Transcript No Slide Title

Health Psychology
Chapter 13:
Smoking Tobacco
Mansfield University
Dr. Craig, Instructor
1
Tobacco Use and Mortality
 400,000 death’s yearly
 20% of deaths directly related to Tobacco Use
 3 leading causes of death

Heart Disease



Cancer



180,000 attributable to smoking
nicotine effect on CV physiology & atherosclerotic effects
150K/annually, 120K from lung cancer
all cancers, especially lung, strongly related to smoking
COPD

85,000 deaths annually; 80% from smoking
 Other Bad Stuff: facial wrinkling, impotence, gum disease,
macular degeneration
Effects of Passive Smoking
 Passive Smoking a/k/a
• Environmental Tobacco Smoke (ETS)
• Second Hand Smoke
• Side Stream Smoke
 Lung Cancer- elevates risk between 20-30%
 Breast Cancer- almost as strong as active smoking!!

a “strong” dose-response relationship

2 hours a day for 25 years, tripled risk

even stronger relationship if exposed as a child
 Heart Disease- increases risk of CHD 20-30%,

of 30-60,000 ETS related deaths annually, 75% from Heart
Disease
Passive Smoking and Children’s Health
 1700 infant mortalities through ETS annually

dose-response relationship between SIDS risk and
number of cigarettes smoked by mother
 Other effects


low-birth weight babies
Smoking around children less than 2 years:
bronchitis, pneumonia, asthma, childhood cancers
& lower respiratory tract infections.
Breathing and Defending Against Particles
 Nasal Passage > Pharynx > Larynx > Trachea >
Bronchi > Bronchioles >

to Alveoli (CO2-O2 exchanged here)
 All prior of alveoli- work to cleanse, warm, and humidify
inspiration
 Sneezing, coughing, swallowing all defensive physiology
against airborne particles
 Mucociliatory Escalator (MCE)- cilia transport mucous
and engulfed particle out of lungs/nasopharynx to be
coughed up/swallowed.
 Smoking effects physiological processes by
obstructing pulmonary (lung) function
Smoking and COPD
 Chronic Bronchitis

smoking increases mucous secretion > MSE
activity decreased> excess mucous collection >
coughing reflex leads to intense coughing fits >
permanent damage/scarring of cilia and respiratory
tissue.
 Emphysema


scar tissue in bronchioles obstructs expiration
O2 oxidizes alveoli walls and obstructs capillaries
delivering blood to alveoli. CO2 not exchanged for
O2, reduced physical functioning.
“What you been smokin’?”
 4000 chemical compound in a burning cigarette
 Nicotine- 30-40 minute half-life (between cigarettes)

Stimulates CNS receptors in pleasure areas of brain
• leads to endorphin and opiate release
• underlying addictive component

Stimulates SNS and general metabolism
 Tars


carcinogens
varying directly with nicotine content (low tar/low
nicotine)
low tar cigarettes and compensating smoking behavior
Who smokes? Part I
 Percent smoker, former, non-smoker 1965-1995
Who Smokes?
Part II
 Smoking and
Education

1966-1994
Who Smokes? Part III
 Smoking in Males and Females

Males smoke a little more than women, but rate of
decline much greater among men… may be smaller
within 10 years or so
 Adolescent Smoking--- the new challenge

rates have markedly increased in the past 10 years
• 10% for women, 25% for men

40% of white adolescents!
 Characteristics- social/health risk takers

dissatisfaction with education, low grade
depression, cluster with unhealthy behaviors
The Key Questions for Scientists, Part I
 1. Why do adolescents start especially when the
hazards of smoking are generally understood?


Optimistic bias regarding health and difficulty
quitting
Present threats are more salient
 Leventhal & Cleary- 3 reasons



tension control (stress/relaxation/pleasure)
rebellion
social pressure- situational factors appear
particularly strong


also sibling, parents
body image needs, weight concerns
 Risk of Addiction- 100 lifetime or 15 a day.
The Key Questions for Scientists, Part II
 Why do people continue to smoke?
 Tomkins and Smoking Behavior



Habitual Smoker- a matter of habit, little attention
or thought to smoking
Positive/Negative Affect Smoker (Pleasure/Taste)increase relaxation and/or decrease feeling of
anxiety or stress etc.
Addicted Smoker- keenly aware of when they are
NOT smoking… can tell you how long since last
and prepare so they are never without
 Also- “environmentally cued smoking”
Why continue to smoke
 Nicotine Addiction Model- suggest that people
continue to smoke to maintain basic level of
nicotine to prevent withdrawal
 support• double-blind studies with high and low nicotine
cigarettes. Smokers adjusted behavior despite not
knowing nicotine content.
• More and deeper “puffs” from low nicotine cigarettes
 Can’t explain why people start though or why
nicotine delivery products (patch) don’t work with
everyone and is still hard for those who succeed.

Nicotine plays a role, but not the only factor!!
Starting and Continuing to Smoke- SLM
 Social Learning Model of Smoking

people learn patterns of behavior that are social reinforced
by other we deem to be important
 The first cigarette, often not pleasant experience

how is this often negative experience overcome?
 Both positive and negative social reinforcement
in action
Deterring Smoking
 information on its own is not a deterrent
 More success: buffering or “innoculation”
programs



taught about situations that pressure to smoke
might be high
role model refusal/counter social pressure
particularly effective when peer-led and combined
with community anti-smoking campaigns
Quitting Smoking
 Cognitive barriers and Addictive Barriers
• refusal to recognize risks
• refusal to personalize risks
• combined addictions: Smoking and Alcohol
 More people quit on their own than through
programs (“cold turkey”)- 60% success rate
• no difference in success rates between light/heavy
smokers
 Programs- eventually, about 60%, lower initially
• Quitting rates should not be based on programs numbers
• tend to attract those w/o success on own
• tendency to fail 1 or 2 times, but succeed by third
Quitting Smoking
 Nicotine Replacement Therapy

gum: 15% to 9% in placebo control


patch 22% to 9% in placebo control


tends to maintain weight better than the patch
w/ bupropion increases to 35% success after 1 year
Effectiveness increased when combined with drugs
and psychological interventions
 Psychological Interventions- deal with affect/ cognitive/social
element that reinforce smoking
• improving self-efficacy- point out previous successive,
note likelihood of success
• sensitizes to environmental cues to smoke
• stress management techniques
Increasing the Odds & Relapse Control
 Married/Supportive S.O.







particularly if supported by spouse/so
Previous attempts
Longer quit attempts
Reducing smokers in social network
Reduce alcohol consumption
Heart disease diagnosis (not cancer though!)
Increase self-efficacy- personal control over smoking
 RELAPSE CONTROL
• identify relapse factors, addresses and control, quit
again.
• Phone follow-ups, social encouragement
What about weight gain? My a** is already fat!
 Research Fact: There is a tendency to gain on average of 9
lbs. for men and 11 lbs. for women while quitting if
sedentary in the first year
 Research Fact: Non-smokers and smokers tend to gain
more than 5 lbs. a year
 Research Fact: After 2 years of abstinence, weight of
quitters and matched-smokers is the same on average.
 Research Fact: Moderate exercise with quitting will
minimize weight gain and increases the metabolism
making weight hard to put on.
 Research Fact: Gain in life expectancy (5-8 years) and
reduce disease risks far outweigh risk associated with
weight gain during quitting.
Health and Bodily Effects of Quitting
 Overall Mortality
• Figure 13.7
 Light Smokers

after 16 years have
same risk as never
smokers for cancer
& CHD, stroke
 Heavy Smokers

dramatically cut
HD risk, stroke, less
so for lung cancer