GSE
Stress, toxins, damaged fats, microbes and NOT enough antioxidants causes inflammation
Stress, toxins, damaged fats, microbes and NOT enough
antioxidants causes inflammation
Inflammation occurs as a result of
Oxidant /Antioxidant Imbalance
A major reason damage occurs to body tissue is
because too many highly reactive, oxidant
ions/molecules introduced into or being produced in the body have
overwhelmed the body's antioxidant
presence -
Uncontrolled
free radicals ,
ROS
(Reactive Oxygen Species),
RNS (Reactive Nitrogen Species)
and other reactive species
are likely to take part in chemical reactions with your body's proteins,
lipids, carbohydrates and DNA.
For more detailed information on Reactive
Oxygen Species (ROS), see:
Life's Oxygen Paradox - Meet Dr. ROS Jeckyll
and Mr. ROS Hyde
ROS
in the body come from various sources - some are
listed on this page, but for more detailed information:
Where do ROS in the body come from?
Reactive oxidants are produced
in the body during metabolism
Energy-producing oxidative metabolism produces
ROS - Oxidative
metabolism is part of the design to extract energy by controlled oxidation
of substrates, at the same time preventing uncontrolled
oxidative damage
via antioxidants - a good analogy is "To use fire for warmth, but not to get burnt".
ROS
in oxidized Lipids / Trans Fats
Oxidized Cholesterol
In fried, cooked, cured, aged, or processed foods,
chiefly meats, eggs and dairy - E.g. powdered eggs/milk, scrambled
eggs. Dietary oxidized cholesterol is equally distributed to both HDL and LDL in
the body. (Univ of
Ca, 2003)
Cholesterol produced by the body or consumed in
food is oxidized in the body - in its antioxidant
role when it comes into contact with free radicals .
(lipid peroxidation induced by ROS/RNS seems
to be involved not only in cardiovascular disease, but also in cancer, rheumatoid
arthritis, and other degenerative health problems, including accelerated aging).
Oxidized
Polyunsaturated ,
Omega-6
and
Omega-3
Fats
These essential fats
are easily oxidized by ROS and
RNS :
-
In food before consumption - E.g. during the usual high-temperature
commercial process of extracting vegetable oils from seeds, or in high-temperature
processed foods. E.g. fried foods.Dietary
omega-3
and
omega-6 fats are essential
to well-being, but need to be consumed undamaged, in balance, together with fat-protective
antioxidants, such as vitamins A, D, E. and K;
-
In the body after consumption - when
antioxidants are deficient;
particularly damaging to cell membranes;
Trans Fats
2005 study of 700 nurses
- found
that those consuming the most trans fats had a significantly higher risk of cardiovascular
diseaseLink
to study
Increase both LDL and Lp(a) - One
study showed significant increases in Lp(a) levels of subjects consuming diets high
in trans fats, but not in those consuming high levels of saturated fats [J
Lipid Res 1992 Oct;33(10):1493-501 ]. Nutritionist/author Dr. Mary Enig
maintains that saturated fats actually LOWER Lp(a) levels. (Lp(a) is a specific
type of LDL cholesterol, implicated in, and an accurate marker for CVD)
Lp(a) - The "Repair
Man"
Decrease HDL
Damaged/Altered,Toxic Fats
ROS produced
by white blood cells when body reacts to an adverse factor
A wound, fever, nervous imbalance
(stress), microbial infection or toxin precipitates
an inflammatory response - in which
radicals, ROS, RNS or other reactive oxidants
are released by immune system white blood cells (E.g. macrophages).
Emotional stress
(Possibly today's main oxidation-causing stressor)
Histamine is produced as a result of Erratic Stress -
Accumulating histamine leads to inflammation and plaque formation. (Bruce H. Lipton's
histamine theory is that erratic stress induces mast cells on blood vessel endothelium
to emit histamine, which causes cells to multiply).
Having a Type-A personality is linked to an increased
risk of CHD - characteristics include time urgency and
competitiveness.
Trauma / Infective Microbes
Physical damage or presence of infectious agents,
such as bacteria, viruses, protozoa, initiates an inflammatory process that leads
to ROS production by phagocytes -
E.g. infectious bacteria Chlamydia pneumoniae and the Herpes simplex virus
have been proposed as initial inflammatory infectious agents in atherosclerosis.
ROS
are released in the synthesis of prostaglandins and leukotrienes - local "messenger"molecules
released from unsaturated fatty acids, produced in response to trauma.
Environmental Toxins
Induce inflammatory response leading to damaging
ROS and
RNS - E.g.cigarette smoking by-products, exhaust fumes, household chemicals,
chlorine, fluoride,
heavy metals, pesticides/herbicides, GMOs, food additives: E.g. dyes, aspartame,
sucralose, MSG, nitrites (used to cure meat such as bacon, bologna, corned beef,
sausages and hot dogs); (Suwa et al, 2002; Pope et
al, 2004a)
ROS produced by hyperglycemia
(chronically high blood sugar levels)
Hyperglycemia induces an inflammatory reaction
in endothelial cells (lining
interior surface of blood vessels), which can cause an increase in the production
of ROS
(reactive oxidants, including free radicals)
(Ceriello et
al, 1996)
Hyperglycemia increases the formation of
oxidized LDL - an important modulating factor
in atherosclerosis and cardiovascular death.
References Ceriello P et al, (April 1996 )High Glucose Induces Antioxidant
Enzymes in Human Endothelial Cells in Culture, Diabetes Vol 45.
Pope CA, III, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D, et al. (2004a)
Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological
evidence of general pathophysiological pathways of disease. Circulation. 109:71-77.
Suwa T, Hogg JC, Quinlan KB, Ohgami A, Vincent R, van Eeden SF. (2002)
Particulate air pollution induces progression of atherosclerosis. J Am Coll Cardiol.
39:935-942. [PubMed ]
Universityof California Study, published Feb. 1, 2003.