Worldwide sperm counts are declining at a rate of 0.70million/ml per year, with some western countries experiencing up to a 72.6% decrease in sperm counts over the past 50 years. Coinciding with the decreased sperm counts is the epidemic increased incidence of metabolic disorders encapsulating; obesity, type II diabetes, high blood pressure, hyperlipidaemia, fatty liver disease, etc. among men of reproductive age, with rates of diagnosis increased by 35% from 1988–1994 to 2007–2012 in many western nations. Obese men in the general population have higher odds ratio of experiencing infertility, while those receiving assisted reproductive treatment for their infertility have lower rates of live birth. There is still conflicting findings in the literature about obesities effects on sperm quality. Our extensive research in animal models of obesity, suggests that increased fat mass is not the driver for the changes in sperm function seen and why conflicting reports still exist in the current literature. It seems that a combination of obesity related co-morbidities (such as, hyperglycaemia, poor nutrition, pro-inflammatory state etc.) are the main culprits. In humans, obese men who present with azoospermia/oligospermia are more likely to have an additional underlying medical condition (i.e. fatty liver disease or hyperglycaemia) than just increased fat mass. Interestingly, in our animal obesity model, when we target just one of these comorbidities i.e. altered glucose control with metformin, or poor nutrition with micronutrient supplementation we can restore sperm function, sperm oxidative DNA damage and fetal growth without a need to reduce adiposity. Therefore, moving forward we must assess obesity related subfertility as a syndrome ensuring we determine the real underlying reasons for their changes in sperm quality, as restoration may require more or less than just telling a man to lose weight.