scholarly journals Metabolic and nutritional approach to older frail people

2017 ◽  
Vol 3 (3) ◽  
Author(s):  
Stefano Volpato ◽  
Giovanni Zuliani

Frailty is a common clinical syndrome in older adults that carries an increased risk for poor health outcomes including falls, incident disability, hospitalization, and mortality. It is characterized by multisystem dysregulations, leading to a loss of dynamic homeostasis, decreased physiologic reserve, and increased vulnerability to stressors. A large body of literature suggests several important multisystem pathophysiologic processes in the pathogenesis of the frailty syndrome, including chronic inflammation and immune activation, insulin resistance and those in musculoskeletal and endocrine systems. Currently, no effective pharmaceutical interventions have been developed for the prevention and treatment of the frailty syndrome. Conversely, epidemiological and intervention studies suggest that adequate nutrition and physical exercise might prevent or postpone the onset of frailty and related clinical manifestations.

2021 ◽  
Author(s):  
Emma Ahlqvist ◽  
Rashmi B Prasad ◽  
Leif Groop

Type 2 diabetes (T2D) is one of the fastest increasing diseases worldwide. Although it is defined by a single metabolite, glucose, it is increasingly recognized as a highly heterogeneous disease with varying clinical manifestations. Identification of different subtypes at an early stage of disease when complications might still be prevented could hopefully allow for more personalized medicine. An important step towards precision medicine would be to target the right resources to the right patients, thereby improving patient health and reducing health costs for the society. More well-defined disease populations also offer increased power in experimental, genetic and clinical studies. In a recent study, we used six clinical variables (GAD autoantibodies, age at onset of diabetes, HbA1c, BMI, and simple measures of insulin resistance and insulin secretion (so called HOMA estimates) to cluster adult-onset diabetes patients into five subgroups. These subgroups have been robustly reproduced in several populations worldwide and are associated with different risks of diabetic complications and responses to treatment. Importantly, the group with severe insulin-deficient diabetes (SIDD) had increased risk of retinopathy and neuropathy, whereas the severe insulin-resistant diabetes (SIRD) group has the highest risk for diabetic kidney disease (DKD) and fatty liver. This emphasizes the key role of insulin resistance in the pathogenesis of DKD and fatty liver in T2D. In conclusion, this novel sub-classification, breaking down T2D in clinically meaningful subgroups, provides the prerequisite framework for expanded personalized medicine in diabetes beyond what is already available for monogenic and to some extent type 1 diabetes.


2018 ◽  
Vol 6 ◽  
pp. 205031211877558 ◽  
Author(s):  
Fairus Asma Mohd Hamidin ◽  
Siti Nur’Asyura Adznam ◽  
Zuriati Ibrahim ◽  
Yoke Mun Chan ◽  
Nur Hafizah Abdul Aziz

Objective: Frailty is a clinical syndrome with increased risk of poor health outcomes and particularly prevalent in older adults and community population. The study’s aim was therefore to determine the prevalence of frailty and its association with sociodemographic and socioeconomic characteristics, health-related status, and anthropometric measurements among community-dwelling older adults. Methods: A total of 279 older adults aged 60 years and above were randomly selected. Respondents were classified as non-frail (<2 criteria) or frail (≥3 criteria) based on the ‘phenotype of frailty’. A binary logistic regression was used to determine predictors of frailty. Results: The prevalence of frailty was 18.3%. The frail older adults were positively associated with advanced age, being unmarried, hospitalisation in the previous year, poor self-rated health, and lower body mass index. Discussion: These results give an overview on underlying effects and guiding actions for prevention programmes functioning to reverse and minimise the adverse effects of frailty syndrome.


2011 ◽  
Vol 64 (7-8) ◽  
pp. 381-385
Author(s):  
Ksenija Bozic ◽  
Ksenija Gebauer-Bukurov ◽  
Petar Slankamenac ◽  
Marija Knezevic-Pogancev ◽  
Slobodan Sekulic

Introduction. Juvenile myoclonic epilepsy is an idiopathic, hereditary form of epilepsy. Although juvenile myoclonic epilepsy is a well defined clinical syndrome, attempts at diagnosing it commonly fail. Etiopathogenesis. The exact cause of juvenile myoclonic epilepsy remains unknown. Clinical, morphological and metabolic data suggest a preferential role for frontal regions in this syndrome. Several major genes for juvenile myoclonic epilepsy have been identified, but these genes account for only a small proportions of juvenile myoclonic epilepsy cases, suggesting multifactorial or complex inheritance in most. Clinical Manifestations. Juvenile myoclonic epilepsy is characterized by the triad of myoclonic jerks on awakening (all patients), generalized tonic-clonic seizures (>90% of patients) and typical absences (about one third of patients). Seizures have an age-related onset, circadian distribution and are frequently precipitated by sleep deprivation, fatigue and alcohol intake. Intelligence is normal. Diagnosis. Juvenile myoclonic epilepsy diagnosis is based upon clinical criteria and typical electroencephalographic findings (generalized pattern of spikes and/or polyspikes and waves). All other tests are normal. Treatment and Prognosis. Both medical treatment and counselling are important in the management of juvenile myoclonic epilepsy. Mono-therapy with valproate is the preferred treatment. Some of the newer antiepileptic drugs have been suggested as possible alternatives. Juvenile myoclonic epilepsy has a good prognosis. Lifelong treatment is usually considered necessary in vast majority of patients due to the increased risk of relapse if treatment is discontinued. Conclusion. Juvenile myoclonic epilepsy is a common, although under-diagnosed epileptic syndrome. The clinician should study the occurrence of myoclonic jerks and should consider atypical presentations.


2018 ◽  
Vol 24 (3) ◽  
pp. 207-214 ◽  
Author(s):  
Madison Caldwell ◽  
Lisa Martinez ◽  
Jennifer G. Foster ◽  
Dawn Sherling ◽  
Charles H. Hennekens

Cardiovascular disease (CVD), principally myocardial infarction (MI) and stroke, is the leading clinical and public health problem in the United States and is rapidly becoming so worldwide. Their primary prevention is promising, in theory, but difficult to achieve in practice. The principal modalities that have demonstrated efficacy include therapeutic lifestyle changes (TLCs) and adjunctive drug therapies under the guidance of the health-care provider and tailored to the individual patient. The prevention and treatment of the pandemic of overweight and obesity and lack of regular physical activity, both of which are alarmingly common in the United States, prevention and treatment of hypertension, avoidance and cessation of cigarette smoking, adoption and maintenance of a healthy diet, and avoidance of heavy alcohol consumption all have proven benefits in decreasing the risks of a first MI and stroke as well as other clinical manifestations of CVD. Although adoption of TLCs would avoid the need for adjunctive drug therapies in many primary prevention subjects, this strategy is difficult to achieve or maintain for most and may be insufficient for many, especially those at high risk with metabolic syndrome. The criteria for metabolic syndrome, affecting over 40% of the adult population older than 40 in the United States, include overweight or obesity, dyslipidemia, hypertension, and insulin resistance, a precursor of diabetes. The adjunctive therapies of proven benefit in the primary prevention of MI and stroke include statins, blood pressure medications, aspirin, and drugs to treat insulin resistance and hyperglycemia. Fortunately, even for patients who prefer prescription of pills to proscription of harmful lifestyles, these drug therapies still have net benefits. The adoption and maintenance of TLCs and adjunctive drug therapies into clinical practice will reduce both the incidence of and mortality from a first MI and stroke as well as other major clinical manifestations of CVD.


Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 1525-1536
Author(s):  
Xiao Wang ◽  
Min Wu

Abstract Frailty is a clinical syndrome caused by homeostasis imbalance. It is characterized by marked vulnerability to endogenous or exogenous stressors, reduced self-care ability, and increased mortality risk. This aging-related syndrome is common in individuals older than 65 years and carries an increased risk for poor health outcomes. These include falls, incident disability, incapacity, and mortality. In addition, it can result in a poor prognosis for other comorbidities. With the aging population, frailty increases the burden of adverse health outcomes. Studies on frailty are at their infancy. In addition, there is a lack of thorough understanding of its pathogenesis. Several studies have suggested that frailty is caused by chronic inflammation due to enhanced intestinal permeability following gut microbiota imbalance as well as pathogen-related antibodies entering the circulation system. These result in musculoskeletal system disorders and neurodegenerative diseases. However, this assumption has not been validated in large cohort-based studies. Several studies have suggested that inflammation is not the only cause of frailty. Hence, further studies are necessary to extend our understanding of its pathogenesis. This review summarizes the research findings in the field and expands on the possible role of the gut microbiota in frailty syndrome.


2013 ◽  
pp. 234-238
Author(s):  
Giovanni Corona ◽  
Francesco Lotti ◽  
Alessandra Sforza ◽  
Mario Maggi ◽  
Valerio Chiarini

Background: A large body of evidences indicates that sexual dysfunction, and in particular erectile dysfunction (ED), may represent an early surrogate marker of different disease states such as diabetes mellitus, hypertension, metabolic syndrome (MetS) and depression. Furthermore, it has been suggested that ED could also be considered the first sign of a forthcoming coronary heart disease (CHD) and an efficient predictor of silent CHD in a diabetic population, independently of glycometabolic control and ED severity. Hypogonadism is frequently associated with MetS both in subjects with or without ED, insulin resistance being the putative pathogenetic link. In subjects with ED hypogonadism can exacerbate sexual dysfunction because of its typical symptoms, such as decreased sexual desire and mood disturbances. However, hypogonadism per se has been associated with an increased risk of cardiovascular and overall mortality. Aim of the study: In this review, a comprehensive literature search was carried out, in order to discuss the relationship between insulin resistance, ED, MetS and hypogonadism, focusing on their possible involvement in the development of cardiovascular diseases.


2016 ◽  
Vol 229 (2) ◽  
pp. R67-R81 ◽  
Author(s):  
Mark E Cleasby ◽  
Pauline M Jamieson ◽  
Philip J Atherton

Insulin resistance (IR) in skeletal muscle is a key defect mediating the link between obesity and type 2 diabetes, a disease that typically affects people in later life. Sarcopenia (age-related loss of muscle mass and quality) is a risk factor for a number of frailty-related conditions that occur in the elderly. In addition, a syndrome of ‘sarcopenic obesity’ (SO) is now increasingly recognised, which is common in older people and is applied to individuals that simultaneously show obesity, IR and sarcopenia. Such individuals are at an increased risk of adverse health events compared with those who are obese or sarcopenic alone. However, there are no licenced treatments for sarcopenia or SO, the syndrome is poorly defined clinically and the mechanisms that might explain a common aetiology are not yet well characterised. In this review, we detail the nature and extent of the clinical syndrome, highlight some of the key physiological processes that are dysregulated and discuss some candidate molecular pathways that could be implicated in both metabolic and anabolic defects in skeletal muscle, with an eye towards future therapeutic options. In particular, the potential roles of Akt/mammalian target of rapamycin signalling, AMP-activated protein kinase, myostatin, urocortins and vitamin D are discussed.


2022 ◽  
Vol 23 (2) ◽  
pp. 786
Author(s):  
Gracia Fahed ◽  
Laurence Aoun ◽  
Morgan Bou Zerdan ◽  
Sabine Allam ◽  
Maroun Bou Zerdan ◽  
...  

Metabolic syndrome (MetS) forms a cluster of metabolic dysregulations including insulin resistance, atherogenic dyslipidemia, central obesity, and hypertension. The pathogenesis of MetS encompasses multiple genetic and acquired entities that fall under the umbrella of insulin resistance and chronic low-grade inflammation. If left untreated, MetS is significantly associated with an increased risk of developing diabetes and cardiovascular diseases (CVDs). Given that CVDs constitute by far the leading cause of morbidity and mortality worldwide, it has become essential to investigate the role played by MetS in this context to reduce the heavy burden of the disease. As such, and while MetS relatively constitutes a novel clinical entity, the extent of research about the disease has been exponentially growing in the past few decades. However, many aspects of this clinical entity are still not completely understood, and many questions remain unanswered to date. In this review, we provide a historical background and highlight the epidemiology of MetS. We also discuss the current and latest knowledge about the histopathology and pathophysiology of the disease. Finally, we summarize the most recent updates about the management and the prevention of this clinical syndrome.


2017 ◽  
Vol 55 (3) ◽  
pp. 262
Author(s):  
M. N. SARIDOMICHELAKIS (Μ. Ν. ΣΑΡΙΔΟΜΙΧΕΛΑΚΗΣ) ◽  
A. F. KOUTINAS (Α.Φ. ΚΟΥΤΙΝΑΣ)

Diabetes mellitus, the clinical syndrome that results form absolute or relative insulin deficiency and/or reduced number or sensitivity of the insulin receptors, is considered one of the most common endocrine diseases in the cat, being secondary only to hypethyroidism. The exact etiology of type I feline diabetes mellitus remains obscure, although in many cases occurs secondarily to chronic pancreatitis. Type II diabetes mellitus, which is very common in the everyday clinical practice, is characterized by relative insulin deficiency, secondary to reduced production of this hormone (chronic pancreatitis, pancreatic amyloidosis), insulin resistance and/or increased glucose production by the liver (obesity, chronic stress, overproduction of amylin). Secondary (type III) diabetes mellitus is the result of various causes, not directly involving pancreatic tissue, that cause insulin resistance, such as hyperadrenocorticism, pheochromocytoma, acromegaly, hyperthyroidism, infections, neoplasia, hyperlipidemia, chronic heart and renal failure and the exogenous administration of glucocorticoids and progestagens. The most common clinical manifestations of feline non-ketotic diabetes mellitus include polyuria, polydipsia, polyphagia, weight loss, hepatomegaly, retinopathy, peripheral polyneuropathy, dry seborrhea and those resulting form the secondary infections, such as cystitis and stomatitis.


Author(s):  
Iskander I. Zaidullin ◽  
Denis O. Karimov ◽  
Lilija K. Karimova ◽  
Milyausha F. Kabirova ◽  
Rasima R. Galimova ◽  
...  

The susceptibility to the development and progression of inflammatory periodontal diseases, which depends on genetic and external factors (smoking, stress, oral hygiene), varies widely. In the development of these diseases, an important role is played not only by the presence of periodontal pathogenic microorganisms, but also by the presence of congenital or acquired immunodeficiency, immunoregulatory defects. The immune system plays a key role in the physiological and pathological processes of periodontal tissues. In this regard, IL17, produced by CD4+ Th cells, which has both Pro-inflammatory and protective activity, is of particular interest in the pathogenesis of periodontitis. The aim of study was to identify the relationship between polymorphic loci of the IL-17A (rs2275913) and MMP-1 (rs1799750) genes and clinical manifestations of chronic periodontitis in petrochemical workers. Dental examination was performed in 92 ethylene oxide production workers with chronic periodontitis and 74 patients with chronic periodontitis who did not come into contact with chemical factors (control group). Genotyping of polymorphisms rs2275913 of the IL17A gene and rs1799750 of the MMP1 gene was performed by allele-specific real-time polymerase chain reaction (PCR). Hygienic assessment of the degree of air pollution of the working area with harmful substances was carried out by gas chromatography according to the guidelines for the determination of harmful substances in the air № 5098-89, № 3119-84. When comparing the results of studies of both groups, there were no statistically significant differences in the frequency distributions of allelic variants and genotypes of the IL-17A and MMP-1 genes. The AA/AG genotypes of the IL-17A gene were associated with an increased risk of severe disease compared to the GG genotype in workers in the main group (OR=6.1; 95% CI 1.33-28.5; p=0.021) and in the control group (OR=7.26; 95% CI 1.34-39.25; p=0.016). Carriers of the A allele in the control group increased the risk of severe chronic periodontitis by 2.4 times compared to carriers of the G allele (OR=2.41; 95% CI 1.19-4.87; p=0.014). During the dental examination of employees of the ethylene oxide plant, the clinical course of periodontal diseases was more severe in comparison with the control group, and the number of patients with severe periodontitis was twice as high. It was found that the AA/AG genotypes of the IL-17A gene and the carrier of the A allele are associated with increased susceptibility to the development of severe chronic periodontitis. The association between the MMP-1 gene polymorphism and the risk of severe forms of chronic periodontitis has not been established. A risk factor for the development of inflammatory periodontal diseases in employees of the petrochemical complex is a complex of harmful production factors.


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