I wasn't aware of the new cookie law, Robert.  Thanks for updating us.
Keep up the good work.

Now, for those on planet Earth:

Such a study is rather odd, in that no thought is given to controlling
the different components of these foods.  Sadly, it seems to be the
rule rather than the exception in "nutritional science" these days.

I have attempted to determine what the key components are over the last
few years.  Here, it is not specified whether the eggs were boiled or
cooked while exposed to air, which makes a big difference (oxidized
cholesterol).  The fried steak would indeed be high in oxidized
cholesterol.  Steak also contains a lot more stearic acid, which
enhances iron absorption, enhancing lipid peroxidation.  Steak also
contains more arachidonic acid than the other meal, and this fatty acid
is bad news (just do a pubmed.com search for arachidonic to see what I
mean).  It's amazing how much is known, but how little any one "expert"
knows.  They defer to each other, instead of attempting to establish an
overall framework, which is what I am doing in my latest book (due out
in a year or less).

The study seems more intent on the LDL lowering effect.  What they must
not be aware of is that lowering LDL means higher risk of cancer, death
from shock, and "bleeding" stroke.  You can read about the history of
this in the book Heart Failure, by Thomas Moore, you can read the
"father" of the "cholesterol hypothesis," namely Ancel Keys, say in his
1979 book, Seven Countries, that the optimum range of cholesterol is
200 to 220 (if you want to live as long as possible), and there are
molecular/cellular level studies, such as the one below:

Free Radic Biol Med. 1995 Oct;19(4):511-6.

Cholesterol protects the phospholipid bilayer from oxidative damage.

Parasassi T, Giusti AM, Raimondi M, Ravagnan G, Sapora O, Gratton E.

Istituto di Medicina Sperimentale, CNR, Roma, Italy.

The measurement of fluorescence lifetime distribution of
1,6-diphenyl-1,3,5-hexatriene is used for the detection of oxidative
damage produced in phospholipid membranes by ionizing radiation. The
recently developed method is based on the linear relationship between
the width of the probe lifetime distribution and the logarithm of the
dose. The molecular origin of the damage resides in the production of
hydroperoxide residues at the level of acyl chains double bonds. A
chemiluminescence assay was used to quantitate the amount of produced
hydroperoxides. Consequences of the produced damages include an
increased disorder in the upper portion of the bilayer, accompanied by
the penetration of water molecules. In the presence of the
physiological concentration of cholesterol in phopholipid bilayers, the
amount of hydroperoxides produced by ionizing radiation is dramatically
reduced. The packing effect of cholesterol in phopholipid bilayers is
well recognized, as well as its influence on the reduction of water
concentration in the bilayer. The dramatic reduction of hydroperoxides
concentration observed when irradiation is performed in the presence of
cholesterol probably originates from a steric hindrance to the radical
chain reaction through the unsaturated lipids due to the presence of
cholesterol.