Healthy Aging

Healthy Aging vs Unhealthy Aging
Part 1
Stephan Betterbodyz van Breenen

Poorer physical functioning with higher
levels of
psychological distress. Better physical
health to help cope more effectively
with challenges.
Maintenance of good physical health in
later life is central to maintaining quality
of life, and providing a resource for
coping and adaptation.

“Human resilience refers to the
processes or patterns of positive
adaptation and development in the
context of
significant threats to an individual’s life
or function”.
Having better physical health, being
more physically and socially active,
having a wider range of hobbies and
interests, and being able to let go of the
unimportant things in life are the most
important factors in the older

Are we living healthier as well as longer
lives, or are our additional years spent
in poor health?
We can affect not only how long we
live, but also how well we can function
with advancing age
The risk of dementia increases sharply
with age and, unless new strategies for
prevention and management are
developed, this syndrome is expected
to place growing demands on health

The number of disabled people in most
developing countries seems certain to
increase as the number of older people
continues to rise
The percentage of people with at least
three of six health risk factors
(physical inactivity, current tobacco
use, heavy
alcohol consumption, a high-risk waist-
hip
ratio, hypertension, or obesity)

Without adequate daily physical
exercise
Older men and women could lose
between one-quarter and one-third of
muscle strength over a 10-year period,
which would make a considerable
impact on quality of life and ability to
remain independent from other people.

Regular physical fitness can slow the
rate of decline in both aerobic and
musculoskeletal systems and hence
improve work ability
Aging results in an increase in body fat,
reduction of muscle strength in both
upper and lower limbs, and lower levels
of flexibility, agility, and endurance.

Mobility impairments in older adults are
a dynamic process characterized by
frequent transitions between being
independent and dependent on others
The high prevalence and major health
impact of mobility impairments,
interventions that target maintaining
recovery during transitional states are
highly needed.

Significant proportion of functional
decline attributed to "aging" in older
adults may be associated with specific
conditions. Identifying and reducing the
impact of these conditions may prove
to be a useful approach to preventing
or minimizing functional loss.
Impaired balance and gait are the 2
most significant risk factors for limited
mobility and falls in the elderly. It is
important to understand the effects of

Muscle mass and motor unit number,
activation, and synchronization are
highly related to strength.
Muscle mass and motor unit number,
activation, and synchronization are
highly related to strength; both
decrease with aging.
Resistance-training is the best way to
increase muscle mass, neural
coordination, and strength.

The importance of exercise to improve
physical performance, and how lifelong
exercise can counteract the effects
associated with the ageing of the
neuromuscular system.
Both muscle contractile and
mitochondrial protein decrease with
aging in sedentary humans.
Endurance training, is the best exercise
to increase/maintain mitochondrial

Age-related declines in health include
decreased energy expenditure at rest
and during exercise, and increased
body fat and its accompanying
increased dyslipidemia and reduced
insulin sensitivity.
Quality of life is affected by reduced
strength and endurance and increased
difficulty in being physically active.

Muscle quality (strength relative to
muscle mass) increases with
resistance training in older adults
possibly for a number of reasons,
including increased ability to neuraly
activate motor units and increased
high-energy phosphate availability.
Resistance training in older adults also
increases power, reduces the difficulty
of performing daily tasks, enhances
energy expenditure and body
composition, and promotes

High intensity resistance training
(HIRT) leads to increased protein
synthesis, along with muscle
hypertrophy measured at the whole
body, whole muscle, and muscle fibre
levels, in older adults.
Stronger active older adults with a
muscle mass sufficient for greater
strength, strength training enables
them to use available muscle mass
more effectively.

Regular performance of resistance
exercises and the habitual ingestion of
adequate amounts of dietary protein
from high-quality sources are two
important ways for older persons to
slow the progression of and treat
sarcopenia, the age-related loss of
skeletal muscle mass and function.

Inadequate protein intake will cause
adverse metabolic and physiological
accommodation responses that include
the loss of fat-free mass and muscle
strength and size.
Endurance exercise increases the
oxidation of essential amino acids and
increases the requirement for dietary
protein, resistance exercise results in a
decrease in nitrogen excretion,
lowering dietary protein needs.

Aging is associated with remarkable
changes in body composition. Loss of
skeletal muscle, a process called
sarcopenia, is a prominent feature of
these changes. In addition, gains in total
body fat and visceral fat content
continue into late life.
The cause of sarcopenia is likely a
result of a number of changes that also
occur with aging. These include
reduced levels of physical activity,
changing endocrine function (reduced

Lifting weight requires that a muscle shorten as
it produces force (concentric contraction).
Lowering the weight, on the other hand, forces
the muscle to lengthen as it produces force
(eccentric contraction). These lengthening
muscle contractions have been shown to
produce ultrastructural damage (microscopic
tears in contractile proteins muscle cells) that
may stimulate increased muscle protein
turnover.
This muscle damage produces a cascade of
metabolic events which is similar to an acute
phase response and includes complement
activation, mobilization of neutrophils, increased

Cigarette smoking reduces life
span by an average of 7 years,
and tobacco consumption
accounts for a shortening of
disease free life by 14 years.
Cigarette smoke chemicals
contribute to the aging of a large
number of organs, making
cigarette smoke a “broad range”

Aging is defined as “the deterioration of
a system with time” smoking clearly
accelerates the aging process of the
system man, by affecting molecules,
cells, and organs.
Cigarette smoke chemicals also
contribute to aging of the brain.
smoking contributes to age-related
brain diseases is the causation of
cerebrovascular dysfunction. The
reduced supply of nutrients and oxygen
is thought to directly account for cell

Smoking-caused cerebrovascular
diseases have been also shown to
accelerate degenerative dementias
such as Alzheimer’s disease.
Smoking causes inflammation and
increased levels of CRP, smoking-
mediated inflammation is also
likely to contribute to brain aging.

By causing continuous cellular
damage, cigarette smoking
contributes to a chronic systemic
inflammatory status, which – apart
from other detrimental effects –
also damages the retina.
Smoking reduces estrogenic
activity. Since estrogens are
important regulators of bone
metabolism, smoking also

Smoking contributes to
osteoporosis by interfering with
calcium (Ca) and vitamin D
homeostasis, which are vital for
bone metabolism.
Oxidative stress (as caused by
smoking) inhibits the differentiation
of osteoblastic cells, resulting in
reduced bone formation

An aging-relevant phenomenon is the
decrease of total estrogen activity in
smokers. By promoting 2-
hydroxyestrogen production, smoking
reduces estrogenic activity and
contributes to the clearance of
estrogen from the circulation.
Reduced estrogen production may
contribute to an earlier onset of
menopause which is associated with
several age-related diseases like
mammary carcinoma, cardiovascular

The functionality of the lung as a selective
filtering system is maintained by a complex
system of maintenance, repair, and cleaning
functions. Cigarette smoke interferes with all
of these systems. Cigarette smoke contains
a high amount of particulate matter, including
small sized particles below 2.5 μm that can
reach the alveoli .
Particulate matter is a part of normal air and
the body has evolved efficient removal
systems (surfactant, lung macrophages, and
cilia). The amount of particles deposited per
time period is increased in smokers, and
thereby the cleaning functions are burdened.

Nitric oxide (NO) is an important
regulator of vascular tone.
Cigarette smoke contains
superoxide radicals– which are
also increasingly generated in
aged cells – that interact with NO
to form peroxynitrite (ONOO).
As a result, NO pools are
decreased and vasomotor function
is reduced reflecting a less

As a result of accelerated vascular
aging by cigarette smoke,
individuals suffer earlier from
vascular associated
events/diseases, like myocardial
infarction, stroke, peripheral
arterial diseases, erectile
dysfunction, and vascular
dementia.

Cigarette smoke contains a large number of
mutagenic compounds including oxidants,
radicals, and PAHs. The mechanisms by
which individual compounds exert their DNA
damaging activity are diverse, but have in
common the alteration of gene sequences to
induce cellular proliferation, inhibit apoptosis,
and to promote immune evasion.
Accumulation of mutations in the nuclear and
mitochondrial genome also occurs during the
normal aging process by exposure of
individuals to naturally occurring mutagens
like radioactivity, UV-light, nutrition-contained
mutagens, and environmental as well as

Smoking increases the rate of
mutations over time which not only
accounts for the carcinogenic activity of
cigarette smoke but also reduces the
functionality of enzymes, cells, and
organs
Mutations in the mitochondrial genome
are, result in defective activity of the
respiratory chain, which in turn leads to
increased intracellular oxidative stress
and damage. These processes which
are accelerated by cigarette smoke

Cigarette smoking cause pre-mature
skin aging. Skin aging, account for a
considerable number of deaths, as
various tumors of the skin e.g.
squamous cell carcinoma, and reduced
wound healing are results of skin
aging.
The most important mechanism is the
reduction of the blood flow in the skin,
resulting in a reduced supply of the
wound with oxygen and nutrients,

The body has evolved a range of
defense mechanisms that counteract
alterations of the physiological state
occurring in the course of aging.
Cigarette smoke chemicals interfere
with these mechanisms in a twofold
fashion.
First, smoke chemicals increase the
number of repairs required from the
defense machinery by increasing the
number of damaged sites. Second,
smoke chemicals interfere with the

Aging, and especially human
aging, can be explained by the
emerging concept of para-
inflammation-driven inflammaging,
i.e. a combination of inflammation
and aging.
Inflammaging posits that aging
either physiologically or
pathologically can be driven by the
pro-inflammatory cytokines and

Humans must maintain
homeostasis as they age
despite incessant attack from
both intrinsic and extrinsic
stimuli/antigens.
These potentially harmful pro
inflammatory signals at a later
stage of life may act
antagonistically to the beneficial

Inflammation, triggered by
harmful stimuli and agents like
infection and tissue injury, is
defined as a wide
variety of adaptive physiological
and pathological processes to
avoid infection and repair
damage, restoring
the organism to the usual state

Inflammation can be defined by:
1. Low-grade.
2. Controlled.
3. Asymptomatic and not
pathological.
4. Chronic.
5. Systemic inflammatory state.
6. Beneficial effects in early life but
detrimental effects in later life for
individuals

The condition of inflammaging
provides a continuous mild
antigenic challenge leading to a
pro-inflammatory condition
associated with the progressive
stimulation/depletion
of the immune system and other
organismal systems

The potential forces that drive
inflammaging are pro-
inflammatory cytokines and
substances .
CRP and fibrinogen, the major
clinical markers of inflammation,
have been significantly associated
with
coronary disease, myocardial

A decreased ability to maintain
homeostasis in response to
external stress in association with
an increased risk of age-associated
diseases and death.
Aging and innate immunity play a
pivotal role of in controlling
longevity of the elderly.

Obesity is closely associated with a
series of sequentially appearing
health
problems including insulin-resistant
type II diabetes mellitus, fatty liver,
atherosclerosis, hypertension,
neurodegenerative Alzheimer's
disease, chronic obstructive lung
disease, and even some cancers

Metabolic syndrome consists of a
combination of abdominal fat
deposition, hypertriglyceridemia,
low high density lipoprotein,
hypertension, and fasting
Hyper-glycaemia that can lead to
diabetes mellitus and
atherosclerosis.
Caloric restriction along with
appropriate

Inflammaging is a pathological
phenomenon and a central concept
that brings together our
understanding of age-related
chronic disease, functional decline
and frailty across the life-course.
It is a consequence of lifelong
exposure of the immune system to
antigenic stimuli and complex
genetic, environmental and age-

Many age-related diseases are initiated
or worsened by systemic inflammation,
including neurodegeneration and
atherosclerosis.
Inflammaging also affects the anabolic-
catabolic balance within myocytes,
causing a shift towards catabolism,
atrophy and progression of sarcopenia;
this is a major contributor to functional
decline and frailty. As with other age-
related disease processes, it is believed
that the degree of shift towards

Inflammaging is implicated in the
progression of osteoporosis and
dementia.
The cumulative consequence of having
a greater degree of inflammaging and
anti-inflammaging is increased
susceptibility to, and a faster
progression of, all age-related diseases.

Higher cortisol levels have been
associated with increased mortality in
patients with stroke , sepsis, heart
failure and sarcopenia.
Cortisol is a glucocorticoid hormone
secreted by the adrenal gland in
response to pituitary secretion of
adrenal cortico-trophic hormone, which
itself is stimulated by corticotrophin
releasing hormone from the
hypothalamus; together these form the
hypothalamic-pituitary-adrenal (HPA)

Ageing is associated with decreases in autophagy
mechanisms, further contributing to proinflammatory
environments. Autophagy is a cellular housekeeping
mechanism that is responsible for the removal of
dysfunctional intracellular protein (for example, dead
organelles, damaged scaffold proteins) via lysomal
degradation.
This prevents the activation of inflammasomes;
intracellular multi-protein sensors that stimulate the
inflammatory response after recognizing danger
signals emanating from proteins, such as the
intracellular danger-associated molecular patterns
that occur as a consequence of either tissue injury or
necrosis.
The consequence of a decline of autophagy with age

The immune system of older people
declines in reliability and efficiency with
age, resulting in greater susceptibility to
pathology as a consequence of
inflammation, for example,
cardiovascular disease, Alzheimer's
disease, auto-reactivity and vaccine
failure, as well as an increased
vulnerability to infectious disease .
These changes are further compounded
by reduced responsiveness and
impaired communication between all

Older population in developed
countries is reflected in an increase
in the number of people suffering
from age-related chronic
inflammatory diseases such as
metabolic syndrome, diabetes,
heart and lung diseases, cancer,
osteoporosis, arthritis, and
dementia.

Human diet have a major influence
on both the development and
prevention of age-related diseases.
Most plant-derived dietary
phytochemicals and macro- and
micronutrients modulate oxidative
stress and inflammatory signaling
and regulate metabolic pathways
and bioenergetics.

The hallmarks of aging are genomic
instability, telomere attrition,
epigenetic alterations, loss of
proteostasis, deregulated nutrient
sensing, mitochondrial dysfunction,
cellular senescence, stem cell
exhaustion, and altered intercellular
communication.

Genome Instability
Genome instability (also "genetic instability" or
"genomic instability") refers to a high
frequency of mutations within the genome of a
cellular lineage.
These mutations can include changes in
nucleic acid sequences, chromosomal
rearrangements or aneuploidy. Genome
instability does occur in bacteria.
In multicellular organisms genome instability
is central to carcinogenesis, and in humans it
is also a factor in some neurodegenerative
diseases such as amyotrophic lateral

Telomere Attrition
As cells divide, the telomere ends of
chromosomes get shorter. Eventually, the
enzyme that adds telomeric repeat
sequences, telomerase, gets silenced and the
telomeres are too short for cells to divide.
Shortened telomeres are associated with
aging cells that are senescent.
Telomeres at the ends of chromosomes, like
all other sections of DNA, are prone to DNA
damage, including double-strand breaks
(DSBs). And unlike the rest of the
chromosome, telomere DSBs aren’t fixed by
the DNA repair pathway, as this would

Loss of Proteostasis
As cells age, environmental stresses add up and
mechanisms responsible for maintaining proper
protein composition start to decline. Proteins lose
their stability, autophagic processes start to fail, and
misfolded proteins accumulate.
Over the years, our bodies are subjected to many
environmental inputs that put thermal stress,
oxidative stress, and osmotic stress on our cells,
causing misfolding of proteins. For example, free
radicals present in polluted air have been identified
as particularly noxious agents in this regard,
contributing to multiple aging-related pathologies. In
younger cells, micro- and macroautophagy pathways,
together with the ubiquitin-proteasome system, take
care of clearing these unfolded proteins. However, in
aging cells, autophagy induction can be gradually

Epigenetic alteration
A heritable change that does not affect the
DNA sequence but results in a change in
gene expression.
Aging
The most prominent feature of aging is a gradual loss
of function—or degeneration—that occurs at the
molecular, cellular, tissue, and organismal levels.
Age-related loss of function is a feature of virtually all
organisms that age, ranging from single-celled
creatures to large, complex animals. In mammals,
age-related degeneration gives rise to well-
recognized pathologies, such as sarcopenia,
atherosclerosis and heart failure, osteoporosis,
macular degeneration, pulmonary insufficiency, renal
failure, neurodegeneration (including prominent

Deregulated nutrient sensing
Metabolic activities can put stress on our cells. Too
much activity, and changes in nutrient availability and
composition cause cells to age faster.
Metabolism and its byproducts, over time, damage
cells via oxidative stress, ER stress, calcium
signaling, and mitochondrial dysfunction. Therefore,
organisms depend on multiple nutrient sensing
pathways to make sure that the body takes in just the
right amount of nutrition – not too much, not too little.
However, these damaging events also deregulate the
nutrient-sensing molecules and downstream
pathways. A misguided hypothalamus may signal for
greater food intake, then, when the body doesn’t
really require it. Age-related obesity, diabetes and
other metabolic syndromes result. To make things
even worse, obesity- and diabetes-related chronic

Deregulated nutrient sensing
Probably because so many interdependent pathways
link metabolism to aging, these are the pathways that
have received the most intense focus in the search
for anti-aging therapeutics. There was much
excitement in the last decade around resveratrol and
caloric restriction, the effects of which have now been
shown to be limited to mice and other model
organisms. Today, intermittent caloric restriction (i.e.,
fasting) is the only intervention that has been shown
to extend human lifespan.

Mitochondrial Disease
Mitochondrial disease is a group of disorders caused
by dysfunctional mitochondria, the organelles that
generate energy for the cell. Mitochondria are found
in every cell of the human body except red blood
cells, and convert the energy of food molecules into
the ATP that powers most cell functions.
Mitochondrial diseases are sometimes (about 15% of
the time) caused by mutations in the mitochondrial
DNA that affect mitochondrial function. Other causes
of mitochondrial disease are mutations in genes of
the nuclear DNA, whose gene products are imported
into the mitochondria (mitochondrial proteins) as well
as acquired mitochondrial conditions. Mitochondrial
diseases take on unique characteristics both because
of the way the diseases are often inherited and
because mitochondria are so critical to cell function.

Cellular Senescence
Cellular senescence is the phenomenon by which
normal diploid cells cease to divide. In culture,
fibroblasts can reach a maximum of 50 cell divisions
before becoming senescent. This phenomenon is
known as "replicative senescence", or the Hayflick
limit. Replicative senescence is the result of telomere
shortening that ultimately triggers a DNA damage
response.
Cells can also be induced to senesce via DNA
damage in response to elevated reactive oxygen
species (ROS), activation of oncogenes and cell-cell
fusion, independent of telomere length. As such,
cellular senescence represents a change in "cell
state" rather than a cell becoming "aged" as the
name confusingly suggests. Nonetheless, the number

Stemcell Exhaustiong
As we age, our stem cells eventually lose their ability
to divide. Furthermore, we are unable to replace the
stem cells that have migrated, differentiated, or died.
As a result, we show outward symbols of aging, such
as grey hair.
While the decrease in the renewal of stem cells
certainly leads to age-related disorders, it is clear that
this “stem cell exhaustion” is really a consequence of
DNA damage, deregulated nutrient sensing,
senescence, and other processes already
mentioned—in other words, it might be argued that it
is not a “true” hallmark. Nevertheless, because of
their unique role in determining cell fate in a tissue-
specific way, stem cells can reveal ways that tissues
interact during the aging of a complex organism and
possibly redirect the fate of aging tissues upon

Altered Intercellular Communication
Cells, as they age, show an increase in self-
preserving signals that result in damage elsewhere.
Altered intercellular communication with aging
contributes to decline in tissue health.
Like the decline in stem cell renewal, the age-
dependent changes in intercellular communication
are integrated effects of the other hallmarks of aging.
In particular, senescent cells trigger chronic
inflammation that can further damage aging tissues.
.
At an organ system level, the aging hypothalamus
drives changes in neurohormone signaling, which in
turn affects food intake and metabolism. Since the
hypothalamus also regulates sleep cycles, these
changes can inhibit DNA repair, exacerbating the
aging phenotype.

A large part of the aging phenotype is
explained by an imbalance between
inflammatory and anti-inflammatory
networks.
Levels of inflammatory mediators
typically increase with age even in the
absence of acute infection or other
physiologic stress.

The aging process is a chronic
smoldering oxidative and inflammatory
stress that leads to the damage of
cellular components, including proteins,
lipids, and DNA, contributing to the age-
related decline of physiological
functions. This is especially evident in
cells that regulate homeostasis, such as
the nervous, endocrine, and immune
systems. It explains their functional
losses observed during aging, with a
resulting increase in morbidity and

The progressive loss of physiological
organismal and cellular integrity is the primary
risk factor for major human pathologies,
including metabolic syndrome, cancer,
diabetes, cardiovascular disorders, and
neurodegenerative diseases.
Due to an imbalance between energy intake
and expenditure, largely attributable to the
increased availability of foods with high caloric
content coupled with the adoption of a
sedentary lifestyle, the continuing increase in
obesity and metabolic disorders such as type
2 diabetes and accelerating aging population
globally will remain the major contributors to

The importance of weight
management and early intervention
with regard to modifiable risk
factors in overweight patients.
To reduce the burden of cardio-
metabolic disorders and early onset
of aging disorders, promoting
exercise with a complementary diet,
supplemented with bioactive
phytochemicals, is expected to

Epigenetic changes in response to
diet and environmental (stress)
conditions complement genetic
mutations and contribute to the
development and progression of
inflammaging diseases such as
rheumatoid arthritis, metabolic
disorders (obesity, type 2 diabetes),
cardiovascular disease, and cancer

Disruption of epigenetic
mechanisms can alter immune
function and that epimutations not
only contribute to certain cancers
but also to lifestyle diseases such
as type 2 diabetes, allergies,
cardiovascular disease, and
rheumatoid arthritis, as well as
unhealthy aging.

To prevent or to reverse adverse
epigenetic alterations associated
with multifactorial aging diseases,
combinatorial therapeutic and/or
nutritional approaches will be
necessary to modulate different
classes of chromatin modifiers

Aging and Alcohol
Brain:
Alcohol interferes with the brain’s
communication pathways, and can
affect the way the brain looks and
works. These disruptions can change
mood and behavior, and make it harder
to think clearly and move with
coordination

Aging and Alcohol
Heart:
Drinking a lot over a long time or too
much on a single occasion can damage
the heart, causing problems including:
Cardiomyopathy – Stretching and
drooping of heart muscle
Arrhythmias – Irregular heart beat
Stroke
High blood pressure

Aging and Alcohol
Liver:
Heavy drinking takes a toll on the liver,
and can lead to a variety of problems
and liver inflammations including:
Steatosis, or fatty liver
Alcoholic hepatitis
Fibrosis
Cirrhosis

Aging and Alcohol
Pancreas:
Alcohol causes the pancreas to produce
toxic substances that can eventually
lead to pancreatitis, a dangerous
inflammation and swelling of the blood
vessels in the pancreas that prevents
proper digestion.

Aging and Alcohol
Cancer:
Drinking too much alcohol can increase
your risk of developing certain cancers,
including cancers of the:
Mouth
Esophagus
Throat
Liver
Breast

Aging and Alcohol
Immune System:
Drinking too much can weaken your
immune system, making your body a
much easier target for disease. Chronic
drinkers are more liable to contract
diseases like pneumonia and
tuberculosis than people who do not
drink too much. Drinking a lot on a
single occasion slows your body’s ability
to ward off infections – even up to 24

Defining obesity in aged humans
and nonhuman primates is difficult
as the physiological changes that
occur with aging are not accounted
for using our current systems (BMI
– body mass index, and BCS –
body condition score

The health consequences of
increased visceral adiposity caused
by a long-term, chronic,
hypercaloric diet is a multi-systemic
deterioration resulting in an
increased risk for developing
metabolic syndrome

Metabolic Syndrome is diagnosed
when 3 or more of the following
characteristics are identified:
1) Enlarged waist circumference,
2) Elevated triglycerides
3) Decreased high density
lipoprotein cholesterol (HDL-c)
4) Elevated blood pressure
5) Increased fasting glucose

Caloric restriction (CR) is
associated with a decreased risk of
age-associated pathologies in
humans and NHPs.
Caloric restriction is studied with
regard to its potential benefits,
increasing health-span and
extending life-span, while obesity
has been linked to diminished

Obesity can exacerbate age-related
decline in physical function.
Activities of daily living, particularly
mobility, is markedly diminished in
the overweight and obese
Physical activity decreases with
increasing age, and it has been
estimated that decreased physical
activity accounts for about one-half
of the decrease in total energy

Obesity causes serious health
complications resulting in morbidity.
The prevalence of several medical
complications, such as diabetes,
hypertension, arthritis,
cardiovascular disease, urinary
incontinence, and various types of
cancers, is associated with obesity
in advancing age.

About 30–50% of the elderly aged
65 years and above are affected by
hypertension.
Obesity and arthritis tend to go together.
If strain is sustained for a long time in
the elderly, it may also lead to
osteoarthritis of weight-bearing joints.
Arthritis is one big cause of physical
immobility in older adults, resulting in
reduced energy expenditure and high
risk of weight gain.

Obesity, particularly abdominal obesity,
is associated with pulmonary function
abnormalities, obesity-hypoventilation
syndrome, and obstructive sleep apnea.
Coronary artery diseases is the major
cause of disability, thus limiting the
activity and eroding the quality of life of
millions of elderly people each year.

Obesity is associated with an increased
risk of several types of cancer (i.e.,
breast, colon, gallbladder, pancreas,
renal, bladder, uterine, cervical, and
prostate cancers)
Obesity contributes to the increase in
prevalence of urinary incontinence in
older persons, and the increase in
urinary incontinence is directly
associated with increased BMI

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