This leads to poor embryo development, with many of the
embryos derived from “obese eggs” failing to develop to the
stage at which they can implant into the uterus.
There is also an inverse correlation between body mass index
and levels of anti-Mullerian hormone, which can be used as a
surrogate measure of oocyte number. Thus obesity may also
cause premature ovarian ageing, with a reduction of the ovarian
reserve effectively shortening the reproductive lifespan for obese
women.
In men, obesity can be associated with lower testosterone,
which leads to impaired semen parameters. Although it’s
contentious whether obesity consistently affects sperm count,
motility and morphology, it’s becoming evident that sperm
quality is poorer in obese men.
Following fertilisation, the newly formed embryo attaches
to the inner lining of the womb, the endometrium, and the
outer cells of the embryo (which go on to form the placenta)
must invade the tissues to gain access to the mother’s blood
supply so that it can access oxygen and essential nutrients. This
attachment and implantation phase of early pregnancy is
governed by a complex dialogue of signals between the embryo
and the mother’s endometrium, and depends on the
endometrium becoming “receptive” to the embryo. Indeed,
two-thirds of pregnancy failures are attributed to the failure
of this intricate process.Compelling evidence from assisted reproduction and miscar-
riage databases shows that obese women are more likely to expe-
rience recurrent miscarriages. As miscarriage often results from
impaired or altered implantation of the embryo into the
mother’s endometrium, it’s possible that obesity affects
maternal–foetal communication during this process. Indeed,
some of the signals between the embryo and the endometrium
are not effectively functioning in obese women.
The impact of obesity on the endometrium has been exam-
ined in studies where oocytes donated by lean women and
fertilised by lean fathers were implanted into obese recipients
to remove the effect of obesity on both the egg and sperm.
When the embryos from lean donors were transplanted into
obese recipients there was a reduced chance of implantation
into the endometrium, fewer live births and an increased risk
of miscarriage, suggesting that obesity also has negative impacts
on the womb.
When implantation of the embryo does occur in an obese
mother there are further adverse consequences, such as inade-
quate placental development that can result in serious compli-
cations. For instance, obesity is currently the leading risk factor
for pre-eclampsia in the developed world.
Thus the intra-uterine environment is vitally important for
pregnancy success, and evidence clearly shows that maternal
obesity disrupts this environment at multiple levels.
More alarmingly, clinical and animal studies demonstrate
that the current obesity epidemic affects not only parents but
also the health of their future generations.
Recent attention given to “three-parent reproduction” has
highlighted the importance of mitochondria in the oocyte.
Mitochondria are the powerhouse of cells, and those in the egg
are transferred to all of the offspring’s tissues. The oocytes and
embryos from obese mothers are often metabolically abnormal,
displaying suboptimal mitochondrial activity that could be
inherited by the offspring and thus placing them at greater risk
of metabolic diseases, including obesity during their life.
Obesity throughout pregnancy or during breastfeeding also
increases the chance of the child becoming obese. This likely
occurs through the supply of excess calories to the child from
the mother, and again demonstrates that obesity and diet can
have negative impacts throughout the entirety of pregnancy
and beyond.
These problems are magnified for obese couples because
obesity-induced changes in sperm also compromise the health
of offspring. Obese men are more likely to father obese chil-
dren, and even their grandchildren have an increased risk of
developing diseases such as diabetes.
Of course, these human studies are heavily confounded by
common genetic predispositions to obesity and cultural factors
involving poor dietary habits, both of which can be passed from24 | JAN/FEB 2016
Figure 1. (a) The percentage of obese men and women in
populations with low fertility rates (USA, Australia and UK) and high
fertility rates (Niger and Burkina Faso). (b) The percentage of obese
boys/girls (<20 years of age) and men/women (>20 years of age) in
Australia.BoysMenGirlsWomenUSA Australia UK Niger Burkina Faso% of population obeseab