Nutrition in multimorbidity

Author(s):  
Dr Sue Kenneally

Poor nutrition can be both a cause, and a consequence, of multimorbidity. Assessing nutrition status is therefore a vital component in the management of people with multimorbidity. Suboptimal diet is a direct contributor to risk of ischaemic heart disease, cerebral ischaemic events, many cancers, diabetes, Alzheimer’s disease and other chronic diseases. Eating a diet based on processed foods throughout life increases the risk of these diseases and multiple nutrient deficiencies, including, for example, iron, vitamin B12, folate and calcium.

2013 ◽  
Vol 170 (2) ◽  
pp. 195-201 ◽  
Author(s):  
Anna-Maija Tolppanen ◽  
Raimo Kettunen ◽  
Riitta Ahonen ◽  
Hilkka Soininen ◽  
Sirpa Hartikainen

1992 ◽  
Vol 26 (6) ◽  
pp. 424-430 ◽  
Author(s):  
Rosely Sichieri ◽  
Cecilia A. de Lolio ◽  
Valmir R. Correia ◽  
James E. Everhart

Mortality due to chronic diseases has been increasing in all regions of Brazil with corresponding decreases in mortality from infectious diseases. The geographical variation in proportionate mortality for chronic diseases for 17 Brazilian state capitals for the year 1985 and their association with socio-economic variables and infectious disease was studied. Calculations were made of correlation coefficients of proportionate mortality for adults of 30 years or above due to ischaemic heart disease, stroke and cancer of the lung, the breast and stomach with 3 socio-economic variables, race, and mortality due to infectious disease. Linear regression analysis included as independent variables the % of illiteracy, % of whites, % of houses with piped water, mean income, age group, sex, and % of deaths caused by infectious disease. The dependent variables were the % of deaths due to each one of the chronic diseases studied by age-sex group. Chronic diseases were an important cause of death in all regions of Brazil. Ischaemic heart diseases, stroke and malignant neoplasms accounted for more than 34% of the mortality in each of the 17 capitals studied. Proportionate cause-specific mortality varied markedly among state capitals. Ranges were 6.3-19.5% for ischaemic heart diseases, 8.3-25.4% for stroke, 2.3-10.4% for infections and 12.2-21.5% for malignant neoplasm. Infectious disease mortality had the highest (p < 0.001) correlation with all the four socio-economic variables studied and ischaemic heart disease showed the second highest correlation (p < 0.05). Higher socio-economic level was related to a lower % of infectious diseases and a higher % of ischaemic heart diseases. Mortality due to breast cancer and stroke was not associated with socio-economic variables. Multivariate linear regression models explained 59% of the variance among state capitals for mortality due to ischaemic heart disease, 50% for stroke, 28% for lung cancer, 24% for breast cancer and 40% for stomach cancer. There were major differences in the proportionate mortality due to chronic diseases among the capitals which could not be accounted for by the social and environmental factors and by the mortality due to infectious disease.


1998 ◽  
Vol 79 (03) ◽  
pp. 495-499 ◽  
Author(s):  
Anna Maria Gori ◽  
Sandra Fedi ◽  
Ludia Chiarugi ◽  
Ignazio Simonetti ◽  
Roberto Piero Dabizzi ◽  
...  

SummarySeveral studies have shown that thrombosis and inflammation play an important role in the pathogenesis of Ischaemic Heart Disease (IHD). In particular, Tissue Factor (TF) is responsible for the thrombogenicity of the atherosclerotic plaque and plays a key role in triggering thrombin generation. The aim of this study was to evaluate the TF/Tissue Factor Pathway Inhibitor (TFPI) system in patients with IHD.We have studied 55 patients with IHD and not on heparin [18 with unstable angina (UA), 24 with effort angina (EA) and 13 with previous myocardial infarction (MI)] and 48 sex- and age-matched healthy volunteers, by measuring plasma levels of TF, TFPI, Prothrombin Fragment 1-2 (F1+2), and Thrombin Antithrombin Complexes (TAT).TF plasma levels in IHD patients (median 215.4 pg/ml; range 72.6 to 834.3 pg/ml) were significantly (p<0.001) higher than those found in control subjects (median 142.5 pg/ml; range 28.0-255.3 pg/ml).Similarly, TFPI plasma levels in IHD patients were significantly higher (median 129.0 ng/ml; range 30.3-316.8 ng/ml; p <0.001) than those found in control subjects (median 60.4 ng/ml; range 20.8-151.3 ng/ml). UA patients showed higher amounts of TF and TFPI plasma levels (TF median 255.6 pg/ml; range 148.8-834.3 pg/ml; TFPI median 137.7 ng/ml; range 38.3-316.8 ng/ml) than patients with EA (TF median 182.0 pg/ml; range 72.6-380.0 pg/ml; TFPI median 115.2 ng/ml; range 47.0-196.8 ng/ml) and MI (TF median 213.9 pg/ml; range 125.0 to 341.9 pg/ml; TFPI median 130.5 ng/ml; range 94.0-207.8 ng/ml). Similar levels of TF and TFPI were found in patients with mono- or bivasal coronary lesions. A positive correlation was observed between TF and TFPI plasma levels (r = 0.57, p <0.001). Excess thrombin formation in patients with IHD was documented by TAT (median 5.2 μg/l; range 1.7-21.0 μg/l) and F1+2 levels (median 1.4 nmol/l; range 0.6 to 6.2 nmol/l) both significantly higher (p <0.001) than those found in control subjects (TAT median 2.3 μg/l; range 1.4-4.2 μg/l; F1+2 median 0.7 nmol/l; range 0.3-1.3 nmol/l).As in other conditions associated with cell-mediated clotting activation (cancer and DIC), also in IHD high levels of circulating TF are present. Endothelial cells and monocytes are the possible common source of TF and TFPI. The blood clotting activation observed in these patients may be related to elevated TF circulating levels not sufficiently inhibited by the elevated TFPI plasma levels present.


1975 ◽  
Vol 34 (01) ◽  
pp. 236-245 ◽  
Author(s):  
I. D Walker ◽  
J. F Davidson ◽  
P Young ◽  
J. A Conkie

SummarySix anabolic steroids were assessed for their ability to enhance plasma fibrinolytic activity in males with ischaemic heart disease. Five 17α-alkylated steroids (Ethyloestrenol, Norethandrolone, Methandienone, Methylandrostenediol and Oxymetholone) were examined and all produced a significant increase in plasma plasminogen activator as measured by the euglobulin lysis time. The only non-17α-alkylated steroid studied (Methenolone acetate) failed to enhance fibrinolysis. The 17α-alkylated steroids studied all deserve more detailed evaluation of their long term effects on plasma fibrinolytic activity.


1975 ◽  
Vol 34 (01) ◽  
pp. 106-114 ◽  
Author(s):  
I. D Walker ◽  
J. F Davidson ◽  
P Young ◽  
J. A Conkie

SummaryThe effect of seven different anabolic steroids (Ethyloestrenol, Methenolone acetate, Norethandrolone, Methylandrostenediol, Oxymetholone, Methandienone, and Stanozolol) on three α-globulin antiprotease inhibitors of thrombin and plasmin was studied in men with ischaemic heart disease. In distinct contrast to the oral contraceptives, five of the six 17-α-alkylated anabolic steroids studied produced increased plasma Antithrombin III levels and five produced decreased levels of plasma α2-macroglobulin. The effect on plasma α1antitrypsin levels was less clear-cut but three of the steroids examined produced significantly elevated levels. The increased plasma fibrinolytic activity which the 17-α-alkylated anabolic steroids induce is therefore unlikely to be secondary to disseminated intravascular coagulation.


1970 ◽  
Vol 19 (2) ◽  
pp. 87-93
Author(s):  
MS Kabir ◽  
AAS Majumder ◽  
AW Chowdhury ◽  
SA Haque ◽  
AQM Reza ◽  
...  

Only one half to two thirds of atherosclerotic vascular diseases can be explained by classical risk factors like smoking, diabetes mellitus, hypertension, dyslipidaemia, family history of premature atherosclerotic vascular diseases, physical inactivity, obesity etc. Some other variables appear to contribute to the development of atherosclerotic vascular diseases which include estrogen deficiency, lipoprotein (a), plasma fibrinogen, plasminogen-activator inhibitor type I, endogenous tissue plasminogen activator (tPA), C-reactive protein and homocysteine. Over the last several years, investigators undertook extensive research work, in home and abroad, to determine the contribution of plasma homocysteine in the pathogenesis of atherosclerotic vascular diseases. So far the research work indicates, raised plasma homocysteine appears to be a potential risk factor for ischaemic heart disease.   doi: 10.3329/taj.v19i2.3158 TAJ 2006; 19(2): 87-93


Sign in / Sign up

Export Citation Format

Share Document