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The incidence of both venous and arterial thrombosis increases exponentially with age in both men and women. Possible reasons include: increasing immobility, trauma, surgery and acute medical illness; increasing prevalence (and/or cumulative effects) of obesity, raised blood pressure, dyslipidaemia and glucose intolerance; increasing prevalence of atherosclerosis; and increasing circulating markers of inflammation (C-reactive protein, CRP) and thrombosis. While arterial thrombosis is less common in women, the relative risk for classical risk factors associated with myocardial infarction is at least as strong in women as in men, in prospective population-based studies using MONICA criteria (e.g. Scottish Heart Health Study, Reykjavik Study). Some of these risk factors (e.g. smoking, cholesterol, triglycerides) show decreasing hazard ratios with age. Ongoing studies of newer potential risk factors for venous and arterial thrombosis (e.g. homocysteine, haemostatic and inflammatory variables) should elucidate their roles in risk prediction, including thrombotic risks of sex hormones which have effects on these variables.
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PMID:Venous and arterial thrombosis: epidemiology and risk factors at various ages. 1506 77

By the turn of the last century, flying in the face of over a hundred years of research and clinical observation to the contrary, medicine abandoned the link between infection and atherogenesis; not because it was ever proven wrong, but because it did not fit in with the trends of a medical establishment convinced that chronic disease such as heart disease must be multifactorial, degenerative and non-infectious. Yet it was the very inability of 'established' risk factors such as hypercholesterolemia, hypertension and smoking to completely explain the incidence and trends in cardiovascular disease that resulted in historically repeated calls to search out an infectious cause, a search that began more than a century ago. Today, half of US heart attack victims have acceptable cholesterol levels and 25% or more have none of the "risk factors" associated with heart disease, including smoking, high blood pressure or obesity, most of which are not inconsistent with being caused by infection. Even the case of the traditionalist's latest 2003 JAMA assault to 'debunk' what they call the "50% risk factor myth" falls woefully short under scrutiny. In one group 30% died of heart disease with a cholesterol of at least 240 mg/dl, a condition which also existed in 21% who did not die during the same period. And the overlap was obvious throughout the so-called risk categories. Under such scrutiny, lead author Greenland conceded that if obesity, inactivity and elevated cholesteriol in the elderly are included, just about everyone has a risk factor and he likened the dilemma of people who do or do not wind up with heart disease akin to the susceptibility of people who are exposed to tuberculosis but do not get the disease. In Infections and Atherosclerosis: New Clues from an old Hypothesis? Nieto stressed the need to extend the possible role of infectious agents beyond the three infections which have in recent years been the focus of research: Cytomegalovirus (CMV) Chlamydia pneumoniae and Helicobactor pylori. Mycobacterial disease shares interesting connections to heart disease. Not only is tuberculosis the only microorganism to depend on cholesterol for its pathogenesis but CDC maps for cardiovascular disease bear a striking similarity to those of State and regional TB case rates. Ellis, Hektoen, Osler, McCallum, Swartz, Livingston and Alexander-Jackson all saw clinical and laboratory evidence of a causative relationship between the mycobacteria and heart disease. And Xu showed that proteins of mycobacterial origin actually led to experimental atherosclerosis in laboratory animals Furthermore present day markers suggested as indicators for heart disease susceptibility such as C-Reactive Protein (CRP), interleukin-6 and homocysteine are all similarly elevated in tuberculosis. It therefore behooves us to explore the link between heart disease and typical and atypical tuberculosis.
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PMID:Heart disease: the greatest 'risk' factor of them all. 1508 5

Poor development in utero may favor the development of obesity in adulthood. Animal studies showed that embryo manipulation in vitro or nutritional insults during the embryonic and fetal stages of development may lead to obesity in adult life. We studied the in vitro proliferation and differentiation of adipocytes to investigate whether early protein restriction may program cell growth and development. In a series of experiments, 2 different low-protein diet protocols were compared. In both cases, pregnant rats were fed a diet with a high (18-20%) or low (8-9%) protein content during gestation and/or lactation. Preadipocytes were isolated from the fetuses, neonates, and weanling offspring. Moderate protein restriction, imposed during either gestation and/or lactation, did not affect the capacity of preadipose cells to divide or store fat. Because previous studies showed that early protein restriction alters the metabolism of sulfur amino acids, we also investigated the effects of methionine, taurine, and homocysteine on proliferation and differentiation of preadipocytes. The supplementation of the diet with methionine or the addition of homocysteine and taurine to the culture media did not influence the development of preadipocytes. We obtained no evidence for the direct reprogramming of the precursor or stem cells and suggest that the subsequent alteration in fat accretion may therefore reflect a change in the neuroendocrine environment.
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PMID:Prenatal protein restriction does not affect the proliferation and differentiation of rat preadipocytes. 1517 17

Several parallels exist between preeclampsia and atherosclerosis. Both are multifactorial diseases that share risk factors such as obesity, insulin resistance, lipid abnormalities, and elevated serum homocysteine. There are also similarities in the biochemical changes seen in both diseases, including elevated serum triglycerides, decreased HDL cholesterol and enhanced formation of small, dense LDL particles as well as vascular atherosclerotic lesions. Chronic infection with Chlamydia pneumoniae has been linked to coronary artery disease. This study evaluated a possible link between the incidence of preeclampsia and infection with C. pneumoniae by examining the rate of seropositivity in 81 women with preeclampsia, and 206 women with normal pregnancies. Although our data confirmed well-known risk factors for preeclampsia such as obesity, diabetes, and hypertension, we found no difference in the rate of seropositivity between preeclampsia and normal pregnancy. On the contrary, the presence of chlamydial antibodies was lower in preeclampsia. Multiparous women with preeclampsia showed a significantly lower rate of seropositivity than multiparous normal women and nulliparous preeclamptics. In addition, women with a history of preeclampsia who developed preeclampsia in the current pregnancy also had a significantly lower rate of seropositivity.
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PMID:Preeclampsia and Chlamydia pneumoniae: is there a link? 1536 46

High total homocysteine (tHcy) concentrations increase coronary disease risk. Therefore, the authors examined the relation between tHcy concentrations and the number of stenotic arteries in patients with ischemic heart disease (IHD). They enrolled 155 patients with IHD (135 men) who had undergone selective coronary angiography during the previous 2 years. These patients were divided into 4 groups according to the number of vessels (0, 1, 2, and 3) with > or = 70% stenosis. They also reviewed the major coronary risk factors for each patient (age, gender, hypertension, diabetes mellitus, dyslipidemia, cigarette smoking, obesity), and measured serum concentrations of tHcy, folate, vitamin B12 and lipids. There was a significant positive correlation (rs = 0.19; p = 0.017; n = 155) between tHcy serum concentration and the extent of coronary atherosclerosis, expressed by the number of coronary arteries with significant stenosis. Moreover, the number of affected vessels displayed a significant positive correlation with the presence of diabetes mellitus (rs = 0.30; p < 0.0001; n = 155) and serum concentrations of lipoprotein (a) (rs = 0.25; p < 0.05; n = 67) and a negative correlation with apolipoprotein A-I serum concentration (rs = -0.27; p < 0.01; n = 67). In this study, the serum concentrations of tHcy correlated with the extent of coronary atherosclerosis, independently of other classical risk factors, with the exception of diabetes mellitus.
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PMID:Association of serum total homocysteine with the extent of ischemic heart disease in a Mediterranean cohort. 1537 14

Recent data on the atherogenic effect of elevated concentrations of homocysteine (Hcy) and a review of published results on the influence of sex hormones, especially estrogens, on plasma Hcy levels are presented. Epidemiological data show that hyperhomocysteinemia as well as a mild elevation in plasma Hcy levels significantly increase cardiovascular risk. Some results do not support this relationship. Recently it was established that onset of menopause and decreases in serum estrogen levels probably increase serum Hcy concentrations. The majority of investigation, based on observational studies and the results of one randomized, double-blind placebo-controlled study, showed that use of estrogen and hormonal replacement therapy lowered HCY concentration. It has been observed that the decrease in Hcy level was greater the higher its concentrations before treatment. These results are in contrast with those of another randomized double-blind placebo-controlled study which showed that the Hcy concentration does not depend on menopause and does not change after hormonal treatment. Individual data showed that dehydroepiandrosterone, an adrenal steroid, probably lowers Hcy level. There were no correlations between serum Hcy concentration and insulin concentration, body mass, and type of obesity. The hypotheses about the influence of sex hormones on Hcy concentration are not clear and need further investigation.
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PMID:[Homocysteine--an underestimated atheromatosis risk factor. Do sex hormones influence homocysteine concentrations?]. 1553 96

Lipid and non-lipid cardiovascular risk parameters (cholesterol, HDL- and LDL-cholesterol, triglycerides, homocysteine, C-reactive protein, insulin resistance) and data about blood pressure, smoking, body mass index were assessed in two ethnic groups aged 19-35 years--the Gypsy group (n=122) and the Slovak group (n=137) of two regions with a high density of Gypsy population. In the Gypsy group, the values of triglycerides, atherogenic index, insulin, insulin resistance were significantly increased and the level of HDL-cholesterol was significantly decreased. The risk value of atherogenic index was found in 27 % of Gypsy vs 13 % of majority subjects, and 28 % vs 24 % of subjects had hypertriglyceridemia. Risk value of insulin resistance (HOMA) was presented in 11 % of the Gypsy vs 5 % of the majority group. More obese subjects (20 % vs 8 %), more smokers (55 % vs 25 %) and more subjects with low education (85 % vs 27 %) were recorded in the minority group. The greater occurrence of dyslipidemia, obesity and insulin resistance in young Gypsy subjects is influenced with lifestyle (nutrition /prevalence of animal fat consumption, low consumption of food with low glycemic index and soluble fibre/, smoking, low physical activity) as well as low educational status. (Tab. 2, Ref. 22.).
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PMID:Cardiovascular risk factors in young Gypsy population. 1554 46

While the incidence of infectious diseases has been on the decline in developing countries, the toll of cardiovascular diseases, including stroke and myocardial infarction, has been increasing. The impression of physicians in certain regions of the western Sahel, including the state of Gombe in northeastern Nigeria, is that macrovascular disease in the indigenous population is on the rise. This study was, therefore, undertaken to compare well-established risk factors for cardiovascular disease in a group of 53 men (n=34) and women (n=19) in the town of Gombe who had suffered a stroke or heart attack with the corresponding parameters in 48 age- and gender-matched healthy adults living in the same environment. The parameters of cardiovascular diseases considered were: overweight and obesity, blood pressure, lipid profiles, and homocysteine. While the male and female patients who had suffered stroke (n=48) or heart attack (n=5) were borderline hypertensive, their mean body mass index values were not different from the corresponding values of their control groups. Although the serum homocysteine levels of the patients and controls were not significantly different, 85% of the stroke patients had serum homocysteine levels greater than 10 microM. These high homocysteine levels could not be accounted for by sub-optimal folate or vitamin B 12 status. The serum levels of HDL-cholesterol and triglyceride were not significantly different between the male and female patients and their respective controls. However, the males, but not the females, with macrovascular disease had significantly higher levels of total cholesterol (161 vs 137 mg/dL, p=0.04) and LDL-cholesterol (91 vs 70 mg/dL, p=0.02). In addition, both female and male stroke/myocardial infarction patients exhibited an elevated LDL-cholesterol/HDL-cholesterol ratio. These results indicate that blood pressure and the LDL-cholesterol/HDL-cholesterol ratio are associated with stroke and myocardial infarction in adults in northern Nigeria, thereby creating potential opportunities for possible public-health interventions.
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PMID:Serum lipid profiles and homocysteine levels in adults with stroke or myocardial infarction in the town of Gombe in northern Nigeria. 1566 67

Alcoholic liver disease is a major cause of illness and death in the United States. In the initial stages of the disease, fat accumulation in hepatocytes leads to the development of fatty liver (steatosis), which is a reversible condition. If alcohol consumption is continued, steatosis may progress to hepatitis and fibrosis, which may lead to liver cirrhosis. Alcoholic fatty liver has long been considered benign; however, increasing evidence supports the idea that it is a pathologic condition. Blunting of the accumulation of fat within the liver during alcohol consumption may block or delay the progression of fatty liver to hepatitis and fibrosis. To achieve this goal, it is important to understand the underlying biochemical and molecular mechanisms by which chronic alcohol consumption leads to fat accumulation in the liver and fatty liver progresses to hepatitis and fibrosis. In addition to alcohol consumption, dietary fatty acids and obesity have been shown to affect the degree of fat accumulation within the liver. Again, it is important to know how these factors modulate the progression of alcoholic liver disease. The National Institute on Alcohol Abuse and Alcoholism and the Office of Dietary Supplements, National Institutes of Health, sponsored a symposium on "Role of Fatty Liver, Dietary Fatty Acid Supplements, and Obesity in the Progression of Alcoholic Liver Disease" in Bethesda, Maryland, USA, October 2003. The following is a summary of the symposium. Alcoholic fatty liver is a pathologic condition that may predispose the liver to further injury (hepatitis and fibrosis) by cytochrome P450 2E1 induction, free radical generation, lipid peroxidation, nuclear factor-kappa B activation, and increased transcription of proinflammatory mediators, including tumor necrosis factor-alpha. Increased acetaldehyde production and lipopolysaccharide-induced Kupffer cell activation may further exacerbate liver injury. Acetaldehyde may promote hepatic fat accumulation by impairing the ability of peroxisome proliferator-activated receptor alpha to bind DNA, and by increasing the synthesis of sterol regulatory binding protein-1. Unsaturated fatty acids (corn oil, fish oil) exacerbate alcoholic liver injury by accentuating oxidative stress, whereas saturated fatty acids are protective. Polyenylphosphatidylcholine may prevent liver injury by down-regulating cytochrome P450 2E1 activity, attenuating oxidative stress, reducing the number of activated hepatic stellate cells, and up-regulating collagenase activity. Nonalcoholic steatohepatitis may develop through several mechanisms, such as oxidative stress, mitochondrial dysfunction and associated impaired fat metabolism, dysregulated cytokine metabolism, insulin resistance, and altered methionine/S-adenosylmethionine/homocysteine metabolism. Obesity (adipose tissue) may contribute to the development of alcoholic liver disease by generating free radicals, increasing tumor necrosis factor-alpha production, inducing insulin resistance, and producing fibrogenic agents, such as angiotensin II, norepinephrine, neuropeptide Y, and leptin. Finally, alcoholic fatty liver transplant failure may be linked to oxidative stress. In vitro treatment of fatty livers with interleukin-6 may render allografts safer for clinical transplantation.
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PMID:Role of fatty liver, dietary fatty acid supplements, and obesity in the progression of alcoholic liver disease: introduction and summary of the symposium. 1567 Jun 59

In hyperandrogenic women, several phenotypes may be observed. This includes women with classic polycystic ovary syndrome (C-PCOS), those with ovulatory (OV) PCOS, and women with idiopathic hyperandrogenism (IHA), which occurs in women with normal ovaries. Where other causes have been excluded, we categorized 290 hyperandrogenic women who were seen consecutively for this complaint between 1993 and 2004 into these three subgroups. The aim was to compare the prevalence of obesity, insulin resistance, and dyslipidemia as well as increases in C-reactive protein and homocysteine in these different phenotypes with age-matched ovulatory controls of normal weight (n = 85) and others matched for body mass index (BMI) with women with C-PCOS (n = 42). Although BMI affected fasting serum insulin and the Quantitative Insulin-Sensitivity Check Index, these markers of insulin resistance were greatest in C-PCOS (n = 204), followed by OV-PCOS (n = 50) and then IHA (n = 33). Androgen levels were similar in OV-PCOS and IHA but were higher in C-PCOS, whereas gonadotropins were similar in all groups. Lipid abnormalities were highest in C-PCOS and OV-PCOS and were normal in IHA. C-reactive protein was elevated in C-PCOS and OV-PCOS but not IHA. Homocysteine was elevated only in C-PCOS. Overall, the prevalence of obesity (BMI > 30) was 29% in C-PCOS, 8% in OV-PCOS, and 15% in IHA and insulin resistance (Quantitative Insulin-Sensitivity Check Index < 0.33) was 68% in C-PCOS, 36% in OV-PCOS, and 26% in IHA. The prevalence of having at least one elevated cardiovascular risk marker was 45% in C-PCOS 38% in OV-PCOS and was not increased on IHA (6%). These results suggest that among hyperandrogenic women the prevalence of abnormal metabolic and cardiovascular risk parameters is greatest in C-PCOS, followed by OV-PCOS and then women with IHA. Moreover, in that in OV-PCOS and IHA, ages and weights were similar yet the prevalence of metabolic and cardiovascular risk was greater in OV-PCOS, the finding of polycystic ovaries may be a significant modifying factor.
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PMID:Phenotypic variation in hyperandrogenic women influences the findings of abnormal metabolic and cardiovascular risk parameters. 1572 3


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