science_stress

In 1994, Dr. Jiankang Liu and his colleagues, based on experimental data, published a
paper in the International Journal of Stress Management entitled “Involvement of reactive
oxygen species in emotional stress: A hypothesis based on the immobilization stress-
nduced oxidative damage and antioxidant defense changes in rat brain, and the effect of
antioxidant treatment with reduced glutathione”. In 1999, Dr. Liu further modified the
hypothesis with more findings in stress and oxidative stress studies and proposed an
“Oxidative damage hypothesis of stress-associated aging acceleration”, published in the
Neurochemical Research. In recent years, a variety of oxidative damage induced by stress
has been demonstrated in the brain and other organs of several animal models. Meanwhile,
protective effect of antioxidants is a current topic not only in stress-related disorders but
also in other age-associated degenerative diseases such as cancer, Parkinson’s and
Alzheimer’s disease. In his most recent review paper, Dr. Liu summarized the recent
advances in stress and oxidative damage studies in supporting his theory, with a focus on
the anti-stress and neuroprotective effects of some natural and nutritional antioxidants.

The Oxidative Damage Theory of Stress-associated Aging Acceleration can be illustrated
in the slide presentation and summarized as: Stress may contribute to aging acceleration and
age-related degenerative diseases. Stress and adaptation to stress require numerous
homeostatic adjustments including hormones, neurotransmitters, oxidants, and other
mediators, such as immune cytokines. The stress-induced hormones, neurotransmitters,
mediators, and oxidants all have beneficial, but also harmful effects if out of balance.
Therefore, the homeostasis of stress and adaptation should be governed by the hormone
balance, neurotransmitter balance, mediator balance, and oxidant balance, as well as the
interactions among these substances. The imbalance and the over-interaction of these
balances may ultimately cause increased oxidant generation from mitochondria and
oxidative damage to biomolecules. This increased oxidative damage may add to the oxidant
burden associated with normal aerobic metabolism, which in itself, generates oxidants,
causes accumulation of oxidative damage in mitochondria, and contributes to normal aging.
Therefore, the stress-associated increase of oxidative damage may, in part, contribute to
stress-associated aging acceleration and age-related neurodegenerative diseases, and anti-
stress agents, including hormones, neurotransmitters, immune regulators, antioxidants,
especially antioxidant mitochondrial nutrients, may be effective in delaying, preventing, and
treating stress-associated aging acceleration and stress-related diseases, such as
depression, chronic fatigue syndrome, digestive disorders, sleep disorders, heart diseases,
cataract, obesity, diabetes, immune dysfunction, memory decline, and neurodegenerative
diseases.