http://www.chronicprostatitis.com/sugar.html

Pain after ingesting sugar-rich foods make many suspect yeast problems. But
is it that simple?

In brief, sugar (in all its forms) does two things which could account for
the pain people frequently experience after ingesting it:

It affects the immune system for a short time (few hours)

It causes a spurt of uric acid to be excreted via the
kidneys/bladder/prostatic urethra, so burning the inflamed tissues there.

Here is the evidence:

Bernstein, J., et al, Depression of lymphocyte transformation following oral
glucose ingestion, Am. J. Clin. Nutr., 30:613, 1977

Sanchez, A., et al, Role of sugars in human neutrophilic phagocytosis, Am.
J. Clin. Nutr., 26:180, 1973.

These studies show that in adults, cell mediated immunity is significantly
depressed after sugar ingestion (75 grams). A 100g portion of sugar can
significantly reduce the capacity of white blood cells to engulf bacteria.
Maximum immune suppression occurs one to two hours after ingestion and
remains suppressed for up to five hours after feeding. Although the studies
concentrate on phagocytosis, it is not hard to see how any suppression of
parts of the immune system could affect inflammatory responses going on,
even if there are no fungi or bacteria.

To prove that sugar consumption causes a burst of uric acid production:

Reiser S et al. Blood lipids, lipoproteins, apoproteins, and uric acid in
men fed diets containing fructose or high-amylose cornstarch. The American
Journal of Clinical Nutrition 1989;49:832-39

...which contains the following paragraph on uric acid, inter alia:

"Uric acid -- The feeding of sucrose, at levels approximating that currently
consumed in this country, as compared with starch has been shown to increase
fasting uric acid levels in hyperinsulinemic subjects and in patients with
NIDDM. The fructose moiety of sucrose appears to be specifically responsible
for these increases. These results are consistent with the findings in the
present study in which fructose as compared with starch feeding produced
both a chronic (fasting level) and acute (response levels) increase in uric
acid levels. The increase in uric acid caused by fructose-containing
carbohydrates is not only a risk factor associated with heart disease but
also appears to be associated with short-term and adaptive changes in
metabolism consistent with decreased hepatic levels of adenosine
triphosphate (ATP), which could potentially affect the myriad of metabolic
processes dependent on ATP."

More evidence:

Some effects, in man, of varying the load of glucose, sucrose, fructose, or
sorbitol and various metabolites in blood I. Macdonald, M.D., D.Sc., Anne
Keyser, and Deborah Pacy, B.Sc. Am. J. Clin. Nutr. 31: 1305- 1311, 1978.

ABSTRACT: Tolerance tests using glucose, sucrose, fructose, or sorbitol each
at 4 dose levels, were carried out in nine healthy young men and during the
90 min after ingestion the plasma serum concentrations of glucose, insulin,
fructose, triglyceride, glycerol, uric acid, lactate, and pyruvate were
estimated. It was confirmed that serum glucose levels are unaffected by the
amount of glucose given. Little fructose seems to be converted to glucose
judging by the serum fructose levels following sucrose and fructose, and by
the small insulin response to oral fructose. The insulin response to a
sucrose meal is half of that after an equivalent amount of glucose. The fall
in serum triglyceride seen after carbohydrate meals is not related to
insulin. Only glucose is not associated with a rise in serum uric acid,
lactate, and pyruvate concentrations after ingestion.

Quotes from study:

"Uric Acid -- There was a significant increase in the concentration of uric
acid at each level of fructose intake, but it did not appear to be dose
related. At three dose levels of sucrose there was a significant mean
increase in uric acid whereas after glucose and sorbitol no significant
change occurred .... The increase in uric acid levels after sucrose and
fructose ingestion and the absence of such an increase after glucose
ingestion supports the view that fructose causes depletion of hepatic
adenine nucleotides and the purine component of these appears as uric acid
and in fact there is a significant correlation between the increase in serum
fructose and uric acid concentrations."

{FYI: each 1g fructose/kg bodyweight gave a 0.6mg/100ml increase in uric
acid}