chronically elevated insulin is common among people that
are thin. This often goes undetected because most people
assume that thinness equals metabolic health—a major error.
There’s even a medical term for normal-weight patients with
metabolic syndrome: metabolically obese, normal-weight
(the nonmedical term is skinny-fat). This illustrates an
important but often confused point: insulin resistance and
obesity are independent conditions. Yes, it is possible to fit
into small sizes and still be “obese” on the inside.
One consequence of elevated insulin for the thin and
overweight alike is that the release of stored fat for fuel—a
process called lipolysis—is blocked. How? Insulin acts like
a one-way valve on your fat cells. This means that when
insulin is elevated, calories can go in, but they can’t come
out. Your fat cells become a Roach Motel, meant as a way
of increasing (and preserving) stored fuels when the body
senses that food is abundant.
Imagine the average person, consuming more than 300
grams of carbohydrate per day, mostly from refined sources
like toaster pastries, commercial breads, sugar-sweetened
beverages, and wheat snacks. For this person, insulin
production is constant. This presents a major problem
because certain organs have evolved to use (and even
prefer) fat for fuel, such as nerve cells of the eye and the
heart muscle, but are prevented from doing so.
New research has shown that, contrary to what was
previously believed, fat can be used as a source of energy
for the photoreceptors of the eye.^4 Published in Nature
Medicine, researchers demonstrated how starving these cells
of fatty acids could drive age-related macular degeneration