Nutrition and reproduction: Is there evidence to support a “Fertility Diet” to improve mitochondrial function?

Abstract

Normal function of mitochondria plays an essential role in enabling reproductive capacity. To date, few studies have investigated the role of promoting mitochondrial health in relation to fertility in humans. Selected nutritional interventions have demonstrated a potential to enhance mitochondrial function, suggesting a promise for future research for fertility treatment. This review summarizes the extant literature and highlights a putative role of particular nutrients in promotion of mitochondrial function, including in vitro, animal and human studies. Strong basis exists to advocate for further investigation of nutritional treatments for infertility patients.

Mitochondria: Participation to infertility as source of energy and cause of senescence

“…To date, few studies have investigated the role of promoting mitochondrial health in relation to fertility in humans (Shaum and Polotsky, 2013). During spermatogenesis there is a significant reduction of mitochondria number per cell due to mtDNA replication arrest.…”

Changes in Body Condition from Prepartum to Postpartum on Health and Reproduction in Dairy Cattle

“…The mitochondria are responsible for converting these fatty acids into ATP for energy. When excessive fatty acid mobilization occurs, the mitochondria often become overloaded and produce reactive oxygen species (ROS), and the peroxisomes become more active alternatively producing hydrogen peroxide and heat (Wathes et al, 2013;Shaum et al, 2013). Excessive lipolysis overloads the liver and mitochondria causing lipid accumulation in these tissues likely leading to damage and apoptosis of the cells (Wathes et al, 2013;Shaum et al, 2013).…”

“…When excessive fatty acid mobilization occurs, the mitochondria often become overloaded and produce reactive oxygen species (ROS), and the peroxisomes become more active alternatively producing hydrogen peroxide and heat (Wathes et al, 2013;Shaum et al, 2013). Excessive lipolysis overloads the liver and mitochondria causing lipid accumulation in these tissues likely leading to damage and apoptosis of the cells (Wathes et al, 2013;Shaum et al, 2013). Studies associated with obese women have shown that accumulation of lipids and oxidative stress in reproductive tissues, such as oocytes, causes a decrease in oocyte development (Shaum et al, 2013).…”

“…Excessive lipolysis overloads the liver and mitochondria causing lipid accumulation in these tissues likely leading to damage and apoptosis of the cells (Wathes et al, 2013;Shaum et al, 2013). Studies associated with obese women have shown that accumulation of lipids and oxidative stress in reproductive tissues, such as oocytes, causes a decrease in oocyte development (Shaum et al, 2013). The stress placed on the mitochondria during this high level of lipolysis in dairy cattle likely causes mitophagy, clearing of damaged mitochondria, due to shortage of nutrients and the oxidative stress placed on the mitochondria resulting in DNA damage and ultimate apoptosis of the organelle (Wathes et al, 2013).…”

“…The stress placed on the mitochondria during this high level of lipolysis in dairy cattle likely causes mitophagy, clearing of damaged mitochondria, due to shortage of nutrients and the oxidative stress placed on the mitochondria resulting in DNA damage and ultimate apoptosis of the organelle (Wathes et al, 2013). Antioxidants convert ROS into water and cofactors, such as vitamin B 12 , facilitate beta oxidation in the mitochondria to control this oxidative stress (Wathes et al, 2013;Shaum et al, 2013). Over/under conditioned dairy cattle were most susceptible to oxidative stress from lipolysis (Wathes et al, 2013).…”