The question really comes down to do you have primary or secondary hypogonadism. If you have primary hypogonadism, you could take all the enclomiphene in the world and it would not adequately raise the testosterone levels to the normal range because the Leydig cells have failed. If you have secondary hypogonadism, then treating the underlying cause of that (obesity, diabetes, etc) would have a greater effect long-term in elevating testosterone levels.

Most men who have hypogonadism do not receive FSH/LH levels in their workup, so population studies are still not adequate, but it is currently believed that testicular failure (Primary hypogonadism) is the prevailing type of hypogonadism, with an increasing number of men with mixed hypogonadism (both direct testicular failure as well as hypothalamus/pituitary dysfunction). Is this due to the effects of microplastics, BPA, or atrazine? Birth control in our city water supplies? No one knows yet because science has only given us clues, without any adequate studies that arent purely observational and anecdotal.

The primary cause for secondary hypogonadism is obesity and metabolic syndrome. This can be treated, but the problem in this case is that once you are in the cycle of having low T due to obesity, the low level of T makes weight loss significantly more difficult as muscle mass (which is the driver of metabolism) is lost along with adipose tissue during calorie restriction in the absence of normal testosterone.

You are not wrong though. In the debate of restoration vs replacement (of T), restoration should always be the first choice when feasible.