Plonk
---
Joan

sorry tommy

but you just plain fail to understand the cause and effect, as it is
currently known
as i wrote before, i prefer to take my information from multiple sources,
of acknowledged researchers, not someone who gleans their understanding
from key word searches in the hopes of somehow bolstering their claims. i
make no claims, i just read and review what is there.

what you have always failed to acknowledge is that others 'do' read studies
and reports, and draw conclusions from  them - that they differ from 'your'
conclusions appears to create angst in your dealings with others.

"Free radicals are highly reactive molecules generated by biochemical redox
reactions that occur as a part of normal cell metabolism (  1  ). These
unstable species may cause oxidative damage to DNA, carbohydrate, proteins
and lipids that are normally counteracted by protective antioxidants.
Oxidative defense is provided by a number of enzymes and vitamins,
including the vitamin E, vitamin C and glutathione (  2  ,  3  ,  4  ). In
times of increased free radical production, individuals may become
deficient in these antioxidants. Excessive free radical production or low
antioxidant level leads to oxidation of cellular lipids, proteins and
nucleic acids, which results in fragmentation and cross-linking. This may
ultimately lead to cell death with widespread pathological consequences (
5  ) The imbalance between protective antioxidants (antioxidant defense)
and increased free radical production, leading to oxidative damage, is
known as oxidative stress. Oxidative stress is caused by a relative
overload of oxidants, i.e., reactive oxygen species. This impairs cellular
functions and contributes to the pathophysiology of many disease"

now:

"The generation of reactive oxygen species (free radicals) is an important
factor in the development and maintenance of rheumatoid arthritis in humans
and animal models. One source of free radicals is nitric oxide produced
within the synoviocytes and chondrocytes and giving rise to the highly
toxic radical peroxynitrite. Several cytokines, including tumour necrosis
factor-alpha (TNFalpha) are involved in the formation of free radicals"

"The polyunsaturated fatty acids (PUFA) include the n-3 compounds, some of
which are precursors of eicosanoid synthesis, and the n-6 group which can
increase formation of the pro-inflammatory cytokines TNFalpha and
interleukin-6, and of reactive oxygen species."
Darlington L.G.1, *; Stone T.W.2

Levels of R proteins (RP) [R immunoreactive proteins] and activity of lipid
peroxidation (LPO) were measured in 209 patients with RA. It was noted that
RP levels and LPO activity correlated with the activity of inflammation. A
rapid RA progression was characterized by higher RP levels and LPO
activity, while polyarthritis by more intensive RP metabolism and LPO. A
comprehensive study of RP and LPO in RA patients may facilitate prognosis
of the destruction rate.
1996;68(12):76-8.

# The antioxidant defense system is compromised in rheumatoid arthritis
patients.
# There is a shift in the oxidant/antioxidant balance in favor of lipid
peroxidation, which could lead to the tissue damage observed in the
disease.
# Oxygen free radicals have been implicated as mediators of tissue damage
in rheumatoid arthritis (RA).
# Therapeutic coadministration of antioxidants along with conventional
drugs to such patients has been considered beneficial
# Patients with RA had lower AOP levels
# which is an indication of reduced antioxidant capacity in these patients
Durak et al (1999)
Indicating that the antioxidant system is impaired and peroxidation
reactions are accelerated in patients with RA

a result of the already impaired function, not the cause...which is of
course, why much of the current development in RA treatment has been along
the lines of tnf control...

but that's really enough of your silly name calling, you will most likely
continue with it,  and since i have no intention of being affected by it,
you will only being crying in the wind.