedures seem better suited to a particular gender. Given the possible differences between males and females, however, the results of such studies may not be generalizable (Denmark, Russo, Frieze, & Sechzer, 1988). Denmark et al. provide an example of studies on contraception practices that use only females because of stereotypical assumptions that only females are responsible for contraception. They also point out several other ways that gender bias may arise in psychological research, including confounding gender with age or job status and selecting response measures that are gender-stereotyped. The solution is to be aware of possible gender differences and include both males and females in our research investigations. Moreover, it is important to recognize the ways that males and females might differentially interpret independent variable manipulations or questions asked in a questionnaire.

Locale

The location that participants are recruited from can also have an impact on a study’s external validity. Participants in one locale may differ from participants in another locale. For example, students at UCLA may differ from students at a nearby state university, who in turn may differ from students at a community college. People in Iowa may differ from people in New York City. Thus, a finding obtained with the students in one type of educational setting or in one geographic region may not generalize to people in other settings or regions. In fact, studies have explored how personality traits like extraversion (the tendency to seek social stimulation) and openness to new experiences vary across geographic areas. Rentfrow, Gosling, and Potter (2008) looked at geographic differences in personality traits among citizens of various U.S. states and found extraversion to vary by state. People in midwestern states tended to be more extraverted than people in northeastern states, and people in western states tended to be more open to new experiences. Thus, a study conducted in one location may not generalize well to another, particularly if the variables in question are related to location in some way.

Culture

Whether theories and research findings generalize across cultures is a critically important issue. Some observers of current psychological research have been very critical of the types of samples employed in behavioral research. Based on analyses of published research by Arnett (2008) and others, Henrich, Heine, and Norenzayan (2010) contend that psychology is built on the study of WEIRD Page 295(Western, Educated, Industrialized, Rich, Democratic) people. In many cases, research samples consist primarily of college students from the United States, other English-speaking countries, and Europe. Ultimately, researchers wish to discover aspects of human behavior that have universal applications but in fact cannot generalize beyond their limited samples. This is, at its heart, a critique of the external validity of behavioral research: Does our human behavioral research generalize to all humans, or is it really a study of the WEIRD?

Clearly, if psychologists want to understand human behavior, they must understand human behavior across and among cultures (Henrich et al., 2010; Miller, 1999). Miller described research on self-concept by Kitayama, Markus, Matsumoto, and Norasakkunkit (1997) to illustrate the benefits of incorporating culture into psychological theory. Traditional theories of self-concept are grounded in the culture of the United States and Western Europe; the “self” is an individualistic concept where people are independent from others and self-enhancement comes from individual achievements. Kitayama and his colleagues take a broader, cultural perspective: In contrast to the U.S. meaning of self, in other cultures the “self” is a collective concept in which self-esteem is derived from relationships with others. Often, Japanese engage in self-criticism, which can be seen as relationship-maintaining, whereas Americans work to maintain and enhance self-esteem—thus, very different activities contribute to a positive self-concept in the two cultures (Kitayama et al., 1997). This is a very common theme in research that incorporates culture in psychological processes: “The significance of self-esteem, however, may be much more specific to a culture than has typically been supposed in the literature” (p. 1262).

Much of this cultural research centers on identifying similarities and differences that may exist in personality and other psychological characteristics, as well as ways that individuals from different cultures respond to the same environments (Matsumoto, 1994). Research by Kim, Sherman, and Taylor (2008) provides another example of the limits of external validity across cultural groups. This research focused on how people from different cultures use social support to cope with stress. In reviewing the research on the topic, they concluded that Asians and Asian Americans might benefit from different styles of social support as compared with European Americans. For example, Asian Americans are more likely to benefit from support that does not involve the sort of intense disclosure of personal stressful events and feelings that is the hallmark of support in many European American groups. Rather, they suggest that Asians and Asian Americans may benefit more from support that comes with the comforts of proximity (being with close friends) rather than sharing.

These examples all focused on differences among cultures. Many studies also find similarities across cultures. Evolutionary psychologists, for instance, often conduct studies in different cultural groups because they are looking for similarities across cultures in order to see if a particular behavior or attitude can be tied to our evolutionary past. For example, Singh, Dixson, Jessop, Morgan, and Dixson (2010) wanted to see if a particular aspect of beauty that is tied to greater reproductive success—namely waist-to-hip ratio (e.g., the ratio for Page 296a 25-inch waist and 35-inch hips is .71), which is related to sex hormones and thus fertility—would be seen as attractive across cultures. Diverse groups from Africa, Samoa, Indonesia, and New Zealand evaluated photographs of females with small and large waist-to-hip ratios. The researchers found that indeed, low waist-to-hip ratio among females was seen as more attractive across all these groups. In this example, the results obtained in one culture do generalize to other cultures.

Nonhuman Animals

We noted in  Chapter 3  that about 7% of psychological research is conducted with nonhuman animals. Almost all of this research is done with rats, mice, and birds. Most research with other species is conducted to study the behavior of those animals directly to gather information that may help with the survival of endangered species and increase our understanding of our bonds with nonhuman animals such as dogs, cats, and horses ( http://www.apa-hai.org/human-animal-interaction ).

The basic research that psychologists conduct with nonhuman animals is usually done with the expectation that the findings can be generalized to humans. This research is important because the research problems that are addressed require procedures such as long-term observation that could not be done with human samples. We do expect that we can generalize as our underlying biological and behavioral patterns are shared. In fact, the value of studying nonhuman animals has been demonstrated by research that does apply to humans. These applications include the biological bases of memory, food preferences, sexual behavior, choice behavior, and drug addictions. The American Psychological Association has prepared a brochure on animal research: ( http://www.apa.org/research/responsible/research-animals.pdf ).

In Defense of College Students

It is easy to criticize research on the basis of subject characteristics, yet criticism by itself does not mean that results cannot be generalized. Although we need to be concerned about the potential problems of generalizing from unique populations such as college students (cf. Sears, 1986), we should also keep several things in mind when thinking about this issue. First, criticisms of the use of any particular type of subject, such as college students, in a study should be backed with good reasons that a relationship would not be found with other types of subjects. College students, after all, arehuman, and researchers should not be blamed for not worrying about generalization to a particular type of subject if there is no good reason to do so. Moreover, college student bodies are increasingly diverse and increasingly representative of the society as a whole (although college students will always be characterized as having the ability and motivation to pursue a college degree). Second, replication of research studies provides a safeguard against the limited external validity of a single study. Studies are replicated at other colleges using different mixes of students, and Page 297many findings first established with college students are later applied to other populations, such as children, aging adults, and people in other countries. It is also worth noting that Internet samples are increasingly used in many types of studies. Although such studies raise their own issues of external validity, they frequently complement studies based on college student samples.

GENERALIZING ACROSS METHODS

The person who actually conducts the experiment is the source of another external validity problem. In most research, only one experimenter is used, and rarely is much attention paid to the personal characteristics of the experimenter (McGuigan, 1963). The main goal is to make sure that any influence the experimenter has on subjects is constant throughout the experiment. There is always the possibility, however, that the results are generalizable only to certain types of experimenters.

Some of the important characteristics of experimenters have been discussed by Kintz and his colleagues (Kintz, Delprato, Mettee, Persons, & Schappe, 1965). These include the experimenter’s personality and gender and the amount of practice in the role of experimenter. A warm, friendly experimenter will almost certainly produce different results from a cold, unfriendly experimenter. Participants also may behave differently with male and female experimenters. It has even been shown that rabbits learn faster when trained by experienced experimenters (Brogden, 1962)! The influence of the experimenter may depend as well on the characteristics of the participants. For example, participants seem to perform better when tested by an experimenter of the other sex (Stevenson & Allen, 1964).

One solution to the problem of generalizing to other experimenters is to use two or more experimenters. A fine example of the use of multiple experimenters is a study by Rubin (1975), who sent several male and female experimenters to the Boston airport to investigate self-disclosure. The experimenters revealed different kinds of information about themselves to both male and female travelers and recorded the passengers’ self-disclosures in return. One interesting result was that women tended to reveal more about themselves to male experimenters, and men tended to reveal more about themselves to female experimenters.

Pretests and Generalization

Researchers are often faced with the decision of whether to give a pretest. Intuitively, pretesting seems to be a good idea. The researcher can be sure that the groups are equivalent on the pretest, and it is often more satisfying to see that individuals changed their scores than it is to look only at group means on a posttest. A pretest also enables the researcher to assess mortality (attrition) effects when it is likely that some participants will withdraw from an experiment. Page 298If you give a pretest, you can determine whether the people who withdrew are different from those who completed the study.

Pretesting, however, may limit the ability to generalize to populations that did not receive a pretest. (cf. Lana, 1969). Simply taking the pretest may cause subjects to behave differently than they would without the pretest. Recall from  Chapter 8  that a Solomon four-group design (Solomon, 1949) can be used in situations in which a pretest is desirable but there is concern over the possible impact of taking the pretest. In the Solomon four-group design, half of the participants are given the pretest; the other half receive the posttest only. That is, the same experiment is conducted with and without the pretest. Mortality effects can be assessed in the pretest conditions. Also, the researcher can examine whether there is an interaction between the independent variable and the pretest: Are posttest scores on the dependent variable different depending on whether the pretest was given? Sometimes, researchers find that it is not feasible to conduct the study with all four groups in a single experiment. In this case, the first study can include the pretest; the study can be replicated later without the pretest.

Generalizing from Laboratory Settings

Research conducted in a laboratory setting has the advantage of allowing the experimenter to study the impact of independent variables under highly controlled conditions. The internal validity of the research is the primary consideration. The question arises, however, as to whether the artificiality of the laboratory setting limits the ability to generalize what is observed in the laboratory to real-life settings.

Mook (1983) articulated one response to the artificiality issue: Generalization to real-life settings is not relevant when the purpose of the study was to investigate causal relationships under carefully controlled conditions. Mook is concerned that a “knee-jerk” criticism of laboratory research on the basis of external validity is too common. Good research is what is most important.

Another response to the laboratory artificiality criticism is to examine the results of field experiments. Recall from  Chapter 4  that in a field experiment, the researcher manipulates the independent variable in a natural setting—a factory, a school, or a street corner, for example.

Anderson, Lindsay, and Bushman (1999) asked whether laboratory and field experiments that examine the same variables do in fact produce the same results. To answer this question, they found 38 pairs of studies for which a laboratory investigation had a field experiment counterpart. The studies were drawn from a variety of research areas including aggression, helping, memory, leadership style, and depression. Results of the laboratory and field experiments were in fact very similar—the effect size of the independent variable on the dependent variable was very similar in the two types of studies. Thus, even though lab and field experiments are conducted in different settings, the results Page 299are complementary rather than contradictory. When findings are replicated using multiple methods, our confidence in the external validity of the findings increases.

SUPPORTING GOOD EXTERNAL VALIDITY

It may seem as if no research can possibly be generalizable! In some ways, this is true. Furthermore, it can be very difficult to understand the extent to which a study is generalizable; external validity is an aspect of a study that we try to assess, but cannot truly know. How, then, can we support good external validity? There are a few ways that external validity can be supported.

The key way that external validity can be supported is related to a study’s methodology. Using a census, or a random sample will always produce better external validity than using a nonrandom sample. This, of course, is not always possible. Next, we will explore a few other ways in which external validity can be supported.

Generalization as a Statistical Interaction

The problem of generalization can be thought of as an interaction in a factorial design (see  Chapter 10 ). An interaction occurs when a relationship between variables exists under one condition but not another or when the nature of the relationship is different in one condition than in another. Thus, if you question the generalizability of a study that used only males, you are suggesting that there is an interaction between gender and the independent variable. Suppose, for example, that a study examines the relationship between crowding and aggression among males and reports that crowding is associated with higher levels of aggression. You might then question whether the results are generalizable to females.

Figure 14.1  shows four potential outcomes of a hypothetical study on crowding and aggression that tested both males and females. In each graph, the relationship between crowding and aggression for males has been maintained. In Graph A, there is no interaction—the behavior of males and females is virtually identical. Thus, the results of the original all-male study could be generalized to females. In Graph B, there is also no interaction; the effect of crowding is identical for males and females. However, in this graph, males are more aggressive than females. Although such a difference is interesting, it is not a factor in generalization because the overall relationship between crowding and aggression is present for both males and females.

Graphs C and D do show interactions. In both, the original results with males cannot be generalized to females. In Graph C, there is no relationship between crowding and aggression for females. In Graph D, the interaction tells us that a positive relationship between crowding and aggression exists for males but that a negative relationship exists for females. As it turns out, Graph D describes the results of several studies on this topic (cf. Freedman, Levy, Buchanan, & Price, 1972).

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FIGURE 14.1

Outcomes of a hypothetical experiment on crowding and aggression

Note: The presence of an interaction indicates that the results for males cannot be generalized to females.

Researchers can address issues of external validity that stem from the use of different populations by including subject type as a variable in the study. By including variables such as gender, age, or ethnic group in the design of the study, the results may be analyzed to determine whether there are interaction effects like the ones illustrated in  Figure 14.1 .

The Importance of Replications

Replication of research is a way of overcoming any problems of generalization that occur in a single study. There are two types of replications to consider: exact replications and conceptual replications.

Exact replications An exact replication is an attempt to replicate precisely the procedures of a study to see whether the same results are obtained. A researcher who obtains an unexpected finding will frequently attempt Page 301a replication to make sure that the finding is reliable. If you are starting your own work on a problem, you may try to replicate a crucial study to make sure that you understand the procedures and can obtain the same results. Often, exact replications occur when a researcher builds on the findings of a prior study. For example, suppose you are intrigued by Singh et al.’s (2010) research on waist-to-hip ratio that was mentioned previously. Singh reports that males rate females with a ratio of .70 as most attractive. In your research, you might replicate the procedures used in the original study and expand on the original research. For example, you might study this phenomenon with males similar to those in the original sample as well as males from different cultures or age groups. When you replicate the original research findings using very similar procedures, your confidence in the external validity of the original findings is increased.

The “Mozart effect” provides us with an interesting example of the importance of replications. In the original study by Rauscher, Shaw, and Ky (1993), college students listened to 10 minutes of a Mozart sonata. These students then showed better performance on a spatial-reasoning measure drawn from the Stanford-Binet Intelligence Scale than students exposed to a relaxation tape or simple silence. This finding received a great deal of attention in the press as people quickly generalized it to the possibility of increasing children’s intelligence with Mozart sonatas. In fact, one state governor began producing Mozart CDs to distribute in maternity wards, and entrepreneurs began selling Mozart kits to parents over the Internet. Over the next few years, however, there were many failures to replicate the Mozart effect (see Steele, Bass, & Crook, 1999). We noted above that failures to replicate may occur because the exact conditions for producing the effect were not used. In this case, Rauscher and Shaw (1998) responded to the many replication failures by precisely describing the conditions necessary to produce the Mozart effect. However, Steele et al. (1999) and McCutcheon (2000) were unable to obtain the effect even though they followed the recommendations of Rauscher and Shaw. Research on the Mozart effect continues. Some recent findings suggest that the effect is limited to music that also increases arousal; it is this arousal that can cause better performance following exposure to the music (Thompson, Schellenberg, & Husain, 2001). Bangerter and Heath (2004) present a detailed analysis of the development of the research on the Mozart effect.

A single failure to replicate does not reveal much, though; it is unrealistic to assume, on the basis of a single failure to replicate, that the previous research is necessarily invalid. Failures to replicate share the same problems as nonsignificant results, discussed in  Chapter 13 . A failure to replicate could mean that the original results are invalid, but it could also mean that the replication attempt was flawed. For example, if the replication is based on the procedure as reported in a journal article, it is possible that the article omitted an important aspect of the procedure. For this reason, it is usually a good idea to write to the researcher to obtain detailed information on all of the materials that were used in the study.

Page 302Several scientific societies are encouraging systematic replications of important scientific findings. The journal Perspectives on Psychological Science (published by the Association for Psychological Science) is sponsoring the publication of Registered Research Replications ( http://www.psychologicalscience.org/index.php/replication ). Multiple groups of researchers will undertake replications of important studies using procedures that are made public before initiating the research. When completed, all of the replications will be described in a single report. In addition to the Psychological Science initiative, the online journal PLOS ONE (Public Library of Science) has developed the Reproducibility Initiative to encourage independent replication of research in the clinical sciences (Pattinson, 2012). Such developments should lead to greater understanding of the generalizability of research findings.

Conceptual replications A conceptual replication is the use of different procedures to replicate a research finding. In a conceptual replication, researchers attempt to understand the relationships among abstract conceptual variables by using new, or different, operational definitions of those variables. Conceptual replications are even more important than exact replications in furthering our understanding of behavior.

In most research, a key goal is to discover whether a relationship between conceptual variables exists. In the original Mozart effect study, researchers examined the effect of exposure to classical music on spatial reasoning. These are conceptual variables; in the actual study, specific operational definitions of the variables were used. Exposure to classical music was operationalized as 10 minutes of exposure to the Mozart Sonata for Two Pianos in D Major. Spatial reasoning was operationalized as performance on a particular spatial reasoning measure.

In a conceptual replication, the same independent variable is operationalized in a different way, and the dependent variable may be measured in a different way, too. Conceptual replications are extremely important in the social sciences because the variables used are complex and can be operationalized in different ways. Complete understanding of any variable involves studying the variable using a variety of operational definitions. A crucial generalization question is whether the relationship holds when other ways of manipulating or measuring the variables are studied. Sometimes the conceptual replication may involve an alternative stimulus (e.g., a different Mozart sonata, a selection by a different composer) or an alternative dependent measure (e.g., a different spatial-reasoning task). Or as we previously noted, the same variables are sometimes studied in both laboratory and field settings. When conceptual replications produce similar results, our confidence in the generalizability of relationships between variables is greatly increased.

This discussion should also alert you to an important way of thinking about research findings. The findings represent relationships between conceptual variables but are grounded in specific operations. You may read about the specific methods employed in a study conducted 20 years ago and question Page 303whether the study could be replicated today. You might also speculate that the methods used in a study are so unusual that they could never generalize to other situations. These concerns are not as serious when placed within the context of conceptual replications because, although operational definitions can change over time, the underlying conceptual variable often remains more consistent. Admittedly, a specific method from a study conducted at one time might not be effective today, given changes in today’s political and cultural climate. A conceptual replication of the manipulation, however, would demonstrate that the relationship between the conceptual theoretical variables is still present. Similarly, the narrow focus of a particular study is less problematic if the general finding is replicated with different procedures.

Evaluating Generalizations via Literature Reviews and Meta-analyses

Researchers have traditionally drawn conclusions about the external validity of research findings by conducting literature reviews. In a literature review, a reviewer reads a number of studies that address a particular topic and then writes a paper that summarizes and evaluates the literature. The Publication Manual of the American Psychological Association provides the following description: “Literature reviews, including research syntheses and meta-analyses, are critical evaluations of material that has already been published.… By organizing, integrating, and evaluating previously published material, authors of literature reviews consider the progress of research toward clarifying a problem” (APA, 2010, p. 10). The literature review provides information that (1) summarizes what has been found, (2) tells the reader which findings are strongly supported and which are only weakly supported in the literature, (3) points out inconsistent findings and areas in which research is lacking, and (4) discusses future directions for research.

Sometimes a review will be a narrative in which the author provides descriptions of research findings and draws conclusions about the literature. The conclusions in a narrative literature review are based on the subjective impressions of the reviewer. Another technique for comparing a large number of studies in an area is meta-analysis (Borenstein, Hedges, Higgins, & Rothstein, 2009). In a meta-analysis, the researcher combines the actual results of a number of studies. The analysis consists of a set of statistical procedures that employ effect sizes to compare a given finding across many different studies. Instead of relying on judgments obtained in a narrative literature review, you can draw statistical conclusions from this material. The statistical procedures need not concern you. They involve examining several features of the results of studies, including the effect sizes and significance levels obtained. The important point here is that meta-analysis is a method for determining the reliability of a finding by examining the results from many different studies.

Stewart and Chambless (2009) conducted a meta-analysis of research on the effectiveness of cognitive-behavioral therapy (CBT) for anxiety disorders. Page 304Both a traditional literature review and a meta-analysis begin with a body of previous research on a topic; in this case, Stewart and Chambless located 56 studies using CBT with adults diagnosed with an anxiety disorder (including panic disorder, social anxiety, post traumatic stress disorder, generalized anxiety disorder, and obsessive-compulsive disorder). Studies that included an additional medication treatment were excluded. The researchers performed a statistical analysis of the results of these studies and concluded that CBT was effective in treating all of the types of anxiety disorders. In a traditional literature review, it can be difficult to provide the type of general conclusion that was reached with the meta-analysis because it is necessary to integrate information from many studies with different experimental designs, disorders, and measures of anxiety.

One of the most important reasons a meta-analysis can lead to clear conclusions is that meta-analysis studies focus on effect size (recall that an effect size represents the extent to which two variables are associated, see  page 256 ). A typical table in a meta-analysis will show the effect size obtained in a number of studies along with a summary of the average effect size across the studies. More important, the analysis allows comparisons of the effect sizes in different types of studies to allow tests of hypotheses. For example, Miller and Downey (1999) analyzed the results of 71 studies that examined the relationship between weight and self-esteem.  Table 14.1  shows a few of the findings. The effect size r averaged across all studies was −.18: Heavier weight is associated with lower self-esteem. However, several variables moderate the relationship between weight and self-esteem. Thus, the effect size is larger when the weight variable is a report of self-perceived rather than actual weight, and the relationship between weight and self-esteem is somewhat larger for females than for males. Finally, the effect is greater among individuals with a high socioeconomic background.

TABLE 14.1 Some meta-analysis findings for weight and self-esteem

 

Page 305Both narrative reviews and meta-analyses provide valuable information and in fact are often complementary. A meta-analysis allows statistical, quantitative conclusions whereas a narrative review identifies trends in the literature and directions for future study—a more qualitative approach. A study by Bushman and Wells (2001) points to an interesting way in which knowledge of meta-analysis can improve the way that we interpret information for literature reviews.

The reviewers in their study were undergraduates who were provided with both titles and information about the findings of 20 studies dealing with the effect of attitude similarity on attraction. Sometimes the titles were salient with respect to the findings (“Birds of a Feather Flock Together”) and others were nonsalient (“Research Studies Who Likes Whom”). Salient titles are obviously easier to remember. When asked to draw conclusions about the findings, naive reviewers with no knowledge of meta-analysis overestimated the size of the similarity–attraction relationship when provided with salient titles. Other reviewers were given brief training in meta-analysis; these reviewers drew accurate conclusions about the actual findings. That is, they were not influenced by the article title. Thus, even without conducting a meta-analysis, a background in meta-analysis can be beneficial when reviewing research findings.

USING RESEARCH TO IMPROVE LIVES

In a presidential address to the American Psychological Association, George Miller (1969) discussed “psychology as a means of promoting human welfare” and spoke of “giving psychology away.” Miller was addressing the broadest issue of generalization, taking what we know about human behavior and allowing it to be applied by many people in all areas of everyday life. Zimbardo’s (2004) presidential address to the American Psychological Association described many ways in which Miller’s call to give psychology away is being honored. The impact of psychological research can be seen in areas such as health (programs to promote health-related behaviors related to stress, heart disease, and sexually transmitted diseases), law and criminal justice (providing data on the effects of 6- versus 12-person juries and showing how law enforcement personnel can improve the accuracy of eyewitness identification), education (providing methods for encouraging academic performance or reducing conflict among different ethnic groups), and work environments (providing workers with more control and improving the ways that people interact with computers and other machines in the workplace). In addition, psychologists are using the Internet to provide the public with information on parenting, education, mental health, and Page 306many other topics—for example, the websites of the American Psychological Association and the Association for Psychological Science ( http://www.apa.org ;  http://www.psychologicalscience.org ), national mental health resource websites ( http://www.mentalhealth.gov/  and  http://www.samhsa.gov/ ), and many individual psychologists who are sharing their expertise with the public.

We have discussed only a few of the ways that basic research has been applied to improve people’s lives. Despite all the potential problems of generalizing research findings that were highlighted in this chapter, the evidence suggests that we can generalize our findings to many aspects of our lives.

ILLUSTRATIVE ARTICLE: GENERALIZING RESULTS

Driving around in a 4,000-pound automobile is a dangerous thing. Motor vehicle accidents are among the leading preventable causes of death in the United States every year. Distraction is one of the most common causes of automobile accidents, and talking to another person is a very common distraction.

In an effort to observe the impact of conversation on driving, Drews, Pasupathi, and Strayer (2008) conducted a study using a driving simulator that tracks errors committed by drivers. The researchers varied the type of conversation. In one condition, participants had a conversation with a passenger; in another condition, participants talked on a cell phone. There was also a no conversation, control condition. As you would expect, having any conversation resulted in more driving errors. However, the number of driving errors was highest in the cell phone condition.

For this exercise, acquire and read the article:

Drews, F., Pasupathi, M., & Strayer, D. (2008). Passenger and cell phone conversations in simulated driving. Journal of Experimental Psychology: Applied, 14, 392–400. doi:10.1037/a0013119

After reading the article, consider the following:

1. Describe how well you think the sample of participants in this study generalizes to other groups of people. What about age? What about sex?

2. In this study, participants were told to have a conversation about a time when “their lives were threatened.” Do you think that the results of this study would be different if the conversation were about something else? How so? Why?

3. Do you think that the findings from this study would generalize to other cultures? Do you think that a sample of college students in Mexico, Italy, and Germany would generate similar results? Why or why not?

4. How well do you think the driving simulator generalizes to real-world driving? What would you change to improve the generalizability of the simulator?Page 307

5. Evaluate the internal validity of this study. Explain your answer.

6. Evaluate the external validity of this study. Explain your answer.

Study Terms

Conceptual replication ( p. 302 )

Exact replication ( p. 300 )

External validity ( p. 292 )

Literature review ( p. 303 )

Meta-analysis ( p. 303 )

Replication ( p. 300 )

Solomon four-group design ( p. 298 )

Review Questions

1. What is external validity?

2. Why should a researcher be concerned about generalizing to other populations?

3. How can the fact that most studies are conducted with college students, volunteers, and individuals from a limited location and culture potentially impact external validity?

4. How does the use of the Internet to recruit subjects and collect data impact external validity?

5. What is the source of the problem of generalizing to other experimenters? How can this problem be solved?

6. Why is it important to pretest a problem for generalization? Discuss the reasons why including a pretest may affect the ability to generalize results.

7. Distinguish between an exact replication and a conceptual replication. What is the value of a conceptual replication?

8. What is a meta-analysis?

Activities

1. It is easy to collect data for experiments and surveys on the Internet. Anyone in the world who is connected to the Internet can participate in an online experiment or survey. Use a search term such as “psychological research on the Internet” to find some studies that are being conducted. Page 308What issues of generalization might arise when interpreting the results of such studies? Does the computer aspect of the research make this research less generalizable than traditional research, or does the fact that people throughout the world can participate make it more generalizable? Could you empirically answer this question?

2. Use PsycINFO to find abstracts of articles that included race, ethnicity, gender, or nationality as a key variable. Consider topics such as body image, rumination, academic achievement, or identity development. What conclusions do the authors of these studies draw about generalization?

3. Find a meta-analysis published in a journal; two good sources are the Review of Educational Research and Psychological Bulletin. What conclusions were drawn from the meta-analysis? How were studies selected for the analysis? How was the concept of effect size discussed in the meta-analysis?

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Unit 3 Study Questions

Chapter 7

1. Nietzsche announces the death of God in a parable about

a. A madman holding a lantern

b. A lonely prophet walking the earth

c. Jesus

d. A desert hermit living in a cave

2. The madman’s proclamation that “God is dead” refers to the fact that

a. He has found incontrovertible proof that God never really existed in the first place

b. God has temporarily withdrawn Himself from the world, only to return at the end of time

c. People have ceased to believe in God

d. None of the above

3. The madman finds the death of God to be so terrifying because

a. All of his contemporaries are grief-stricken at the sudden disappearance of God, and do not know how to recover from this frightening piece of news

b. Without God human life is devoid of any intrinsic purpose, value, and meaning

c. Both A and B

d. None of the above

4. Shakespeare’s Macbeth says that life “is a tale told by an idiot, full of sound and fury, signifying nothing.” This would be an example of

a. Theism

b. Virtue ethics

c. Hedonism

d. Nihilism

5. “Life itself is essentially appropriation, injury, conquest of the strange and weak, suppression, severity…and at the least…exploitation.” Nietzsche here refers explicitly to

(HINT: see page 86, 89, paragraph 3!)

a. The Will to Power

b. Slave Morality

c. Judeo-Christianity

d. The German people

6. Each of the following is a characteristic of an aristocratic society EXCEPT:

(HINT: see pages 88-90!)

a. They come into being through conquest

b. Master Morality

c. They are the embodiment of will-to-power

d. They champion full equality among all members of society

7. Master morality is to slave morality as

(HINT: see pages 86-88, 90-91!)

a. nobility is to baseness

b. higher is to lower

c. affirmation of life is to negation of life

d. All of the above

8. The “good” of master morality is to the “good” of slave morality as

a. Noble is to despicable

b. Mediocrity is to excellence

c. Despicable is to noble

d. Rare is to exceptional

9. The “evil” of slave morality is to the “bad” of master morality as

a. cowardly is to heroic

b. lover is to beloved

c. self-glorification is to resentment

d. mediocrity is to excellence

10. The “good” of master morality is to the “evil” of slave morality as

a. resentment is to honor

b. hero is to coward

c. base is to noble

d. They are one and the same thing

11. According to Nietzsche, the modern liberal democratic ideal

a. encourages slavishness

b. is the only honorable value to be found in Judeo-Christianity

c. is embraced by master morality

d. is shunned by slave morality

12. Nihilism is the belief that

a. God is Good

b. Nothingness is an illusion of the mind

c. If we remain ignorant we will annihilate ourselves

d. The world is utterly meaningless

13. According to Nietzsche, the slavish individual expresses _________ for the noble types.

a. admiration

b. resentment

c. a feeling of kinship

d. affection

14. According to Nietzsche, slave morality originates from

(HINT: see page 87, 91!)

a. a feeling of superiority

b. the need for slaves to survive

c. economic inequality

d. faith in a higher power

15. According to Nietzsche, master morality originates from

a. the aristocratic man’s spontaneous self-glorification

b. resentment toward other aristocratic men

c. the need to combat low self-esteem

d. a will to the denial of life

Chapter 8

1. Ortega can best be described as

a. a nihilist

b. an elitist

c. a feminist

d. an egalitarian

2. According to Ortega, the masses have begun to insinuate themselves in each of the following areas EXCEPT:

a. politics

b. education

c. the priesthood

d. the arts

3. According to Ortega, the phenomenon of the “masses” as a concentrated group gaining power and influence in all sectors of society

a. is nothing new

b. is consistent with the rise of fascism in Spain

c. is a recent phenomenon

d. is a cause for great celebration

4. Each of the following is true about the mass man EXCEPT:

a. he is the “average” man

b. he belongs exclusively to the working class

c. he is comfortable in his mediocrity

d. he is not particularly ambitious

5. Each of the following is true about the “select individual” EXCEPT:

a. he snobbishly believes that he is simply superior to everyone else

b. he sets very high standards for himself

c. he assigns himself great tasks

d. his presence is not limited to any particular socio-economic stratum of society

6. The select individual is to the mass man

a. as higher is to lower

b. as rare is to common

c. as noble is to vulgar

d. all of the above

7. Before the advent of the “crowd phenomenon,” artistic, political, and intellectual enterprises were directed by

(HINT: see page 101, paragraph 10!)

a. anybody who wanted to take part

b. only those who were select individuals

c. only those who were qualified or at least claimed to be qualified

d. all of the above

8. According to Ortega, hyperdemocracy

a. is a threat to liberal democracy

b. is the mass man’s way of imposing itself on the rest of society

c. is the mass man’s way of stifling human excellence

d. all of the above

9. Each of the following is a characteristic of the “select individual” EXCEPT:

a. judges himself against a high standard.

b. complacency

c. qualified for intellectual, aesthetic, and political endeavors

d. runs the risk of being crushed under the weight of the mass

Chapter 9

1. Sartre’s phrase “existence precedes essence” means that

(HINT: see pages 107-108!)

a. God created man as a “blank slate” on which he can make his own essence.

b. Man created God in his own image

c. Man first has an essence, and then he confers on himself existence

d. Man exists in a godless universe, without any determinate nature or essence: he creates his own essence through his actions.

2. According to Sartre, when you choose how to live, you are choosing

(HINT: see pages 108-110!)

a. for your loved ones

b. for all mankind

c. for nobody but oneself

d. none of the above

3. In Sartre’s view, the existentialist finds the fact that God does not exist

(HINT: see pages 110-111!)

a. deeply distressing

b. liberating

c. insignificant

d. absurd to the point of being comical

4. Sartre argues that when he speaks of anguish, he is referring to

a. the feeling of having been abandoned by God

b. the fact that we are not responsible for our actions

c. man’s feeling of total and deep responsibility for all mankind

d. all of the above

5. According to Sartre, each human being is the sum total of his/her

a. hopes

b. actions

c. beliefs

d. ambitions

6. Sartre argues that when he speaks of forlornness, he means that

a. We are not responsible for our actions

b. We can never truly understand human nature

c. God does not exist, so we must face all of the consequences of this

d. all of the above.

7. Sartre criticizes certain atheists in the 1880s that wanted to create an atheist ethics on the grounds that

a. without God, there can be no a priori standard of good to which everyone is bound to conform.

b. there can be no salvation without embracing our Lord and Savior Jesus Christ

c. atheists are generally very immoral people

d. none of the above

8. Sartre argues that when he speaks of despair, he means that

(HINT: see pages 112-113!)

a. when one chooses, one chooses for oneself only

b. one should reckon only with what depends on our will

c. life is a tale told by an idiot

d. all of the above

9. According to Sartre, the value of one’s feeling is determined by

(HINT: see page 111!)

a. the way one feels

b. what one believes

c. the way one acts

d. all of the above

10. Each of the following is true for Sartre EXCEPT:

a. You are the sum total of your hopes and dreams

b. Responsibility for one’s actions involves being responsible for everyone

c. Man’s situation is characterized by anguish, forlornness, and despair

d. We are “condemned to be free”

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05994 Topic: Discussion 2

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1. Meeting and diagnosing the guests of an imagined party (10 points) chapters 9-12

July 2, 2025/in Psychology Questions /by Besttutor

Meet and Diagnose:

2. The invitation contains a description and picture of each guest.

3. Each guest has some type of personality disorder (must be a personality disorder). 

4. Read over the descriptions carefully as your task is to try and diagnose each guest. chapters 9-12

5. After reading the material, SEE ATTACHED WORD DOC called “party guest diagnosis.”

6. Fill out your diagnosis sheet and submit the completed form

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Hunger, Eating, and Health Why Do Many People Eat Too Much?

12.1 Digestion, Energy Storage, and Energy Utilization

12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives

12.3 Factors That Determine What, When, and How Much We Eat

12.4 Physiological Research on Hunger and Satiety

12.5 Body Weight Regulation: Set Points versus Settling Points

12.6 Human Obesity: Causes, Mechanisms, and Treatments

12.7 Anorexia and Bulimia Nervosa

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source of serious personal and health problems. Most eating-related health problems in industrialized

nations are associated with eating too much—the average American consumes 3,800 calories per day, about twice the average daily requirement (see Kopelman, 2000). For

example, it is estimated that 65% of the adult U.S. popu- lation is either overweight or clinically obese, qualifying

this problem for epidemic status (see Abelson & Kennedy, 2004; Arnold, 2009). The resulting financial and personal costs are huge. Each year in the United States, about $100 billion is spent treating obesity-related disorders (see Ol- shansky et al., 2005). Moreover, each year, an estimated 300,000 U.S. citizens die from disorders caused by their excessive eating (e.g., diabetes, hypertension, cardiovas- cular diseases, and some cancers). Although the United States is the trend-setter when it comes to overeating and obesity, many other countries are not far behind (Sofsian, 2007). Ironically, as overeating and obesity have reached epidemic proportions, there has been a related increase in disorders associated with eating too little (see Polivy & Herman, 2002). For example, almost 3% of American adolescents currently suffer from anorexia or bulimia, which can be life-threatening in extreme cases.

The massive increases in obesity and other eating- related disorders that have occurred over the last few decades in many countries stand in direct opposition to most people’s thinking about hunger and eating. Many people—and I assume that this includes you—believe that hunger and eating are normally triggered when the

body’s energy resources fall below a prescribed optimal level, or set point. They ap- preciate that many factors in-

fluence hunger and eating, but they assume that the hunger and eating system has evolved to supply the body with just the right amount of energy.

This chapter explores the incompatibility of the set- point assumption with the current epidemic of eating disorders. If we all have hunger and eating systems

whose primary function is to maintain energy resources at optimal levels, then eating disorders should be rare. The fact that they are so prevalent suggests that hunger and eating are regulated in some other way. This chapter will repeatedly challenge you to think in new ways about issues that impact your health and longevity and will provide new insights of great personal relevance—I guarantee it.

Before you move on to the body of the chapter, I would like you to pause to consider a case study. What would a severely amnesic patient do if offered a meal

shortly after finishing one? If his hunger and eating were controlled by energy set points, he would refuse the sec- ond meal. Did he?

The Case of the Man Who Forgot Not to Eat

R.H. was a 48-year-old male whose progress in graduate school was interrupted by the development of severe am- nesia for long-term explicit memory. His amnesia was similar in pattern and severity to that of H.M., whom you met in Chapter 11, and an MRI examination revealed bilateral damage to the medial temporal lobes.

The meals offered to R.H. were selected on the basis of interviews with him about the foods he liked: veal parmi- giana (about 750 calories) plus all the apple juice he wanted. On one occasion, he was offered a second meal about 15 minutes after he had eaten the first, and he ate it. When offered a third meal 15 minutes later, he ate that, too. When offered a fourth meal he rejected it, claiming that his “stomach was a little tight.”

Then, a few minutes later, R.H. announced that he was going out for a good walk and a meal. When asked what he was going to eat, his answer was “veal parmigiana.”

Clearly, R.H.’s hunger (i.e., motivation to eat) did not result from an energy deficit (Rozin et al., 1998). Other cases like that of R.H. have been reported by Higgs and colleagues (2008).

12.1 Digestion, Energy Storage, and Energy Utilization

The primary purpose of hunger is to increase the proba- bility of eating, and the primary purpose of eating is to supply the body with the molecular building blocks and energy it needs to survive and function (see Blackburn, 2001). This section provides the foundation for our con- sideration of hunger and eating by providing a brief overview of the processes by which food is digested, stored, and converted to energy.

Digestion The gastrointestinal tract and the process of digestion are illustrated in Figure 12.1 on page 300. Digestion is the gastrointestinal process of breaking down food and ab- sorbing its constituents into the body. In order to appre- ciate the basics of digestion, it is useful to consider the body without its protuberances, as a simple living tube

29912.1 ■ Digestion, Energy Storage, and Energy Utilization

Thinking CreativelyThinking Creatively

Clinical Clinical Implications Implications

Eating is a behavior that is of interest to virtuallyeveryone. We all do it, and most of us derive greatpleasure from it. But for many of us, it becomes a

Watch You Are What You Eat www.mypsychlab.com

Watch Thinking about Hunger www.mypsychlab.com

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(a simple sugar that is the breakdown product of complex carbohydrates, that is, starches and sugars).

The body uses energy continuously, but its consump- tion is intermittent; therefore, it must store energy for use in the intervals between meals. Energy is stored in three forms: fats, glycogen, and proteins. Most of the body’s energy reserves are stored as fats, relatively little as glycogen and proteins (see Figure 12.2). Thus, changes in the body weights of adult humans are largely a conse- quence of changes in the amount of their stored body fat.

Why is fat the body’s preferred way of storing energy? Glycogen, which is largely stored in the liver and muscles, might be expected to be the body’s preferred mode of energy storage because it is so readily converted to glucose—the body’s main directly utilizable source of energy. But there

300 Chapter 12 ■ Hunger, Eating, and Health

Chewing breaks up food and mixes it with saliva.1 Saliva lubricates food and begins its digestion.2 Swallowing moves food and drink down the esophagus to the stomach.3 The primary function of the stomach is to serve as a storage reservoir. The

hydrochloric acid in the stomach breaks food down into small particles, and pepsin begins the process of breaking down protein molecules to amino acids.

4

The stomach gradually empties its contents through the pyloric sphincter into the

duodenum, the upper portion of the intestine, where most of the absorption takes place.

5

Digestive enzymes in the duodenum, many of them from the gall bladder and pancreas,

break down protein molecules to amino acids, and starch and complex sugar molecules to simple sugars. Simple sugars and amino acids readily pass through the duodenum wall into the bloodstream and are carried to the liver.

6

Fats are emulsified (broken into droplets) by bile, which is manufactured in the liver and

stored in the gall bladder until it is released into the duodenum. Emulsified fat cannot pass through the duodenum wall and is carried by small ducts in the duodenum wall into the lymphatic system.

7

Most of the remaining water and electrolytes are absorbed from the waste in

the large intestine, and the remainder is ejected from the anus.

8

Steps in Digestion

Parotid gland

Salivary glands

Esophagus

Liver

Stomach

Gall bladder

Pyloric sphincter

Pancreas

Duodenum

Large intestine or colon

Small intestine

Anus

with a hole at each end. To supply itself with energy and other nutrients, the tube puts food into one of its two holes—the one with teeth—and passes the food along its internal canal so that the food can be broken down and partially absorbed from the canal into the body. The leftovers are jettisoned from the other end. Although this is not a particularly appetizing description of eating, it does serve to illustrate that, strictly speaking, food has not been consumed until it has been digested.

Energy Storage in the Body As a consequence of digestion, energy is delivered to the body in three forms: (1) lipids (fats), (2) amino acids (the breakdown products of proteins), and (3) glucose

FIGURE 12.1 The gastrointestinal tract and the process of digestion.

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are two reasons why fat, rather than glycogen, is the pri- mary mode of energy storage: One is that a gram of fat can store almost twice as much energy as a gram of glyco- gen; the other is that glycogen, unlike fat, attracts and holds substantial quantities of water. Consequently, if all your fat calories were stored as glycogen, you would likely weigh well over 275 kilograms (600 pounds).

Three Phases of Energy Metabolism There are three phases of energy metabolism (the chem- ical changes by which energy is made available for an

organism’s use): the cephalic phase, the absorptive phase, and the fasting phase. The cephalic phase is the preparatory phase; it often begins with the sight, smell, or even just the thought of food, and it ends when the food starts to be absorbed into the bloodstream. The absorptive phase is the period during which the energy absorbed into the bloodstream from the meal is meet- ing the body’s immediate energy needs. The fasting phase is the period during which all of the unstored en- ergy from the previous meal has been used and the body is withdrawing energy from its reserves to meet its immediate energy requirements; it ends with the begin- ning of the next cephalic phase. During periods of rapid weight gain, people often go directly from one absorp- tive phase into the next cephalic phase, without experi- encing an intervening fasting phase.

The flow of energy during the three phases of energy metabolism is controlled by two pancreatic hormones: insulin and glucagon. During the cephalic and absorptive phases, the pancreas releases a great deal of insulin into the bloodstream and very little glucagon. Insulin does three things: (1) It promotes the use of glucose as the pri- mary source of energy by the body. (2) It promotes the conversion of bloodborne fuels to forms that can be stored: glucose to glycogen and fat, and amino acids to proteins. (3) It promotes the storage of glycogen in liver and muscle, fat in adipose tissue, and proteins in muscle. In short, the function of insulin during the cephalic phase is to lower the levels of bloodborne fuels, primarily glucose, in anticipation of the impending influx; and its function during the absorptive phase is to minimize the increasing levels of bloodborne fuels by utilizing and storing them.

In contrast to the cephalic and absorptive phases, the fasting phase is characterized by high blood levels of glucagon and low levels of insulin. Without high levels of insulin, glucose has difficulty entering most body cells; thus, glucose stops being the body’s primary fuel. In effect, this saves the body’s glucose for the brain, because insulin is not required for glucose to enter most brain cells. The low levels of insulin also promote the conversion of glycogen and protein to glucose. (The conversion of protein to glucose is called gluconeogenesis.)

On the other hand, the high levels of fasting-phase glucagon promote the release of free fatty acids from adi- pose tissue and their use as the body’s primary fuel. The high glucagon levels also stimulate the conversion of free fatty acids to ketones, which are used by muscles as a source of energy during the fasting phase. After a pro- longed period without food, however, the brain also starts to use ketones, thus further conserving the body’s re- sources of glucose.

Figure 12.3 summarizes the major metabolic events as- sociated with the three phases of energy metabolism.

30112.1 ■ Digestion, Energy Storage, and Energy Utilization

Fat in adipose tissue (85%)

Protein in muscle (14.5%)

Glycogen in muscle and liver (0.5%)

FIGURE 12.2 Distribution of stored energy in an average person.

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12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives

One of the main difficulties I have in teaching the funda- mentals of hunger, eating, and body weight regulation is the set-point assumption. Although it dominates most people’s thinking about hunger and eating (Assanand, Pinel, & Lehman, 1998a, 1998b), whether they realize it or not, it is inconsistent with the bulk of the evidence. What exactly is the set-point assumption?

Set-Point Assumption Most people attribute hunger (the motivation to eat) to the presence of an energy deficit, and they view eating as the means by which the energy resources of the body are returned to their optimal level—that is, to the energy set point. Figure 12.4 summarizes this set-point assumption. After a meal (a bout of eating), a person’s energy resources are assumed to be near their set point and to decline there- after as the body uses energy to fuel its physiological processes. When the level of the body’s energy resources falls far enough below the set point, a person becomes motivated by hunger to initiate another meal. The meal continues, ac- cording to the set-point assumption, until the energy level

302 Chapter 12 ■ Hunger, Eating, and Health

Cephalic Phase Preparatory phase, which is initiated by the sight, smell, or expectation of food

Absorptive Phase Nutrients from a meal meeting the body’s immediate energy requirements, with the excess being stored

Fasting Phase Energy being withdrawn from stores to meet the body’s immediate needs

Promotes • Utilization of blood glucose as a source

of energy • Conversion of excess glucose to

glycogen and fat • Conversion of amino acids to proteins • Storage of glycogen in liver and muscle,

fat in adipose tissue, and protein in muscle

Inhibits • Conversion of glycogen, fat, and protein

into directly utilizable fuels (glucose, free fatty acids, and ketones)

Promotes • Conversion of fats to free fatty acids

and the utilization of free fatty acids as a source of energy

• Conversion of glycogen to glucose, free fatty acids to ketones, and protein to glucose

Inhibits • Utilization of glucose by the body but

not by the brain • Conversion of glucose to glycogen and

fat, and amino acids to protein • Storage of fat in adipose tissue

Glucagon levels low

Insulin levels high

Glucagon levels high

Insulin levels low

FIGURE 12.3 The major events associated with the three phases of energy metabolism: the cephalic, absorptive, and fasting phases.

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returns to its set point and the person feels satiated (no longer hungry).

Set-point models assume that hunger and eating work in much the same way as a thermostat- regulated heating system in a cool climate. The heater increases the house temperature until it reaches its set point (the thermo- stat setting). The heater then shuts off, and the temperature of the house gradually de- clines until it becomes low enough to turn the heater back on. All set-point systems have three components: a set- point mechanism, a detector mechanism, and an effector mechanism. The set-point mechanism defines the set point, the detector mechanism detects deviations from the set point, and the effector mechanism acts to eliminate the deviations. For example, the set-point, detector, and ef- fector mechanisms of a heating system are the thermo- stat, the thermometer, and the heater, respectively.

All set-point systems are negative feedback systems— systems in which feedback from changes in one direction elicit compensatory effects in the opposite direction. Negative feedback systems are common in mammals be- cause they act to maintain homeostasis—a stable internal environment—which is critical for mammals’ survival (see Wenning, 1999). Set-point systems combine negative feedback with a set point to keep an internal environment fixed at the prescribed point. Set-point systems seemed necessary when the adult human brain was assumed to be immutable: Because the brain couldn’t change, energy re- sources had to be highly regulated. However, we now know that the adult human brain is plastic and capable of considerable adaptation. Thus, there is no longer a logical imperative for the set-point regulation of eating. Through- out this chapter, you will need to put aside your precon- ceptions and base your thinking about hunger and eating entirely on the empirical evidence.

Glucostatic and Lipostatic Set-Point Theories of Hunger and Eating In the 1940s and 1950s, researchers working under the as- sumption that eating is regulated by some type of set- point system speculated about the nature of the regulation. Several researchers suggested that eating is

regulated by a system that is designed to maintain a blood glucose set point—the idea being that we become hungry when our blood glucose levels drop significantly below their set point and that we become satiated when eating returns our blood glucose levels to their set point. The various versions of this theory are collectively referred to as the glucostatic theory. It seemed to make good sense that the main purpose of eating is to defend a blood glu- cose set point, because glucose is the brain’s primary fuel.

The lipostatic theory is another set-point theory that was proposed in various forms in the 1940s and 1950s. According to this theory, every person has a set point for body fat, and deviations from this set point produce com- pensatory adjustments in the level of eating that return levels of body fat to their set point. The most frequently cited support for the theory is the fact that the body weights of adults stay relatively constant.

The glucostatic and lipostatic theories were viewed as complementary, not mutually exclusive. The glucostatic theory was thought to account for meal initiation and ter- mination, whereas the lipostatic theory was thought to account for long-term regulation. Thus, the dominant view in the 1950s was that eating is regulated by the inter- action between two set-point systems: a short-term glu- costatic system and a long-term lipostatic system. The simplicity of these 1950s theories is appealing. Remark- ably, they are still being presented as the latest word in some textbooks; perhaps you have encountered them.

Problems with Set-Point Theories of Hunger and Eating Set-point theories of hunger and eating have several seri- ous weaknesses (see de Castro & Plunkett, 2002). You have already learned one fact that undermines these the- ories: There is an epidemic of obesity and overweight,

30312.2 ■ Theories of Hunger and Eating: Set Points versus Positive Incentives

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which should not occur if eating is regulated by a set point. Let’s look at three more major weaknesses of set-

point theories of hunger and eating.

● First, set-point theories of hunger and eating are in- consistent with basic eating-related evolutionary pressures as we understand them. The major eating- related problem faced by our ancestors was the incon-

sistency and unpredictability of the food supply. Thus, in order to survive, it was im- portant for them to eat large quantities of

good food when it was available so that calories could be banked in the form of body fat. Any ancestor— human or otherwise—that stopped feeling hungry as soon as immediate energy needs were met would not have survived the first hard winter or prolonged drought. For any warm-blooded species to survive under natural conditions, it needs a hunger and eating system that prevents energy deficits, rather than one that merely responds to them once they have devel- oped. From this perspective, it is difficult to imagine how a set-point hunger and feeding system could have evolved in mammals (see Pinel, Assanand, & Lehman, 2000).

● Second, major predictions of the set-point theories of hunger and eating have not been confirmed. Early studies seemed to support the set-point theories by showing that large reductions in body fat, produced by starvation, or large reductions in blood glucose, pro- duced by insulin injections, induce increases in eating in laboratory animals. The problem is that reductions in blood glucose of the magnitude needed to reliably induce eating rarely occur naturally. Indeed, as you have already learned in this chapter, about 65% of U.S. adults have a significant excess of fat deposits when they begin a meal. Conversely, efforts to reduce meal size by having subjects consume a high-calorie drink before eating have been largely unsuccessful; indeed, beliefs about the caloric content of a premeal drink often influence the size of a subsequent meal more than does its actual caloric content (see Lowe, 1993).

● Third, set-point theories of hunger and eating are de- ficient because they fail to recognize the major influ- ences on hunger and eating of such important factors as taste, learning, and social influences. To convince yourself of the importance of these factors, pause for a minute and imagine the sight, smell, and taste of your favorite food. Perhaps it is a succulent morsel of lobster meat covered with melted garlic butter, a piece of chocolate cheesecake, or a plate of sizzling home- made french fries. Are you starting to feel a bit hun- gry? If the homemade french fries—my personal weakness—were sitting in front of you right now, wouldn’t you reach out and have one, or maybe the whole plateful? Have you not on occasion felt discomfort

after a large main course, only to polish off a substan- tial dessert? The usual positive answers to these ques- tions lead unavoidably to the conclusion that hunger and eating are not rigidly controlled by deviations from energy set points.

Positive-Incentive Perspective The inability of set-point theories to account for the basic phenomena of eating and hunger led to the development of an alternative theoretical perspective (see Berridge, 2004). The central assertion of this perspective, com- monly referred to as positive-incentive theory, is that humans and other animals are not normally driven to eat by internal energy deficits but are drawn to eat by the an- ticipated pleasure of eating—the anticipated pleasure of a behavior is called its positive-incentive value (see Bolles, 1980; Booth, 1981; Collier, 1980; Rolls, 1981; Toates, 1981). There are several different positive-incentive theo- ries, and I refer generally to all of them as the positive- incentive perspective.

The major tenet of the positive-incentive perspective on eating is that eating is controlled in much the same way as sexual behavior: We engage in sexual behavior not because we have an internal deficit, but because we have evolved to crave it. The evolutionary pressures of unexpected food shortages have shaped us and all other warm-blooded an- imals, who need a continuous supply of energy to main- tain their body temperatures, to take advantage of good food when it is present and eat it. According to the positive- incentive perspective, it is the presence of good food, or the anticipation of it, that normally makes us hungry, not an energy deficit.

According to the positive-incentive perspective, the de- gree of hunger you feel at any particular time depends on the interaction of all the factors that influence the positive- incentive value of eating (see Palmiter, 2007). These in- clude the following: the flavor of the food you are likely to consume, what you have learned about the effects of this food either from eating it previously or from other peo- ple, the amount of time since you last ate, the type and quantity of food in your gut, whether or not other people are present and eating, whether or not your blood glucose levels are within the normal range. This partial list illus- trates one strength of the positive-incentive perspective. Unlike set-point theories, positive-incentive theories do not single out one factor as the major determinant of hunger and ignore the others. Instead, they acknowledge that many factors interact to determine a person’s hunger at any time, and they suggest that this interaction occurs through the influence of these various factors on the positive-incentive value of eating (see Cabanac, 1971).

In this section, you learned that most people think about hunger and eating in terms of energy set points and

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were introduced to an alternative way of thinking—the positive-incentive perspective. Which way is correct? If you are like most people, you have an attachment to familiar ways of thinking and a resistance to new ones. Try to put this tendency aside and base your views about this impor- tant issue entirely on the evidence.

You have already learned about some of the major weaknesses of strict set-point theories of hunger and eat- ing. The next section describes some of the things that biopsychological research has taught us about hunger and eating. As you progress through the section, notice the su- periority of the positive-incentive theories over set-point theories in accounting for the basic facts.

12.3 Factors That Determine What, When, and How Much We Eat

This section describes major factors that commonly deter- mine what we eat, when we eat, and how much we eat. No- tice that energy deficits are not included among these factors. Although major energy deficits clearly increase hunger and eating, they are not a common factor in the eating behavior of people like us, who live in food-replete societies. Although you may believe that your body is short of energy just before a meal, it is not. This miscon- ception is one that is addressed in this section. Also, notice how research on nonhumans has played an important role in furthering understanding of human eating.

Factors That Determine What We Eat Certain tastes have a high positive-incentive value for vir- tually all members of a species. For example, most hu- mans have a special fondness for sweet, fatty, and salty tastes. This species-typical pattern of human taste prefer- ences is adaptive because in nature sweet and fatty tastes

are typically characteristic of high-energy foods that are rich in vitamins and miner- als, and salty tastes are characteristic of

sodium-rich foods. In contrast, bitter tastes, for which most humans have an aversion, are often associated with toxins. Superimposed on our species-typical taste prefer- ences and aversions, each of us has the ability to learn specific taste preferences and aversions (see Rozin & Shulkin, 1990).

Learned Taste Preferences and Aversions Animals learn to prefer tastes that are followed by an infusion of calories, and they learn to avoid tastes that are followed by illness (e.g., Baker & Booth, 1989; Lucas & Sclafani, 1989; Sclafani, 1990). In addition, humans and other animals learn what to eat from their conspecifics. For example,

rats learn to prefer flavors that they experience in mother’s milk and those that they smell on the breath of other rats (see Galef, 1995, 1996; Galef, Whishkin, & Bielavska, 1997). Similarly, in humans, many food prefer- ences are culturally specific—for example, in some cul- tures, various nontoxic insects are considered to be a delicacy. Galef and Wright (1995) have shown that rats reared in groups, rather than in isolation, are more likely to learn to eat a healthy diet.

Learning to Eat Vitamins and Minerals How do an- imals select a diet that provides all of the vitamins and minerals they need? To answer this question, researchers have studied how dietary deficiencies influence diet selec- tion. Two patterns of results have emerged: one for sodium and one for the other essential vitamins and min- erals. When an animal is deficient in sodium, it develops an immediate and compelling preference for the taste of sodium salt (see Rowland, 1990). In contrast, an animal that is deficient in some vitamin or mineral other than sodium must learn to consume foods that are rich in the missing nutrient by experiencing their positive effects; this is because vitamins and minerals other than sodium normally have no detectable taste in food. For example, rats maintained on a diet deficient in thiamine (vitamin B1) develop an aversion to the taste of that diet; and if they are offered two new diets, one deficient in thiamine and one rich in thiamine, they often develop a preference for the taste of the thiamine-rich diet over the ensuing days, as it becomes associated with improved health.

If we, like rats, are capable of learning to select diets that are rich in the vitamins and minerals we need, why are dietary deficiencies so prevalent in our society? One reason is that, in order to maximize profits, manufacturers produce foods that have the tastes we prefer but lack many of the nutrients we need to maintain our health. (Even rats prefer chocolate chip cookies to nutritionally complete rat chow.) The second reason is illustrated by the classic study of Harris and associates (1933). When thiamine-deficient rats were offered two new diets, one with thiamine and one without, almost all of them learned to eat the complete diet and avoid the deficient one. However, when they were offered ten new diets, only one of which contained the badly needed thiamine, few developed a preference for the complete diet. The number of different substances, both nutritious and not, con- sumed each day by most people in industrialized societies is immense, and this makes it difficult, if not impossible, for their bodies to learn which foods are beneficial and which are not.

There is not much about nutrition in this chapter: Although it is critically important to eat a nutritious diet, nutrition seems to have little direct effect on our feelings of hunger. However, while I am on the topic, I would like to direct you to a good source of information

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about nutrition that could have a positive effect on your health: Some popular books on nutrition are dan-

gerous, and even governments, inordinately influenced by economic considerations and special-interest groups, often do not provide the best nutritional advice (see Nestle, 2003). For sound research-based advice on nutrition, check out an article by Willett and Stampfer (2003) and the book on which it is based, Eat, Drink, and Be Healthy by Willett, Skerrett, and Giovannucci (2001).

Factors That Influence When We Eat Collier and his colleagues (see Collier, 1986) found that most mammals choose to eat many small meals (snacks)

each day if they have ready access to a continuous supply of food. Only when there are physical costs involved in initiat-

ing meals—for example, having to travel a considerable distance—does an animal opt for a few large meals.

The number of times humans eat each day is influ- enced by cultural norms, work schedules, family routines, personal preferences, wealth, and a variety of other fac- tors. However, in contrast to the usual mammalian pref- erence, most people, particularly those living in family groups, tend to eat a few large meals each day at regular times. Interestingly, each person’s regular mealtimes are the very same times at which that person is likely to feel most hungry; in fact, many people experience attacks of malaise (headache, nausea, and an inability to concen- trate) when they miss a regularly scheduled meal.

Premeal Hunger I am sure that you have experienced attacks of premeal hunger. Subjectively, they seem to pro- vide compelling support for set-point theories. Your body seems to be crying out: “I need more energy. I cannot function without it. Please feed me.” But things are not al- ways the way they seem. Woods has straightened out the confusion (see Woods, 1991; Woods & Ramsay, 2000; Woods & Strubbe, 1994).

According to Woods, the key to understanding hunger is to appreciate that eating meals stresses the body. Before a meal, the body’s energy reserves are in reasonable homeostatic balance; then, as a meal is consumed, there is a homeostasis-disturbing influx of fuels into the bloodstream. The body does what it can to defend its homeostasis. At the first indication that a person will soon be eating—for example, when the usual mealtime approaches—the body enters the cephalic phase and takes steps to soften the impact of the impending homeostasis- disturbing influx by releasing insulin into the blood and thus reducing blood glucose. Woods’s message is that the strong, unpleasant feelings of hunger that you may expe- rience at mealtimes are not cries from your body for food; they are the sensations of your body’s preparations for the expected homeostasis-disturbing meal. Mealtime

hunger is caused by the expectation of food, not by an en- ergy deficit.

As a high school student, I ate lunch at exactly 12:05 every day and was overwhelmed by hunger as the time approached. Now, my eating schedule is different, and I never experience noontime hunger pangs; I now get hungry just before the time at which I usually eat. Have you had a similar experience?

Pavlovian Conditioning of Hunger In a classic series of Pavlovian conditioning experiments on laboratory rats, Weingarten (1983, 1984, 1985) provided strong sup- port for the view that hunger is often caused by the expec- tation of food, not by an energy deficit. During the conditioning phase of one of his experiments, Weingarten presented rats with six meals per day at irregular inter- vals, and he signaled the impending delivery of each meal with a buzzer-and-light conditional stimulus. This condi- tioning procedure was continued for 11 days. Through- out the ensuing test phase of the experiment, the food was continuously available. Despite the fact that the subjects were never deprived during the test phase, the rats started to eat each time the buzzer and light were presented— even if they had recently completed a meal.

Factors That Influence How Much We Eat The motivational state that causes us to stop eating a meal when there is food remaining is satiety. Satiety mecha- nisms play a major role in determining how much we eat.

Satiety Signals As you will learn in the next section of the chapter, food in the gut and glucose entering the blood can induce satiety signals, which inhibit subse- quent consumption. These signals depend on both the volume and the nutritive density (calories per unit vol- ume) of the food.

The effects of nutritive density have been demon- strated in studies in which laboratory rats have been maintained on a single diet. Once a stable baseline of consumption has been estab- lished, the nutritive density of the diet is changed. Some rats learn to adjust the volume of food they consume to keep their caloric intake and body weights relatively stable. However, there are major limits to this adjustment: Rats rarely increase their intake suffi- ciently to maintain their body weights if the nutritive density of their conventional laboratory feed is reduced by more than 50% or if there are major changes in the diet’s palatability.

Sham Eating The study of sham eating indicates that satiety signals from the gut or blood are not necessary to terminate a meal. In sham-eating experiments, food is chewed and swallowed by the subject; but rather than

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passing down the subject’s esophagus into the stomach, it passes out of the body through an implanted tube (see Figure 12.5).

Because sham eating adds no energy to the body, set-point theories predict that all sham-eaten meals should be huge. But this is not the case. Weingarten and Kulikovsky (1989) sham fed rats one of two differently flavored diets: one that the rats had naturally eaten many times before and one that they had never eaten before. The first sham meal of the rats that had previously eaten the diet was the same size as the previously eaten meals of that diet; then, on ensuing days they began to sham eat more and more (see Figure 12.6). In contrast, the rats that were presented with the unfamiliar diet

sham ate large quantities right from the start. Weingarten and Kulikovsky concluded that the amount we eat is in- fluenced largely by our previous experience with the par- ticular food’s physiological effects, not by the immediate effect of the food on the body.

Appetizer Effect and Satiety The next time you at- tend a dinner party, you may experience a major weak- ness of the set-point theory of satiety. If appetizers are served, you will notice that small amounts of food consumed before a meal actually in- crease hunger rather than reducing it. This is the appetizer effect. Presumably, it occurs because the con- sumption of a small amount of food is particularly effec- tive in eliciting cephalic-phase responses.

Serving Size and Satiety Many experiments have shown that the amount of consumption is influenced by serving size (Geier, Rozin, & Doros, 2006). The larger the servings, the more we tend to eat. There is even evidence that we tend to eat more when we eat with larger spoons.

Social Influences and Satiety Feelings of satiety may also depend on whether we are eating alone or with others. Redd and de Castro (1992) found that their sub- jects consumed 60% more when eating with others. Laboratory rats also eat substantially more when fed in groups.

30712.3 ■ Factors That Determine What, When, and How Much We Eat

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In humans, social factors have also been shown to reduce consumption. Many people eat less than they would like in order to achieve their society’s ideal of slenderness, and others refrain from eating large amounts in front of oth- ers so as not to appear gluttonous. Unfortunately, in our culture, females are influenced by such pressures more than males are, and, as you will learn later in the chapter, some develop serious eating disorders as a result.

Sensory-Specific Satiety The number of different tastes available at each meal has a major effect on meal size. For example, the effect of offering a laboratory rat a varied diet of highly palatable foods—a cafeteria diet—is dramatic. Adults rats that were offered bread and choco- late in addition to their usual laboratory diet increased their average intake of calories by 84%, and after 120 days they had increased their average body weights by 49% (Rogers & Blundell, 1980). The spectacular effects of cafe- teria diets on consumption and body weight clearly run counter to the idea that satiety is rigidly controlled by in- ternal energy set points.

The effect on meal size of cafeteria diets results from the fact that satiety is to a large degree sensory-specific. As you eat one food, the positive-incentive value of all foods de- clines slightly, but the positive-incentive value of that par- ticular food plummets. As a result, you soon become satiated on that food and stop eating it. However, if another food is offered to you, you will often begin eating again.

In one study of sensory-specific satiety (Rolls et al., 1981), human subjects were asked to rate the palatability of eight different foods, and then they ate a meal of one of them. After the meal, they were asked to rate the palata- bility of the eight foods once again, and it was found that their rating of the food they had just eaten had declined substantially more than had their ratings of the other seven foods. Moreover, when the subjects were offered an unexpected second meal, they consumed most of it unless it was the same as the first.

Booth (1981) asked subjects to rate the momentary pleasure produced by the flavor, the smell, the sight, or just the thought of various foods at different times after consuming a large, high-calorie, high-carbohydrate liquid meal. There was an immediate sensory-specific decrease in the palatability of foods of the same or similar flavor as soon as the liquid meal was consumed. This was followed by a general decrease in the palatability of all substances about 30 minutes later. Thus, it appears that signals from taste receptors produce an immediate decline in the positive-incentive value of similar tastes and that signals associated with the postingestive consequences of eating produce a general decrease in the positive-incentive value of all foods.

Rolls (1990) suggested that sensory-specific satiety has two kinds of effects: relatively brief effects that influence the selection of foods within a single meal, and relatively enduring effects that influence the selection of foods from

meal to meal. Some foods seem to be relatively immune to long-lasting sensory-specific satiety; foods such as rice, bread, potatoes, sweets, and green salads can be eaten al- most every day with only a slight decline in their palata- bility (Rolls, 1986).

The phenomenon of sensory-specific satiety has two adaptive consequences. First, it encourages the consump- tion of a varied diet. If there were no sensory-specific sati- ety, a person would tend to eat her or his preferred food and nothing else, and the re- sult would be malnutrition. Second, sensory- specific satiety encourages animals that have access to a variety of foods to eat a lot; an animal that has eaten its fill of one food will often begin eating again if it encoun- ters a different one (Raynor & Epstein, 2001). This en- courages animals to take full advantage of times of abundance, which are all too rare in nature.

This section has introduced you to several important properties of hunger and eating. How many support the set-point assump- tion, and how many are inconsistent with it?

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Are you ready to move on to the discussion of the physiol- ogy of hunger and satiety in the following section? Find out by completing the following sentences with the most appropriate terms. The correct answers are provided at the end of the exercise. Before proceeding, review material related to your incorrect answers and omissions.

1. The primary function of the ______ is to serve as a storage reservoir for undigested food.

2. Most of the absorption of nutrients into the body takes place through the wall of the ______, or upper intestine.

3. The phase of energy metabolism that is triggered by the expectation of food is the ______ phase.

4. During the absorptive phase, the pancreas releases a great deal of ______ into the bloodstream.

5. During the fasting phase, the primary fuels of the body are ______.

6. During the fasting phase, the primary fuel of the brain is ______.

7. The three components of a set-point system are a set-point mechanism, a detector, and an ______.

8. The theory that hunger and satiety are regulated by a blood glucose set point is the ______ theory.

9. Evidence suggests that hunger is greatly influenced by the current ______ value of food.

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10. Most humans have a preference for sweet, fatty, and ______ tastes.

11. There are two mechanisms by which we learn to eat diets containing essential vitamins and minerals: one mechanism for ______ and another mechanism for the rest.

12. Satiety that is specific to the particular foods that produce it is called ______ satiety.

Do the observed reductions in blood glucose before a meal lend support to the glucostatic theory of hunger? I think not, for five reasons:

● It is a simple matter to construct a situation in which drops in blood glucose levels do not precede eating (e.g., Strubbe & Steffens, 1977)—for example, by unex- pectedly serving a food with a high positive-incentive value.

● The usual premeal decreases in blood glucose seem to be a response to the intention to start eating, not the other way round. The premeal decreases in blood glu- cose are typically preceded by increases in blood in- sulin levels, which indicates that the decreases do not reflect gradually declining energy reserves but are actively produced by an increase in blood levels of insulin (see Figure 12.7).

● If an expected meal is not served, blood glucose levels soon return to their previous homeostatic level.

● The glucose levels in the extracellular fluids that sur- round CNS neurons stay relatively constant, even when blood glucose levels drop (see Seeley & Woods, 2003).

● Injections of insulin do not reliably induce eating un- less the injections are sufficiently great to reduce blood glucose levels by 50% (see Rowland, 1981), and large premeal infusions of glucose do not suppress eating (see Geiselman, 1987).

Myth of Hypothalamic Hunger and Satiety Centers In the 1950s, experiments on rats seemed to suggest that eating behavior is controlled by two different re- gions of the hypothalamus: satiety by the ventromedial

30912.4 ■ Physiological Research on Hunger and Satiety

Scan Your Brainanswers: (1) stomach, (2) duodenum, (3) cephalic, (4) insulin, (5) free fatty acids, (6) glucose, (7) effector, (8) glucostatic, (9) positive- incentive, (10) salty, (11) sodium, (12) sensory-specific.

12.4 Physiological Research on Hunger and Satiety

Now that you have been introduced to set-point theories, the positive-incentive perspective, and some basic factors that affect why, when, and how much we eat, this section introduces you to five prominent lines of research on the physiology of hunger and satiety.

Role of Blood Glucose Levels in Hunger and Satiety As I have already explained, efforts to link blood glucose levels to eating have been largely unsuccessful. However, there was a renewed interest in the role of glucose in the regulation of eating in the 1990s, following the develop- ment of methods of continually monitoring blood glucose levels. In the classic experiment of Campfield and Smith (1990), rats were housed individu- ally, with free access to a mixed diet and water, and their blood glucose levels were continually monitored via a chronic intravenous catheter (i.e., a hypodermic needle located in a vein). In this situation, baseline blood glucose levels rarely fluctuated more than 2%. However, about 10 minutes before a meal was initiated, the levels suddenly dropped about 8% (see Figure 12.7).

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hypothalamus (VMH) and feeding by the lateral hypo- thalamus (LH)—see Figure 12.8. This theory turned out to be wrong, but it stimulated several important discoveries.

VMH Satiety Center In 1940, it was discovered that large bilateral electrolytic lesions to the ventromedial hypothala- mus produce hyperphagia (excessive eating) and extreme obesity in rats (Hetherington & Ranson, 1940). This VMH syndrome has two different phases: dynamic and static. The dynamic phase, which begins as soon as the subject regains consciousness after the operation, is characterized by several weeks of grossly excessive eating and rapid weight gain. However, after that, consumption gradually declines to a level that is just sufficient to maintain a stable level of obe- sity; this marks the beginning of the static phase. Figure 12.9 illustrates the weight gain and food intake of an adult rat with bilateral VMH lesions.

The most important feature of the static phase of the VMH syndrome is that the animal maintains its new

body weight. If a rat in the static phase is deprived of food until it has lost a substantial amount of weight, it will re- gain the lost weight once the deprivation ends; conversely, if it is made to gain weight by forced feeding, it will lose the excess weight once the forced feeding is curtailed.

Paradoxically, despite their prodigious levels of con- sumption, VMH-lesioned rats in some ways seem less hungry than unlesioned controls. Although VMH-lesioned rats eat much more than normal rats when palatable food is readily available, they are less willing to work for it (Teitelbaum, 1957) or to consume it if it is slightly un- palatable (Miller, Bailey, & Stevenson, 1950). Weingarten, Chang, and Jarvie (1983) showed that the finicky eating of VMH-lesioned rats is a consequence of their obesity, not a primary effect of their lesion; they are no less likely to consume unpalatable food than are unlesioned rats of equal obesity.

LH Feeding Center In 1951,Anand and Brobeck reported that bilateral electrolytic lesions to the lateral hypothala- mus produce aphagia—a complete cessation of eating. Even rats that were first made hyperphagic by VMH le- sions were rendered aphagic by the addition of LH le- sions. Anand and Brobeck concluded that the lateral region of the hypothalamus is a feeding center. Teitelbaum and Epstein (1962) subsequently discovered two impor- tant features of the LH syndrome. First, they found that the aphagia was accompanied by adipsia—a complete cessa- tion of drinking. Second, they found that LH-lesioned rats partially recover if they are kept alive by tube feeding. First, they begin to eat wet, palatable foods, such as chocolate chip cookies soaked in milk, and eventually they will eat dry food pellets if water is concurrently available.

Reinterpretation of the Effects of VMH and LH Lesions The theory that the VMH is a satiety center crumbled in the face of two lines of evidence. One of these lines showed that the primary role of the hypothalamus is the regulation of energy metabolism, not the regulation of eating. The initial interpretation was that VMH-lesioned animals become obese because they overeat; however, the evidence suggests the converse—that they overeat because they become obese. Bilateral VMH le- sions increase blood insulin levels, which increases lipogenesis (the pro- duction of body fat) and decreases lipolysis (the break- down of body fat to utilizable forms of energy)—see Powley et al. (1980). Both are likely to be the result of the increases in insulin levels that occur following the lesion. Because the calories ingested by VMH-lesioned rats are converted to fat at a high rate, the rats must keep eating to ensure that they have enough calories in their blood to meet their immediate energy requirements (e.g., Hustvedt & Løvø, 1972); they are like misers who run to the bank each time they make a bit of money and deposit it in a sav- ings account from which withdrawals cannot be made.

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Pituitary

Ventricles Lateral hypothalamus

Ventromedial hypothalamus

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FIGURE 12.8 The locations in the rat brain of the ventro- medial hypothalamus and the lateral hypothalamus.

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The second line of evidence that undermined the theory of a VMH satiety center has shown that many of the effects of VMH lesions are not at- tributable to VMH damage. A large fiber bundle, the ventral noradrener- gic bundle, courses past the VMH and is thus inevitably damaged by large electrolytic VMH lesions; in particu- lar, fibers that project from the nearby paraventricular nuclei of the hypothalamus are damaged (see Figure 12.10). Bilateral lesions of the noradrenergic bundle (e.g., Gold et al., 1977) or the paraventricular nu- clei (Leibowitz, Hammer, & Chang, 1981) produce hyperphagia and obe- sity, just as VMH lesions do.

Most of the evidence against the notion that the LH is a feeding cen-

31112.4 ■ Physiological Research on Hunger and Satiety

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ter has come from a thorough analysis of the effects of bi- lateral LH lesions. Early research focused exclusively on the aphagia and adipsia that are produced by LH lesions, but subsequent research has shown that LH lesions pro- duce a wide range of severe motor disturbances and a general lack of responsiveness to sensory input (of which food and drink are but two examples). Consequently, the idea that the LH is a center specifically dedicated to feed- ing no longer warrants serious consideration.

Role of the Gastrointestinal Tract in Satiety One of the most influential early studies of hunger was published by Cannon and Washburn in 1912. It was a perfect collaboration: Cannon had the ideas, and Wash- burn had the ability to swallow a balloon. First, Washburn swallowed an empty balloon tied to the end of a thin tube. Then, Cannon pumped some air into the balloon and connected the end of the tube to a water-filled glass U-tube so that Washburn’s stomach contractions pro- duced a momentary increase in the level of the water at

FIGURE 12.10 Location of the paraventricular nucleus in the rat hypothalamus. Note that the section through the hypothala- mus is slightly different than the one in Figure 12.8.

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the other end of the U-tube. Washburn re- ported a “pang” of hunger each time that a large stomach contraction was recorded (see Figure 12.11).

Cannon and Washburn’s finding led to the theory that hunger is the feeling of contractions caused by an empty stomach, whereas satiety is the feeling of stomach dis- tention. However, support for this theory and interest in the role of the gastroin- testinal tract in hunger and satiety quickly waned with the discovery that human pa- tients whose stomach had been surgically removed and whose esophagus had been hooked up directly to their duodenum (the first segment of the small intestine, which normally carries food away from the stomach) continued to report feelings of hunger and satiety and continued to maintain their normal body weight by eating more meals of smaller size.

In the 1980s, there was a resurgence of interest in the role of the gastrointestinal tract in eating. It was stimulated by a se- ries of experiments that indicated that the gastrointestinal tract is the source of satiety signals. For example, Koopmans (1981) transplanted an extra stomach and length of intes- tine into rats and then joined the major arteries and veins of the implants to the recipients’ circulatory systems (see Figure 12.12). Koopmans found that food injected into the transplanted stomach and kept there by a noose around the pyloric sphincter decreased eating in propor- tion to both its caloric content and volume. Because the transplanted stomach had no functional nerves, the gas- trointestinal satiety signal had to be reaching the brain through the blood. And because nutrients are not ab- sorbed from the stomach, the bloodborne satiety signal could not have been a nutrient. It had to be some chemi- cal or chemicals that were released from the stomach in response to the caloric value and volume of the food— which leads us nicely into the next subsection.

Hunger and Satiety Peptides Soon after the discovery that the stomach and other parts of the gastrointestinal tract release chemical signals to the brain, evidence began to accumulate that these chemicals

were peptides, short chains of amino acids that can func- tion as hormones and neurotransmitters (see Fukuhara et al., 2005). Ingested food interacts with receptors in the gastrointestinal tract and in so doing causes the tract to release peptides into the bloodstream. In 1973, Gibbs, Young, and Smith injected one of these gut peptides, cholecystokinin (CCK), into hungry rats and found that they ate smaller meals. This led to the hypothesis that circulating gut peptides provide the brain with information about the quantity and nature of food in the gastrointestinal tract and that this information plays a role in satiety (see Bad- man & Flier, 2005; Flier, 2006).

There has been considerable support for the hypothesis that peptides can function as satiety signals (see Gao & Horvath, 2007; Ritter, 2004). Several gut peptides have been shown to bind to receptors in the brain, particularly in areas of the hypothalamus involved in energy metabolism, and a dozen or so (e.g., CCK, bombesin, glucagon, alpha- melanocyte-stimulating hormone, and somatostatin) have been reported to reduce food intake (see Batterham et al., 2006; Zhang et al., 2005). These have become known as satiety peptides (peptides that decrease appetite).

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FIGURE 12.11 The system developed by Cannon and Washburn in 1912 for measuring stomach contractions. They found that large stomach contractions were related to pangs of hunger.

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In studying the appetite-reducing effects of peptides, researchers had to rule out the possibility that these ef- fects are not merely the consequence of illness (see Moran, 2004). Indeed, there is evidence that one pep- tide in particular, CCK, induces illness: CCK adminis- tered to rats after they have eaten an unfamiliar substance induces a conditioned taste aversion for that substance, and CCK induces nausea in human subjects. However, CCK reduces appetite and eating at doses substantially below those that are required to induce taste aversion in rats, and thus it qualifies as a legitimate satiety peptide.

Several hunger peptides (peptides that increase appetite) have also been discovered. These peptides tend to be syn- thesized in the brain, particularly in the hypothalamus. The most widely studied of these are neuropeptide Y, galanin, orexin-A, and ghrelin (e.g., Baird, Gray, & Fischer, 2006; Olszewski, Schiöth & Levine, 2008; Williams et al., 2004).

The discovery of the hunger and satiety peptides has had two major effects on the search for the neural mechanisms of hunger and satiety. First, the sheer number of these hunger and satiety peptides indicates

that the neural system that controls eating likely reacts to many different signals (Nogueiras & Tschöp, 2005; Schwartz & Azzara, 2004), not just to one or two (e.g., not just to glucose and fat). Second, the discovery that many of the hunger and satiety peptides have receptors in the hypothalamus has renewed interest in the role of the hypothalamus in hunger and eating (Gao & Horvath, 2007; Lam, Schwartz, & Rossetti, 2006; Luquet et al., 2005). This interest was further stimulated by the dis- covery that microinjection of gut peptides into some sites in the hypothalamus can have major effects on eat- ing. Still, there is a general acceptance that hypothalamic circuits are only one part of a much larger system (see Berthoud & Morrison, 2008; Cone, 2005).

Serotonin and Satiety The monoaminergic neurotransmitter serotonin is an- other chemical that plays a role in satiety. The initial evi- dence for this role came from a line of research in rats. In these studies, serotonin- produced satiety was found to have three major properties (see Blundell & Halford, 1998):

● It caused the rats to resist the powerful attraction of highly palatable cafeteria diets.

● It reduced the amount of food that was consumed during each meal rather than reducing the number of meals (see Clifton, 2000).

● It was associated with a shift in food preferences away from fatty foods.

This profile of effects suggested that serotonin might be useful in combating obesity in humans. Indeed, serotonin agonists (e.g., fenfluramine, dexfenfluramine, fluoxetine) have been shown to reduce hunger, eating, and body weight under some conditions (see Blundell & Halford, 1998). Later in this chapter, you will learn about the use of serotonin to treat human obesity (see De Vry & Schreiber, 2000).

Prader-Willi Syndrome: Patients with Insatiable Hunger Prader-Willi syndrome could prove critical in the discov- ery of the neural mechanisms of hunger and satiety (Goldstone, 2004). Individuals with Prader-Willi syn- drome, which results from an accident of chromosomal replication, experience insatiable hunger, little or no sati- ety, and an exceptionally slow metabolism. In short, the Prader-Willi patient acts as though he or she is starving. Other common physical and neurological symptoms in- clude weak muscles, small hands and feet, feeding diffi- culties in infancy, tantrums, compulsivity, and skin picking. If untreated, most patients become extremely obese, and they often die in early adulthood from dia- betes, heart disease, or other obesity-related disorders. Some have even died from gorging until their stomachs

31312.4 ■ Physiological Research on Hunger and Satiety

Transplant connected to the recipient’s lower intestine

Recipient’s own gastrointestinal tract

Transplanted stomach and intestine

Food injected here

Strings pulled to tighten noose around pyloric sphincter

FIGURE 12.12 Transplantation of an extra stomach and length of intestine in a rat. Koopmans (1981) im- planted an extra stomach and length of intestine in each of his experimental subjects. He then connected the major blood vessels of the implanted stomachs to the circulatory systems of the recipients. Food injected into the extra stomach and kept there by a noose around the pyloric sphincter decreased eating in pro- portion to its volume and caloric value.

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split open. Fortunately, Miss A. was diagnosed in infancy and received excellent care, which kept her from becom- ing obese (Martin et al., 1998).

Prader-Willi Syndrome: The Case of Miss A.

Miss A. was born with little muscle tone. Because her sucking reflex was so weak, she was tube fed. By the time she was 2 years old, her hypotonia (below-normal muscle tone) had resolved itself, but a number of characteristic deformities and developmental delays began to appear.

At 31/2 years of age, Miss A. suddenly began to display a voracious appetite and quickly gained weight. Fortu- nately, her family maintained her on a low-calorie diet and kept all food locked away.

Miss A. is moderately retarded, and she suffers from psychiatric problems. Her major problem is her tendency to have tantrums any time anything changes in her envi- ronment (e.g., a substitute teacher at school). Thanks largely to her family and pediatrician, she has received ex- cellent care, which has minimized the complications that arise with Prader-Willi syndrome—most notably those related to obesity and its pathological effects.

Although the study of Prader-Willi syndrome has yet to provide any direct evidence about the neural mecha- nisms of hunger and eating, there has been a marked surge in its investigation. This increase has been stimu- lated by the recent identification of the genetic cause of the condition: an accident of reproduction that deletes or disrupts a section of chromosome 15 coming from the fa- ther. This information has provided clues about genetic factors in appetite.

12.5 Body Weight Regulation: Set Points versus Settling Points

One strength of set-point theories of eating is that they explain body weight regulation. You have already learned that set-point theories are largely inconsistent with the facts of eating, but how well do they account for the reg- ulation of body weight? Certainly, many people in our culture believe that body weight is regulated by a body-fat set point (Assanand, Pinel, & Lehman, 1998a, 1998b). They believe that when fat deposits are below a person’s set point, a person becomes hungrier and eats more, which results in a return of body-fat levels to that person’s set point; and, conversely, they believe that when fat de- posits are above a person’s set point, a person becomes less hungry and eats less, which results in a return of body-fat levels to their set point.

Set-Point Assumptions about Body Weight and Eating You have already learned that set-point theories do a poor job of explaining the characteristics of hunger and eating. Do they do a better job of accounting for the facts of body weight regulation? Let’s begin by looking at three lines of evidence that challenge fundamental aspects of many set- point theories of body weight regulation.

Variability of Body Weight The set-point model was expressly designed to explain why adult body weights re- main constant. Indeed, a set-point mechanism should make it virtually impossible for an adult to gain or lose large amounts of weight. Yet, many adults experience large and lasting changes in body weight (see Booth, 2004). Moreover, set-point thinking crumbles in the face of the epidemic of obesity that is currently sweeping fast- food societies (Rosenheck, 2008).

Set-point theories of body weight regulation suggest that the best method of maintaining a constant body weight is to eat each time there is a motivation to eat, be- cause, according to the theory, the main function of hunger is to defend the set point. However, many people avoid obesity only by resisting their urges to eat.

Set Points and Health One implication of set-point theories of body weight regulation is that each person’s set point is optimal for that person’s health—or at least not incompatible with good health. This is why popular psychologists commonly advise people to “listen to the wisdom of their bodies” and eat as much as they need to satisfy their hunger. Experimental results indicate that this common prescription for good health could not be further from the truth.

Two kinds of evidence suggest that typical ad libitum (free-feeding) levels of consumption are unhealthy (see Brownell & Rodin, 1994). First are the results of studies of humans who consume fewer calories than others. For ex- ample, people living on the Japanese island of Okinawa seemed to eat so few calories that their eating habits be- came a concern of health officials. When the health offi- cials took a closer look, here is what they found (see Kagawa, 1978). Adult Okinawans were found to consume, on average, 20% fewer calories than other adult Japanese, and Okinawan school children were found to consume 38% fewer calories than recommended by public health officials. It was somewhat surprising then that rates of morbidity and mortality and of all aging-related diseases were found to be substantially lower in Okinawa than in other parts of Japan, a country in which overall levels of caloric intake and obesity are far below Western norms. For example, the death rates from stroke, cancer, and heart disease in Okinawa were only 59%, 69%, and 59%, respectively, of those in the rest of Japan. Indeed, the pro- portion of Okinawans living to be over 100 years of age

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was up to 40 times greater than that of inhabitants of var- ious other regions of Japan.

The Okinawan study and the other studies that have reported major health benefits in humans who eat less (e.g., Manson et al., 1995; Meyer et al., 2006; Walford &

Walford, 1994) are not controlled experiments; therefore, they must be interpreted with caution. For ex-

ample, perhaps it is not simply the consumption of fewer calories that leads to health and longevity; per- haps in some cultures people who eat less tend to eat healthier diets.

Controlled experimental demonstrations in over a dozen different mammalian species, including monkeys (see Coleman et al., 2009), of the beneficial effects of calo-

rie restriction constitute the second kind of evidence that ad libitum levels of con- sumption are unhealthy. Fortunately, the

results of such controlled experiments do not present the same problems of interpretation as do the findings of the Okinawa study and other similar correlational studies in humans. In typical calorie-restriction experiments, one group of subjects is allowed to eat as much as they choose, while other groups of subjects have their caloric intake of the same diets substantially reduced (by between 25% and 65% in various studies). Results of such experiments have been remarkably consistent (see Bucci, 1992; Masoro, 1988; Weindruch, 1996; Weindruch & Walford, 1988): In experiment after experiment, substantial reductions in the caloric intake of balanced diets have improved nu- merous indices of health and increased longevity. For ex- ample, in one experiment (Weindruch et al., 1986), groups of mice had their caloric intake of a well-balanced commercial diet reduced by either 25%, 55%, or 65% after weaning. All levels of dietary restriction substantially improved health and increased longevity, but the benefits

were greatest in the mice whose intake was reduced the most. Those mice that con- sumed the least had the lowest incidence of

cancer, the best immune responses, and the greatest maxi- mum life span—they lived 67% longer than mice that ate as much as they liked. Evidence suggests that dietary restriction can have beneficial effects even if it is not initi- ated until later in life (Mair et al., 2003; Vaupel, Carey, & Christensen, 2003).

One important point about the results of the calorie- restriction experiments is that the health benefits of the restricted diets may not be entirely attributable to loss of body fat (see Weindruch, 1996). In some dietary restric- tion studies, the health of subjects has improved even if they did not reduce their body fat, and there are often no significant correlations between amount of weight loss and improvements in health. This suggests excessive en- ergy consumption, independent of fat accumulation, may accelerate aging with all its attendant health problems (Lane, Ingram, & Roth, 2002; Prolla & Mattson, 2001).

Remarkably, there is evidence that dietary restriction can be used to treat some neurological conditions. Caloric restriction has been shown to reduce seizure susceptibility in human epileptics (see Maalouf, Rho, & Mattson, 2008) and to improve memory in the elderly (Witte et al., 2009). Please stop and think about the impli- cations of all these findings about calorie restriction. How much do you eat?

Regulation of Body Weight by Changes in the Effi- ciency of Energy Utilization Implicit in many set- point theories is the premise that body weight is largely a function of how much a person eats. Of course, how much someone eats plays a role in his or her body weight, but it is now clear that the body controls its fat levels, to a large degree, by changing the efficiency with which it uses energy. As a person’s level of body fat declines, that person starts to use energy resources more efficiently, which lim- its further weight loss (see Martin, White, & Hulsey, 1991); conversely, weight gain is limited by a progressive decrease in the efficiency of energy utilization. Rothwell and Stock (1982) created a group of obese rats by main- taining them on a cafeteria diet, and they found that the resting level of energy expenditure in these obese rats was 45% greater than in control rats.

This point is illustrated by the progressively declining effectiveness of weight-loss programs. Initially, low-calorie diets produce substantial weight loss. But the rate of weight loss diminishes with each successive week on the diet, until an equilibrium is achieved and little or no fur- ther weight loss occurs. Most dieters are familiar with this disappointing trend. A similar effect occurs with weight- gain programs (see Figure 12.13 on page 316).

The mechanism by which the body adjusts the effi- ciency of its energy utilization in response to its levels of body fat has been termed diet-induced thermogenesis. Increases in the levels of body fat produce increases in body temperature, which require additional energy to maintain them—and decreases in the level of body fat have the opposite effects (see Lazar, 2008).

There are major differences among humans both in basal metabolic rate (the rate at which energy is utilized to maintain bodily processes when resting) and in the ability to adjust the metabolic rate in response to changes in the levels of body fat. We all know people who remain slim even though they eat gluttonously. However, the re- search on calorie-restricted diets suggests that these peo- ple may not eat with impunity: There may be a health cost to pay for overeating even in the absence of obesity.

Set Points and Settling Points in Weight Control The theory that eating is part of a system designed to de- fend a body-fat set point has long had its critics (see

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Booth, Fuller, & Lewis, 1981; Wirtshafter & Davis, 1977), but for many years their arguments were largely ignored and the set-point assumption ruled. This situa- tion has been changing: Several promi- nent reviews of research on hunger and weight regulation generally acknowledge that a strict set-point model cannot ac-

count for the facts of weight regulation, and they argue for a more

flexible model (see Berthoud, 2002; Mercer & Speakman, 2001; Woods et al., 2000). Because the body-fat set-point model still dominates the thinking of many people, I want to review the main advantages of an alternative and more flexible regulatory model: the settling-point model. Can you change your thinking?

According to the settling-point model, body weight tends to drift around a natu- ral settling point—the level at which the various factors that influence body weight achieve an equilibrium. The idea is that as body-fat levels increase, changes occur that tend to limit further increases until a balance is achieved between all factors that encourage weight gain and all those that discourage it.

The settling-point model provides a loose kind of homeostatic regulation, without a set-point mechanism or mechanisms to return body weight to a set point. Ac- cording to the settling-point model, body weight remains stable as long as there are no long-term changes in the factors that influence it; and if there are such changes, their impact is limited by negative feedback. In the settling- point model, the negative feedback merely limits further changes in the same direction, whereas in the set-point model, negative feedback triggers a return to the set point. A neuron’s resting potential is a well-known bio- logical settling point—see Chapter 4.

The seductiveness of the set-point mechanism is attrib- utable in no small part to the existence of the thermostat model, which provides a vivid means of thinking about it. Figure 12.14 presents an analogy I like to use to think about the settling-point mechanism. I call it the leaky-barrel model: (1) The amount of water entering the hose is analogous to the amount of food available to the subject; (2) the water pressure at the nozzle is analogous to the

positive-incentive value of the available food; (3) the amount of water entering the barrel is analogous to the amount of

energy consumed; (4) the water level in the barrel is analo- gous to the level of body fat; (5) the amount of water leak- ing from the barrel is analogous to the amount of energy being expended; and (6) the weight of the barrel on the hose is analogous to the strength of the satiety signal.

The main advantage of the settling-point model of body weight regulation over the body-fat set-point model is that it is more consistent with the data. Another advan- tage is that in those cases in which both models make the same prediction, the settling-point model does so more parsimoniously—that is, with a simpler mechanism that requires fewer assumptions. Let’s use the leaky-barrel analogy to see how the two models account for four key facts of weight regulation.

● Body weight remains relatively constant in many adult animals. On the basis of this fact, it has been argued that body fat must be regulated around a set point. However, constant body weight does not require, or even imply, a set point. Consider the leaky-barrel model. As water from the tap begins to fill the barrel, the weight of the water in the barrel increases. This in- creases the amount of water leaking out of the barrel and decreases the amount of water entering the barrel by increasing the pressure of the barrel on the hose. Eventually, this system settles into an equilibrium where the water level stays constant; but because this level is neither predetermined nor actively defended, it is a settling point, not a set point.

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● Many adult animals experience enduring changes in body weight. Set-point systems are designed to main- tain internal constancy in the face of fluctuations of the external environment. Thus, the fact that many adult animals experience long-term changes in body weight is a strong argument against the set-point model. In contrast, the settling-point model predicts that when there is an enduring change in one of the parameters that affect body weight—for example, a major increase in the positive-incentive value of available food—body weight will drift to a new settling point.

● If a subject’s intake of food is reduced, metabolic changes that limit the loss of weight occur; the oppo- site happens when the subject overeats. This fact is often cited as evidence for set-point regulation of body weight; however, because the metabolic changes merely limit further weight changes rather than eliminating those that have occurred, they are more consistent with a settling-point model. For example, when water intake in the leaky-barrel model is reduced, the water

level in the barrel begins to drop; but the drop is lim- ited by a decrease in leakage and an increase in inflow attributable to the falling water pressure in the barrel. Eventually, a new settling point is achieved, but the re- duction in water level is not as great as one might ex- pect because of the loss-limiting changes.

● After an individual has lost a substantial amount of weight (by dieting, exercise, or the surgical removal of fat), there is a tendency for the original weight to be re- gained once the subject returns to the previous eating- and energy-related lifestyle. Although this finding is often offered as irrefutable evidence of a body-weight set point, the settling-point model readily accounts for it. When the water level in the leaky-barrel model is reduced—by temporarily decreasing input (dieting), by temporarily increasing output (exercising), or by scoop- ing out some of the water (surgical removal of fat)— only a temporary drop in the settling point is produced. When the original conditions are reinstated, the water level inexorably drifts back to the original settling point.

31712.5 ■ Body Weight Regulation: Set Points versus Settling Points

1The amount of water entering the hose is analogous to the amount of available food.

2 The water pressure at the nozzle is analogous to the incentive value of the available food.

3 The amount of water entering the barrel is analogous to the amount of consumed energy.

4 The water level in the barrel is analogous to the level of body fat.

5 The amount of water leaking from the barrel is analogous to the amount of energy being expended.

6 The weight of the barrel on the hose is analogous to the strength of the satiety signal.

FIGURE 12.14 The leaky-barrel model: a settling-point model of eating and body weight homeostasis.

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Does it really matter whether we think about body weight regulation in terms of set points or settling points— or is making such a distinction just splitting hairs? It cer- tainly matters to biopsychologists: Understanding that

body weight is regulated by a settling- point system helps them better under- stand, and more accurately predict,

the changes in body weight that are likely to occur in vari- ous situations; it also indicates the kinds of physiological mechanisms that are likely to mediate these changes. And it should matter to you. If the set-point model is correct, at- tempting to change your body weight would be a waste of time; you would inevitably be drawn back to your body- weight set point. On the other hand, the leaky-barrel model suggests that it is possible to permanently change your body weight by permanently changing any of the factors that influence energy intake and output.

11. ______ models are more consistent with the facts of body-weight regulation than are set-point models.

12. ______ are to set points as leaky barrels are to settling points.

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Are you ready to move on to the final two sections of the chapter, which deal with eating disorders? This is a good place to pause and scan your brain to see if you under- stand the physiological mechanisms of eating and weight regulation. Complete the following sentences by filling in the blanks. The correct answers are provided at the end of the exercise. Before proceeding, review material related to your incorrect answers and omissions.

1. The expectation of a meal normally stimulates the release of ______ into the blood, which reduces blood glucose.

2. In the 1950s, the ______ hypothalamus was thought to be a satiety center.

3. A complete cessation of eating is called ______. 4. ______ is the breakdown of body fat to create usable

forms of energy. 5. The classic study of Washburn and Cannon was the

perfect collaboration: Cannon had the ideas, and Washburn could swallow a ______.

6. CCK is a gut peptide that is thought to be a ______ peptide.

7. ______ is the monoaminergic neurotransmitter that seems to play a role in satiety.

8. Okinawans eat less and live ______. 9. Experimental studies of ______ have shown that typi-

cal ad libitum (free-feeding) levels of consumption are unhealthy in many mammalian species.

10. As an individual grows fatter, further weight gain is minimized by diet-induced ______.

Scan Your Brainanswers: (1) insulin, (2) ventromedial, (3) aphagia, (4) Lipolysis, (5) balloon, (6) satiety, (7) Serotonin, (8) longer, (9) calorie restriction, (10) thermogenesis, (11) Settling-point, (12) Thermostats.

12.6 Human Obesity: Causes, Mechanisms, and Treatments

This is an important point in this chapter. The chapter opened by describing the current epidemic of obesity and overweight and its adverse effects on health and longevity and then went on to discuss behavioral and physiological factors that influence eating and weight. Most importantly, as the chapter progressed, you learned that some common beliefs about eating and weight regulation are incompati- ble with the evidence, and you were challenged to think about eating and weight regulation in unconventional ways that are more consistent with current evidence. Now, the chapter completes the circle with two sections on eat- ing disorders: This section focuses on obesity, and the next covers anorexia and bulimia. I hope that by this point you realize that obesity is currently a major health problem and will appreciate the relevance of what you are learning to your personal life and the lives of your loved ones.

Who Needs to Be Concerned about Obesity? Almost everyone needs to be concerned about the prob- lem of obesity. If you are currently overweight, the reason for concern is obvious: The relation between obesity and poor health has been repeatedly documented (see Eilat- Adar, Eldar, & Goldbourt, 2005; Ferrucci & Alley, 2007; Flegal et al., 2007; Hjartåker et al., 2005; Stevens, McClain, & Truesdale, 2006). Moreover, some studies have shown that even individuals who are only a bit overweight run a greater risk of developing health problems (Adams et al., 2006; Byers, 2006; Jee et al., 2006), as do obese individuals who manage to keep their blood pressure and blood cho- lesterol at normal levels (Yan et al., 2006). And the risk is not only to one’s own health: Obese women are at in- creased risk of having infants with health problems (Nohr et al., 2007).

Even if you are currently slim, there is cause for con- cern about the problem of obesity. The incidence of obe- sity is so high that it is almost certain to be a problem for somebody you care about. Furthermore, because weight tends to increase substantially with age, many people who are slim as youths develop serious weight problems as they age.

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There is cause for special concern for the next genera- tion. Because rates of obesity are increasing in most parts of the world (Rosenheck, 2008; Sofsian, 2007), public health officials are concerned about how they are going to handle the growing problem. For example, it has been es- timated that over one-third of the children born in the United States in 2000 will eventually develop diabetes, and 10% of these will develop related life-threatening conditions (see Haslam, Sattar, & Lean, 2006; Olshansky et al., 2005).

Why Is There an Epidemic of Obesity? Let’s begin our analysis of obesity by considering the pressures that are likely to have led to the evolution of our eating and weight-regulation systems (see Flier & Maratos-Flier, 2007; Lazar, 2005; Pinel et al., 2000). Dur-

ing the course of evolution, inconsistent food supplies were one of the main threats to survival. As a result, the fittest individu-

als were those who preferred high-calorie foods, ate to ca- pacity when food was available, stored as many excess calories as possible in the form of body fat, and used their stores of calories as efficiently as possible. Individuals who did not have these characteristics were unlikely to survive a food shortage, and so these characteristics were passed on to future generations.

The development of numerous cultural practices and beliefs that promote consumption has augmented the ef- fects of evolution. For example, in my culture, it is com- monly believed that one should eat three meals per day at regular times, whether one is hungry or not; that food should be the focus of most social gatherings; that meals should be served in courses of progressively increasing palatability; and that salt, sweets (e.g., sugar), and fats (e.g., butter or cream) should be added to foods to im- prove their flavor and thus increase their consumption.

Each of us possesses an eating and weight-regulation system that evolved to deal effectively with periodic food shortages, and many of us live in cultures whose eating- related practices evolved for the same purpose. However, our current environment differs from our “natural” envi- ronment in critical food-related ways. We live in an envi- ronment in which an endless variety of foods of the highest positive-incentive and caloric value are readily and continuously available. The consequence is an ap- pallingly high level of consumption.

Why Do Some People Become Obese While Others Do Not? Why do some people become obese while others living under the same obesity-promoting conditions do not? At a superficial level, the answer is obvious: Those who are obese are those whose energy intake has exceeded their energy output; those who are slim are those whose energy intake

has not exceeded their energy output (see Nestle, 2007). Although this answer provides little insight, it does serve to emphasize that two kinds of individual differences play a role in obesity: those that lead to differences in energy input and those that lead to differences in energy output.

Differences in Consumption There are many factors that lead some people to eat more than others who have comparable access to food. For example, some people consume more energy because they have strong prefer- ences for the taste of high-calorie foods (see Blundell & Finlayson, 2004; Epstein et al., 2007); some consume more because they were raised in families and/or cultures that promote excessive eating; and some consume more because they have particu- larly large cephalic-phase re- sponses to the sight or smell of food (Rodin, 1985).

Differences in Energy Expenditure With respect to energy output, people differ markedly from one another in the degree to which they can dissipate excess consumed energy. The most obvious difference is that people differ substantially in the amount of exercise they get; however, there are others. You have already learned about two of them: differences in basal metabolic rate and in the ability to react to fat increases by diet-induced thermogenesis. The third factor is called NEAT, or nonexercise activity thermo- genesis, which is generated by activities such as fidgeting and the maintenance of posture and muscle tone (Ravussin & Danforth, 1999) and can play a small role in dissipating excess energy (Levine, Eberhardt, & Jensen, 1999; Ravussin, 2005).

Genetic Differences Given the number of factors that can influence food consumption and energy metabolism, it is not surprising that many genes can influence body weight. Indeed, over 100 human chromosome loci (regions) have already been linked to obesity (see Fischer et al., 2009; Rankinen et al., 2006). However, because body weight is influenced by so many genes, it is proving difficult to under- stand how their interactions with one another and with ex- perience contribute to obesity in healthy people. Although it is proving difficult to unravel the various genetic factors that influence variations in body weight among the healthy, single gene mutations have been linked to pathological con- ditions that involve obesity. You will encounter an example of such a condition later in this section.

Why Are Weight-Loss Programs Typically Ineffective? Figure 12.15 describes the course of the typical weight- loss program. Most weight-loss programs are unsuccess- ful in the sense that, as predicted by the settling-point model, most of the lost weight is regained once the dieter

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stops following the program and the original conditions are reestablished. The key to permanent weight loss is a permanent lifestyle change.

Exercise has many health-promoting effects; however, despite the general belief that exercise is the most effective method of losing weight, several studies have shown that it often contributes little to weight loss (e.g., Sweeney et al., 1993). One reason is that physical exercise normally accounts for only a small proportion of total en- ergy expenditure: About 80% of the energy you expend is used to maintain the resting physiological processes of your body and to digest your food (Calles-Escandon & Horton, 1992). Another reason is that our bodies are effi- cient machines, burning only a small number of calories during a typical workout. Moreover, after exercise, many people feel free to consume extra drinks and foods that contain more calories than the relatively small number that were expended during the exercise.

Leptin and the Regulation of Body Fat Fat is more than a passive storehouse of energy; it actively releases a peptide hormone called leptin. The discovery of leptin has been extremely influential (see Elmquist & Flier, 2004). The following three subsections describe (1) the discovery of leptin, (2) how its discovery has fu- eled the development of a new approach to the treatment

of human obesity, and (3) how the understanding that leptin (and insulin) are feedback signals led to the discov- ery of a hypothalamic nucleus that plays an important role in the regulation of body fat.

Obese Mice and the Discovery of Leptin In 1950, a spontaneous genetic mutation occurred in the mouse colony being maintained in the Jackson Laboratory at Bar Harbor, Maine. The mutant mice were homozygous for the gene (ob), and they were grossly obese, weighing up to three times as much as typical mice. These mutant mice are commonly referred to as ob/ob mice. See Figure 12.16.

Ob/ob mice eat more than control mice; they convert calories to fat more efficiently; and they use their calories more efficiently. Coleman (1979) hypothesized that ob/ob mice lack a critical hormone that normally inhibits fat production and maintenance.

In 1994, Friedman and his colleagues characterized and cloned the gene that is mutated in ob/ob mice (Zhang et al., 1994). They found that this gene is expressed only in fat cells, and they characterized the protein that it nor- mally encodes, a peptide hormone that they named leptin. Because of their mutation, ob/ob mice lack leptin. This finding led to an exciting hypothesis: Perhaps leptin is a negative feedback signal that is normally released from fat

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1 Weight lossoccurs rapidly at beginning of diet

2 As weightdeclines, the amount of energy “leakage” is automatically reduced, and this reduces the rate of weight loss

3 Gradually thereduced rate of intake is matched by the reduced energy output, and a new stable settling point is achieved

4 When the dietis terminated, weight gain is rapid because of the high incentive value of food and the low level of energy leakage

5 As weightaccumulates, the incentive value of food gradually decreases and the energy leakage increases until the original settling point is regained

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stores to decrease appetite and increase fat metabolism. Could leptin be administered to obese humans to reverse the current epidemic of obesity?

Leptin, Insulin, and the Arcuate Melanocortin System There was great fanfare when leptin was dis- covered. However, it was not the first peptide hormone to be discovered that seems to function as a negative feed- back signal in the regulation of body fat (see Schwartz, 2000; Woods, 2004). More than 25 years ago, Woods and colleagues (1979) suggested that the pancreatic peptide hormone insulin serves such a function.

At first, the suggestion that insulin serves as a negative feedback signal for body fat regulation was viewed with skepticism. After all, how could the level of insulin in the body, which goes up and then comes back down to nor- mal following each meal, provide the brain with infor- mation about gradually changing levels of body fat? It turns out that insulin does not readily penetrate the blood–brain barrier, and its levels in the brain were found to stay relatively stable—indeed, high levels of glu- cose are toxic to neurons (Tomlinson & Gardiner, 2008). The following findings supported the hypothesis that in- sulin serves as a negative feedback signal in the regula- tion of body fat:

● Brain levels of insulin were found to be positively cor- related with levels of body fat (Seeley et al., 1996).

● Receptors for insulin were found in the brain (Baura et al., 1993).

● Infusions of insulin into the brains of laboratory ani- mals were found to reduce eating and body weight (Campfield et al., 1995; Chavez, Seeley, & Woods, 1995).

Why are there two fat feedback signals? One reason may be that leptin levels are more closely correlated with subcutaneous fat (fat stored under the skin), whereas insulin levels are more closely correlated with visceral

fat (fat stored around the internal organs of the body cavity)—see Hug & Lodish (2005). Thus, each fat signal provides different information. Visceral fat is more common in males than females and poses the greater threat to health (Wajchenberg, 2000). Insulin, but not leptin, is also involved in glucose regulation (see Schwartz & Porte, 2005).

The discovery that leptin and insulin are signals that provide information to the brain about fat levels in the body provided a means for discovering the neural cir- cuits that participate in fat regulation. Receptors for both peptide hormones are located in many parts of the nervous system, but most are in the hypothalamus, par- ticularly in one area of the hypothalamus: the arcuate nucleus.

A closer look at the distribution of leptin and insulin receptors in the arcuate nucleus indicated that these re- ceptors are not randomly distributed throughout the nu- cleus. They are located in two classes of neurons: neurons that release neuropeptide Y (the gut hunger peptide that you read about earlier in the chapter), and neurons that release melanocortins, a class of peptides that includes the gut satiety peptide α-melanocyte-stimulating hormone (alpha-melanocyte-stimulating hormone). Attention has been mostly focused on the melanocortin-releasing neurons in the arcuate nucleus (often referred to as the melanocortin system) because injections of α-melanocyte-stimulating hormone have been shown to suppress eating and pro- mote weight loss (see Horvath, 2005; Seeley & Woods, 2003). It seems, however, that the melanocortin system is only a minor component of a much larger system: Elimi- nation of leptin receptors in the melanocortin system produces only a slight weight gain (see Münzberg & Myers, 2005).

Leptin as a Treatment for Human Obesity The early studies of leptin seemed to confirm the hypothesis that it could function as an effective treatment for obesity. Re- ceptors for leptin were found in the brain, and injecting it into ob/ob mice reduced both their eating and their body fat (see Seeley & Woods, 2003). All that remained was to prove leptin’s effectiveness in human patients.

However, when research on leptin turned from ob/ob mice to obese humans, the program ran into two major snags. First, obese humans—unlike ob/ob mice—were found to have high, rather than low, levels of leptin (see Münzberg & Myers, 2005). Second, injections of leptin did not reduce either the eating or the body fat of obese humans (see Heymsfield et al., 1999).

Why the actions of leptin are different in humans and ob/ob mice has yet to be explained. Nevertheless, efforts to use leptin in the treatment of human obesity have not been a total failure. Although few obese humans have a genetic mutation to the ob gene, leptin is a panacea for those few who do. Consider the following case.

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FIGURE 12.16 An ob/ob mouse and a control mouse.

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The Case of the Child with No Leptin

The patient was of normal weight at birth, but her weight soon began to increase at an excessive rate. She demanded food continually and was disruptive when denied food. As a result of her extreme obesity, deformities of her legs de- veloped, and surgery was required.

She was 9 when she was referred for treatment. At this point, she weighed 94.4 kilograms (about 210 pounds), and her weight was still increasing at an alarming rate. She was found to be homozygous for the ob gene and had no detectable leptin. Thus, leptin therapy was com- menced.

The leptin therapy immediately curtailed the weight gain. She began to eat less, and she lost weight steadily over the 12-month period of the study, a total of 16.5 kilograms (about 36 pounds), almost all in the form of fat. There were no obvious side effects (Farooqi et al., 1999).

Treatment of Obesity Because obesity is such a severe health problem, there have been many efforts to develop an effective treatment. Some of these—such as the leptin treatment you just read about—have worked for a few, but the problem of obesity continues to grow. The following two subsections discuss two treatments that are at different stages of de- velopment: serotonergic agonists and gastric surgery.

Serotonergic Agonists Because—as you have already learned—serotonin agonists have been shown to reduce food consumption in both human and nonhuman sub- jects, they have considerable potential in the treatment of obesity (Halford & Blundell, 2000a). Serotonin agonists seem to act by a mechanism different from that for leptin and insulin, which produce long-term satiety signals based on fat stores. Serotonin agonists seem to increase short-term satiety signals associated with the consump- tion of a meal (Halford & Blundell, 2000b).

Serotonin agonists have been found in various studies of obese patients to reduce the following: the urge to eat high- calorie foods, the consumption of fat, the subjective inten-

sity of hunger, the size of meals, the number of between-meal snacks, and bingeing. Because of this extremely posi-

tive profile of effects and the severity of the obesity problem, serotonin agonists (fenfluramine and dexfenfluramine) were rushed into clinical use. However, they were subse- quently withdrawn from the market because chronic use was found to be associated with heart disease in a small, but significant, number of users. Currently, the search is on for serotonergic weight-loss medications that do not have dan- gerous side effects.

Gastric Surgery Cases of extreme obesity sometimes warrant extreme treatment. Gastric bypass is a surgical treatment for extreme obesity that involves short-circuiting the normal path of food through the digestive tract so that its absorption is reduced. The first gastric bypass was done in 1967, and it is currently the most commonly pre- scribed surgical treatment for extreme obesity. An alter- native is the adjustable gastric band procedure, which involves surgically positioning a hollow silicone band around the stomach to reduce the flow of food through it; the circumference of the band can be adjusted by inject- ing saline into the band through a port that is implanted in the skin. One advantage of the gastric band over the gastric bypass is that the band can readily be removed.

The gastric bypass and adjustable gastric band are illustrated in Figure 12.17. A meta-analysis of studies comparing the two procedures found both to be highly effective (Maggard et al., 2005). However, neither proce- dure is effective unless patients change their eating habits.

12.7 Anorexia and Bulimia Nervosa

In contrast to obesity, anorexia nervosa is a disorder of underconsumption (see Södersten, Bergh, & Zandian, 2006). Anorexics eat so little that they experience health- threatening weight loss; and despite their emaciated appearance, they often perceive themselves as fat (see Benning- hoven et al., 2006). Anorexia nervosa is a serious condition; In approximately 10% of diagnosed cases, complications from starvation result in death (Birmingham et al., 2005), and there is a high rate of suicide among anorexics (Pompili et al., 2004).

Anorexia nervosa is related to bulimia nervosa. Bulimia nervosa is a disorder characterized by periods of not eating interrupted by bingeing (eating huge amounts of food in short periods of time) followed by efforts to immediately eliminate the consumed calories from the body by voluntary purging (vomiting); by excessive use of laxatives, enemas, or diuretics; or by extreme exercise. Bu- limics may be obese or of normal weight. If they are un- derweight, they are diagnosed as bingeing anorexics.

Relation between Anorexia and Bulimia Are anorexia nervosa and bulimia nervosa really different disorders, as current convention dictates? The answer to this question depends on one’s perspective. From the perspec- tive of a physician, it is important to distinguish between these disorders because starvation pro- duces different health problems than does repeated bingeing and purging.

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For example, anorexics often require treatment for reduced metabolism, bradycardia (slow heart rate), hypotension (low blood pressure), hypothermia (low body temperature), and anemia (deficiency of red blood cells) (Miller et al., 2005). In contrast, bulimics often require treatment for irritation and inflammation of the esophagus, vitamin and mineral defi- ciencies, electrolyte imbalance, dehydration, and acid reflux.

Although anorexia and bulimia nervosa may seem like very different disorders from a physician’s perspective, sci- entists often find it more appropriate to view them as vari- ations of the same disorder. According to this view, both anorexia and bulimia begin with an obsession about body image and slimness and extreme efforts to lose weight. Both anorexics and bulimics attempt to lose weight by strict diet- ing, but bulimics are less capable of controlling their ap- petites and thus enter into a cycle of starvation, bingeing, and purging (see Russell, 1979). The following are other similarities that support the view that anorexia and bulimia are variants of the same disorder (see Kaye et al., 2005):

● Both anorexics and bulimics tend to have distorted body images, seeing themselves as much fatter and

less attractive than they are in reality (see Grant et al., 2002).

● In practice, many patients seem to straddle the two di- agnoses and cannot readily be assigned to one or the other categories and many patients flip-flop between the two diagnoses as their circumstances change (Lask & Bryant-Waugh, 2000; Santonastaso et al., 2006; Ten- coni et al., 2006).

● Anorexia and bulimia show the same pattern of distri- bution in the population. Although their overall inci- dence in the population is low (lifetime incidence estimates for American adults are 0.6% and 1.0% for anorexia and bulimia, respectively; Hudson et al., 2007), both conditions occur more commonly among educated females in affluent cultural groups (Lind- berg & Hjern, 2003).

● Both anorexia and bulimia are highly correlated with obsessive-compulsive disorder and depression (Kaye et al., 2004; O’Brien & Vincent, 2003).

● Neither disorder responds well to existing therapies. Short-term improvements are common, but relapse is usual (see Södersten et al., 2006).

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From esophagus From esophagusStaples create a smaller stomach pouch

Stitches

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Adjustable band slows passage of food through stomach

Skin

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Anorexia and Positive Incentives The positive-incentive perspective on eating suggests that the decline in eating that defines both anorexia (and bulimia) is likely a consequence of a corresponding de- cline in the positive-incentive value of food. However, the

positive-incentive value of food for anorexia patients has received little attention—in part, because anorexic

patients often display substantial interest in food. The fact that many anorexic patients are obsessed with food— continually talking about it, thinking about it, and preparing it for others (Crisp, 1983)—seems to suggest that food still holds a high positive-incentive value for them. However, to avoid confusion, it is necessary to keep in mind that the positive-incentive value of interacting with food is not necessarily the same as the positive-incentive value of eating food—and it is the positive-incentive value of eating food that is critical when considering anorexia nervosa.

A few studies have examined the positive-incentive value of various tastes in anorexic patients (see, e.g., Drewnowski et al., 1987; Roefs et al., 2006; Sunday & Halmi, 1990). In general, these studies have found that the positive-incentive value of various tastes is lower in anorexic patients than in control participants. However, these studies grossly under- estimate the importance of reductions in the positive- incentive value of food in the etiology of anorexia nervosa, because the anorexic participants and the normal-weight control participants were not matched for weight—such matching is not practical.

We can get some insight into the effects of starvation on the positive-incentive value of food by studying starva- tion. That starvation normally triggers a radical increase in the positive-incentive value of food has been best docu- mented by the descriptions and behavior of participants voluntarily undergoing experimental semistarvation. When asked how it felt to starve, one participant replied:

I wait for mealtime. When it comes I eat slowly and make the food last as long as possible. The menu never gets mo- notonous even if it is the same each day or is of poor quality. It is food and all food tastes good. Even dirty crusts of bread in the street look appetizing. (Keys et al., 1950, p. 852)

Anorexia Nervosa: A Hypothesis The dominance of set-point theories in research into the regulation of hunger and eating has resulted in wide- spread inattention to one of the major puzzles of anorexia: Why does the adaptive massive increase in the positive-incentive value of eating that occurs in victims of starvation not occur in starving anorexics? Under condi- tions of starvation, the positive-incentive value of eating normally increases to such high levels that it is difficult to imagine how anybody who was starving—no matter how

controlled, rigid, obsessive, and motivated that person was—could refrain from eating in the presence of palat- able food. Why this protective mechanism is not activated in severe anorexics is a pressing question about the etiol- ogy of anorexia nervosa.

I believe that part of the answer lies in the research of Woods and his colleagues on the aversive physiological effects of meals. At the beginning of meals, people are nor- mally in reasonably homeostatic bal- ance, and this homeostasis is disrupted by the sudden infusion of calories. The other part of the answer lies in the finding that the aversive effects of meals are much greater in people who have been eating little (Brooks & Melnik, 1995). Meals, which produce adverse, but tolerable, effects in healthy individuals, may be extremely aversive for individuals who have undergone food deprivation. Evidence for the extremely noxious effects that eating meals has on starving humans is found in the re- actions of World War II concentration camp victims to refeeding—many were rendered ill and some were even killed by the food given to them by their liberators (Keys et al., 1950; see also Soloman & Kirby, 1990).

So why do severe anorexics not experience a massive in- crease in the positive-incentive value of eating, similar to the increase experienced by other starving individuals? The answer may be meals—meals forced on these patients as a result of the misconception of our society that meals are the healthy way to eat. Each meal consumed by an anorexic may produce a variety of conditioned taste aversions that reduce the motivation to eat. This hypothesis needs to be addressed because of its implication for treatment: Anorexic patients—or anybody else who is severely under- nourished—should not be encouraged, or even permitted, to eat meals. They should be fed—or infused with—small amounts of food intermittently throughout the day.

I have described the preceding hypothesis to show you the value of the new ideas that you have encountered in this chapter: The major test of a new theory is whether it leads to innovative hypotheses. A while ago, as I was perusing an article on global famine and malnutrition, I noticed an in- triguing comment: One of the clinical complications that results from feeding meals to famine victims is anorexia (Blackburn, 2001). What do you make of this?

The Case of the Anorexic Student In a society in which obesity is the main disorder of con- sumption, anorexics are out of step. People who are struggling to eat less have difficulty understanding those who have to struggle to eat. Still, when you stare anorexia in the face, it is diffi- cult not to be touched by it.

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She began by telling me how much she had been enjoy- ing the course and how sorry she was to be dropping out of the university. She was articulate and personable, and her grades were high—very high. Her problem was anorexia; she weighed only 82 pounds, and she was about to be hospitalized.

“But don’t you want to eat?” I asked naively.“Don’t you see that your plan to go to medical school will go up in smoke if you don’t eat?”

“Of course I want to eat. I know I am terribly thin— my friends tell me I am. Believe me, I know this is wreck- ing my life. I try to eat, but I just can’t force myself. In a strange way, I am pleased with my thinness.”

She was upset, and I was embarrassed by my insensi- tivity. “It’s too bad you’re dropping out of the course be- fore we cover the chapter on eating,” I said, groping for safer ground.

“Oh, I’ve read it already,” she responded. “It’s the first chapter I looked at. It had quite an effect on me; a lot of things started to make more sense. The bit about posi-

tive incentives and learning was really good. I think my problem began when eating started to lose its positive- incentive value for me—in my mind, I kind of associ- ated eating with being fat and all the boyfriend problems I was having. This made it easy to diet, but every once in a while I would get hungry and binge, or my parents would force me to eat a big meal. I would eat so much that I would feel ill. So I would put my fin- ger down my throat and make myself throw up. This kept me from gaining weight, but I think it also taught my body to associate my favorite foods with illness— kind of a conditioned taste aversion. What do you think of my theory?”

Her insightfulness impressed me; it made me feel all the more sorry that she was going to discontinue her studies. After a lengthy chat, she got up to leave, and I walked her to the door of my office. I wished her luck and made her promise to come back for a visit. I never saw her again, but the image of her emaciated body walking down the hallway from my office has stayed with me.

325Think about It

Themes Revisited

Three of the book’s four themes played prominent roles in this chapter. The thinking creatively theme was prevalent as you were challenged to critically evaluate your own beliefs and ambiguous research findings, to consider the

scientific implications of your own experiences, and to think in new ways about phenomena with major personal

and clinical implications. The chapter ended by using these new ideas to develop a potentially important hypothesis about the etiology of anorexia nervosa. Because of its emphasis on thinking, this chapter is my personal favorite.

Both aspects of the evolutionary perspective theme were emphasized repeatedly. First, you saw how thinking about hunger and eating from an evolutionary perspective leads to important insights. Second, you saw how controlled research on nonhuman species has contributed to our current understanding of human hunger and eating.

Finally, the clinical implications theme pervaded the chapter, but it was featured in the cases of the man who forgot not to eat, the child with Prader-Willi syndrome, the child with no leptin, and the anorexic student.

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Think about It

1. Set-point theories suggest that attempts at permanent weight loss are a waste of time. On the basis of what you have learned in this chapter, design an effective and per- manent weight-loss program.

2. Most of the eating-related health problems of people in our society occur because the conditions in which we live are different from those in which our species evolved. Discuss.

3. On the basis of what you have learned in this chapter, de- velop a feeding program for laboratory rats that would lead to obesity. Compare this program with the eating habits prevalent in your culture.

4. What causes anorexia nervosa? Summarize the evidence that supports your view.

5. Given the weight of evidence, why is the set-point theory of hunger and eating so prevalent?

IS B

N 0-

55 8-

78 57

1- 9

Biopsychology, Eighth Edition, by John P.J. Pinel. Published by Allyn & Bacon. Copyright © 2011 by Pearson Education, Inc.

 

 

326 Chapter 12 ■ Hunger, Eating, and Health

Set point (p. 299)

12.1 Digestion, Energy Storage, and Energy Utilization Digestion (p. 299) Lipids (p. 300) Amino acids (p. 300) Glucose (p. 300) Cephalic phase (p. 301) Absorptive phase (p. 301) Fasting phase (p. 301) Insulin (p. 301) Glucagon (p. 301) Gluconeogenesis (p. 301) Free fatty acids (p. 301) Ketones (p. 301)

12.2 Theories of Hunger and Eating: Set Points versus Positive Incentives Set-point assumption (p. 302) Negative feedback systems

(p. 303)

Homeostasis (p. 303) Glucostatic theory (p. 303) Lipostatic theory (p. 303) Positive-incentive theory

(p. 304) Positive-incentive value (p. 304)

12.3 Factors That Determine What, When, and How Much We Eat Satiety (p. 306) Nutritive density (p. 306) Sham eating (p. 306) Appetizer effect (p. 307) Cafeteria diet (p. 308) Sensory-specific satiety (p. 308)

12.4 Physiological Research on Hunger and Satiety Ventromedial hypothalamus

(VMH) (p. 309) Lateral hypothalamus (LH)

(p. 310) Hyperphagia (p. 310)

Dynamic phase (p. 310) Static phase (p. 310) Aphagia (p. 310) Adipsia (p. 310) Lipogenesis (p. 310) Lipolysis (p. 310) Paraventricular nuclei (p. 311) Duodenum (p. 312) Cholecystokinin (CCK) (p. 312) Prader-Willi syndrome (p. 313)

12.5 Body Weight Regulation: Set Points versus Settling Points Diet-induced thermogenesis

(p. 315) Basal metabolic rate (p. 315) Settling point (p. 316) Leaky-barrel model (p. 316)

12.6 Human Obesity: Causes, Mechanisms, and Treatments NEAT (p. 319) Leptin (p. 320)

Ob/ob mice (p. 320) Subcutaneous fat (p. 321) Visceral fat (p. 321) Arcuate nucleus (p. 321) Neuropeptide Y (p. 321) Melanocortins (p. 321) Melanocortin system (p. 321) Gastric bypass (p, 322) Adjustable gastric band

procedure (p. 322)

12.7 Anorexia and Bulimia Nervosa Anorexia nervosa (p. 322) Bulimia nervosa (p. 322)

Key Terms

Test your comprehension of the chapter with this brief practice test. You can find the answers to these questions as well as more practice tests, activities, and other study resources at www.mypsychlab.com.

1. The phase of energy metabolism that often begins with the sight, the smell, or even the thought of food is the a. luteal phase. b. absorptive phase. c. cephalic phase. d. fasting phase. e. none of the above

2. The ventromedial hypothalamus (VH) was once believed to be a. part of the hippocampus. b. a satiety center. c. a hunger center. d. static. e. dynamic.

3. Patients with Prader-Willi syndrome suffer from a. anorexia nervosa. b. bulimia. c. an inability to digest fats. d. insatiable hunger. e. lack of memory for eating.

4. In comparison to obese people, slim people tend to a. have longer life expectancies. b. be healthier. c. be less efficient in their use of body energy. d. all of the above e. both a and b

5. Body fat releases a hormone called a. leptin. b. glucagon. c. insulin. d. glycogen. e. serotonin.

Quick Review

IS B

N 0-558-78571-9

Biopsychology, Eighth Edition, by John P.J. Pinel. Published by Allyn & Bacon. Copyright © 2011 by Pearson Education, Inc.

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