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THE EFFECT OF STRESS ON HUMAN LIFE

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ADALYA JOURNAL ISSN NO: 1301-2746

THE EFFECT OF STRESS ON HUMAN LIFE

CH. B. Praveena Devi 1*, M. Anisha Reddy 2, Onaiza Zahan 2, JVC Sharma1

1
Department of Pharmacy, Joginpally B.R Pharmacy College, Yenkapally (V) Moinabad (M),
Hyderabad, Telangana, India, 500075.

2
Department of Pharmacy Practice, Joginpally B.R Pharmacy College, Yenkapally (V)
Moinabad (M), Hyderabad, Telangana, India 500075.

* Corresponding Author:

CH. B. Praveena Devi,

Assistant Professor,

Department of Pharmacy,

Joginpally B.R. Pharmacy College,

Hyderbad, Telangana,

India, 500075.

e-mail: praveenadeviv@gmail.com

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INTRODUCTION

STRESS AND STRESS SYNDROME

All vital physiologic systems of the body are inherently programmed, through rigorous
fine-tuning achieved during evolution, to preserve a predefined steady state, i.e.
homeostasis or eustasis, which is essential for life and well-being [1, 2]. This optimal
equilibrium is constantly challenged by adverse forces which are intrinsic or extrinsic, real or
even perceived, and are described as stressors. Thus, stress is defined as a state of
disharmony, i.e. cacostasis or allostasis, and is counteracted by an intricate repertoire of
physiologic and behavioural responses which aim to maintain/re-establish the threatened
homeostasis (adaptive stress response). The stress response is mediated by a complex and
interconnected neuroendocrine, cellular and molecular infrastructure which consists of the stress
system and is located in both the central nervous system (CNS) and the periphery [1, 2]. The
adaptive response of each individual to stress is determined by a multiplicity of genetic,
environmental and developmental factors. Changes in the ability to effectively respond to
stressors (e.g. inadequate, excessive and/or prolonged reactions) may lead to disease. Moreover,
highly potent and/or chronic stressors can have detrimental effects on a variety of physiologic
functions, including growth, reproduction, metabolism and immune competence, as well as on
behaviour and personality development. Of note, prenatal life, infancy, childhood and
adolescence are critical periods in the process of forming the matrix of the adaptive stress
response, characterized by high plasticity of the stress system and increased vulnerability to
stressors.

The stress system receives and integrates a great diversity of neurosensory (i.e. visual,
auditory, somatosensory, nociceptive, and visceral), blood-borne, and limbic signals which arrive
at the various stress system centres / stations through distinct pathways. Acute stress system
activation triggers a cluster of time-limited changes, both behavioural and physical, which are
rather consistent in their qualitative presentation and are collectively defined as the stress
syndrome [1-4]. Under normal conditions these changes are adaptive and improve the chances of
survival. Initially, the stimulation of the stress system components follows a stressor-specific
mode; however as the potency of the stressor (s) increases the specificity of the adaptive

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response decreases in order to eventually present the relatively nonspecific stress syndrome
phenomenology which follows exposure to potent stressors.

Behavioural adaptation includes enhanced arousal, alertness, vigilance, cognition,

focused attention and analgesia, whilst there is concurrent inhibition of vegetative functions,
such as feeding and reproduction. In parallel, physical adaptation mediates an adaptive
redirection of energy and body resources. As such, increases in the cardiovascular tone,
respiratory rate and intermediate metabolism (gluconeogenesis and lipolysis) work in concert to
promote this redirection of vital substrates, while energy consuming functions (e.g. digestion,
reproduction, growth and immunity) are temporally suppressed. Thus, oxygen and nutrients are
primarily shunted to the CNS and to stressed body site(s) where they are needed the most.

In addition to the adaptive stress response, restraining forces are also activated during
stress to prevent a potential excessive response of the various stress system components [1, 2].
The ability to timely and precisely develop restraining forces is equally essential for a successful
outcome against the imposed stressor (s), since prolonging the mobilized adaptive stress
response can turn maladaptive and contribute to the development of disease.

Interestingly, the mobilization of the stress system is often of a magnitude and nature that allows
the perception of control by the individual. Under such conditions, stress can be rewarding and
pleasant, or even exciting, providing positive stimuli to the individual for emotional and
intellectual growth and development [5].

STRESS
Stress is your body’s way of responding to any kind of demand or threat. When you
sense danger-whether its real or imagine the body's defenses into high gear into rapid, automatic
process known as fight or flight reaction or the stress response. The stress response is the body’s
way of protecting you. When working properly, it helps you to stay focused, energetic and alert.
In emergency situations, stress can save your life-giving you extra strength to defend yourself.
Stress can also help you rise to meet challenges, sharpens your concentration. But
beyond a certain point stress stops being helpful and starts causing major damage to your health,
your mood, your productivity and your quality of your life.

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Fight or flight responds what happens in the body when you feel threatened, your
nervous system responds by releasing a flood of stress hormones, including adrenaline and
cortisol, which rouse the body of emergency action. Your heart pounds faster, muscle tighten,
blood pressure rises, breath quickens digestive system slows down immune activity decreases, a
heightened state of alertness prevents sleep and your senses becomes sharper. These physical
changes increase your strength and stamina, speed your reaction time and enhance your focus-
preparing u to either fight or flee from danger at hand.
Factors of the environment that trigger this reaction are called as stressors. Example:
noises, aggressive behavior, speeding car, scary movements etc. The physical system includes
dizziness, general aches and pains, grinding teeth and clenched jaw, headaches, indigestion,
increase or lose of hepatitis, muscle tension in neck face or shoulders, problems sleeping, raising
heart, cold, sweaty palms, tiredness, trembling or shacking or weight gain or lose, upset stomach
diarrhea, sexual difficulties.
Stress is both physical and emotional. Stress that continues without relief can lead to
condition called distress-a negative stress reaction which disturbs the body's internal balance or
equilibrium leading to physical symptoms such as headaches and upset stomach, elevated blood
pressure, chest pain, sexual dysfunction and problems in sleeping, emotional problems include
depression, anxiety and panic attack. Stress is linked to the leading causes of death. There are
few problems associated with stress disorder.
 Heart diseases
 Cancer
 Lung ailments
 Obesity
 Diabetes
 Depression and Anxiety
 Alzheimer’s disease
 Premature deaths
TYPES OF STRESS
 Acute stress
 Episodic stress
 Chronic stress

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Acute stress is the most common type. Acute stress that occurs frequently is called
periodical stress. This type of stress is common in people whose lives are extremely busy and
disorganized and in those who tend to worry excessively. Chronic stress is the serious condition
which occurs when a stressful situation is prolonged and continuous, often causes severe
physical and emotional symptoms post-traumatic stress disorder- is a psychiatric condition that
can occur following life threating events such as military actions natural disasters terrorist
attacks.
RISK FACTORS AND CAUSES OF STRESS
 External factors eg: Events situations environment
 Internal factors: Expectations, Attitudes, Feelings
 Physical causes: Illness or injury
 Psychological causes: Anxiety or fear
 Being under lots of pressure
 Facing big changes
 Worrying about something
 Not having much or any control over the outcome of a situation
 Having responsibilities that you’re finding overwhelming
 Times of uncertainty
 Busy schedule

SYMPTOMS
Emotional symptoms
 Become easily agitated, frustrated and moody
 Feeling overwhelmed, like your losing control or need to control
 Having difficulty relaxing and quieting your mind
 Feeling bad about yourself, depressed
 Avoiding others
Physical symptoms
 Low energy
 Headaches
 Chest pain and rapid heart beats

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 Insomnia
 Frequent cold and infections
 Loss of sexual desires and ability
 Nervousness and shaking, ringing in the ear
 Dry mouth and difficulty swallowing
COGNITIVE SYMPTOMS
 Constant worrying
 Racing thoughts
 Disorganization
 Inability to focus
 Poor judgment
BEHAVIORAL SYMPTOMS
 Changes in appetite
 Procrastinating and avoiding responsibilities
 Use of alcohol drugs or cigarettes
 Nail biting fidgeting and pacing

BIOLOGICAL RESPONSES TO STRESSORS

Acute Stress Responses

Following the perception of an acute stressful event, there is a cascade of changes in

the nervous, cardiovascular, endocrine, and immune systems. These changes constitute the stress
response and are generally adaptive, at least in the short term [6]. Two features in particular
make the stress response adaptive. First, stress hormones are released to make energy stores
available for the body’s immediate use. Second, a new pattern of energy distribution emerges.
Energy is diverted to the tissues that become more active during stress, primarily the skeletal
muscles and the brain. Cells of the immune system are also activated and migrate to “battle
stations” [7]. Less critical activities are suspended, such as digestion and the production of
growth and gonadal hormones. Simply put, during times of acute crisis, eating, growth, and
sexual activity may be a detriment to physical integrity and even survival.

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Stress hormones are produced by the SNS and hypothalamic-pituitary adrenocortical axis. The
SNS stimulates the adrenal medulla to produce catecholamines (e.g., epinephrine). In parallel,
the paraventricular nucleus of the hypothalamus produces corticotropin releasing factor, which in
turn stimulates the pituitary to produce adrenocorticotropin. Adrenocorticotropin then stimulates
the adrenal cortex to secrete cortisol. Together, catecholamines and cortisol increase available
sources of energy by promoting lipolysis and the conversion of glycogen into glucose (i.e., blood
sugar). Lipolysis is the process of breaking down fats into usable sources of energy (i.e., fatty
acids and glycerol [8].

Energy is then distributed to the organs that need it most by increasing blood
pressure levels and contracting certain blood vessels while dilating others. Blood pressure is
increased with one of two hemodynamic mechanisms [9]. The myocardial mechanism increases
blood pressure through enhanced cardiac output; that is, increases in heart rate and stroke volume
(i.e., the amount of blood pumped with each heart beat). The vascular mechanism constricts the
vasculature, thereby increasing blood pressure much like constricting a hose increases water
pressure. Specific stressors tend to elicit either myocardial or vascular responses, providing
evidence of situational stereotypy [10]. Laboratory stressors that call for active coping strategies,
such as giving a speech or performing mental arithmetic, require the participant to dosomething
and are associated with myocardial responses. In contrast, laboratory stressors that call for more
vigilant coping strategies in the absence of movement, such as viewing a distressing video or
keeping one’s foot in a bucket of ice water, are associated with vascular responses. From an
evolutionary perspective, cardiac responses are believed to facilitate active coping by shunting
blood to skeletal muscles, consistent with the fight-or-flight response. In situations where
decisive action would not be appropriate, but instead skeletal muscle inhibition and vigilance are
called for, a vascular hemodynamic response is adaptive. The vascular response shunts blood
away from the periphery to the internal organs, thereby minimizing potential bleeding in the case
of physical assault.

Finally, in addition to the increased availability and redistribution of energy, the

acute stress response includes activation of the immune system. Cells of the innate immune
system (e.g., macrophages and natural killer cells), the first line of defense, depart from
lymphatic tissue and spleen and enter the bloodstream, temporarily raising the number of

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immune cells in circulation (i.e., leukocytosis). From there, the immune cells migrate into tissues
that are most likely to suffer damage during physical confrontation (e.g., the skin). Once at
“battle stations,” these cells are in position to contain microbes that may enter the body through
wounds and thereby facilitate healing [11].

Chronic Stress Responses

The acute stress response can become maladaptive if it is repeatedly or continuously

activated. For example, chronic SNS stimulation of the cardiovascular system due to stress leads
to sustained increases in blood pressure and vascular hypertrophy [12]. That is, the muscles that
constrict the vasculature thicken, producing elevated resting blood pressure and response
stereotypy, or a tendency to respond to all types of stressors with a vascular response.
Chronically elevated blood pressure forces the heart to work harder, which leads to hypertrophy
of the left ventricle [13]. Over time, the chronically elevated and rapidly shifting levels of blood
pressure can lead to damaged arteries and plaque formation.

The elevated basal levels of stress hormones associated with chronic stress also
suppress immunity by directly affecting cytokine profiles. Cytokines are communicatory
molecules produced primarily by immune cells [14]. There are three classes of cytokines.
Proinflammatory cytokines mediate acute inflammatory reactions. Th1 cytokines mediate
cellular immunity by stimulating natural killer cells and cytotoxic T cells, immune cells that
target intracellular pathogens (e.g., viruses). Finally, Th2 cytokines mediate humoral immunity
by stimulating B cells to produce antibody, which “tags” extracellular pathogens (e.g., bacteria)
for removal. In a meta-analysis of over 30 years of research, [15] found that intermediate
stressors, such as academic examinations, could promote a Th2 shift (i.e., an increase in Th2
cytokines relative to Th1 cytokines). A Th2 shift has the effect of suppressing cellular immunity
in favor of humoral immunity. In response to more chronic stressors (e.g., long-term caregiving
for a dementia patient), Segerstrom & Miller found that proinflammatory, Th1, and Th2
cytokines become dysregulated and lead both to suppressed humoral and cellular immunity.
Intermediate and chronic stressors are associated with slower wound healing and recovery from
surgery, poorer antibody responses to vaccination, and antiviral deficits that are believed to
contribute to increased vulnerability to viral infections (e.g., reductions in natural killer cell
cytotoxicity [16]

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Chronic stress is particularly problematic for elderly people in light of

immunosenescence, the gradual loss of immune function associated with aging. Older adults are
less able to produce antibody responses to vaccinations or combat viral infections [17], and there
is also evidence of a Th2 shift [18]. Although research has yet to link poor vaccination responses
to early mortality, influenza and other infectious illnesses are a major cause of mortality in the
elderly, even among those who have received vaccinations [19]

PSYCHOSOCIAL STRESSORS AND HEALTH

Cardiovascular Disease

Both epidemiological and controlled studies have demonstrated relationships

between psychosocial stressors and disease. The underlying mediators, however, are unclear in
most cases, although possible mechanisms have been explored in some experimental studies. An
occupational gradient in coronary heart disease (CHD) risk has been documented in which men
with relatively low socioeconomic status have the poorest health outcomes [20]. Much of the risk
gradient in CHD can be eliminated, however, by taking into account lack of perceived job
control, which is a potent stressor [21]. Other factors include risky behaviors such as smoking,
alcohol use, and sedentary lifestyle [22], which may be facilitated by stress. Among men [23]
and women [24], work stress has been reported to be a predictor of incident CHD and
hypertension [25]. However, in women with existing CHD, marital stress is a better predictor of
poor prognosis than is work stress [26].

Although the observational studies cited thus far reveal provocative associations
between psychosocial stressors and disease, they are limited in what they can tell us about the
exact contribution of these stressors or about how stress mediates disease processes. Animal
models provide an important tool for helping to understand the specific influences of stressors on
disease processes. This is especially true of atherosclerotic CHD, which takes multiple decades
to develop in humans and is influenced by a great many constitutional, demographic, and
environmental factors. It would also be unethical to induce disease in humans by experimental
means.

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Perhaps the best-known animal model relating stress to atherosclerosis was

developed by [27]. Their study was carried out on male cynomolgus monkeys, who normally live
in social groups. The investigators stressed half the animals by reorganizing five-member social
groups at one- to three-month intervals on a schedule that ensured that each monkey would be
housed with several new animals during each reorganization. The other half of the animals lived
in stable social groups. All animals were maintained on a moderately atherogenic diet for 22
months. Animals were also assessed for their social status (i.e., relative dominance) within each
group. The major findings were that (a) socially dominant animals living in unstable groups had
significantly more atherosclerosis than did less dominant animals living in unstable groups; and
(b) socially dominant male animals living in unstable groups had significantly more
atherosclerosis than did socially dominant animals living in stable groups. Other important
findings based upon this model have been that heart-rate reactivity to the threat of capture
predicts severity of atherosclerosis [28] and that administration of the SNS-blocking agent
propranolol decreases the progression of atherosclerosis [29]. In contrast to the findings in males,
subordinate premenstrual females develop greater atherosclerosis than do dominant females
because they are relatively estrogen deficient, tending to miss ovulatory cycles [30]
Whereas the studies in cynomolgus monkeys indicate that emotionally stressful behaviour can
accelerate the progression of atherosclerosis, [31] provided evidence that affiliative social
behaviour can slow the progression of atherosclerosis in the Watanabe heritable hyperlipidemic
rabbit. This rabbit model has a genetic defect in lipoprotein clearance such that it exhibits
hypercholesterolemia and severe atherosclerosis. The rabbits were assigned to one of three social
or behavioural groups: (a) an unstable group in which unfamiliar rabbits were paired daily, with
the pairing switched each week; (b) a stable group, in which littermates were paired daily for the
entire study; and (c) an individually caged group. The stable group exhibited more affiliative
behaviour and less agonistic behaviour than the unstable group and significantly less
atherosclerosis than each of the other two groups. The study emphasizes the importance of
behavioural factors in atherogenesis, even in a model of disease with extremely strong genetic
determinants.

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Upper Respiratory Diseases

The hypothesis that stress predicts susceptibility to the common cold received support
from observational studies [33]. One problem with such studies is that they do not control for
exposure. Stressed people, for instance, might seek more outside contact and thus be exposed to
more viruses. Therefore, in a more controlled study, people were exposed to a rhinovirus and
then quarantined to control for exposure to other viruses [34]. Those individuals with the most
stressful life events and highest levels of perceived stress and negative affect had the greatest
probability of developing cold symptoms. In a subsequent study of volunteers inoculated with a
cold virus, it was found that people enduring chronic, stressful life events (i.e., events lasting a
month or longer including unemployment, chronic underemployment, or continued interpersonal
difficulties) had a high likelihood of catching cold, whereas people subjected to stressful events
lasting less than a month did not [35].

Human Immunodeficiency Virus

The impact of life stressors has also been studied within the context of human
immunodeficiency virus (HIV) spectrum disease. [36] followed men with HIV for up to 7.5
years and found that faster progression to AIDS was associated with higher cumulative stressful
life events, use of denial as a coping mechanism, lower satisfaction with social support, and
elevated serum cortisol.

Inflammation, the Immune System, and Physical Health

Despite the stress-mediated immunosuppressive effects reviewed above, stress has

also been associated with exacerbations of autoimmune disease [37] and other conditions in
which excessive inflammation is a central feature, such as CHD [38]. Evidence suggests that a
chronically activated, dysregulated acute stress response is responsible for these associations.
Recall that the acute stress response includes the activation and migration of cells of the innate
immune system. This effect is mediated by proinflammatory cytokines. During periods of
chronic stress, in the otherwise healthy individual, cortisol eventually suppresses
proinflammatory cytokine production. But in individuals with autoimmune disease or CHD,

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prolonged stress can cause proinflammatory cytokine production to remain chronically activated,
leading to an exacerbation of pathophysiology and symptomatology.

[39] proposed the glucocorticoid-resistance model to account for this deficit in

proinflammatory cytokine regulation. They argue that immune cells become “resistant” to the
effects of cortisol (i.e., a type of glucocorticoid), primarily through a reduction, or down
regulation, in the number of expressed cortisol receptors. With cortisol unable to suppress
inflammation, stress continues to promote proinflammatory cytokine production indefinitely.
Although there is only preliminary empirical support for this model, it could have implications
for diseases of inflammation. For example, in rheumatoid arthritis, excessive inflammation is
responsible for joint damage, swelling, pain, and reduced mobility. Stress is associated with
more swelling and reduced mobility in rheumatoid arthritis patients [40]. Similarly, in multiple
sclerosis (MS), an overactive immune system targets and destroys the myelin surrounding
nerves, contributing to a host of symptoms that include paralysis and blindness. Again, stress is
associated with an exacerbation of disease. Even in CHD, inflammation plays a role. The
immune system responds to vascular injury just as it would any other wound: Immune cells
migrate to and infiltrate the arterial wall, setting off a cascade of biochemical processes that can
ultimately lead to a thrombosis (i.e., clot; [41]. Elevated levels of inflammatory markers, such as
C-reactive protein (CRP), are predictive of heart attacks, even when controlling for other
traditional risk factors (e.g., cholesterol, blood pressure, and smoking; [42]. Interestingly, a
history of major depressive episodes has been associated with elevated levels of CRP in men.

Inflammation, Cytokine Production, and Mental Health

In addition to its effects on physical health, prolonged proinflammatory cytokine

production may also adversely affect mental health in vulnerable individuals. During times of
illness (e.g., the flu), proinflammatory cytokines feed back to the CNS and produce symptoms of
fatigue, malaise, diminished appetite, and listlessness, which are symptoms usually associated
with depression. It was once thought that these symptoms were directly caused by infectious
pathogens, but more recently, it has become clear that proinflammatory cytokines are both
sufficient and necessary (i.e., even absent infection or fever) to generate sickness behaviour.

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Sickness behaviour has been suggested to be a highly organized strategy that

mammals use to combat infection. Symptoms of illness, as previously thought, are not
inconsequential or even maladaptive. On the contrary, sickness behaviour is thought to promote
resistance and facilitate recovery. For example, an overall decrease in activity allows the sick
individual to preserve energy resources that can be redirected toward enhancing immune activity.
Similarly, limiting exploration, mating, and foraging further preserves energy resources and
reduces the likelihood of risky encounters (e.g., fighting over a mate). Furthermore, decreasing
food intake also decreases the level of iron in the blood, thereby decreasing bacterial replication.
Thus, for a limited period, sickness behaviour may be looked upon as an adaptive response to the
stress of illness.

Much like other aspects of the acute stress response, however, sickness behaviour can
become maladaptive when repeatedly or continuously activated. Many features of the sickness
behaviour response overlap with major depression. Indeed, compared with healthy controls,
elevated rates of depression are reported in patients with inflammatory diseases such as MS or
CH [43]. Granted, MS patients face a number of stressors and reports of depression are not
surprising. However, when compared with individuals facing similar disability who do not have
MS (e.g., car accident victims), MS patients still report higher levels of depression. In both MS
[44] and CHD [45], indicators of inflammation have been found to be correlated with depressive
symptomatology. Thus, there is evidence to suggest that stress contributes to both physical and
mental disease through the mediating effects of proinflammatory cytokines.

DIAGNOSIS
 Hormonal test
 Exercise stress test
 ECG
TREATMENT
 Talking treatment
 Medication
 Eco therapy
 Complimentary and alternating therapies

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TALKING TREATMENT

Talking with trained professional can help you learn to deal with stress, which
include COGNITIVE BEHAVIOURAL THERAPY (CBT) which helps you understand your
thought patterns, recognize your trigger points and identify positive actions.

MINDFULLNESS
Based Stress Reduction (MBSR) which combines mindfullness, meditation and yoga with
particular focus on reducing stress.
MEDICATION
CELEXA- Citalopram is an antidepressant drug of the selective serotonin reuptake inhibitors
class. This medication works by helping to restore the balance of a certain natural substance
(SEROTONIN) in the brain.
SIDE EFFECTS
Nausea, Vomiting, Dry mouth, Loss of interest in sex, Drowsiness, Blurred vision, Yawning
PROZAC- Fluoxetine is used to treat depression, panic attacks and obsessive compulsive
disorder. This medication improves sleep, appetite and energy levels and decrease anxiety and
other thoughts
SIDE EFFECTS: Nausea, Drowsiness, Dizziness, loss of appetite, tiredness, sweating, thoughts
of suicide, weight loss, decreased interest in sex.
BENZODIAZEPAM-DIAZEPAM: These are used to treat anxiety, but are effective in treating
several conditions like anxiety and panic attacks, seizures, insomnia or trouble sleeping and
muscle relaxation.
SIDE EFFECTS- Sedation, dizziness, weakness and unsteadiness, headache and memory
impairment in severe cases.

HERBAL MEDICINES
 PASSION FLOWER- It is a folk remedy for anxiety and insomnia which are
comparable to benzodiazepines class which is used to treat stress. This works by

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increasing levels of the GABA in the brain .This lowers the activity of the brain cells,
making the person feeling relaxed.

 LAVENDER ESSENTIAL OIL- Lavender oil helps alleviate anxiety and stress by
inducing a calming effect on the central nervous system.

 CINNAMON ESSENTIAL OIL- It has anti –inflammatory properties and works

wonders for soothing and aching muscles and produces calming effects.

 ASHWAGANDHA- It is a traditional medicinal herb with multiple health benefits. It

can reduce anxiety and stress, helps fight depression, boost fertility. The medicinal part is
the root. It acts by balancing the hormones and also depresses the brain.

 TULSI OR BASIL LEAVES- It is a powerful anti-oxidant and its most significant

might be for stress–relief and relaxation which acts by depressing the CNS activity. [6]

ECOTHERAPY
It is a way of improving your wellbeing and self-esteem by spending time in nature. This can
include physical exercise in green spaces or taking part in a gardening or conservation project

COMPLIMENTARY THERAPIES
Yoga, Meditation, Exercise, Sleep, Acupuncture, Aromatherapy Massage

NON PHARMACOLOGICAL THERAPY

 Massage: It is used to relax tense muscles, reduce pain and improve circulation.
 Meditation: The small amount of peace in your day can help you to deal with or even
release stress.

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 Exercise: It works in the same way as mediation because it gives you time to be with
yourself to calm out the running thoughts, where endorphins are released into the brain
and improve the mood and blood circulation.
 Organize your life: Organization offers sense of control and peace of mind, where it
improves the quality of life by putting a correct schedule.
 Eat healthy: It’s proven that the junk food can make us depressed so cleaning our dies is
important. Healthy foods like whole grains, protein can improve the mood and give long-
lasting energy to tackle. Aloe extra caffeine should also be cut down as it stimulates the
brain cells and make anxious.
 Limit the use of cellphones and internet: By turning away from the internet and
shutting off our cellphone, we can at least block some of the channels which cause stress.
It is particularly important to cut off electronic use before sleep, which can cut down on
insomnia-related problems.
 Vitamin B: These are known to promote proper functioning of the brain and nervous
system as well as help inducing relaxation and fight fatigue. In fact it indicates B
deficiency include irritability, depression and apathy.
 Sleep: Sleep is the most important natural stress reducer of them. Too little sleep leaves
us cranky, irritable and on edge. Too much sleep can leave us sluggish and depressed.
Right balance should be maintained. Sleep can be promoted by bed time rituals, warm
bath before sleep and foods like carbohydrates, peanuts, bananas, figs, diary and turkey
which contain tryptophan and precursor for creating melatonin. ( ref 7&8)

REFERENCES

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3. http://www.healthcommunities.com/stress/overview-types-of-stress-risk-factors.shtml

4. https://www.webmd.com/balance/stress-management/stress-symptoms-effects_of-stress-
on-the-body#

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