1.13: web.health/diet/gout prevention:
. an acquaintance thought oats worsen gout;
what is a diet that reduces gout risk?
. certain foods contain more purines,
which break down into uric acid,
that may form crystals in joints;
but gout doesn't correlate exactly with purines.
. fructose is metabolized into uric acid [JASN 2010].
. milk products may reduce risk despite purines;
but milk protein may be inflammatory due to Neu5Gc,
a sialic acid found in non-human mammal protein.
ehow.com's list of purines per 100g grain
oats 94 mg
Barley 94 mg
wheat 51 mg
Rye 51 mg
-- most beer comes from barley;
whiskey often contains wheat or rye.
. purines from meat clearly increase risk of gout,
while purines from vegetables are not a problem;
and dairy foods (despite containing purines)
actually lower one's risk of gout. [whfoods.com]
. Mayo clinic's gout diet allows
plant-based purines, including peas, beans;
and excludes sugar(fructose), beer, and some liquors.
(grain liquors [potato vodka would be ok]).
Limit daily fish and poultry to 4 - 6 ounces;
milk products are a safer source of animal protein
easy on the high-fructose fruits:
. fructose may be bad for gout in 2 ways:
it breaks down into uric acid,
and it might reduce the kidney's ability to
remove the uric acid from the blood stream.
. fructose is a major source of kidney dysfunction:
Fructose may be a "risk factor for kidney disease
that includes glomerular hypertension, renal inflammation,
and tubulointerstitial injury" [JASN 2010]
"Fructose, but not dextrose, accelerates'
the progression of chronic kidney disease:"
"Glomerular sclerosis, tubular atrophy, tubular dilatation,
and cellular infiltration appeared markedly worse";
a high-fructose diet causes "insulin resistance
dyslipidemia, hypertension and hyperuricemia"
[Am J Physiology - Renal Physiology 2007].
. fructose causes dysfunction of mitochondria;
and is a main source of the insulin resistance
that is causing leptin resistance .
. fructose increases the uric acid load
that can drive a hypertension condition .
[Dr Lustig 2010 (transcribed here)].
"One feature that is common to metabolic syndrome
is an elevated uric acid.
Although often considered to be
secondary to hyperinsulinemia [high insulin],
recent evidence supports a primary role for uric acid
in mediating this syndrome. Specifically, fructose,
which rapidly can cause metabolic syndrome in rats,
also raises uric acid;
and, lowering uric acid in fructose-fed rats
prevents features of the metabolic syndrome.
. Mild hyperuricemia in normal rats
induces systemic hypertension,
renal vasoconstriction, glomerular hypertension
and hypertrophy, and tubulointerstitial injury
independent of intrarenal[inside-kidney] crystal formation.
Lowering uric acid in fructose-fed rats
ameliorates much of the metabolic syndrome,
including a reduction in BP[blood pressure],
serum triglycerides, hyperinsulinemia, and weight gain .
. Uric acid also can accelerate renal disease
in experimental animals
and epidemiologically is associated with
progressive renal disease in humans.
It is proposed that fructose- and purine-rich foods
that have in common the raising of uric acid
may have a role in the epidemic of metabolic syndrome
and renal disease that is occurring throughout the world.
. fructose intake correlates well with
the recent rise in the epidemic of metabolic syndrome,
diabetes, hypertension, and kidney disease .
The main pathophysiologic mechanism by which
uric acid causes these conditions involves an inhibition of
endothelial nitric oxide bioavailability
(which may induce insulin resistance),
activation of the renin angiotensin system,
and direct actions on endothelial cells
and vascular smooth muscle cells .
[J Am Soc Nephrol 2006]
go humans: "nonsense mutations" inside!:
"Urate oxidase converts uric acid to allantoin,
which is 5-10 times more soluble than uric acid.
Homo sapiens cannot express urate oxidase
because of a nonsense mutation."