sugar and doesn’t cause a rise in insulin—at least not
initially. Food companies commonly exploit this difference
to sell products sweetened with fructose to health-conscious
consumers and diabetics.
Once in the liver, fructose induces lipogenesis—literally,
fat creation. In truth, all carbohydrates when consumed in
excess are capable of stimulating lipogenesis, but fructose
may be the most efficient at doing so. One short-term study
published in the journal Obesity demonstrated nearly double
the increase in liver fat when healthy humans on high-
calorie diets supplemented with fructose compared to
glucose (113 percent versus 59 percent, respectively).^21
After fructose fills your liver to its capacity with fat, it
spills over into your bloodstream as triglycerides.
Consuming fat also leads to a short post-meal triglyceride
spike, but lipogenesis due to fructose consumption can
dump more fat into your blood than even the highest-fat-
containing meal—following a high-fructose snack, your
blood can actually take on the appearance of pink cream for
this very reason. This is also why fasting triglyceride levels
(a marker used to assess metabolic health and heart disease
risk) are nearly universally influenced by carbohydrate
consumption, and by fructose in particular.
While fructose has a negligible immediate effect on
blood sugar, frequent consumption will eventually cause
blood sugar to rise because the stress on the liver creates
inflammation, impairing the ability of cells to “suck up”
glucose from the blood. This may have been an adaptation
to help us store more fat when fruit was in season, and yet
now explains why sugar consumption dovetails with