25 October 2010
Lecture 17-RHEUMATOID ARTHRITIS AND NUTRITION
ARTHRITIS-
The influence of diet and nutraceuticals
Rheumatoid
arthritis
protein energy malnutrition
a) cytokine mediated metabolism
b) anorexia
c) gastrointestinal involvement
i) malabsorption
iron
zinc
copper
selenium
vitamin C
vitamin B6
vitamin E
histidine
elimination
therapy
4) Functional foods
5) Nutraceuticals
supplementation
therapy
w6 and w3
Protein energy
malnutrition
Widespread in
RA patients- poor prognosis and rehospitalisation and increased mortality rate
Cytokine mediated
metabolism
Lean body mass (LBM) decreases due to
PEM- most of metabolic activity in LBM this gives rise to deficient immune
competence and elevated IL-1 and
TNF-a via unknown mechanism associated with
hypermetabolism that is to say elevated energy metabolism
elevated
IL-1 and TNF-a
via unknown mechanism associated with
hypermetabolism that is to say elevated energy metabolism
More prevalent during active disease
Elevated
IL-1 and TNF-a
produce
anorexia in animals
Inverse
relation in humans between dietary intake and blood levels of these 2 inflammatory
cytokines
Gastrointestinal
tract involvement
malabsorption
-this gives rise to a decrease in nutrient uptake
Iron
Anemia- most
common cause is a cytokine mediated failure of the bone marrow to increase red blood cell
production in response to erythropoetin and impaired release of iron from reserves
lots of
iron in synovial tissue- possible
mediator of
inflammation-oxidation
-iron
chelators stops iron mediated oxidation in animal models
zinc
decreased levels in rheumatoid arthritis patients
Zinc supplementation comes with risks
-risks of zinc
supplementation
-impairment
of lymphocyte/neutrophil functions
-increased
LDL-c/HDL-c ratio
copper
Theory- Cu/Zn in superoxide dismutase
However copper levels in synovial
fluid and
plasma and correlate positively with disease activity
pharmacologic
treatment improves disease and brings copper
levels down
selenium
anti-inflammatory and immunomodulatory
down in rheumatoid arthritis patients
plasmas
however- most Se supplementation
trials no
real improvement in disease even when normal plasma levels restored
Vitamin C
Essential to
collagen synthesis -RA leads to collagen breakdown faster than collagen synthesis
Vitamin C supplementation leads to no clinical improvement in RA
Vitamin B6
down in
RA patients plasma
suppression
correlated with degree of
inflammation
and levels of pro-inflammatory cytokines
however supplementation- no clinical improvement
some studies
lower serum levels of vitamin E compared to healthy controls
other studies
suggest lower levels in synovial fluid compared to paired serum samples in RA patients
antioxidant-
synovium- vitamin E supplementation shows no clinical improvement
low serum levels in RA
correlates with disease activity (clinical and laboratory measures)
supplementation
does not work
Elimination therapy
Dong diet
Eliminating
additives preservatives red meat, herbs, dairy products, spices, carbonated drinks and
ethanol
Eat seafood, vegetables and rice
No difference
in RA clinical outcome between dong and placebo diets for RA patients
Other dietary elimination studies have come up with same thing
Role of diet
is controversial because existing studies do not give clear cut results
Food intolerances
Potential food antigens absorbed through the GI tract
Dairy,
cereals, maize, wheat gluten, tartrazine and certain dyes (azo dyes) have been speculated
upon as potential food antigens causing or promoting rheumatoid arthritis
-debatable as
to whether elimination of such antigens would have any impact whatsoever on cause or
promotion of RA
Supplementation therapy-functional foods
Novel supplements
New Zealand green lipped mussel extract
Devils
claw
(Harpagophytum root extract)
Sea kelp
ginseng
lactobacillus
Novel
supplements are all unproven
Functional
foods
Fish
Sulphur containing foods
Peppers
FISH-
only fish oils supported for clinical use
SULPHUR CONTAINING FOODS
Asparagus, eggs, onion, garlic- sulphur
necessary for building bone cartilage and connective tissue-no evidence to support
clinical use
PEPPERS
Capsaicin- anti-pain-reduces neural sensitivity
No
clinical evidence to support the use of peppers
Supplementation
therapy-Nutraceuticals
w6 and w3 foods to
reduce inflammation
reminder of pathways
Evening primrose oil
Borage oil
Blackcurrant oil
Fungal oil
Chrondroitin sulphate
Glucosamine
EVENING PRIMROSE OIL-SEE CLASS HANDOUT
BORAGE OIL-SEE CLASS HANDOUT
BLACKCURRANT OIL-SEE CLASS HANDOUT
FUNGAL OIL-Nothing
done to date but there is potential for
improvement
CHONDROITIN SULPHATE -no evidence to support clinical use