► Western diets tend to be high in saturated fat and simple carbohydrates (HFS). ► This review examines the impact of HFS diets on the human brain. ► HFS diets impair several aspects of cognition and ...damage associated brain areas. ► HFS diets may cause such damage via several established mechanisms. ► HFS diets also seem to contribute to the onset of neurodegenerative conditions.
Animal work over the last three decades has generated a convincing body of evidence that a Western diet – one high in saturated fat and refined carbohydrates (HFS diet) – can damage various brain systems. In this review we examine whether there is evidence for this in humans, using converging lines of evidence from neuropsychological, epidemiological and neuroimaging data. Using the animal research as the organizing principal, we examined evidence for dietary induced impairments in frontal, limbic and hippocampal systems, and with their associated functions in learning, memory, cognition and hedonics. Evidence for the role of HFS diet in attention deficit disorder and in neurodegenerative conditions was also examined. While human research data is still at an early stage, there is evidence of an association between HFS diet and impaired cognitive function. Based upon the animal data, and a growing understanding of how HFS diets can disrupt brain function, we further suggest that there is a causal link running from HFS diet to impaired brain function in humans, and that HFS diets also contribute to the development of neurodegenerative conditions.
Ductular reaction (DR) is characterized by the proliferation of reactive bile ducts induced by liver injuries. DR is pathologically recognized as bile duct hyperplasia and is commonly observed in ...biliary disorders. It can also be identified in various liver disorders including nonalcoholic fatty liver disease. DR is associated with liver fibrosis and damage, and the extent of DR parallels to patient mortality. DR raises scientific interests because it is associated with transdifferentiation of liver cells and may play an important role in hepatic regeneration. The origin of active cells during DR can be cholangiocytes, hepatocytes, or hepatic progenitor cells, and associated signaling pathways could differ depending on the specific liver injury or animal models used in the study. Although further studies are needed to elucidate detailed mechanisms and the functional roles in liver diseases, DR can be a therapeutic target to inhibit liver fibrosis and to promote liver regeneration. This review summarizes previous studies of DR identified in patients and animal models as well as currently understood mechanisms of DR.
There is strong epidemiological evidence that poor diet is associated with depression. The reverse has also been shown, namely that eating a healthy diet rich in fruit, vegetables, fish and lean ...meat, is associated with reduced risk of depression. To date, only one randomised controlled trial (RCT) has been conducted with elevated depression symptoms being an inclusion criterion, with results showing that a diet intervention can reduce clinical levels of depression. No such RCTs have been performed in young adults. Young adults with elevated levels of depression symptoms and who habitually consume a poor diet were randomly allocated to a brief 3-week diet intervention (Diet Group) or a habitual diet control group (Control Group). The primary and secondary outcome measures assessed at baseline and after the intervention included symptoms of depression (Centre for Epidemiological Studies Depression Scale; CESD-R; and Depression Anxiety and Stress Scale- 21 depression subscale; DASS-21-D), current mood (Profile of Mood States), self-efficacy (New General Self-Efficacy Scale) and memory (Hopkins Verbal Learning Test). Diet compliance was measured via self-report questionnaires and spectrophotometry. One-hundred-and-one individuals were enrolled in the study and randomly assigned to the Diet Group or the Control Group. Upon completion of the study, there was complete data for 38 individuals in each group. There was good compliance with the diet intervention recommendations assessed using self-report and spectrophotometry. The Diet group had significantly lower self-reported depression symptoms than the Control Group on the CESD-R (p = 0.007, Cohen's d = 0.65) and DASS-21 depression subscale (p = 0.002, Cohen's d = 0.75) controlling for baseline scores on these scales. Reduced DASS-21 depression subscale scores were maintained on follow up phone call 3 months later (p = .009). These results are the first to show that young adults with elevated depression symptoms can engage in and adhere to a diet intervention, and that this can reduce symptoms of depression. The findings provide justification for future research into the duration of these benefits, the impacts of varying diet composition, and their biological basis.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Human and animal data suggest that the hippocampus plays certain roles in regulating food intake. However, its actual role may be far broader than currently envisaged, a claim suggested by the ...centrality of the hippocampus to so many aspects of human/animal cognition. Understanding these ingestion-related functions is especially significant. This is because some degree of hippocampal impairment may be quite common, resulting for example from a Western-style diet, insomnia, diabetes, and depression-among many other causes. One potential consequence of hippocampal impairment could be a loosening of food intake regulation, leading in the longer-term to weight gain and its health-related impacts. Here we review known, suspected and newly hypothesized hippocampal-dependent functions involved in regulating human food intake: (a) declarative memory processes, and their use in explicitly evaluating when, what and how much to eat; (b) interoception, as it relates to hunger, fullness and thirst; (c) inhibitory processes, especially as applied to physiological state, place, and time, and their role in modulating memory retrieval; (d) craving and imagery for food; (e) perception of time and its role in preparing the body for food intake and estimating meal length; (f) trace conditioning and nutrient-related learning; and (g) inhibition of the hypothalamic-pituitary-adrenal stress response and stress-related eating. For each we present evidence for hippocampal involvement, describe the putative regulatory role, and the hypothesized effects of hippocampal impairment. We conclude that the hippocampus is intimately involved in regulating human food intake via multiple interconnected pathways, many of which are unstudied and understudied.
In animals, a Western style diet-high in saturated fat and added sugar-causes impairments in hippocampal-dependent learning and memory (HDLM) and perception of internal bodily state (interoception). ...In humans, while there is correlational support for a link between Western-style diet, HDLM, and interoception, there is as yet no causal data. Here, healthy individuals were randomly assigned to consume either a breakfast high in saturated fat and added sugar (Experimental condition) or a healthier breakfast (Control condition), over four consecutive days. Tests of HDLM, interoception and biological measures were administered before and after breakfast on the days one and four, and participants completed food diaries before and during the study. At the end of the study, the Experimental condition showed significant reductions in HDLM and reduced interoceptive sensitivity to hunger and fullness, relative to the Control condition. The Experimental condition also showed a markedly different blood glucose and triglyceride responses to their breakfast, relative to Controls, with larger changes in blood glucose across breakfast being associated with greater reductions in HDLM. The Experimental condition compensated for their energy-dense breakfast by reducing carbohydrate intake, while saturated fat intake remained consistently higher than Controls. This is the first experimental study in humans to demonstrate that a Western-style diet impacts HDLM following a relatively short exposure-just as in animals. The link between diet-induced HDLM changes and blood glucose suggests one pathway by which diet impacts HDLM in humans.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
•Animal data finds that a Western-style (WS) diet impairs hippocampal function (HF).•There is emerging data for a similar effect of WS-diet in humans.•We report the first systematic review and ...meta-analyses of these human data.•We find a small significant pooled-effect size, for the effect of a WS-diet on HF.•We explore why the human data are so heterogenous.
Paralleling animal research, there is emerging evidence that a Western-style (WS) diet – high in saturated fat and added sugar – impairs human hippocampal functioning. However, the conditions under which this occurs are not fully understood and there have been published failures to detect such effects. To date, there has been no systematic review or meta-analysis of relevant human studies. We undertook a systematic database search and review. Twenty studies were identified, two experimental, with the remainder correlational. The latter were included in a meta-analyses on the impact of WS-diet and its macronutrient components on human hippocampal function. Effects of age and sex were also examined. A WS-diet adversely impacted human hippocampal volume and functioning, with a small-pooled effect size. No effects were found for individual macronutrients. There was a high-level of study heterogeneity, which was not fully explained by study/sample characteristics. This may arise via the wide range of assessment tools used to measure both dietary intake and hippocampal functioning. Overall, a WS-diet clearly impacts human hippocampal functioning as in animals.
Background and Aims
Lipopolysaccharides (LPS) is increased in nonalcoholic fatty liver disease (NAFLD), but its relationship with liver inflammation is not defined.
Approach and Results
We studied ...Escherichia coli LPS in patients with biopsy‐proven NAFLD, 25 simple steatosis (nonalcoholic fatty liver) and 25 nonalcoholic steatohepatitis (NASH), and in mice with diet‐induced NASH. NASH patients had higher serum LPS and hepatocytes LPS localization than controls, which was correlated with serum zonulin and phosphorylated nuclear factor‐κB expression. Toll‐like receptor 4 positive (TLR4+) macrophages were higher in NASH than simple steatosis or controls and correlated with serum LPS. NASH biopsies showed a higher CD61+ platelets, and most of them were TLR4+. TLR4+ platelets correlated with serum LPS values. In mice with NASH, LPS serum levels and LPS hepatocyte localization were increased compared with control mice and associated with nuclear factor‐κB activation. Mice on aspirin developed lower fibrosis and extent compared with untreated ones. Treatment with TLR4 inhibitor resulted in lower liver inflammation in mice with NASH.
Conclusions
In NAFLD, Escherichia coli LPS may increase liver damage by inducing macrophage and platelet activation through the TLR4 pathway.
Regulation of energy intake depends in part on both memory for prior food intake and internal signals of hunger and satiety. These functions are both mediated by the hippocampus, a brain structure ...that animal studies have shown to be impaired after maintenance on high fat and refined sugar (HFS) diets. Study 1, using a cross-sectional design, revealed that self-reported HFS diet was associated with poorer performance on hippocampal sensitive memory tasks but not other neuropsychological control measures. Study 2 replicated this finding in two groups selected to differ in HFS intake, additionally showing that this effect is specific to hippocampal functioning and does not extend to measures of prefrontal cortex function. Furthermore, in a laboratory-based test of food intake, the HFS rich diet groups were less accurate in recalling what they had previously eaten and evidenced reduced sensitivity to internal signals of hunger and satiety, relative to a group consuming less HFS rich diets. Together, these findings reveal an association between HFS consumption and poorer hippocampal function in human participants, consistent with findings from animal-based studies. Moreover, our results suggest that this may be related to impaired regulation of energy intake via less accurate tracking of prior food intake and reduced sensitivity to hunger and satiety signals.
Human Hunger as a Memory Process Stevenson, Richard J.; Yeomans, Martin R.; Francis, Heather M.
Psychological review,
01/2024, Letnik:
131, Številka:
1
Journal Article
Recenzirano
Odprti dostop
Hunger refers to (1) the meaning of certain bodily sensations; (2) a mental state of anticipation that food will be good to eat; and (3) an organizing principal, which prioritizes feeding. ...Definitions (1) and (2) are the focus here, as (3) can be considered their consequent. Definition (1) has been linked to energy-depletion models of hunger, but these are no longer thought viable. Definition (2) has been linked to learning and memory (L&M) models of hunger, but these apply just to palatable foods. Nonetheless, L&M probably forms the basis for hunger generally, as damage to declarative memory can eradicate the experience of hunger. Currently, there is no general L&M model of hunger, little understanding of how physiology intersects with a L&M approach, and no understanding of how Definitions (1) and (2) are related. We present a new L&M model of human hunger. People learn associations between internal (e.g., tummy rumbles) and external cues (e.g., brand names) and food. These associations can be to specific foods (episodic memories) or food-related categories (semantic memories). When a cue is encountered, it may lead to food-related memory retrieval. If retrieval occurs, the memory's affective content allows one to know if food will be good to eat now-hunger-a cognitive operation learned in childhood. These memory processes are acutely inhibited during satiety, and chronically by multiple biological parameters, allowing physiology to modulate hunger. Implications are considered for the process of making hunger judgments, thirst, the cephalic phase response, and motivational and lay theories of hunger.
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