Prevalence of and factors associated with frailty and disability in older adults from China, Ghana, India, Mexico, Russia and South Africa.

BACKGROUND: The severe burden imposed by frailty and disability in old age is a major challenge for healthcare systems in low- and middle-income countries alike. The current study aimed to provide estimates of the prevalence of frailty and disability in older adult populations and to examine their relationship with socioeconomic factors in six countries. METHODS: Focusing on adults aged 50+ years, a frailty index was constructed as the proportion of deficits in 40 variables, and disability was assessed using the World Health Organization Disability Assessment Schedule (WHODAS 2.0), as part of the Study on global AGEing and adult health (SAGE) Wave 1 in China, Ghana, India, Mexico, Russia and South Africa. RESULTS: This study included a total of 34,123 respondents. China had the lowest percentages of older adults with frailty (13.1%) and with disability (69.6%), whereas India had the highest percentages (55.5% and 93.3%, respectively). Both frailty and disability increased with age for all countries, and were more frequent in women, although the sex gap varied across countries. Lower levels of both frailty and disability were observed at higher levels of education and wealth. Both education and income were protective factors for frailty and disability in China, India and Russia, whereas only income was protective in Mexico, and only education in South Africa. CONCLUSIONS: Age-related frailty and disability are increasing concerns for older adult populations in low- and middle-income countries. The results indicate that lower levels of frailty and disability can be achieved for older people, and the study highlights the need for targeted preventive approaches and support programs.

Learning-by-doing, population pressure, and the theory of demographic transition.

PIP: The long-term effects of two interdependent relations between economic growth and population growth are discussed. The empirical work of Boserup (1981) was utilized, which focused on rural, sparsely populated economies with low income per capita. According to the formulation of the population-push hypothesis, learning-by-doing effects in production lead to increasing returns to scale and, therefore, to a positive correlation between economic and population growth. In accordance with the theory of demographic transition, the population growth rate initially increases with rising income levels and then declines. The approach originating from Cigno (1984) modified the economic model, which allowed the establishment of two different stable equilibria. Regarding this relationship, the existence and stability of low-income and high-income equilibrium was shown in a neoclassical growth model. Under plausible conditions a demo-economic transition from the first to the second steady-state took place. The instability of the Malthusian steady-state is also possible when a country develops along a path of economic growth which is compatible with the demographic transition. In this context, learning means the application of new techniques of agrarian production. In developed economies with a stable population the learning-or-doing decision lead to accumulation of human capital and the invention of new technologies and goods. The interdependence of income-determined population growth and learning-by-doing may serve as an explanation for the weak and partly controversial empirical support for an overall correlation between income and population growth. The result yielded a meaningful interpretation of the population-push hypothesis, which is consistent with the empirical findings on the correlation between economic and population growth.^ieng

Different accessibility from the artery and the portal vein of alpha- and beta-receptors involved in the sympathetic nerve action on glycogenolysis and hemodynamics in perfused rat liver.

In perfused rat liver perivascular nerve stimulation (7.5 Hz, 20 V, 2 ms, 5 min) at the liver hilus caused an increase in glucose and lactate output and a decrease in flow. The influence of the alpha 1-receptor blocker prazosine and the beta-blocker propranolol on these nerve effects was studied in the isolated rat liver perfused classically via the portal vein only and, as developed recently, via both the hepatic artery and the portal vein. 1) In livers perfused via the portal vein only the nerve stimulation-dependent metabolic alterations were nearly completely inhibited by prazosine (5 microM), but not influenced by propranolol (10 microM). The hemodynamic changes were lowered to only 33% by prazosine and not altered by propranolol either. 2) In livers perfused via the hepatic artery (100 mm Hg, 20-40% of flow) and the portal vein (10 mm Hg, 80-60% of flow)--similar to portal perfusions--the nerve stimulation--dependent metabolic alterations were almost completely blocked by arterial, portal or simultaneously applied arterial and portal prazosine. However--in contrast to portal perfusions--the metabolic alterations were reduced to about 20% (glucose) and 50% (lactate) also by propranolol independently of its site of application. The decrease in flow was reduced by prazosine to about 60%, 50% and 30% when applied via the artery, the portal vein or via both vessels, respectively. The hemodynamic alterations were not influenced by propranolol. These results allow the following conclusions: A subpopulation of beta-receptors can play a permissive role in the alpha 1-receptor-mediated sympathetic nerve action on glucose and lactate metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Nervous control of glycogenolysis and blood flow in arterially and portally perfused liver.

In a recently developed model for the simultaneous perfusion of isolated rat liver via both the hepatic artery (120 mmHg, 20-35% flow) and the portal vein (10 mmHg, 80-65% flow), the arterial and portal nerve plexuses were stimulated (20 V, 2 ms, 2.5-20 Hz for 0.33-5 min) either jointly in the liver hilus or separately at the common hepatic artery and the mesenteric vein, respectively. Stimulation of the arterial plexus alone caused an increase of glucose output, a shift from lactate uptake to output, and a decrease of arterial and, "transhepatically," also of portal flow. Stimulation of the portal plexus alone elicited the same yet clearly smaller metabolic and transhepatic hemodynamic effects. The sum of the metabolic actions of single arterial and portal stimulations but not the sum of the hemodynamic actions was equal to the effects of simultaneous separate stimulations of the hepatic artery and mesenteric vein or joint stimulations in the liver hilus. Half-maximal and maximal effects were reached during 5-min stimulation periods within the physiological range of frequencies, i.e., at 5-6 and 10 Hz for metabolic alterations and at 8 and 20 Hz for hemodynamic changes. At a frequency of 10 Hz, half-maximal and maximal effects were observed with stimulation periods of 0.5 and 1 min for metabolic alterations and with 2 and 5 min for hemodynamic changes. The described model of isolated rat liver perfusion is well suited for the study of the complex metabolic and hemodynamic actions of the arterial and portal nerves, their mutual interactions, and modulations by circulating factors.

A portal-arterial glucose concentration gradient as a signal for an insulin-dependent net glucose uptake in perfused rat liver.

Since in the usual perfusion of isolated rat liver via the portal vein an insulin-dependent increase of hepatic glucose uptake could not be demonstrated, the possibility was considered that hepatic glucose uptake might not be a function of the absolute concentration of this substrate but of its concentration gradient between the portal vein and the hepatic artery. Therefore a new method was established for the simultaneous perfusion of isolated rat liver via both the hepatic artery (20-35% flow) and the portal vein (80-65% flow). When glucose was offered in a concentration gradient, 9.5 mM in the portal vein and 6 mM in the hepatic artery, insulin given via both vessels caused a shift from net glucose release to uptake. This insulin-dependent shift was not observed when glucose was offered without a gradient or with an inverse gradient, 6 mM in the portal vein and 9.5 mM in the hepatic artery. Using a portal-arterial glucose gradient as a signal the liver might be able to differentiate between endogenous and exogenous glucose.