Our findings indicates that women with secondary infertility were older and had longer duration of infertility compared with those with primary infertility. This finding is consistent with the findings of Seth et al.,  and highlights the independent role of age in fertility function of women . This age phenomenon suggests decreased fecundity in secondary infertile women who have been successful in having their previous pregnancies. Ages beyond 32-years reflects decrease in egg quality in association with a gradual increase in circulating level of FSH, declines in circulating anti-müllerian hormone and inhibin B concentrations .
One important finding of this study was that fertility hormones including FSH and LH were higher and above normal range in women with primary infertility compared with secondary infertility. Additionally, although not significant, levels of progesterone and prolactin were high in women with primary infertility compared with secondary infertility. This finding aligns the findings of Al-Turki . Generally, FSH stimulates several follicles to mature and LH kindles ovulation by causing the dominant follicle to burst and release its eggs into the fallopian tube. High LH and FSH levels increase ovarian testosterone production, alter oestrogen production, and causes abnormalities with ovulation. The levels of LH and FSH, observed among primary infertile women is suggestive of a possible primary ovarian failure and poor pregnancy outcomes [18, 20].
Another significant finding in this study was the direct association observed between LH and the central adiposity index (WHR) in both primary and secondary infertile women. Besides, no association was observed between any adiposity index and FSH levels in both primary and secondary infertile women. This findings deviates from previous report, which reported a positive association between central adiposity indices and FSH levels but not LH . De Pergola et al.,  also reported an inverse of adiposity indices with LH and FSH levels, which deviates from our present finding. In our findings, central adiposity indices (WC and WHtR) were positively correlated with LH levels among PCOS associated infertile. In line with a previous study  women with PCOS are most likely to have central fat distribution, which is associated with hyperandrogenaemia. Also, a neuroendocrine mark of PCOS is persistently rapid LH (GnRH) pulsatility, which favours pituitary synthesis of LH over that of FSH and contributes to the increased LH concentrations .
This study also observed a negative association between central adiposity indices (WC and WHtR) and prolactin levels in both primary and secondary fertility. This finding is incongruent with a previous finding , which rather observed a positive association. The unique finding of this study was that prolactin levels of women with tubal factors as the cause of infertility showed negative association with central adiposity indices (WC and WHtR). Women with unexplained causes of infertility showed positive association between WC and WHtR and prolactin levels, which suggest possible obesity-induce hyperprolactinemia and poor fertility outcomes. Thus, we speculated that the association between central adiposity and prolactin levels is influenced by the underlying causes of infertility which merits future investigations.
Among hyperprolactinemia-associated infertility, a positive association was found between FSH levels and markers of central adiposity (WC and WHtR). Hyperprolactinemia affects GnRH neurons and pituitary gland function to reduce secretion of LH and FSH, which represents an ovulatory disorder often associated with secondary amenorrhea or oligomenorrhea [24, 25]. Also, the interplay between fertility and obesity is the effect of obesity on menstrual disturbances [9, 10]. Thus, hypothesised an investigative associations of serum measures of ovarian reserve and ultrasound measurements of antral follicle counts with body size especially in hyperprolactinemia-associated infertility.
Our findings suggest a direct association between adiposity indices and various hormonal derangements, which is largely dependent on the aetiology of infertility. Intervention undertaken to control central and visceral obesity would definitely provide a beneficial effect by correcting the hormonal imbalance. Therefore, we recommend that an effective weight-management intervention among infertile women is beneficial for their hormonal milieu, more appropriate for fertility.
Tests including thyroid stimulating hormones, glucose and lipids as well as oestrogen and testosterone would have beneficial to clearly explain some of the findings between obesity and hormone levels. This is because obesity is associated with the stimulating effects on hormones and metabolism, which has all been implicated in infertility.