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In the liver, fructose bypasses the two highly regulated steps of glycolysis, catalyzed by glucokinase/hexokinase and phosphofructokinase both of which are inhibited by increasing concentrations of their byproducts. Instead, fructose enters the pathway at a level that is not regulated and is metabolized to fructose-1-phosphate primarily by fructokinase or ketohexokinase

Fructokinase has no negative feedback system, and ATP is used for the phosphorylation process. As a result, continued fructose metabolism results in intracellular phosphate depletion, activation of AMP deaminase, and uric acid generation which is harmful at the cellular level

Uric acid, a byproduct of fructose degradation,

Uric acid inhibits endothelial NO both in vivo and in vitro, [15] and directly induces adipocyte dysfunction

Serum uric acid increases rapidly after ingestion of fructose, resulting in increases as high as 2 mg/dL within 1 hour

Uncontrolled fructose metabolism leads to postprandial hypertriglyceridemia, which increases visceral adipose deposition. Visceral adiposity contributes to hepatic triglyceride accumulation, protein kinase C activation, and hepatic insulin resistance by increasing the portal delivery of free fatty acids to the liver

Several reviews have concluded that intake of both fructose and HFCS by children and adults was associated with an increased risk of obesity and metabolic syndrome

Sucrose is a disaccharide that is comprised of fructose and glucose

Figure 2

An alcohol-induced rise in estrogens as a consequence of alcohol catabolism in the liver has been reported

The only study that looked at the association between alcohol and wine consumption in healthy women did not report a clear association

smoking has been reported to increase induction of the 2-hydroxylation metabolic pathway (24). However, the few epidemiological studies conducted on healthy women showed no difference in estrogen metabolites with smoking status (22) or smoking dose (20), in line with our findings.

Family history of a first-degree family member with breast cancer confers a 2- to 4-fold risk of developing breast cancer

16% of breast cancers are due to unidentified hereditary factors

Estrogen metabolism occurs through enzymes whose activity is determined by the presence of specific genetic polymorphisms, thus can be defined as unique to each individual.

the metabolism is also influenced by a number of environmental factors, which change over a lifetime

significantly lower 2:16 OHE ratio in women who have known breast cancer risk factors compared with healthy women

There was an additional significant association specifically with BMI and alcohol use, which also supports the evidence that these factors affect estrogen metabolism

Profiling estrogen metabolites may identify women who are more likely to develop breast cancer within a population of women with known risk factors