Differences in coronary heart disease risk markers among apparently healthy individuals of African ancestry.

OBJECTIVE: This study identified and compared coronary heart disease (CHD) risk factors among foreign-born Afro Caribbeans (FBAC), U.S.-born Afro-Caribbean Americans (USBAC) and African Americans. METHODS: Sixty-six FBAC living in the United States for <10 years, 62 USBAC and 61 African-American adults (18-40 years) were recruited. Sociodemographic, behavioral and biochemical data were collected and analyzed. RESULTS: More USBAC (26.2%) and African-American (23.7%) participants compared to the FBAC (10.8%) participants had significantly (p < 0.05) poorer diet scores and were significantly (p < 0.05) more obese (17.7% and 23.0% vs. 7.6%). These differences remained significant between the male ethnic groups but not the females. Also, more USBAC and African-American participants compared to FBAC participants watched television often/very often (54.8% and 49.2% vs. 45.5%), played less sports (56.5% and 55.7% vs. 40.9%) and smoked cigarettes (4.8% and 6.6% vs. 0.0%). In general, USBAC and African-American participants were more likely to have elevated blood glucose (BG), total cholesterol (TC), low-density-lipoprotein cholesterol (LDL-C) and high-sensitivity C-reactive protein (hs-CRP) levels compared to FBAC participants. More FBAC than USBAC and African-American participants had elevated blood pressure (BP) and low levels of high-density-lipoprotein cholesterol (HDL-C). However, the differences were not significant. CONCLUSION: This study demonstrated that there are differences in risk factors for CHD among ethnic groups (FBAC, USBAC and African-American participants) of persons with African ancestory.

Behavioral risk profiles for coronary heart disease among apparently healthy individuals of African ancestry.

OBJECTIVE: Mortality from coronary heart disease (CHD) is lower in foreign-born Blacks compared to their US-born counterparts. The purpose of this study was to determine if behavioral risk factors for CHD are different between foreign-born Afro Caribbeans (FBAC) and their US-born counterparts (US-born Afro Caribbean Americans, USBAC and African Americans, AA). DESIGN AND PARTICIPANTS: For a cross-sectional study, 66 FBAC (31 males; 35 females) living in the United States <10 years, 62 USBAC (30 males; 32 females), and 61 AA (30 males; 31 females) adults (18-40 years) were recruited. Dietary, anthropometric, physical activity, cigarette smoking, and alcohol consumption data were collected and analyzed. MAIN OUTCOME MEASURE: Risk factors for CHD. RESULTS: Significantly (P<.05) more USBAC (50.0%) and AA (31.0%) males consumed an unhealthy diet compared to the FBAC (16.7%) males. Also, significantly (P<.05) more USBAC and AA males compared to FBAC males were obese (20.0% and 33.3% vs 6.5%). No significant differences were observed between the female ethnic groups. Although less USBAC and AA males and females compared to FBAC males and females played sports, the differences were not significant. More USBAC and AA males compared to FBAC (10.0% and 3.3% vs 0.0%) smoked cigarettes and consumed alcoholic beverages (43.3% and 63.3% vs 16.1%). Among the female ethnic groups, only the AA smoked cigarettes. Significantly (P<.05) more USBAC (36.7%) and AA (33.3%) males compared to FBAC (3.2%) males had poorer behavioral habits, with no significant differences observed between the female ethnic groups. CONCLUSIONS: Our study showed significant differences in CHD risk behaviors among individuals of African decent. The FBAC participants had more favorable behaviors in preventing CHD compared to their US-born counterparts.

Relationship between hepatic glutathione and fatty liver in weanling rats on a low protein diet

Weanling rats were fed on one of four diets: laboratory chow, PLC; 23 percent casein protein, CC; 8 percent casein protein, LP; 8 percent casein protein with supplemental cysteine to the level found in CC diet, LPC. Liver and blood glutathione (GSH), total liver fat and hepatic triglyceride were measured at 6, 12 and 20 days. On the PLC diet the increase in body weight, liver weight and liver GSH were significantly greater than on the CC diet (p<0.01). After 20 days on the LP diet rats showed a significant increase in liver triglyceride and total fat. The addition of cysteine to the low protein diet was associated with a significant increase in body weight and liver GSH and prevented liver triglyceride and total fat from increasing. GSH levels in extrahepatic tissues were not affected to the same extent as in the liver. There was a significant negative linear correlation between hepatic GSH and both liver triglyceride and liver total fat. A low dietary cysteine can cause fatty infiltration of the liver and this may be mediated through a fall in liver GSH (AU)

Relationship between hepatic glutathione and fatty infiltration of the liver

One of the most serious complications of severe protein-energy malnutrition (PEM) is hepatic failure, which is usually associated with fatty infiltration of the liver. The precise biochemical cause of fatty liver is unknown. This study was designed to investigate the relationship between hepatic glutathione (GSH) and fat accumulation in the liver. Also, the experiment was designed in such a way as to determine the effects of different sources of dietary protein. Twenty-one days old weanling rats were fed for 20 days on diets containing adequate protein (Purina Laboratory Chow) (PLC) and Casein (CC - 23 percent protein), low protein (LP - 7 percent Casein), low protein supplemented with cysteine (LPC) to the level in the CC diet and, choline deficient diet (CD). The animals were weighed on the days of weaning and sacrifice. On the day of sacrifice, the blood, liver and kidney were rapidly removed, liver and kidney blotted on filter paper, weighed and GSH and fat measured using standard procedures. Animals on the CD diet lost weight and had twice the hepatic GSH levels compared to rats on the LP diet. However, they did not develop fatty livers as expected due to the deterioration of the diet in storage. Rats on the PLC diet had significantly gretaer body weight gains (p<0.01), higher liver GSH and cysteine values and lower liver triglyceride (TG) values than rats on the CC diet. Thus, the CC diet was used as the reference diet since the test diets were casein-based formulae. Rats on the LP diet showed reduced body weight gain and fat-free dry liver weight (FFDLW) values compared to the control. Liver glutathione (GSH) and cysteine concentrations were also reduced but there was no significant change in kidney and blood GSH concentrations. Liver fat and triglyceride (TG) values were significantly increased compared to the control (p<0.01). The addition of cysteine to the LP diet, dramatically increased liver GSH, FFDLW and body weight values and prevented liver fat and TG levels from increasing. It is concluded that the hepatic GSH and fat levels in weanling rats depend not only on the cysteine content of the diet but, also on the quality and composition of protein in the diet. Also, that cysteine directly or by maintaining liver GSH levels, prevented the increase of liver fat found in weanling rats on the LP diet (AU)

The relationship between glutathione and fatty infiltration of the liver in weanling rats - abstract

One of the most serious complications of severe malnutrition is hepatic failure, which is usually associated with fatty infiltration. The cause of fatty liver is unknown. We have speculated that a low hepatic glutathione (GSH) content may predispose to its development. Weanling rats have been fed low-protein diets, with and without supplemental cysteine, and the effect on gepatic GSH and fat measured. Three casein-based diets were fed for 20 days. The control diet contained 23 percent protein (C), the low-protein diet 6 percent (LP), and the supplemented diet was similar to the low protein diet with cysteine added to the level in the control diet (LPC). On the day of sacrifice, the liver was rapidly removed, weighed and GSH and fat measured using standard methods. By day 20, the rats on the LP diet had a significantly reduced body weight. GSH was significantly reduced, and fat significantly increased. These differences were almost completely reversed by adding cysteine to the diet. There was an inverse linear relationship between liver triglyceride and GSH (r=-o.76). A limited dietary availability of cysteine promotes a low hepatic GSH and fat accumulation. As GSH may be seen as an intracellular store for cysteine, it is not possible to imute a direct causal relationship between GSH level and fat accumulation. The results could be explained on the basis of cysteine being limiting for the synthesis of the apoprotein required for the formation of hepatic export lipoproteins. Alternatively, a low GSH may be directly responsible for hepatic fat accumulation as this tripeptide plays a central role in cellular detoxification, oxidation/reduction reactions and amino-acid transport. As we have shown that children with oedematous malnutrition have a reduced blood GSH, the findings of this study may be of relevance in clinical practice (AU)