Patients with similar audiograms often experience varying levels of difficulty in understanding speech in noisy environments, despite using state-of-the-art hearing aids. With audibility largely restored by amplification, these divergent suprathreshold outcomes are often attributed to reduced frequency selectivity (i.e., broadening of the so-called “tip” of cochlear frequency tuning curves) associated with sensorineural hearing loss (SNHL), and to non-peripheral factors such as attention, working memory, and executive function. However, our ongoing cross-species studies on neural coding in SNHL suggest that distorted tonotopy—a phenomenon where hypersensitive tails of cochlear tuning curves dominate and drive the response in the basal half of the cochlea—can significantly contribute to the degraded neural coding of sounds. This effect is particularly pronounced with naturalistic stimuli, such as speech, which contain intense low-frequency components alongside softer but highly informative high-frequency content. Going from bad to worse, this effect is further exacerbated in noisy backgrounds with pink-like spectral characteristics (e.g., background talkers, environmental noises). Specifically, in a chinchilla model of SNHL with noise-induced permanent threshold shifts, auditory-nerve single-unit measurements revealed that hypersensitive tuning-curve tails were the primary contributor to the severe degradation of speech-envelope coding through the masking effects of low-frequency energy on basal responses, manifesting both as impaired representation of higher vowel formants and near erasure of transient responses to high-frequency consonants. In parallel human studies of individuals with mild or moderate SNHL, we utilized behavioral measures, otoacoustic emissions, and electroencephalography (EEG) to characterize distorted tonotopy. Results indicate that humans with SNHL also exhibit hypersensitive tuning-curve tails, even with mild-moderate SNHL. Furthermore, EEG measurements revealed that these hypersensitive tails are linked to impaired tracking of speech envelopes. Importantly, variations in the estimated degree of distorted tonotopy were also predictive of the large individual differences in speech-in-noise outcomes that persist despite prescriptive amplification. Taken together, our results suggest that distorted tonotopy is a prominent contributor to suprathreshold deficits in SNHL in both laboratory animals and in human listeners. Additionally, in both species, non-invasive assays offer promise towards providing useful indices of distorted tonotopy that may, in the long run, be developed and leveraged for clinical use.