Was Feuerbach right: are we what we eat?

Cizza, Giovanni; Rother, Kristina I.

doi:10.1172/jci58595

Cited by 11 publications

(10 citation statements)

References 20 publications

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“…As a final point let us briefly examine the human digestive system, which has long been known to have a somewhat enigmatic relationship with our emotional health . A connection between persistent stress and an increased risk of suffering gastrointestinal disorders has become so established that these maladies are often treated with anti‐depressants or behavioural therapies .…”

Section: Gut Feelings: Immunity Emotion and The Digestive Systemmentioning

confidence: 99%

“…As a final point let us briefly examine the human digestive system, which has long been known to have a somewhat enigmatic relationship with our emotional health. [82][83][84][85] A connection between persistent stress and an increased risk of suffering gastrointestinal disorders has become so established that these maladies are often treated with anti-depressants or behavioural therapies. 83,[86][87][88] This brain-gut axis, as it is often described, [89][90][91] has experienced a recent upsurge in research focus, with one group going so far as to examine the validity of that commonly given advice to 'follow your gut' (the conclusion being 'yes' albeit with several provisos).…”

Section: Gut Feelings: Immunity Emotion and The Digestive Systemmentioning

confidence: 99%

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‘As above, so below’ examining the interplay between emotion and the immune system

et al. 2014

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SummaryWhile the concept of a palpable relationship between our mental and physical well-being is certainly not new, it is only in the light of modern scientific research that we have begun to realize how deeply connected our emotional and immune states may be. We begin this review with a series of studies demonstrating how four fundamental emotional responses: anger, anxiety, mirth and relaxation are able modulate cytokine production and cellular responses to a variety of immune stimuli. These modulations are shown to be either detrimental or beneficial to a patient's health dependent on the context and duration of the emotion. We also discuss the reverse, highlighting research demonstrating how the loss of key immune cells such as T lymphocytes in clinical and animal studies can negatively impact both emotional well-being and cognition. Additionally, to give a more complete picture of the manifold pathways that link emotion and the immune system, we give a brief overview of the influence the digestive system has upon mental and immunological health. Finally, throughout this review we attempt to highlight the therapeutic potential of this burgeoning field of research in both the diagnosis and treatment of immune and disorders. As well as identifying some of the key obstacles the field must address in order to put this potential into practice.

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Section: Gut Feelings: Immunity Emotion and The Digestive Systemmentioning

confidence: 99%

Section: Gut Feelings: Immunity Emotion and The Digestive Systemmentioning

confidence: 99%

‘As above, so below’ examining the interplay between emotion and the immune system

et al. 2014

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“…In the presence of insulin, cortisol promotes triglyceride accumulation, especially in visceral adipocytes thereby leading to an increase in central fat [29]. Additionally, HPA-axis hyperactivation may lead to adiposity through increases in food intake, as artificially-induced stress, exogenous ovine CRH administration and decreased response to dexamethasone suppression led to increases in appetite, especially for more palatable foods [30]. Functional MRI studies indicate that the sensitivity of the central reward system is diminished by stress, possibly upregulating the craving for “comfort foods” [31].…”

Section: The Hpa-axis and Obesitymentioning

confidence: 99%

The Hypothalamic-Pituitary-Adrenal Axis, Obesity, and Chronic Stress Exposure: Sleep and the HPA Axis in Obesity

Lucassen

Cizza

2012

Curr Obes Rep

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Obesity, exposure to stress and inadequate sleep are prevalent phenomena in modern society. In this review we focus on their relationships and critically evaluate causality. In obese individuals, one of the main stress systems, the hypothalamic-pituitary-adrenal axis, is altered, and concentrations of cortisol are elevated in adipose tissue due to elevated local activity of 11β-hydroxysteroid dehydrogenase (HSD) type 1. Short sleep and decreased sleep quality are also associated with obesity. In addition, experimental sleep curtailment induces HPA-axis alterations which, in turn, may negatively affect sleep. These findings implicate that obesity, stress and sleep loss are all related in a vicious circle. Finally, we discuss new strategies to combat obesity through modulating cortisol levels in adipose tissue by 11β-HSD1 inhibitors or by improving sleep duration.

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“…). Together these studies start to provide a mechanistic framework for understanding the way that homeostatic and hedonic systems controlling food intake might interact, as well as providing a basis for understanding the mechanisms of so called ‘comfort feeding’ (Cizza & Rother, ).…”

Section: Introductionmentioning

confidence: 97%

Gastrointestinal hormones and the dialogue between gut and brain

Dockray

2014

The Journal of Physiology

154

107

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The landmark discovery by Bayliss and Starling in 1902 of the first hormone, secretin, emerged from earlier observations that a response (pancreatic secretion) following a stimulus (intestinal acidification) occurred after section of the relevant afferent nerve pathway. Nearly 80 years elapsed before it became clear that visceral afferent neurons could themselves also be targets for gut and other hormones. The action of gut hormones on vagal afferent neurons is now recognised to be an early step in controlling nutrient delivery to the intestine by regulating food intake and gastric emptying. Interest in these mechanisms has grown rapidly in view of the alarming global increase in obesity. Several of the gut hormones (cholecystokinin (CCK); peptide YY 3-36 (PYY 3-36 ); glucagon-like peptide-1 (GLP-1)) excite vagal afferent neurons to activate an ascending pathway leading to inhibition of food intake. Conversely others, e.g. ghrelin, that are released in the inter-digestive period, inhibit vagal afferent neurons leading to increased food intake. Nutrient status determines the neurochemical phenotype of vagal afferent neurons by regulating a switch between states that promote orexigenic or anorexigenic signalling through mechanisms mediated, at least partly, by CCK. Gut-brain signalling is also influenced by leptin, by gut inflammation and by shifts in the gut microbiota including those that occur in obesity. Moreover, there is emerging evidence that diet-induced obesity locks the phenotype of vagal afferent neurons in a state similar to that normally occurring during fasting. Vagal afferent neurons are therefore early integrators of peripheral signals underling homeostatic mechanisms controlling nutrient intake. They may also provide new targets in developing treatments for obesity and feeding disorders.

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Was Feuerbach right: are we what we eat?

Cited by 11 publications

References 20 publications

‘As above, so below’ examining the interplay between emotion and the immune system

‘As above, so below’ examining the interplay between emotion and the immune system

The Hypothalamic-Pituitary-Adrenal Axis, Obesity, and Chronic Stress Exposure: Sleep and the HPA Axis in Obesity

Gastrointestinal hormones and the dialogue between gut and brain

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