[Carbohydrate intake and prevention of nutrition-related diseases]. / Kohlenhydratzufuhr und Prävention ausgewählter ernährungsmitbedingter Krankheiten.

The relative contribution of nutrition-related chronic diseases to the total disease burden of the society and the healthcare costs have risen continuously over the last decades. This challenge requires to explore and use the potential of dietary prevention of diseases such as obesity, type 2 diabetes, dyslipidaemia, cardiovascular disease and cancer. This evidence-based guideline systematically assessed the potential role of carbohydrates in the primary prevention of these diseases. The major findings were: a high consumption of sugar-sweetened beverages increases the risk of obesity and type 2 diabetes (strength of evidence: probable), whereas a high dietary fibre intake, mainly from whole-grain products, reduces the risk of obesity, type 2 diabetes, dyslipidaemia, hypertension, coronary heart disease and colorectal cancer (strength of evidence: probable and convincing, respectively). The practical consequences for current dietary recommendations are presented.

Alcohol consumption and its relation to cardiovascular risk factors in Germany.

OBJECTIVE: To analyse the association of alcohol consumption and blood lipids, haemostatic factors, and homocysteine in German adults by gender and age groups. DESIGN: Cross-sectional population-based survey. SETTING: Data from the German National Health Interview and Examination Survey 1998, representative for age, gender, community size, and federal state. SUBJECTS: From a sample of 7124 Germans between 18 and 79 y old, 2420 women and 2365 men were selected. Only individuals who were not currently receiving medical treatment or did not have disorders related to cardiovascular disease were selected for this study. RESULTS: Using analyses of variance, mean blood levels of total cholesterol, HDL cholesterol, HDL/total cholesterol ratio, total glycerides, fibrinogen, antithrombin III, and homocysteine adjusted for age, socioeconomic status, East/West Germany residence, body mass index, tobacco use, sports activity, and coffee consumption, if appropriate are presented by alcohol consumption groups (0, >0-10, >10-20, >20-30 and >30 g/day). The HDL/total cholesterol ratio increased with higher alcohol groups up to 10-20 g/day (+15%) for women and >30 g/day (+18%) for men, showing the strongest rise among men aged 55-79 y. Fibrinogen decreased with higher alcohol groups up to 10-20 g/day for women and 20-30 g/day for men. Among women, homocysteine levels showed a U-shaped curve with a minimum of 8.49 mmol/l at 10-20 g alcohol/day (-8%, reference: nondrinking), whereas an inverse association was observed for men. CONCLUSIONS: Moderate alcohol consumption is associated with favourable levels of several cardiovascular risk factors. The most favourable cardiovascular risk factor profile among women was observed among those drinking 10-20 g alcohol/day. Beneficial effects seem to be more pronounced among older men.

Lowering of homocysteine concentrations in elderly men and women.

B-vitamin supplementation has previously been shown to lower the concentration of plasma total homocysteine, a risk factor for cardiovascular disease. Little is known about the homocysteine-lowering effects of low-dose B-vitamins in elderly individuals, who are prone to higher homocysteine levels due to advanced age and a greater frequency of impaired vitamin status. We aimed to identify if and to what extent B-vitamins lower total homocysteine and its subfractions in elderly individuals. Men and women (> or = 60 years) received either B-vitamins (400 micrograms folic acid + 1.65 mg pyridoxine + 3 micrograms cyanocobalamin) or a placebo daily for 4 weeks. Subjects in the vitamin group showed a significant decrease in plasma total homocysteine during the first 2 weeks; thereafter, total homocysteine only slightly decreased further resulting in a geometric mean reduction of -16.3% (95% CI: -11.3% to -21.0%) over the entire treatment period. Free homocysteine decreased as well. However, the observed higher ratio of free/total homocysteine after 4 weeks of supplementation suggest a more pronounced reduction in protein-bound homocysteine. Low-dose B-vitamin supplementation is effective in lowering homocysteine in elderly individuals. Further studies are needed to be able to depict the effect of B-vitamin supplementation on different homocysteine sub-fractions in plasma.

Availability of food folate in humans.

The aim of our study was to determine whether the area-under-the-plasma-response-curve method with the positive area (AUC+) as primary analysis variable is suitable to evaluate the availability of food folate in humans. Healthy volunteers (n = 20) received four test meals in a randomized, four-period cross-over design as follows: meal A, 600 g spinach; meal B, 300 g spinach; meal C, 0.4 mg folic acid in water; meal D, folate-free control meal. Blood samples were drawn before administration of the test meals and up to 10 h postprandially. Plasma folate was significantly increased for up to 6 h after uptake of spinach and folic acid (P < 0.007), whereas the response curve after the control meal decreased slightly but significantly (P < 0.007). To calculate the net increase of plasma folate, the values were corrected by the individual predose concentrations. The AUC+ was calculated with these corrected values. The mean AUC+ was highest after consumption of meal A (71.2 +/- 24.0 h x nmol/L) followed by meal C (61.8 +/- 23. 8 h x nmol/L) and meal B (41.4 +/- 19.4 h x nmol/L). The AUC+ after meal B was significantly lower than after the other two meals (P < 0. 05). The results suggest that the AUC method with multiple blood sampling is useful for assessing the availability of food folate in humans.

Effects of folic acid and combinations of folic acid and vitamin B-12 on plasma homocysteine concentrations in healthy, young women.

BACKGROUND: Elevated plasma homocysteine concentrations are considered to be a risk factor for vascular disease and fetal malformations such as neural tube defects. Recent studies have shown that plasma homocysteine can be lowered by folic acid in amounts corresponding to 1-2 times the recommended dietary allowance. Preliminary evidence indicates that vitamin B-12 may be beneficial when included in supplements or in a food-fortification regimen together with folic acid. OBJECTIVE: We aimed to compare the homocysteine-lowering potential of a folic acid supplement with that of 2 supplements containing different doses of vitamin B-12 in addition to folic acid. DESIGN: Female volunteers of childbearing age (n = 150) received a placebo for 4 wk followed by a 4-wk treatment with either 400 microg folic acid, 400 microg folic acid + 6 microg vitamin B-12, or 400 microg folic acid + 400 microg vitamin B-12. RESULTS: Significant reductions (P < 0.001) in plasma homocysteine were observed in all groups receiving vitamin treatment. The effect observed with the combination of folic acid + 400 microg vitamin B-12 (total homocysteine, -18%) was significantly larger than that with a supplement containing folic acid alone (total homocysteine, -11%) (P < 0.05). Folic acid in combination with a low vitamin B-12 dose (6 microg) affected homocysteine as well (-15%). CONCLUSIONS: These results suggest that the addition of vitamin B-12 to folic acid supplements or enriched foods maximizes the reduction of homocysteine and may thus increase the benefits of the proposed measures in the prevention of vascular disease and neural tube defects.

Vitamins B12, B6 and folate as determinants of homocysteine concentration in the healthy population.

The metabolism of a substrate is closely linked to that of its cofactor(s). In the case of homocysteine, the vitamins B12, B6 and folic acid are involved in its metabolism, acting as coenzymes. To evaluate the role of these vitamins as determinants of homocysteine concentration in the healthy population, only data from this group should be considered. Studies dealing with vitamin deficiency and the occurrence of elevated homocysteine levels as well as with the treatment of elevated homocysteine levels by supplementing one or more of the vitamins have to be omitted. In the healthy population with "normal" homocysteine levels and a vitamin status currently regarded as adequate, folate seems to play the most important role in determining the blood homocysteine level. This has been derived from supplementation studies as well as from statistical correlation analysis regarding the relationship of the three vitamins to homocysteine. Until now, recommended dietary allowances for folate have been defined on the basis of the absence of clinical signs of deficiency as well as morphological alterations of blood cells indicating an early stage of folate deficiency. However, these recommended dietary allowance values do not seem to be sufficient when looking at homocysteine as a functional parameter of folate status. Due to the important role of folate status as a determinant of homocysteine concentration, it may be necessary to redefine an adequate blood folate level and probably reformulate dietary allowances for this B-vitamin.

The role of homocysteine, folate and other B-vitamins in the development of atherosclerosis.

Recently, elevated homocysteine blood concentrations have been identified as an independent risk factor for the development of atherosclerotic lesions. The amino acid homocysteine is metabolized in the human body involving the vitamins folic acid, B12 and B6 as essential cofactors and coenzymes, respectively. There is an inverse relationship between the status of the relevant B-vitamins and the homocysteine blood concentration. Supplementation of these vitamins results in a significant reduction of the homocysteine level. Nutritive amounts seem to be sufficient to obtain this reduction, even in the case of elevated homocysteine levels.

Causes and consequences of hyperhomocyst(e)inemia.

Increased plasma concentrations of the sulfur-containing amino acid homocyst(e)ine are designated as hyperhomocyst(e)inemia. Various definitions have been used to derive cut-off levels for hyperhomocyst(e)inemia. The classification by Kang is now generally used distinguishing moderate, intermediate and severe hyperhomocyst(e)inemia. A variety of causes are discussed for the etiology of the disease which can be grouped into genetic and nongenetic factors. Severe hyperhomocyst(e)inemia is accompanied by homocystinuria and several other symptoms occurring early in life. Treatment is mandatory for normal development and prevention of premature atherosclerosis. Even less severe forms of hyperhomocyst(e)inemia imply a substantially elevated risk for vascular diseases. Etiology and severity of defect(s) leading to hyperhomocyst(e)inemia are the basis for treatment. In genetic defects, supplementation with the cofactor(s) of the affected enzyme is used to enhance enzyme activity. Alternative routes in the pathway may also be enhanced. Nongenetic hyperhomocyst(e)inemia often requires correction of suboptimal vitamin concentrations. Nutritive doses of the vitamins may be sufficient for treatment of less severe forms as well as for prevention of hyperhomocyst(e)inemia.

Homocysteine and cardiovascular diseases.

Elevated homocysteine blood concentrations have been identified as an independent risk factor for the development of atherosclerotic lesions. The metabolism of the amino acid homocysteine in the human body involves the vitamins folic acid, B-12 and B-6 as essential cofactors and coenzymes, respectively. There is an inverse relationship between the status of the relevant B-vitamins and the homocysteine blood concentration. Supplementation of these vitamins results in a significant reduction of the homocysteine level. However, nutritive amounts seems to be sufficient to obtain this reduction, even in the case of elevated homocysteine levels.