Infertility Management May Benefit from Both Increased BDNF Lifestyle and Increased PPAR Agonist Activity

Peroxisome Proliferator-Activated Receptors in Female Reproduction and Fertility 

http://downloads.hindawi.com/journals/ppar/2016/4612306.pdf

PPAR system is an amplifier of other nuclear transcription products.  In this review article, the implications of PPAR dysfunction as it affects fertility is discussed.  In essence, PPAR activity is important for stimulation of  2 types of cells in the ovary and is implicated in ova maturation, ova release, luteal cyst formation, trophoblast implantation in early pregnancy.  However, PPAR activity is diminished relatively later during pregnancy and lactation!

What is implied by early high and late low PPAR activity in pregnancy and lactation is my conjecture of the day.

The metabolic health of cells, their resistance to cell death and malignant transformation is directly correlated to BDNF levels directly and other "starvation set" genes by proxy.
Since PPAR genes can only amplify and co promote other nuclear transcription genes, BDNF et al are the genes they promote along with healthy sex hormone and viable eggs and sperm for procreation.  One must have BOTH BDNF et al gene expression for health and procreation AND PPAR  gene expression to amplify these effects for early pregnancy.

Why then is PPAR activity diminished by pregnancy and lactation?
Why is pregnancy an immune suppression state?

My conjecture is that pregnancy occurs to allow a genetically different body to live in the host or mother albeit in a protected environment with placental barrier.  There must be further immune system protections to prevent the rejection of the genetically different baby or allograft.

In addition to down regulated nuclear gene transcription of immune function there is down regulated nuclear transcription of co promoter or amplifiers.  Hence the decreased PPAR activity levels in the time around pregnancy.

ACTION:  BDNF increasing lifestyle should increase fertility and PPAR effects as a team.

Polycystic ovary syndrome is a syndrome of obesity, insulin resistance, ovarian follicular cysts and infertility.  Infertility is treated by reversing insulin resistance, a PPAR action and by use of fertility medications.

I wonder if BDNF et al gene expression would improve metabolic and fertility issues in Polycystic ovary syndrome.  If true, then raising BHB by any means and using PPAR agonists should improve fertility.

BHB is increased by the following:

Fasting. Restricted interval feeding.  ( This is 80% of metabolic health, based on studies including poor diets and limited exercise likely because the time duration of BHB is prolonged in contrast to the BHB time duration of either exercise and MCT oil consumption.)
Exercise,
MCT oil and coconut oil metabolism.
Ursolic acid. (UA increases PPAR alpha nuclear transcription which increases fatty acid metabolism within cells and increases PGC-1 alpha levels.  The latter amplifies the effect of BHB nuclear transcription of BDNF and has a force multiplying effect for fasting, exercise and MCT oil consumption.)