Stress versus depression

Lechín, Fuad; Dijs, Bertha van der; Benaim, M E

doi:10.1016/0278-5846(96)00075-9

Cited by 46 publications

(24 citation statements)

References 138 publications

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“…Again, although changes in HPA regulation under stress, anxiety and depression have been widely studied, they are not completely understood yet due to the high degree of overlap among the 3 conditions. Lechin et al [65] pointed out that the inability to cope with stress leads to raised plasma cortisol whereas depression shows an opposite profile consisting in adrenomedullary gland hyporesponsiveness. Nevertheless, contradicting results on depression and cortisol have been described in the literature.…”

Section: Discussionmentioning

confidence: 99%

Impaired Immune Function in a Homeless Population with Stress-Related Disorders

Arranz

Vicente²,

Muñoz³

et al. 2009

Neuroimmunomodulation

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Objective: Homeless people suffer high levels of psychological distress. The aim of the present work was to study the immune function in a group of homeless people with stress-related disorders and compare it with that of healthy non-homeless controls. Methods: We included in the study 40 homeless persons and 40 housed controls recruited from the population of Madrid and matched for age and gender. Samples from peripheral blood were collected and we studied several leukocyte functions previously described as good health and survival markers [adherence, chemotaxis, phagocytosis, superoxide anion levels, lymphocyte proliferation in response to phytohemagglutinin, NK activity and cytokine (IL-2, TNF-α) levels], as well as other related parameters, such as plasma cortisol levels and total antioxidant capacity. Results: There was a strongly suppressed immune response in the homeless group, with decreased adherence, chemotaxis, phagocytosis, superoxide levels, lymphoproliferation and NK activity. IL-2 and plasma antioxidant levels were also impaired. Conclusions: These findings suggest an altered immune function in the homeless population that might be responsible for the higher morbidity and mortality of homeless people. In addition, the present work points out directions for future research attempting to increase the quality of life and health status of homeless individuals, since it shows that oxidative stress seems to play a key role in this immune function impairment.

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Section: Discussionmentioning

confidence: 99%

Impaired Immune Function in a Homeless Population with Stress-Related Disorders

Arranz

Vicente²,

Muñoz³

et al. 2009

Neuroimmunomodulation

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“…This abrupt adrenergic response, registered during acute stress periods is not registered in elderly people because of the hyporesponsiveness of their adrenal cortical glands. These facts explain the different neurohormonal stress profiles registered in young and elderly mammals [3, 16,17,148].…”

Section: Pathophysiological Evidencementioning

confidence: 99%

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Lechín¹,

Dijs²

2008

TONEURJ

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Abstract:The assessment of circulating neurotransmitters: noradrenaline, adrenaline, dopamine, platelet serotonin, plasma serotonin and plasma tryptophan before and after many types of stressor agents and neuropharmacological drugs carried out over the last thirty years allowed us to accumulate information dealing with the central nervous system (CNS) versus the peripheral autonomic nervous system (ANS) interactions in healthy as well as diseased mammals. Furthermore, the accurate knowledge about the CNS circuitry disorders which underlie both the CNS and peripheral clinical syndromes, has allowed us to prescribe successful neuropharmacological therapeutical strategies for many types of illnesses. In addition, the demonstration that the clinical improvement was always paralleled by the normalization of the neurochemical, hormonal, immunological and clinical profiles affords strong support to our point of view. According to all the above, the authors postulate the existence of two types of diseases: type A and Type N, which are underlain by two opposite CNS + ANS disorders. Type A diseases should be associated with the "uncoping stress" syndrome and are underlain by hyperactivity of the adrenocortical glands plus the CNS disorder characterized by the predominance of the C1(adrenergic) + DR(serotonergic) axis over the A5(noradrenergic) + MR(serotonergic) binomial, whereas the type N diseases depends on the opposite profile: "endogenous depression" syndrome. Finally, we quoted exhaustive evidence showing that the well known fading of both the A6(noradrenergic) + C1(adrenergic) CNS nuclei activity occurring during aging is responsible for the ANS + CNS disorder which is similar to that underlying psychosis, Alzheimer, post-traumatic stress disorder and deficit-attention hyperactive disorder.

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“…This neuroendocrine disorder is responsible for mammary and ovary cysts, frequently observed in women affected by hyperinsulinism [92] and depression [93]. …”

Section: Cns Circuitry Underlying the Hyperinsulinism Syndromementioning

confidence: 99%

Central Nervous System Circuitry Involved in the Hyperinsulinism Syndrome

Lechín¹,

Dijs²

2006

Neuroendocrinology

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Raised plasma levels of insulin, glucose and glucagon are found in patients affected by ‘hyperinsulinism’. Obesity, hypertension, mammary plus ovary cysts and rheumatic symptoms are frequently observed in these patients. Sleep disorders and depression are also present in most subjects affected by this polysymptomatic disorder. The simultaneous increases of glucose, insulin and glucagon plasma levels seen in these patients indicate that the normal crosstalk between A cells, B cells and D cells is disrupted. With respect to this, it is well known that glucose excites B cells (which secrete insulin) and inhibits A cells (which secrete glucagon), which in turn excites D cells (which secrete somatostatin). Gastrointestinal hormones (incretins) modulate this crosstalk both directly and indirectly throughout pancreatic and hepatobiliary mechanisms. The above factors depend on autonomic nervous system mediation. For instance, acetylcholine released from parasympathetic nerves excites both B and A cells. Noradrenaline released from sympathetic nerves and adrenaline secreted from the adrenal glands inhibit B cells and excite A cells, which are crowded with β₂- and α₂-receptors, respectively. Noradrenaline released from sympathetic nerves also excites A cells by acting at α₁-receptors located at this level. According to this, the excessive release of noradrenaline from these nerves should provoke an enhancement of glucagon secretion which will result in overexcitation of insulin secretion from B cells. That is the disorder seen in the so-called ‘hyperinsulinism’, in which raised plasma levels of glucose, insulin and glucagon coexist. Taking into account that neural sympathetic activity is positively correlated to the A5 noradrenergic nucleus and median raphe serotonergic neurons, and negatively correlated to the A6 noradrenergic, the dorsal raphe serotonergic and the C1 adrenergic neurons, we postulate that this unbalanced central nervous system circuitry is responsible for the hyperinsulinism syndrome.

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Stress versus depression

Cited by 46 publications

References 138 publications

Impaired Immune Function in a Homeless Population with Stress-Related Disorders

Impaired Immune Function in a Homeless Population with Stress-Related Disorders

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Central Nervous System Circuitry Involved in the Hyperinsulinism Syndrome

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