As for the atherogenicity of coconut oil:

Taken from an article written by Conrado S. Dayrit in the Philippine
Journal Of Cardiology entitled “Coconut Oil: Atherogenic or Not?”:

According to the universally accepted Lipid-Heart Theory, high
saturated fats causehypercholesterolemia and coronary heart disease.
Coronary morbidity and mortality are said to be highest in the
countries and peoples consuming the highest amounts of saturated fats.
Coconut oil, with its saturated medium chain fats, has been especially
condemned for this reason. The true facts are just the opposite. The
countries consuming the highest amounts of coconut oil – the
Polynesians, Indonesians, Sri Lankans, Indians, Filipinos have not
only low serum cholesterol but also low coronary heart disease rates.

The reason why coconut oil cannot be atherogenic is basic. Coco oil
consistspredominantly of 65% medium chain fatty acids (MCFA) and MCFAs
are metabolized rapidly in the liver to energy and do not participate
in the biosynthesis and transport of cholesterol. Coconut oil, in
fact, tends to raise the HDL and lower the LDL:HDL ratio. Coco oil is
not deposited in adipose tissues and therefore does not lead to
obesity. It is primarily an energy supplier and as fast a supplier of
energy as sugar. MCFAs therefore differ in their metabolism from all
the long chain fatty acids, whether saturated or unsaturated.

The pathogenesis of atherosclerosis has recently taken a complete
paradigm shift – from a simple deposition of cholesterol and
cholesterol esters to an inflammatory condition where numerous
genetically dependent factors – dyslipoproteinemias, dysfunctions of
endothelial and other cells leading to invasions of the subendothelial
region by macrophages, smoothmuscle cells, leukocytes and T cells –
all interplay in a scenario still not fully understood.

Taka

Another thumbs up for coconut oil having medicinal properties. BPH is
an extremely common problem for aging men, and this seems to be a
viable treatment option (if it is repeatable in humans):

Effects of coconut oil on testosterone-induced prostatic hyperplasia
in Sprague-Dawley rats.

Benign prostatic hyperplasia (BPH) is the benign uncontrolled growth
of the prostate gland, leading to difficulty with urination. Saw
palmetto lipid extracts (SPLE), used to treat BPH, have been shown to
inhibit prostate 5a-reductase, and some major components, such as
lauric, myristic and oleic acids also inhibit this enzyme. Coconut oil
(CO) is also rich in fatty acids, mainly lauric and myristic acids. We
investigated whether CO prevents testosterone-induced prostate
hyperplasia (PH) in Sprague-Dawley rats. Animals were distributed into
seven groups (10 rats each). A negative control group were injected
with soya oil; six groups were injected with testosterone (3 mg
kg(-1)) to induce PH: a positive control group, and five groups
treated orally with SPLE (400 mg kg(-1)), CO or sunflower oil (SO)
(400 and 800 mg kg(-1)). Treatments were given for 14 days. Rats were
weighed before treatment and weekly thereafter. Rats were then killed
and the prostates were removed and weighed. CO (400 and 800 mg
kg(-1)), SPLE (400 mg kg(-1)) and SO at 800 mg kg(-1), but not at 400
mg kg(-1), significantly reduced the increase in prostate weight (PW)
and PW:body weight (BW) ratio induced by testosterone (% inhibition
61.5%, 82.0%, 43.8% and 28.2%, respectively). Since CO and SPLE, but
not SO, contain appreciable concentrations of lauric and myristic
acids, these results could be attributed to this fact. In conclusion,
this study shows that CO reduced the increase of both PW and PW:BW
ratio, markers of testosterone-induced PH in rats.
PMID: 17637195

Taka