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by claude@2026-07, 2026-07-13
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This study tested whether Western diet exposure during early- (postnatal days 26–41) versus late-adolescence (postnatal days 41–56) produces long-lasting hippocampal-dependent memory impairments in male and female rats, using a free-access Western diet model with high-fat and/or high-sugar items. Rats were later assessed after either a short or long period of returning to healthy standard chow, to determine persistence of cognitive deficits far beyond the initial dietary insult. The authors found that, after a short healthy-diet intervention, both sexes exposed to Western diet during either adolescent window showed hippocampal-dependent memory deficits, but after the longer intervention only male rats with early-adolescent Western diet (WD-EA) retained impairments while female rats’ impairments were reversed in both windows; no body weight or composition differences were observed across groups. The paper’s caveat is that it uses an animal Western diet paradigm and behavioral endpoints without directly mapping mechanisms to specific hippocampal pathways. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.
Abstract
Early life Western diet (WD) consumption leads to impaired memory function, particularly for processes mediated by the hippocampus. However, the precise critical developmental window(s) during which WD exposure negatively impacts hippocampal function are unknown. Here, we exposed male and female rats to a WD model involving free access to a variety of high-fat and/or high-sugar food and drink items during either the early-adolescent period (postnatal days [PN] 26-41; WD-EA) or late-adolescent period (PN 41-56; WD-LA). Control (CTL) rats were given healthy standard chow throughout both periods. To evaluate long-lasting memory capacity well beyond the early life WD exposure periods, we performed behavioral assessments after both a short (4 weeks for WD-EA, 2 weeks for WD-LA) and long (12 weeks for WD-EA, 10 weeks for WD-LA) period of healthy diet intervention. Results revealed no differences in body weight or body composition between diet groups, regardless of sex. Following the shorter period of healthy diet intervention, both male and female WD-EA and WD-LA rats showed deficits in hippocampal-dependent memory compared to CTL rats. Following the longer healthy diet intervention period, memory impairments persisted in male WD-EA but not WD-LA rats. In contrast, in female rats the longer healthy diet intervention reversed the initial memory impairments in both WD-EA and WD-LA rats. Collectively, these findings reveal that early-adolescence is a critical period of long-lasting hippocampal vulnerability to dietary insults in male but not female rats, thus highlighting developmental- and sex-specific effects mediating the relationship between the early life nutritional environment and long-term cognitive health.
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Abstract
Early life Western diet (WD) consumption leads to impaired memory function, particularly for processes mediated by the hippocampus. However, the precise critical developmental window(s) during which WD exposure negatively impacts hippocampal function are unknown. Here, we exposed male and female rats to a WD model involving free access to a variety of high-fat and/or high-sugar food and drink items during either the early-adolescent period (postnatal days [PN] 26-41; WD-EA) or late-adolescent period (PN 41-56; WD-LA). Control (CTL) rats were given healthy standard chow throughout both periods. To evaluate long-lasting memory capacity well beyond the early life WD exposure periods, we performed behavioral assessments after both a short (4 weeks for WD-EA, 2 weeks for WD-LA) and long (12 weeks for WD-EA, 10 weeks for WD-LA) period of healthy diet intervention. Results revealed no differences in body weight or body composition between diet groups, regardless of sex. Following the shorter period of healthy diet intervention, both male and female WD-EA and WD-LA rats showed deficits in hippocampal-dependent memory compared to CTL rats. Following the longer healthy diet intervention period, memory impairments persisted in male WD-EA but not WD-LA rats. In contrast, in female rats the longer healthy diet intervention reversed the initial memory impairments in both WD-EA and WD-LA rats. Collectively, these findings reveal that early-adolescence is a critical period of long-lasting hippocampal vulnerability to dietary insults in male but not female rats, thus highlighting developmental- and sex-specific effects mediating the relationship between the early life nutritional environment and long-term cognitive health.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Declarations of interest: none
Abbreviations
- ANOVA
- analysis of variance
- BDNF
- brain-derived neurotrophic factor
- CTL
- control
- DCX+
- doublecortin+
- HFCS
- high-fructose corn syrup
- HFD
- high-fat diet
- HFHSD
- high-fat high-sugar diet
- kcal
- kilocalories
- HPC
- hippocampus
- NOIC
- Novel Object in Context
- NOR
- Novel Object Recognition
- NMR
- nuclear magnetic resonance
- PN
- postnatal day
- SEM
- standard error of the mean
- WD
- Western diet
- WD-EA
- early-adolescent WD exposure
- WD-LA
- late-adolescent WD exposure.
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