The longer chain saturated fatty acids may induce apoptosis of cells
required for reproduction, but these are not prevalent in coconut oil:

Endocrinology. 2001 Aug;142(8):3590-7.

Saturated FFAs, palmitic acid and stearic acid, induce apoptosis in
human granulosa cells.

Mu YM, Yanase T, Nishi Y, Tanaka A, Saito M, Jin CH, Mukasa C, Okabe
T, Nomura M, Goto K, Nawata H.
Third Department of Internal Medicine, Faculty of Medicine, Kyushu
University, Higashi-ku, Fukuoka 812-8582, Japan.

Obesity is associated with insulin resistance and some reproductive
abnormalities. Circulating FFAs are often elevated in obese subjects
and are also closely linked to insulin resistance. In this study, we
demonstrated that saturated FFAs, such as palmitic acid and stearic
acid, markedly suppressed the granulosa cell survival in a time- and
dose-dependent manner. Polyunsaturated FFA, arachidonic acid, had no
effect on the cell survival, even at supraphysiological
concentrations. The suppressive effect of saturated FFAs on cell
survival was caused by apoptosis, as evidenced by DNA ladder formation
and annexin V-EGFP/propidium iodide staining of the cells. The
apoptotic effects of palmitic acid and stearic acid were unrelated to
the increase of ceramide generation or nitric oxide production and
were also completely blocked by Triacsin C, an inhibitor of
acylcoenzyme A synthetase. In addition, acylcoenzyme A,
pamitoylcoenzyme A, and stearylcoenzyme A markedly suppressed
granulosa cell survival, whereas arachidonoylcoenzyme A had no such
effect, and this finding was consistent with the effect of the
respective FFA form. Surprisingly, arachidonic acid instead showed a
protective effect on palmitic acid- and stearic acid-induced cell
apoptosis. A Western blot analysis showed the apoptosis of the
granulosa cells induced by palmitic acid to be accompanied by the down-
regulation of an apoptosis inhibitor, Bcl-2, and the up-regulation of
an apoptosis effector, Bax. These results indicate that saturated FFAs
induce apoptosis in human granulosa cells caused by the metabolism of
the respective acylcoenzyme A form, and the actual composition of
circulating FFAs may thus play a critical role in the apoptotic events
of human granulosa cells. These effects of FFAs on granulosa cell
survival may be a possible mechanism for reproductive abnormalities,
such as amenorrhea, which is frequently observed in obese women.
PMID: 11459807

Biochem Biophys Res Commun. 2003 Apr 18;303(4):1002-7.

Saturated free fatty acids, palmitic acid and stearic acid, induce
apoptosis by stimulation of ceramide generation in rat testicular
Leydig cell.

Lu ZH, Mu YM, Wang BA, Li XL, Lu JM, Li JY, Pan CY, Yanase T, Nawata
H.
Department of Endocrinology, Chinese PLA General Hospital, 28 Fu Xing
Road, Beijing 100853, PR China.

In men, obesity has generally been associated with reduced plasma
testosterone levels and with elevation of the plasma free fatty acids
(FFAs). In this study, we investigated the effects of saturated FFAs
including palmitic acid (PA) and stearic acid (SA), and
polyunsaturated FFA arachidonic acid (AA) on the survival of rat
testicular Leydig cell cultured in vitro. PA and SA markedly
suppressed Leydig cell survival in a time- and dose-dependent manner.
In contrast, AA stimulated the cell proliferation at 5-10 times of
physiological concentration. The suppressive effect of PA and SA on
cell survival was caused by apoptosis evidenced by DNA ladder
formation and Annexin V-EGFP/propidium iodide staining of the cells.
The apoptotic effect of PA was possibly mediated by ceramide
generation because it could be completely blocked by ceramide synthase
inhibitor fumonisin B1 and exogenous ceramide itself could directly
induce apoptosis in vitro. Surprisingly, the apoptosis induced by PA
could be partly prevented by AA. These results indicate that PA and SA
induce apoptosis in testicular Leydig cells by ceramide production and
these apoptotic effects may be a possible mechanism for reproductive
abnormalities in obese men, and AA can partly prevent the apoptotic
effect induced by saturated FFA.
PMID: 12684033

And AA may be better than Viagra:

FASEB J. 2006 Mar;20(3):539-41. Epub 2006 Jan 13.

Cytochrome P450 epoxygenases provide a novel mechanism for penile
erection.

Jin L, Foss CE, Zhao X, Mills TM, Wang MH, McCluskey LP, Yaddanapud
GS, Falck JR, Imig JD, Webb RC.
Department of Physiology,Medical College of Georgia, Augusta, Georgia,
USA. ljin8@jhmi.edu

Erectile dysfunction (ED) is estimated to affect more than 30 million
American men and 152 million men worldwide. Therapeutic agents
targeting the nitric oxide/cyclic GMP signaling pathway have
successfully treated patients with ED; however, the efficacies of
these treatments are significantly lower in specific populations such
as patients with diabetes. The goal of this study was to discover and
identify new endothelium-derived relaxing factors involved in the
regulation of erectile function, providing alternative therapeutic
targets for treatment of ED. Immunoblotting results showed that
protein expressions of epoxygenases from cytochrome P450 (CYP)2B, 2C
and 2J subfamilies, as well as NADPH CYP reductase were present in rat
corpora cavernosa, which was confirmed by immunohistochemical
analysis. Furthermore, CYP2C was localized in cavernosal endothelial
cells using double immunolabeling. CYP epoxygenase activity was
analyzed by reverse-phase high-pressure liquid chromatography; and the
results showed that 11,12- epoxyeicosatrienoic acid (EET) was the
major product metabolized by CYP epoxygenases in rat corpora
cavernosa. Inhibition of EETs function by injection of an EETs
antagonist into rat penis significantly decreased intracavernosal
pressure-induced by electrical stimulation of the major pelvic
ganglion in vivo. In conclusion, our results suggest that EETs,
produced by CYP epoxygenases, in penile endothelial cells serve as
vasodilators. Inhibition of this pathway attenuated erectile function,
suggesting that EETs are required for normal erection.
PMID: 16415108

Proc Natl Acad Sci U S A. 1986 Jun;83(12):4346-9.

The arachidonic acid cascade is involved in the masculinizing action
of testosterone on embryonic external genitalia in mice.

Gupta C, Goldman AS.

We have evaluated whether the arachidonic acid cascade may be involved
in the folding and fusion of the penis and scrotum in masculine
differentiation, a possibility raised by recent observations of the
involvement of the arachidonic acid cascade in the analogous embryonic
processes of elevation and fusion of the palatal shelves and of
folding and fusion of the neural tube. To test this hypothesis, during
embryonic masculine differentiation in mice of the B10.A strain, we
administered certain agents that produce blockade of masculinization.
We report that arachidonic acid can reverse the inhibition of
masculine development in male embryos produced by estradiol-17 beta or
by cyproterone acetate, an androgen receptor-site blocker, and that
such reversal can be prevented by an inhibitor of cyclooxygenase, such
as indomethacin. We have also found that agents that block the
arachidonic acid cascade at the level of phospholipase A2 (cortisone,
phenytoin) or at the level of cyclooxygenase (indomethacin, aspirin)
also block masculine differentiation and that such antimasculinization
is reversed by arachidonic acid. The masculinization of male embryos
is inhibited by indomethacin and aspirin, and the masculinization of
female embryos produced by exogenous testosterone is prevented by
indomethacin. These findings provide evidence that the mechanism by
which testosterone organizes the genitalia involves a role of the
arachidonic acid cascade leading to prostaglandins at a critical
period of development and that interference with testosterone
synthesis or action leads to a teratogenic deficiency of arachidonic
acid during this time in the genital anlagen.
PMID: 3086881