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According to Zimmet et al. An abnormality of serotonergic neurotransmission localized in pre-synaptic and post-synaptic areas plays an important thought not the only one role in the pathogenesis of depression the so-called serotonin hypothesis of depression. Substances which have a serotonergic effect serotonin precursors, fenfluramine, SSRIs conditioned a clinically significant improvement in depressive symptoms. The positive effect of serotonergic substances on depressive mood as well as on a number of disease parameters of diabetes points to a possible etiological relationship.

The conjoined occurrence of depression and diabetes is not a chance phenomenon which evokes consideration about their possible relationship. Scientific authorities present several hypothetical interpretations: 1. Depression arises as a primary consequence of neurochemical — biochemical changes which associate with diabetes; 2. Depression is a consequence of psychosocial factors which associate with the disease or its treatment; 3. Depression is an independent risk factor for the origin of diabetes.

Current knowledge supports the presence of a relationship between depression, depressive symptoms and possible growth of the risk for the development of type 2 diabetes. In contrast, type 1 diabetes leads to the later development of depression. Kovacs et al. Lustman et al. In double-blind randomized studies the hypoglycemic effect of antidepressant treatment was confirmed. The origin of depression is a later result of type 2 diabetes, but depression can increase the risk of its development. Results are similar for type 1 diabetes. Control of DM improves simultaneously with the remission of depression, but also without a clear explanation of the mechanism for this assumption.

In a 5-year monitoring Lustman et al. No differences between type 1 diabetes and type 2 diabetes in this regard were observed. According to all, a longer duration of the depressive phase is more associated with type 1 diabetes, although the differences between type 1 diabetes and type 2 diabetes were not observed in relation to inducing remission after the first depressive episode. On the other hand Lustman et al. They found a higher risk for longer duration of depression only in patients with type 2 diabetes who were not treated with insulin.

Wellset al.

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In a study carried out by Davis et al. A significant relationship was shown between overall and specific social support and depressive symptoms with diabetes Littelfield et al. The presence of positive family history of depression occurs more often in patients with depression in comparison with individuals with diabetes without depression 27 vs. A significant relationship was consequently found between depression and control of glycaemia by measuring the HbA1c values, which were persistently higher on average by 0.

Akbaralya et al. They found that the presence of metabolic syndrome was linked with the increased risk of possible depressive symptoms OR, 1. Central obesity, increased triglycerides and HDL but not other components of metabolic syndrome were predictors of manifestation of depressive symptoms. These findings are thus consistent with the hypothesis that depressive symptoms could be a consequence as well as the reason for metabolic syndrome.

In a study by Backes et al. These findings support the existence of a relationship between the two diseases — diabetes and depression — namely, that both are frequent during gravidity and after birth, and it is relevant, that post-partum depression is treatable but often goes unrecognized.

It is known that women with diabetes keeping in mind the non use of insulin have during gravidity approximately two-times the risk of depression arising versus women without diabetes OR 1. This is similar with the occurrence of depression in women with diabetes in the post-partum period OR 1.

We can say that particularly late rising of depression could be the result of micro or macrovascular changes, and the origin of depression often precedes predominately type 2 diabetes by a number of years. The newest findings support the consideration regarding the reciprocal interaction among depression and diabetes, because depressive symptoms could increase the risk of origin of type 2 diabetes and the diabetic complications associated with it. Referring to some evidence that depression has an adverse psychological impact than the "well being" as a diabetes, we can say that the treatment of depression in diabetes can directly improve the psychological as well as medical parameters.

Improving depressive symptoms and induce remission, the main objectives related to psychological parameters. The treatment of diabetes involves improving glycaemic control and reducing the risk for the occurrence of either short or long-term complications of diabetes and premature mortality. Based on mainly anecdotal evidence and a handful of randomized controlled trials, monoamine oxidase inhibitors MAOIs and tricyclic antidepressants TCAs are considered to have a hyperglycaemic effect, which is in keeping with their noradrenergic and or appetitogenic effects, while selective serotonin reuptake inhibitors SSRIs , such as fluoxetine and sertraline, are more likely to be anorectic, improve insulin sensitivity and reduce glucose levels, probably because the central serotoninergic pathways are important in the regulation of food intake and food preferences Ismail, The common mechanisms etiopathogenetic diabetes and depression to some extent highlights the fact that intensive treatment of depression leads to improved disease manifestations diabetes eg.

Selective serotonin reuptake inhibitors SSRIs - sertraline, paroxetine, fluoxetine, fluvoxamine, citalopram due to a beneficial effect on a number of pathological parameters diabetes - decrease glucose levels, weight loss, decreased serum cholesterol and triglycerides - and given the antidepressant effect comparable with TCAs and MAOIs are in the treatment of depression in diabetes first-line drugs. The use of TCAs in patients with diabetes is mainly limited to their cardiotoxicity. TCAs may increase serum concentrations of glucose and increased craving for sweets.

Considerably better is to use antidepressants - SSRIs or SNRIs later, while in patients with diabetes on this treatment was demonstrated the hypoglycaemic effect. The use of antidepressants was associated with hyperglycaemia ROR 1. Connection with hyperglycaemia was risky for antidepressants with affinity for serotonergic reuptake transporter Derijks, Meyboom et al.

Paroxetine abdominal obesity leads to more frequent administration than other SSRI antidepressants Reader, Bjelland et al. The other antidepressants should mention bupropion, venlafaxine and nefazodone, which are favorable for their pharmacological properties in terms of comorbid conditions also convenient - to have a neutral effect on body weight and glucose metabolism. Among the nine antidepressants especially in pursuit of their effects on the gastrointestinal, central nervous system and sexual life come out with the best profile of bupropion and soon fluvoxamine Dewan, Ananad, Weight gain is a common adverse side effect of acute and long-term treatment with antidepressants.

Also, paroxetine causes higher weight gain compared to other SSRIs preparation for longer-term therapy and bupropion or nefazodone cause less weight gain over the longer-term treatment Fava, According to several studies being less effective in patients with depression and diabetes mirtazapine, in view of a higher risk of gaining weight. The case study series of patients receiving doses of mirtazapine and 15 mg were observed gain weight during 5 months 16 kg, with obesity and by all important risk factor for glucose dysregulation Fisfalen, Hsiung et al.

TCAs are associated with weight gain Nakra, Rutland et al.


TCAs can worsen hyperglycaemia and glycaemic control during longer treatment Nickelson, Box , Carney, and their anticholinergic, cardiovascular and musculoskeletal adverse side effects may worsen symptoms in relation to diabetes constipation associated with diabetic gastroparesis Carney, , Lane, In addition, treatment with MAOIs is associated with weight gain and the need for strict dietary restrictions, which certainly complicates the diet such as in patients with diabetes Carney, In 80 patients with depression Kopf, Westpal et al.

The main findings were that patients with depression and weight in the standard have insulin resistance corresponding to the HPA axis, overweight patients had total and LDL cholesterol out of standard antidepressant treatment led to an improvement in lipoprotein and cholesterol levels, changes in triglyceride metabolism affected by the treatment and weight three important factors control lipid parameters depending on the presence of the metabolic state: weight, hypercorticolism and insulin resistance.

This study first examined the detailed lipid profile in patients with diabetes and depression. Bupropion contrast in patients with diabetes suited to the fact that side does not sexual reactions and decreases body weight in obese patients had more than placebo Jain, Kaplan et al. Lustman, Williams et al.

Metabolic Syndrome and Psychiatric Illness Interactions, Pathophysiology, Assessment & Treatment

Sawhney et al. Patients with diabetes tend to be older, and recent primary care data have shown that the average length of an episode of depression in older primary care patients is approximately 18 months, whereas in mixed-aged populations the mean length of an episode is approximately 4 - 6 months Vuorilehto et al, The tendency for depressive symptoms to be chronic in patients with diabetes is also shown by recent data from a five-year follow-up study of approximately patients with diabetes. Several systematic reviews have been completed exploring effect sizes of psychotherapeutic as well as pharmacological treatments of patients with comorbid depression and diabetes Petrak ; van der Feltz-Cornelis et al.

Efficacy trials generally evaluate intensive treatment of a carefully selected patient group by highly trained staff. Patients with clinically significant psychiatric comorbidities, such as panic disorder of medical comorbidities, are often excluded from these trials. An important question for researchers and clinicians is whether evidence-based pharmacotherapies and psychotherapies that have proven effective in populations of patients with depression with minimal medical illness would be as efficacious in patients with diabetes.

A systematic review of efficacy trials performed in yielded 11 randomized clinical trials, five on psychotherapeutic interventions and six on pharmacological treatments. Most trials were small, with only one recruiting more than patients and the others including 60 or fewer patients. Most trials were completed on patients with type 2 diabetes with serious depressive symptoms or major depressive disorder, and effect sizes were specified for depressive symptom severity as well as for glycaemic control. As shown Table 4 , the pharmacotherapeutic interventions had moderate effects on depressive symptoms, and small effects on glycaemic control.

The effect on depressive outcomes was very similar, but the effect on glycaemic control was smaller than that of the psychotherapeutic studies, many of which had explicit interventions aimed at improving glycaemic control. The pharmacologic trials were also small, mostly under patients enrolled. The small numbers of patients enrolled in both psychotherapy and pharmacologic efficacy trials limits the generalizability of the findings. Due to the lack of data in our conditions in relation to the comorbidity of depression and disorders related to glucose and lipid metabolism and at the same time of the presented high prevalence independently existing of these disorders, we decided to work-up a pilot study on the impact of antidepressants primarily on glucose and lipid metabolism in patients with depression.

Similar, the results in study Songar et al. The HDL cholesterol values have improved after six months antidepressive treatment in both groups 1. These findings are particularly important because from this one that is most closely connected with cardiovascular risks play mainly LDL and HDL components. On the other hand can not draw definite causal conclusions regarding the limitations on file size and especially the length of the monitoring itself.

The effect size of the psychotherapeutic interventions were moderate to large for improvement of depressive symptoms, and moderate to large for improvement of glycaemic control. Three of the five psychotherapy trials compared an evidence-based depression psychotherapy and diabetes education to diabetes education alone. Therefore, it is unclear whether improvements in glycaemic control were due to the beneficial effect of the depression-focused psychotherapy or the combination of both depression therapy and diabetes education.

The probability of the occurrence of depression in patients with diabetes is higher, because depression in patients with diabetes is often unrecognized and therefore also untreatable and the association between depression and glycaemic control is small in cross-sectional studies and almost disappears in most of the handful of prospective studies Lustman et al.

It is interesting that complications associated with diabetes and mortality are already observed with less serious depressive displays Black et al. The comorbidity of depression and obesity worsens the course of diabetes, and furthermore, depression worsens the adherence to a diabetic diet and treatment and predicts low compliance in diabetological programs McKellar et al.

From the results of several studies Katon et al. From several studies it follows that the course of depression in individuals with diabetes is not causally dependent on diabetes. Depression in individuals with diabetes represents a more complex phenomena following from interactions between genetic, biological and psychosocial factors, which could significantly influence the recurrence and longer duration of depression.

Prenatal stress-induced alterations in major physiological systems correlate with gut microbiota composition in adulthood. Psychoneuroendocrinology ; 60 : 58— Jansson T, Powell TL. Role of the placenta in fetal programming: underlying mechanisms and potential interventional approaches. Clin Sci Lond ; : 1— Maternal stress alters endocrine function of the feto-placental unit in rats.

Chronic maternal stress inhibits the capacity to up-regulate placental 11beta-hydroxysteroid dehydrogenase type 2 activity. J Endocrinol ; : R7—R Association between maternal and amniotic fluid cortisol is moderated by maternal anxiety. Psychoneuroendocrinology ; 34 : — The developmental role of serotonin: news from mouse molecular genetics. Nat Rev Neurosci ; 4 : — Serotonin depletion during synaptogenesis leads to decreased synaptic density and learning deficits in the adult rat: a possible model of neurodevelopmental disorders with cognitive deficits.

Brain Res ; : 68— Maternal serotonin is crucial for murine embryonic development. Engelhardt B. Development of the blood-brain barrier. Cell Tissue Res ; : — The gut microbiota influences blood-brain barrier permeability in mice. Sci Transl Med ; 6 ra Anderson GM. Genetics of childhood disorders: XLV. Autism, part 4: serotonin in autism. Microbiota and neurodevelopmental windows: implications for brain disorders. Trends Mol Med ; 20 : — Neurobiological bases of behavioral development in the first year. Neuropediatrics ; 28 : — Extraordinary neoteny of synaptic spines in the human prefrontal cortex.

Karmarkar D, Rock KL. Microbiota signalling through MyD88 is necessary for a systemic neutrophilic inflammatory response. Immunology ; : — Commensal bacteria calibrate the activation threshold of innate antiviral immunity. Immunity ; 37 : — Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation.

Artis D. Epithelial-cell recognition of commensal bacteria and maintenance of immune homeostasis in the gut. Nat Rev Immunol ; 8 : — The role of microbes in developmental immunologic programming. Pediatr Res ; 69 : — Priming for health: gut microbiota acquired in early life regulates physiology, brain and behaviour. Goulet O. Potential role of the intestinal microbiota in programming health and disease. Nutr Rev ; 73 : 32— The intestinal microbiome in early life: health and disease. Front Immunol ; 5 : Microbiota is essential for social development in the mouse.

Commensal microbiota is fundamental for the development of inflammatory pain. Effects of intestinal microbiota on anxiety-like behavior. Commun Integr Biol ; 4 : — Delivery mode shapes the acquisition and structure of the initial microbiota across multiple body habitats in newborns. Mode of delivery affects the bacterial community in the newborn gut.

Early Hum Dev ; 86 : 13— Perinatal factors and the development of autism: a population study. Arch Gen Psychiatry ; 61 : — Caesarean delivery on maternal request and childhood psychopathology: a retrospective cohort study in China. BJOG ; : 42— The impact of obstetric mode of delivery on childhood behavior. Soc Psychiatry Psychiatr Epidemiol ; 50 : — Adv Exp Med Biol ; : — Can nutritional modulation of maternal intestinal microbiota influence the development of the infant gastrointestinal tract? J Nutr ; : — Influences of dietary and environmental stress on microbial populations in the murine gastrointestinal tract.

Infect Immun ; 9 : — Alterations in the vaginal microbiome by maternal stress are associated with metabolic reprogramming of the offspring gut and brain. Maternal prenatal stress is associated with the infant intestinal microbiota. Psychoneuroendocrinology ; 53 : — Microbial manipulation of the rat dam changes bacterial colonization and alters properties of the gut in her offspring.

Antibiotic treatment of pregnant non-obese diabetic mice leads to altered gut microbiota and intestinal immunological changes in the offspring. Scand J Immunol ; 80 : — Impact of maternal intrapartum antibiotics, method of birth and breastfeeding on gut microbiota during the first year of life: a prospective cohort study. BJOG ; doi: Influence of antibiotic exposure in the early postnatal period on the development of intestinal microbiota.

The microbiota regulates neutrophil homeostasis and host resistance to Escherichia coli K1 sepsis in neonatal mice. Nat Med ; 20 : — Disturbance of the gut microbiota in early-life selectively affects visceral pain in adulthood without impacting cognitive or anxiety-related behaviors in male rats. Gut microbiota depletion from early adolescence in mice: implications for brain and behaviour. Brain Behav Immun ; 48 : — Delayed physical and neurobehavioral development and increased aggressive and depression-like behaviors in the rat offspring of dams fed a high-fat diet.

Int J Dev Neurosci ; 31 : — Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin. Induction of anxiety-like behavior in mice during the initial stages of infection with the agent of murine colonic hyperplasia Citrobacter rodentium. Physiol Behav ; 89 : — Psychoactive bacteria Lactobacillus rhamnosus JB-1 elicits rapid frequency facilitation in vagal afferents.

Dantzer R. Cytokine, sickness behavior, and depression. Immunol Allergy Clin North Am ; 29 : — Macfarlane S, Macfarlane GT. Regulation of short-chain fatty acid production. Proc Nutr Soc ; 62 : 67— Short-chain fatty acids and ketones directly regulate sympathetic nervous system via G protein-coupled receptor 41 GPR Neurobiological effects of intraventricular propionic acid in rats: possible role of short chain fatty acids on the pathogenesis and characteristics of autism spectrum disorders.

Behav Brain Res ; : — Effects of the enteric bacterial metabolic product propionic acid on object-directed behavior, social behavior, cognition, and neuroinflammation in adolescent rats: relevance to autism spectrum disorder. Behav Brain Res ; : 47— Macfabe DF.

Short-chain fatty acid fermentation products of the gut microbiome: implications in autism spectrum disorders. Microb Ecol Health Dis ; 23 ; doi: Altered gut microbiota and activity in a murine model of autism spectrum disorders. Brain Behav Immun ; 37 : — Host microbiota constantly control maturation and function of microglia in the CNS. Nat Neurosci ; 18 : — Microglial physiology: unique stimuli, specialized responses.

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Annu Rev Immunol ; 27 : — Physiology of microglia. Physiol Rev ; 91 : — Prinz M, Priller J. Microglia and brain macrophages in the molecular age: from origin to neuropsychiatric disease. Nat Rev Neurosci ; 15 : — The gut microbiota reduces leptin sensitivity and the expression of the obesity-suppressing neuropeptides proglucagon Gcg and brain-derived neurotrophic factor Bdnf in the central nervous system.

Cameron J, Doucet E. Appl Physiol Nutr Metab ; 32 : — Gut hormones and appetite control. Erspamer V. Pharmacology of indole-alkylamines. Pharmacol Rev ; 6 : — Release of 5-hydroxytryptamine from the mucosa is not required for the generation or propagation of colonic migrating motor complexes. Mechanisms underlying distension-evoked peristalsis in guinea pig distal colon: is there a role for enterochromaffin cells? Gut serotonin is a regulator of obesity and metabolism.

Analysis of the responses of myenteric neurons in the small intestine to chemical stimulation of the mucosa. Am J Physiol ; : G—G Autistic children and their first-degree relatives: relationships between serotonin and norepinephrine levels and intelligence. J Neuropsychiatry Clin Neurosci ; 2 : — Whole blood serotonin and plasma beta-endorphin in autistic probands and their first-degree relatives. Biol Psychiatry ; 45 : — Hyperserotonemia in adults with autistic disorder. J Autism Dev Disord ; 37 : — Platelet serotonin levels in pervasive developmental disorders and mental retardation: diagnostic group differences, within-group distribution, and behavioral correlates.

Serotonergic responsivity in male young adults with autistic disorder. Results of a pilot study. Arch Gen Psychiatry ; 46 : — Detection of neurotransmitter amines in microorganisms with the use of high-performance liquid chromatography. Dokl Biochem ; : — J Appl Microbiol ; : — PLoS One ; 7 : e Stephenson M, Rowatt E. The production of acetylcholine by a strain of Lactobacillus plantarum. J Gen Microbiol ; 1 : — Bile acids and the gut microbiome. Curr Opin Gastroenterol ; 30 : — Suppression of the HPA axis during cholestasis can be attributed to hypothalamic bile acid signaling.

Mol Endocrinol ; 29 : — Tryptophan metabolism, from nutrition to potential therapeutic applications. Amino Acids ; 41 : — Tryptophan metabolism in the central nervous system: medical implications. Expert Rev Mol Med ; 8 : 1— Kynurenines in the mammalian brain: when physiology meets pathology. Serotonin signalling in the gut—functions, dysfunctions and therapeutic targets. Nat Rev Gastroenterol Hepatol ; 10 : — Spiller R. Serotonin and GI clinical disorders.

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Neuropharmacology ; 55 : — Gershon MD. Curr Opin Endocrinol Diabetes Obes ; 20 : 14— Growth and amino acid requirements of various strains of group B streptococci. J Clin Microbiol ; 7 : 28— Li G, Young KD. Indole production by the tryptophanase TnaA in Escherichia coli is determined by the amount of exogenous tryptophan. Microbiology ; : — Phenotypic and physiological alterations by heterologous acylhomoserine lactone synthase expression in Pseudomonas putida.

Serotonin function and the mechanism of antidepressant action. Reversal of antidepressant-induced remission by rapid depletion of plasma tryptophan. Arch Gen Psychiatry ; 47 : — Acute tryptophan depletion. Part I: rationale and methodology. Aust N Z J Psychiatry ; 39 : — Inflammasome signaling affects anxiety- and depressive-like behavior and gut microbiome composition.

Mol Psychiatry in press. Mol Psychiatry ; doi: Development of the human gastrointestinal microbiota and insights from high-throughput sequencing. Salthouse TA. Decomposing age correlations on neuropsychological and cognitive variables. J Int Neuropsychol Soc ; 15 : — Effects of polyphenols on brain ageing and Alzheimer's disease: focus on mitochondria. Mol Neurobiol ; 46 : — Cognitive decline, dietary factors and gut-brain interactions. Mech Ageing Dev ; : 59— Through ageing, and beyond: gut microbiota and inflammatory status in seniors and centenarians. PLoS One ; 5 : e Composition, variability, and temporal stability of the intestinal microbiota of the elderly.

An evolutionary perspective on immunosenescence. Ann N Y Acad Sci ; : — Griffin WS. Neuroinflammatory cytokine signaling and Alzheimer's disease. N Engl J Med ; : — Overweight in midlife and risk of dementia: a year follow-up study. Int J Obes Lond ; 33 : — Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease.

Arch Neurol ; 62 : — Cognitive stimulation during hospitalization improves global cognition of older Taiwanese undergoing elective total knee and hip replacement surgery. J Adv Nurs ; 68 : — An update on type 2 diabetes, vascular dementia and Alzheimer's disease.

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Exp Gerontol ; 47 : — Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nat Rev Neurosci ; 10 : — The expanded biology of serotonin. Annu Rev Med ; 60 : — Fidalgo AR. Experimental insights into age-exacerbated cognitive dysfunction after peripheral surgery.

Aging Cell ; 12 : — Gut microbiota composition correlates with diet and health in the elderly. Mediterranean diet habits in older individuals: associations with cognitive functioning and brain volumes. Exp Gerontol ; 48 : — Spatial cognition in adult and aged mice exposed to high-fat diet. The critical need to promote research of aging and aging-related diseases to improve health and longevity of the elderly population.

Aging Dis ; 6 : 1—5. Health in an ageing world—what do we know? Lancet ; : — Health, functioning, and disability in older adults—present status and future implications. Effects of the probiotic Bifidobacterium infantis in the maternal separation model of depression. Chronic gastrointestinal inflammation induces anxiety-like behavior and alters central nervous system biochemistry in mice. The anxiolytic effect of Bifidobacterium longum NCC involves vagal pathways for gut-brain communication. Probiotics prevent bacterial translocation and improve intestinal barrier function in rats following chronic psychological stress.

Gut ; 55 : — Prevention of gut leakiness by a probiotic treatment leads to attenuated HPA response to an acute psychological stress in rats. Psychoneuroendocrinology ; 37 : — Consumption of fermented milk product with probiotic modulates brain activity. The probiotic Bifidobacteria infantis : an assessment of potential antidepressant properties in the rat. J Psychiatr Res ; 43 : — Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites. Increased plasma d-lactic acid associated with impaired memory in rats.

Prebiotic feeding elevates central brain derived neurotrophic factor, N-methyl-D-aspartate receptor subunits and D-serine. Neurochem Int ; 63 : — Brain Behav Immun ; 52 : — Prebiotic intake reduces the waking cortisol response and alters emotional bias in healthy volunteers. N-3 polyunsaturated fatty acids PUFAs reverse the impact of early-life stress on the gut microbiota. Mental Health Foundation, Among the contributing factors that are discussed are genetics, habitual intake of high glycemic index carbohydrates, fructose, saturated fats, trans fatty acids, vitamins, micronutrients, obesity, smoking, and lack of exercise.

The author describes the actual mechanisms by which Metabolic Syndrome progresses and causes damage in the body, including the action of insulin and the pathophysiology of insulin resistance. Details are provided on what occurs in the liver, pancreas, muscle, fat cells, and immune system as Metabolic Syndrome progresses. New findings are presented on fat cells, including the fact that they are beginning to be considered as endocrine cells.

There is a substantive discussion of leptin, which is one of the important adipocytokines. Also carbohydrate, 'bad fats', inflammation, oxidative damage, over-stimulation of the 'fight or flight' system, and high levels of the stress hormone cortisol can actually cause the manifestations of Metabolic Syndrome.

These explanations set the stage for an explanation of the inter-relationships between Metabolic Syndrome, psychiatric illness, dementia and effects of not only diet and life choices, but also the effects of psychiatric medications. Finally, there is an important and unique section on the relationship between Metabolic Syndrome and various psychiatric illnesses, and how they exacerbate each other. The significance of Metabolic Syndrome in Major Depression, Bipolar Affective Disorder, Schizophrenia, fibromyalgia and Polycystic Ovary Disease is vast and it is important to realise the effects of psychiatric medications on Metabolic Syndrome.

The author discusses antidepressants, mood stabilizers and the new atypical antipsychotics. There are dramatic differences among medications in the way they affect Metabolic Syndrome and pharmaceutical companies will want to promote patient awareness with this book. Wie bewerten Sie den Artikel? Bitte geben Sie Daten ein: Name oder Pseudonym.