Aging and Health Advanced Adult Development Select a 3-4 of critical thinking questions from each chapter and answer them in written format, summarizing ke

Aging and Health Advanced Adult Development Select a 3-4 of critical thinking questions from each chapter and answer them in written format, summarizing key ideas, evaluating information, and relating it to real life experiences. Note: The critical thinking questions appear in blue in the margins of pages throughout each chapter, not at the end of chapters. lhysical
lhanges
M I -rwN
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l,/)(.JI
, Nicholas, was 5, I was
writ-
child development. I wanted to open each chapter with
M:f
sonal story that would introduce the topic (much as
hr
{icholas was a rich source of material.
p,itive processes, and
ke value. They
I
was
I
a
am
writing about
I knew that at 5, they tend to judge
are convinced that the glass
with the highest
rde holds the most, regardless of how narrow the diameter is.
rc of
d-
M&Ms
has the most candy, regardless of
how far aparr
And people who are taller are older, period.
lNicholas who was older, Grandma or Dad. He quickly
Dad (who is 5′ 11″) is certainly older than Grandma (who is
!
he aiso knew that Dad was Grandma’s son. He knew that
rd Grandma was 54, and that 54 is more than 30, but logic
mt at 5. I was pleased-so far, he was perfectly illustrating
@ncepts in my textbook chapter.
od-‘How do you tell how old a person is?” I expected him to
re
height or fie color of their hair. But I was surprised when he
mk at their hands.” Hands? 7ell, I thought, I
guess
that’s true.
ilder people have dark spots and larger knuckles. Adolescents
r& in proponion to their other body parts. And infants
have
dmed in reflexive fists. I thought he may be onto something
I adrcd, “7hat do you look for when you look at their hands?”
I
Chapter 2
“Their fingers,” he said patiently. He held up one hand with outstretched fingers ar
said, “You ask someone how old they are and when they hold up their fingers, you cour
rhem. See, I’m five.”
Nicholas’s hypothesis of determining age by looking at hands may hold up wit
kids up to the age of 10, but it’s not much use in adulthood. In fact, the further we g
from “holding up fingers” to tell our ages, the more difficult it is to determine age ju
by looking at someone. One of the reasons is that we have two processes of aging goir
on. Primary aging, which is the topic of this chapter, consists of the gradual, inevitab
changes that will happen to most of us as we go through adulthood. Research over tL
last feu’ decades has given us two major facts about primary aging: first, that it can L
differentiated from disease, and second, that there are many different “normal” time linr
for priman-aging (National Institutes of Health, 2008). S€€ordaqt’ryhg, which will L
rhe ropic of the follorving chapter, refers to the changes that happen more suddenly an
thar are usua.llv the result of disease, injury, or some environmental event.
I *-ill beein this chapter with some of the theories of primary aging and then describ
the changes in rhe major systems of the body most adults experience as they age. Then
s-ill discuss the effecrs of primary aging on complex behaviors like sleep and sexual actir
in-. Finalir-. I *’ill cover some of the individual differences that are found in primary agin
parrerns and anss-er rhe age-old question, “Can we turn back the clock?”
Theories of Primary Aging
\hl
do l.’e agel This has been the subject of speculation for centuries, but the technol
og]- necessan’ ro evaluate it is fairly new. As a result, the biology of aging is a relativel
l’ouns
t-ield ri’rrh a plethora of data
but no grand theories on which
a significant numbe
e I Finch & Austad, 200 1). Instead, a hundred or more fledgling theorie
of scientisrs
har.e been o*ered br- r.arious biologists. As behavior geneticists Gerald McClearn an,
Debra Heller r1000) suggested, “The scientific pessimist might lament the absence of
compeilins unirred rheon’; the scientific optimist wili revel in the richness of the empirice
data and the diversin-of the current theoretical propositions” (p. 1). I have selected a fer
of the more re cent rheories to describe here, along with suppor and criticism for each.
aqre
.)
I
Oxidative Damage
One theon- of priman’aging is based on random damage that takes place on the cellula
J
a
a
i
a
c
in 1956, involve
the release of free radicals, molecules, or atoms that possess an unpaired electron and ar
bv-producrs oinormal body metabolism as well as a response to diet, sunlight, X-rays, an
air pollurion. These molecules enter into many potentially damaging chemical reactionr
mosr oi ri-hich the healthy body can resist or repair. But, according to this theory, ou
resisrance and repair functions decline as we age, the oxidative damage increases, and th
result is priman’aging. We now have over 60 years of research showing that oxidative darr
age ltccontp{tTties agtng, but we still are not able to state thatit causes aging (Bengston, Ganr
Putner’, et al., 2009). The most researchers are willing to say is that oxidative damage is on
of ser.eral factors involved in primary aging (Lustgarten, Muller, & Van Remmen, 2011
A number of vitamins and vitamin-like substances have been identified as anti
oxidants, substances with properties that protect against oxidative damage. Some c
these are vitamins E and C, coenzyme Q10, beta-cafotene, and creatine. Many nutritioni
supplements on the market contain large doses of these substances and advertise therr
selves as having antioxidant properties. However, there is no evidence that they can dela
Ier.el. This process. first identified by biogerontoiogist Denham Harmon
I rrlDlla
g in humans or extend the life span. Most people in developed countries
e supplies of these nutrients in their diets, and no benefit has been shown
rn-recommended doses.
ts
Tofgenetic limits centers on the observation that every species has a characterrm life span. Something between 110 and 120 years appears to be the effecE life span for humans, whereas for turtles it is far longer, and for chickens
rcars, or cows, or most other mammals) it is far shorter. Such observadons
tl-ologist Leonard Hayflick (1977,1994) to propose that there is a genetic
ping the upper age limit of each species. Hayflick showed that when human
Lere placed in nutrient solutions and observed over a period of time, the cells
ptout 50 times, after which they stop dividing and enter a state known as
tscscerce (Hornsby, 2001). Furthermore, cells from the embryos of longerFsrch as the Galdpagos tortoise double perhaps 100 times, whereas chicken
)a””U. only about 25 times. The number of divisions a species will undergo
EIE replicative senescence is known as its Hayflick limit, and there is a posih between that number and the species’ longeviry. According to the genetic
bpr-r.1, aging results when we approach the Hayflick limit for the human
hiry our cells’ abiliry to replicate themselves.
Lr.d mechanism behind the genetic limits theory of aging comes from the
hchromosomes in many human body cells (and those of some other species,
Iadr rips, lengths of repeating DNA called telomeres. Telomeres are neces]-pfication and appear to serve as timekeepers for the cells. On average, the
of a middle-aged adult are shorter than those of a young adult; the
}:”at
tsdd.r adult are shorter still. And once the telomeres are used up, the cell
},ln addition, telomere lengths for males and females are the same at birth,
Ed” fiey are longer in females than in males, Ieading some to ask whether
Se fact that women live about 6 years longer than men in developed
!t
}HtJ^
0″.r, related to both primary and
seconda
ry
aging.people who
,:i::
JxXx*:.;::i:’Tn3f::ililT:”‘t:::’:.’,’j.”.T::’i:’if
group
a
of mothers who were caregivers for children with
If-,.
mrdy,
foond ,J hrrr. telomere lengths equivalent Io women 10 years older
tT,Hi:1il^i.,1Tilil’lfi’:f :HlH;;’*;i?3?i:TTf I;
r-trs’ down the loss of telomere length in one’s celis? This was the
:redical researcher Tim D. Spector and his colleagues (Cherkas,
. 1008), rvho interviewed over 2,400 individuals berween 18 and 81
=:r leisure time exercise. Following the interview, a sample of blood
– rarticipant, and the telomeres from their white blood cells were
j-ners found that those in the light, moderate, and heary exercise
., significantly longer telomeres than those in the inactive group.
:=’.r’exercise group had telomere lengths similar to the people in the
,.
=ie 10 years younger. The hear.y exercise group averaged about 30
. ;-.-,’: rhe inactive group averaged just over 2 minutes a day. It was
“leisure time exercise.” tiThen
=,..rcise described in this study was

Chapter 2
researchers examined the amount of work-related exercise the participants got (such as
stocking shelves in a grocery store), the results were not significant. This suggests that the
“leisure” mode is a key feature of beneficial exercise.
It seems that shorter telomere lengths are good predictors of premature aging and
age-related diseases. It also seems that shorter telomere lengths go hand in hand with
poor health habits such as obesiry, cigarette smoking, and a sedentary lifesryle. None of
this research shows that telomere length determines the rate of aging, but the relationships
are very strong (Aviv, 2011). Again, the advice to take away from this research is to eat
healthy, find ways to reduce or cope with chronic stressors, and enjoy leisure time exercise
regularly. I will discuss the relationship berween stress and health in Chapter 10.
Caloric Restriction
One of the most promising explanations of why we age is that aging is connected with
6u1 dls15-not so much what we eat, but how many calories we metabolize per day. This
idea was first suggested 50 years ago when researchers studied the effects ofcaloric restriction (CR) on lab animals by feeding them diets drastically reduced in calories (600/o to
70o/o of normal diets), but containing all the necessary nutrients. Early researchers found
that animals put on these diets shortly after weaning stayed youthful longer, suffered
I
t
fewer late-life diseases, and lived significantly longer than their normally fed counterparts
(McCay, Crowell, & Maynard, 1935) .More recent studies have supported these findings.
For example, studies with rhesus monkeys show that animals on caloric restriction show
a lower incidence of age-related disease, including qpe 2 diabetes, cancer, heart disease,
and brain atrophy (Colman, Anderson, Johnson, et al., 2009).
Would caloric restriction increase human longevity? One problem is that to receive
maximum benefits, we would have to reduce our caloric intake 6y 30o/o. People eating
a 2,000-calorie diet would need to cut back to 1,400 calories-difficult enough for a
few months, but close to impossible as a lifetime regimen. Limited studies using human
subjects on CR have shown some positive health benefits such as protection against
type 2 diabetes and heart disease and a reduction in cancer incidence and cancer deaths
(Fontana, Colman, Holloszy, et a1.,2011); however, a number of adverse effects have
also been documented. These include cold intolerance, increases in stress hormones,
decreases in sex hormones, and the psychological effeos of extreme hunger-obsessive
thoughts about food, social withdrawal, irritabiliry, and loss of interest
in sex. If the goals of caloric restriction are longeviry and freedom from
disease, this practice seems successful. But if the goals are qualiry of life,
7hat would a daily meal plan be for
severely restricting calories does not seem to be the answer, especially in
someone on a diet of 1,400 calories per
the developed countries of the world, where food cues are abundant and
day?
attractive (Polivy, Herman, 8r Coelho, 2008).
Scientists have now turned
to finding a substance that provides the
same health and longeviry as caloric restriction without reducing normal food intake.
Several candidates have been found, such as resueratrzl, a substance found in red wine
that extended the life spans of yeast, worms, and flies. However, the results on mammals
were disappointing. Another substance, rapamycin, has been more promising (Kapahi &
Kockel, 2011). Originally found in soil collected on Easter Island, rapamycin inhibits cell
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t
growth and was first used as an antirejection medication for organ transplant patients.
Studies of the effects of rapamycin on mice extended maximum life span by some 12%o
(Miller, Harrison, Astle, et al.,20L 1), including some mice that were the human equivalent of 50 years of age (Harrison, Strong, Sharp, et al., 2009). Rapamycin works to
block the effects of a protein called TOR, which scientists believe is implicated in many
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Physical
,.:rs primary aging itself. TOR has the effect of sensing the
:.lrism. and in times of plenty, it becomes active and directs
– . ”l-he n lbod is scarce (as in caloric restriction), TOR reduces
-:.. and one of the results seems to be increased longeviry
-.-,’. rapamvcin itself has side effects that rule it out for human
::,-r)r compelling evidence I have seen that aging in mammals
ll,
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mr
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someday be slowed by a pharmaceutical product.
efPti-.ryAging
ein not to expect that any single theory will be proven to be the
ser ro the question of why we age. In fact, the “separate” theories
nning to cross boundaries and merge. For example, researchers
rc res[iction may reduce the neuronal damage of Alzheimer’s
;dis€ase explain that the mechanism for this is that it protects
in rhe DNA of neurons, an explanation that blends the dietary
i&tive srress theory. And the study of high-stressed women with
ndomeres also reports that these women had more free radical
nwomen in the control group-a finding that combines genetic
SL
s is dearly a good example of the process of scientific investiga-
competition over which theory is right, but different researchers
rrction, “Why do we age?” with their own methods and theories,
ilsrrrrs that bring us closer to the truth.
During Adulthood
ook cover changes in thinking abilities, personaliry, spiritualiry,
ring adulthood. This one deals with the physical aspect of adult
gwirh outward appearance and working through the senses, vari. and ending with a discussion of individual differences in primary
nd
about our outward appearance and how it will change as we
lukhood. Many of the most obvious signs of aging belong in this
and grandparents, in our friends, and sometimes
“rn in our parents
d€cred rwo categories for this 5sglien-wsight and body composiEse are concerns for adults ofall ages, including textbook authors.
rcition. Studies of adults in the United States show that changes
h*, p”,,.rn over adulthood, as you can see Figure 2. 1, first risi’ng
r staving level into the 50s and 60s, then declining in the 70s, folgraph of an inverted U (Rossi, 2004). The upswing in weight that
ns adulthood and middle age can be attributed to our tendency to
re rdentary during that dme without changing our eating habits
o- 2011). The downturn in total body weight that takes place in
ro loss of bone densiry and muscle tissue (Florido, Tchkonia, &
Chapter 2
Women
170
tb3
160
2.1 Both men
and women gain
Figure
weight in young adulthood and middle adulthood, losing in the late
50s, but in slightly different patterns.
I55
a
!o
a
E
C
f,
tao
(L
o_
174
135
130
125
Source; Adapted from Rossi
12004).
140
120
il
2s-2s 30 3e
‘*’Jl;il.i’;1155-5e
60-6e
70-74
25-2e 30-3e
*”‘Ji,;il.i’;54
55-5e 60-6e 70-74
Along with changes in total body weight, there are also changes in where thr
weight is distributed; starting in middle age, fat slowly leaves the face and extremities
and begins to accumulate around the abdomen, resulting in a loss of plump cheeks
and lips, a loss of protective padding on the soles of the feet, and a gain in waistline
circumference.
7hen a person’s total body weight is more than is considered optimally healthy for
their height, they are considered overweight. This is a concern for adults of all ages,
and rightly so-almost two thirds of us in the United States are above optimal weight.
Being overweight can impair movement and flexibility, and it can alter appearance.
Our society does not generally view overweight individuals as healthy and attractive,
and this can result in social and economic discrimination (Lillis, Levin, & Hayes,
2011).
-il/hen
I
a
I
t
L
4
(‘t-1
the weight-to-height ratio increases to the point that it has an adverse effect on
the person’s health, it is a medical condition known as obesity. Over one third of adults
in the United States have this condition-or half of the overweight people in this country
have total body weight that puts them at risk for numerous health disorders.
How do you stand in the body composition evaluation? Ta61e2.l shows how to find your
body mass index (BMI) by finding your height (in inches) in the far Ieft column and moving
across that row to find your weight. The number at the top of the column
is your BMI. According to the Centers for Disease Control and Prevention
(CDC, 2011b), BMIs less than 19 are considered underweighr, 19 o 24 are
lWhere do some of the people on the
considered normal weight, 25 ro 29 are overweight, and 30 and above are
“Ten Most Beautiful” lists rank on the
obese. This is not a perfect system because some healthy, very muscular people
BMI scale?
would be assigned the “overweight” label based on their height and weight,
but the BMI is used by most health organizations and medical researchers
around the world to evaluate body composition.
Adults who are 60 and over are slighdy more likely to be obese, but as you can see in
Figure 2.2, the proportion of obese adults in other age groups is not much lower (Ogden,
Carroll, Kit, et aJ., 2012). Still, the fact remains that over one third of all aduits (and 17o/o
of children) have tota.l body weight that is considered a serious medical condition (CDC,
201 1b).
‘fi{hat can be done about age-related changes in body composition? An active lifestyle
in young adulthood and middle adulthood will help minimize age-related weight gain and
the amount of fat that accumulates in the abdomen at middle age. Strength training and
flexibiliry exercises throughout adulthood will help maintain bone densiry and muscle.
Healthy eating habits can reduce excess fat. However, nothing has been found thar will
i ,r,r
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l’/(il(llll.
BMI
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lritrrrl r:olrrrrrrr Movr: it(:tr):j:; tow l{) ;t (llv(jn w(il(lltl Ilrc nurrrbr.:r itl lltu tol) ol tltu colunlt ts tll0 [JMl al tlral lrerglrl antl
Normal Weight
22 23
Height (!nches)
58
59
60
74
‘148
63
64
65
66
67
68
69
70
71
72
75
76
152
156
120
111
115
118
122
126
124
r30
106
109
1
13
116
147
134
138
142
146
150
154
151
i59
121
131
135
139
143
1
55
160
164
116
120
124
128
132
136
r40
144
r49
153
157
162
166
163 171
‘t68 176
172 180
122
126
130
134
138
142
146
151
121
131
135
140
144
150
r48
155
132
136
141
145
137
142
146
151
156
‘t61
129
133
138
143
147
152
157
162
167
153 159 166 172
158 164 111 117
I55 162 169 116 182
160 167 174 181 188
165 172 179 186 193
169 177 184 191 199
114 182 r89 191 204
179 186 194 202 210
184 192 200 208 216
189 197 205 213 271
Source.-Centers for Disease Control and Prevention (201 1 b)
0bese
25262128n303t
1
73
62
24
91 96 100 105 110 115 119 124
94 99 104 109 114 19 124 128
9’1 102 107 112 118 123 128 133
100
104
107
110
114
118
121
125
128
132
136
140
144
61
Overweight
134 138 143
148
138 143 I4B 153
143 148 153 158
148 153 158 164
153 r58 164 169
158 163 169 115
163 109 174 180
168 174 180 186
173 179 186 192
178 185 191 1S8
184 1S0 197 204
189 196 203 210
195 202 209 216
200 208 215 222
206 213 221 228
212 219 221 235
218 225 233 241
274 232 240 248
230 238 246 254
32
33 34 35 36 37 38 39
153
158
158 163
163 168
169 174
175 180
180 186
186 192
192 198
198 204
204 21’.1
210 216
216 223
222 229
229 236
235 242
242 250
249 256
256 264
263 271
162
168
174
180
86
19i
1
167
173
179
185
‘,lgt
197
197 204
204 210
210 216
211 223
223 230
230 236
236 743
243 250
250 258
257 265
264 272
212 279
219 287
172
177
178 183
184 189
190 r95
190 242
203…
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