Could this be true?  Are the refrigerators killing us with heart
disease?  See here:

http://www.thincs.org/discuss.cordainagain.htm#Leib
http://www.thincs.org/discuss.atherosclerosis.htm#Leib2

QUOTE:
Another consequence of leaving milk fat to sour is that the
cholesterol contained therein undergoes some spontaneous oxidation,
forming oxysterols. Oxysterols have the property of preventing
crystallization of cholesterol from supersaturated solution. I believe
it is the crystallization of cholesterol from the plasma lipids that
are deposited in the arterial intima that renders that cholesterol
atherogenic; and that adequate oxysterols in the diet could prevent
that from happening.

I should add that meat has been preserved for millenia by allowing it
to dry in the air.The same oxidative changes occur in the cholesterol
in meat

In my view, the critical change in the human diet with relevance to
atherogenesis was the alteration in food handling techniques allowed
by refrigeration, introduced in the developed world early in the 20th
century. This inadvertently largely eliminated the spontaneous
generation of oxysterols in foods of animal origin, removing these
compounds from the human diet.

Raising the spectre of oxidized cholesterol does give me the
opportunity to plug my views. Oxysterols, as distinct from
cholesterol, were first conceptually implicated in experimental
atherogenesis by Altschul around 1946. Since then it has over the
years been reported by several groups of workers, including work by
Altschul, that oxysterols do the reverse. They in fact attenuate
lesion formation in cholesterol fed animals. The work implicating
oxysterols in atherogenesis would seem to be questionable.

I have postulated that cholesterol from plasma becomes a pathogenic
moiety in the arterial wall when it takes on its native character,
which is that of a crystalline solid. In this state cholesterol cannot
be cleared from tissue and it is sclerogenic. Thus factors that
promote or prevent the crystallization of cholesterol determine its
role in atherogenesis. This view is based on observations originally
made by chance, namely, that oxysterols prevent the crystallization of
cholesterol in in vitro systems, and that glucose promotes the
crystallization of cholesterol. In addition, oxysterols implanted
subcutaneously in rats together with cholesterol results in the
solubilization and clearance of a large mass of cholesterol, leaving
little residual fibrosis. Implanted pure cholesterol is rapidly
sequestrated by fibrous tissue, no cholesterol is cleared and it
remains sequestrated in a seemingly permanent granuloma.

The possible relevance of oxysterols to atherogenesis in humans was
attributed to their progressive elimination from the human diet since
the advent of refrigeration, which prevents the spontaneous oxidation
of cholesterol in foods of animal origin. Oxysterols must have been
invariably generated in such foods by the techniques practiced for
preservation of these foods prior to the development of refrigeration.
Oxysterols would have been progressively eliminated from the human
diet with progressive application of modern technology in preservation
and handling of foods.

You can find references, should you want to follow up on these
matters, in: Krut L H. Med. Hypotheses 1979;5:533-548, Atherosclerosis
1982:43;95-104 and 1982:43; 105-118. Recent Res. Devel. in Lipids Res
2, 1998:299-318. Amer J Cardiol 1998:81;1045-1046. Atherosclerosis
supplements 2004;5/1:36. Wilkens and Krut. J. Atheroscler Res
1963:3:15-23 and 1965:5;516-523.
UNQUOTE.