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[discostu]

Så lenge du bestiller fra EU og ikke USA blir det ikke stoppet i tollen, derfor lønner det seg å sjekke ebay.co.uk og ikke ebay.com.

 

Logga inn på ebayprofilen nå, men fant ikke liste over kjøp...

 

Wow, er dette virkelig sant? Uansett hva man kjøper liksom?

 

I teorien ja, så lenge det er lovlig. Du kan ikke hamstre knark feks. Og kun til eget bruk så er en grense på dosering.

[Dufen]

Nøkkelhullmerket viser hvilken variant som er sunnest i hver kategori. Helmelk er ikke sunnest, fordi det er mer fett i den.

Forbanna fjott...

[Uncle Scrooge]

Nøkkelhullmerket viser hvilken variant som er sunnest i hver kategori. Helmelk er ikke sunnest, fordi det er mer fett i den.

Forbanna fjott...

 

Fordi? H-melk har et høyere innhold av mettet fett og blir derfor ikke nøkkelhullmerket. Sier ikke at H-melk nødvendigvis er dårligere enn annen melk (kommer selvfølgelig ann på formålet), men for de kriteriene det stilles for nøkkelhullmerket er det dårligere.

[joakimz]

jo mindre mat er prosessert jo bedre er det, derfor er melk rett fra kua best. Den nest beste varianten er h-melk.

[Dufen]

Nøkkelhullmerket viser hvilken variant som er sunnest i hver kategori. Helmelk er ikke sunnest, fordi det er mer fett i den.

Forbanna fjott...

 

Fordi? H-melk har et høyere innhold av mettet fett og blir derfor ikke nøkkelhullmerket. Sier ikke at H-melk nødvendigvis er dårligere enn annen melk (kommer selvfølgelig ann på formålet), men for de kriteriene det stilles for nøkkelhullmerket er det dårligere.

Og HVOR hen har du det fra at mettet fett er dårligere enn umettet fett? Jeg bare lurer...

[Matsemann]

Herregud Robert, ro deg litt ned..

 

Utifra nøkkelhullsmerkingen sine krav er H-melk mindre sunt. Om du er uenig i det ta det opp med dem vel.

[Dufen]

Man skriver ikke ting som "Helmelk er ikke sunnest, fordi det er mer fett i den." og presenterer det som fakta uten å kunne begrunne det.

Noe som i og for seg er umulig med tanke på helmelk...

[justinvernon]

Nøkkelhullmerket viser hvilken variant som er sunnest i hver kategori. Helmelk er ikke sunnest, fordi det er mer fett i den.

Forbanna fjott...

http://www.nejm.org/doi/full/10.1056/NEJM199711203372102

"Dietary Fat Intake and the Risk of Coronary Heart Disease in Women"

 

Each increase of 5 percent of energy intake from saturated fat, as compared with equivalent energy intake from carbohydrates, was associated with a 17 percent increase in the risk of coronary disease (relative risk, 1.17; 95 percent confidence interval, 0.97 to 1.41; P = 0.10). As compared with equivalent energy from carbohydrates, the relative risk for a 2 percent increment in energy intake from trans unsaturated fat was 1.93 (95 percent confidence interval, 1.43 to 2.61; P<0.001); that for a 5 percent increment in energy from monounsaturated fat was 0.81 (95 percent confidence interval, 0.65 to 1.00; P = 0.05); and that for a 5 percent increment in energy from polyunsaturated fat was 0.62 (95 percent confidence interval, 0.46 to 0.85; P = 0.003). Total fat intake was not significantly related to the risk of coronary disease (for a 5 percent increase in energy from fat, the relative risk was 1.02; 95 percent confidence interval, 0.97 to 1.07; P = 0.55). We estimated that the replacement of 5 percent of energy from saturated fat with energy from unsaturated fats would reduce risk by 42 percent (95 percent confidence interval, 23 to 56; P<0.001) and that the replacement of 2 percent of energy from trans fat with energy from unhydrogenated, unsaturated fats would reduce risk by 53 percent (95 percent confidence interval, 34 to 67; P<0.001).

 

CONCLUSIONS

Our findings suggest that replacing saturated and trans unsaturated fats with unhydrogenated monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease in women than reducing overall fat intake."

 

 

Jeg mener fortsatt at det finnes mer som tyder på at mye mettet fett er uheldig. Det å velge skummet/lett istedenfor H-melk er noe som mange kan ha godt av, men det beror jo på resten av kostholdet, generell helse osv...

[Dufen]

Og så var det en undersøkelse som påviste at å drikke helmelk rett etter en treningsøkt ikke førte til økt fettlagring kontra skummetmelk... Sååååehhh...

[Matsemann]

Jeg sier ikke du har feil, Doofen. Men litt ironisk at du maser om kilder, får en kilde, og så svarer på den måten.

[discostu]

Selvfølgelig er skummet og ekstra lett bedre enn H-melk når det kommer til vektnedgang. Og det er vektnedgang folk tenker på når de skal spise sunt.

 

Desuten, som Matsemann sier stiller ikke H-melk opp til nøkkelhullkravene. Så liten vits i å krangle om det.

[Uncle Scrooge]

Fordi? H-melk har et høyere innhold av mettet fett og blir derfor ikke nøkkelhullmerket. Sier ikke at H-melk nødvendigvis er dårligere enn annen melk (kommer selvfølgelig ann på formålet), men for de kriteriene det stilles for nøkkelhullmerket er det dårligere.

Og HVOR hen har du det fra at mettet fett er dårligere enn umettet fett? Jeg bare lurer...

 

Er du blind eller? Skriver at i forhold til de kriteriene nøkkelhullsmerket stiller er lettere meieriprodukter bedre.

 

http://www.nokkelhullsmerket.no/nokkelhull/

[storken]

Nøkkelhullmerket viser hvilken variant som er sunnest i hver kategori. Helmelk er ikke sunnest, fordi det er mer fett i den.

Forbanna fjott...

http://www.nejm.org/...199711203372102

"Dietary Fat Intake and the Risk of Coronary Heart Disease in Women"

 

Each increase of 5 percent of energy intake from saturated fat, as compared with equivalent energy intake from carbohydrates, was associated with a 17 percent increase in the risk of coronary disease (relative risk, 1.17; 95 percent confidence interval, 0.97 to 1.41; P = 0.10). As compared with equivalent energy from carbohydrates, the relative risk for a 2 percent increment in energy intake from trans unsaturated fat was 1.93 (95 percent confidence interval, 1.43 to 2.61; P<0.001); that for a 5 percent increment in energy from monounsaturated fat was 0.81 (95 percent confidence interval, 0.65 to 1.00; P = 0.05); and that for a 5 percent increment in energy from polyunsaturated fat was 0.62 (95 percent confidence interval, 0.46 to 0.85; P = 0.003). Total fat intake was not significantly related to the risk of coronary disease (for a 5 percent increase in energy from fat, the relative risk was 1.02; 95 percent confidence interval, 0.97 to 1.07; P = 0.55). We estimated that the replacement of 5 percent of energy from saturated fat with energy from unsaturated fats would reduce risk by 42 percent (95 percent confidence interval, 23 to 56; P<0.001) and that the replacement of 2 percent of energy from trans fat with energy from unhydrogenated, unsaturated fats would reduce risk by 53 percent (95 percent confidence interval, 34 to 67; P<0.001).

 

CONCLUSIONS

Our findings suggest that replacing saturated and trans unsaturated fats with unhydrogenated monounsaturated and polyunsaturated fats is more effective in preventing coronary heart disease in women than reducing overall fat intake."

 

 

Jeg mener fortsatt at det finnes mer som tyder på at mye mettet fett er uheldig. Det å velge skummet/lett istedenfor H-melk er noe som mange kan ha godt av, men det beror jo på resten av kostholdet, generell helse osv...

 

Det er vel få som benekter de dårlige virkningene transfettsyrer har på kroppen. Så lite som 2% av ditt totale energiinntak fra transfettsyrer øker flere markører for betennelse i kroppen betydelig. Det er uheldig at mettet fett dras inn som en synder i denne studien. Studien er også en epidemistudie som ikke tar hensyn til individuelle foskjeller, generelt er slike studier usikre når det kommer til å dra konklusjoner som dras her. Det blir litt som å bruke BMI på en befolkning, det fungerer for et samfunn - men det kan være store forskjeller mellom helsa på folk av lik BMI.

 

 

Litt mer om trans-fett: Disse fettsyrene har en annerledes struktur som gjør at kroppen benytter seg av dem dårlig. Prosseserte matvarer inneholder mye transfett, slik kan de holde en lang holdbarhet.

 

Mettet fett er en hel haug med forskjellige fettsyrer som generaliseres inn i denne gruppen. Noen er veldig bra for kroppen, andre er ikke like bra. Derfor blir "mettet fett er dårlig" en alt for generell påstand. Under legger jeg en spoiler med ENORMT mye informasjon, leser du gjennom den der kommer du til å forstå mer om mettet fett enn 99% av norges befolkning.

 

 

 

 

HEALTH EFFECTS OF SATURATED FATTY ACIDS

The approach of many mainstream investigators in studying the effect of consuming saturated fats has been narrowly focused to produce and evaluate evidence in support of the hypothesis that dietary saturated fat elevates LDL cholesterol and thus the risk of CAD. The evidence is not strong, and, overall, dietary intervention by lowering saturated fat intake does not lower the incidence of nonfatal CAD; nor does such dietary intervention lower coronary disease or total mortality (31, 61). Unfortunately, the overwhelming emphasis on the role of saturated fats in the diet and the risk of CAD has distracted investigators from studying any other effects that individual saturated fatty acids may have on the body. If saturated fatty acids were of no value or were harmful to humans, evolution would probably not have established within the mammary gland the means to produce saturated fatty acids—butyric, caproic, caprylic, capric, lauric, myristic, palmitic, and stearic acids—that provide a source of nourishment to ensure the growth, development, and survival of mammalian offspring.

 

Fatty acids are essential parts of all body tissues, where they are a major part of the phospholipid component of cell membranes. Saturated fatty acids have been suggested to be the preferred fuel for the heart (62). Fatty acids are used as a source of fuel during energy expenditure, and heavy exercise is associated with decreases in the plasma concentrations of all free fatty acids. In light exercise, fat metabolism may be controlled to favor adipose tissue lipolysis and extraction of free fatty acids from the circulation by muscle, whereas in heavy exercise, adipose tissue lipolysis is inhibited and hydrolysis of muscle triacylglycerols may play a more important part (63). In the absence of sufficient dietary fat, the body synthesizes the fatty acids that it needs from carbohydrates. The major fatty acid synthesized de novo via fatty acid synthase is palmitate, which undergoes elongation involving acyl-CoA and malonyl-CoA to form longer-chain saturated fatty acids. Desaturation via fatty acyl-CoA desaturases introduces unsaturation at C4, C5, C6, or C9. The lack of capability to desaturate past C9 makes dietary linoleic acid an essential fatty acid (for review see reference 64). Synthesis of palmitic acid is also increased by consumption of very-low-fat diets with a high ratio of sugar to starch (14).

 

Based on the controversy over the effects of fat in the diet, the question most often addressed is, What are the relative cholesterolemic effects of the major saturated fatty acids in the diet? However, the evidence suggests that caproic, caprylic, and capric acids are neutral with respect to cholesterol-increasing properties and their ability to modulate LDL metabolism; lauric, myristic, and palmitic acids are approximately equivalent in their cholesterol-increasing potential, and stearic acid appears to be neutral in its cholesterol-increasing potential (65; for review see reference 66). A limited number of controlled studies suggest that myristic acid is the most potent cholesterolemic dietary saturated fatty acid (for review see reference 67). However, there is evidence that the increase in chlolesterol is related to an increase in both LDL and HDL cholesterol (68). Aside from the reported effects on plasma cholesterol concentrations, there are other properties and functions of the individual saturated fatty acids that support beneficial roles in the body. Some of these roles are briefly discussed below.

 

Butyric acid

Short-chain fatty acids are hydrolyzed preferentially from triacylglycerols and absorbed from the intestine to the portal circulation without resynthesis of triacylglycerols. These fatty acids serve as a ready source of energy, and there is only a low tendency for them to form adipose (69). Butyric acid (4:0) is the shortest saturated fatty acid and is present in ruminant milk fat at 2–5% by weight (70), which on a molar basis is approximately one-third the amount of palmitic acid. Human milk contains a lower percentage (≈0.4%) of butyric acid. No other common food fat contains this fatty acid.

 

Butyrate is a well-known modulator of genetic regulation (71, 72), and it also may play a role in cancer prevention (73). Published information thus far indicates that butyric acid exhibits contradictory and paradoxical behavior (74). Although butyric acid is an important energy source for the normal colonic epithelium, is an inducer of the growth of colonic mucosa, and is a modulator of the immune response and inflammation, it also functions as an antitumor agent by inhibiting growth and promoting differentiation and apoptosis (75).

 

Caproic, caprylic, and capric acids

In bovine and human milk, caproic acid (6:0) is present at ≈1% and 0.1% of milk fat, respectively, and caprylic acid (8:0) and capric acid (10:0) are present at ≈0.3% and 1.2% of milk fat, respectively. Goat milk contains the highest percentage of caprylic acid, at 2.7% of milk fat. These 3 fatty acids have similar biological activities. Both caprylic acid and capric acid have antiviral activity, and when formed from capric acid in the animal body, monocaprin has antiviral activity against HIV (76, 77). Caprylic acid has also been reported to have antitumor activity in mice (78). Negative effects of these fatty acids on CAD and cholesterol have not been a dietary issue.

 

Lauric acid

Lauric acid (12:0) is a medium-chain fatty acid that is present in human and bovine milk at ≈5.8% and 2.2% of milk fat, respectively. This fatty acid has been recognized for its antiviral (79) and antibacterial (80, 81) functions. Recent results suggest that Helicobacter pylori present in stomach contents (but not necessarily within the mucus barrier) should be rapidly killed by the millimolar concentrations of fatty acids and monoacylglycerols that are produced by preintestinal lipases acting on suitable triacylglycerols, such as those present in milk fat (82). Lauric acid is also effective as an anticaries and antiplaque agent (83). Medium-chain saturated fatty acids and their monoacylglycerol derivatives can have adverse effects on various microorganisms, including bacteria, yeast, fungi, and enveloped viruses, by disrupting the lipid membranes of the organisms and thus inactivating them (84, 85). This deactivation process also occurs in human and bovine milk when fatty acids are added to milk (86, 87). The release of monolaurin from milk lipids by human milk lipases may be involved in the resulting antiprotozoal functions (88, 89). One study indicated that one antimicrobial effect against bacteria is related to the interference of monolaurin with signal transduction or toxin formation (90). In addition to disrupting membranes to inactivate viruses, lauric acid has an effect on virus reproduction by interfering with assembly and maturation, ie, cells make the components of the virus, but their assembly is inhibited (79).

 

Myristic acid

Bovine milk fat contains 8–14% myristic acid (14:0), and in human milk, myristic acid averages 8.6% of milk fat. As stated above, myristic acid is one of the major saturated fatty acids that have been associated with an increased risk of CAD, and human epidemiologic studies have shown that myristic acid and lauric acid are the saturated fatty acids most strongly related to average serum cholesterol concentrations. However, in healthy subjects, although myristic acid is hypercholesterolemic, it increased both LDL- and HDL-cholesterol concentrations compared with oleic acid (68).

 

Palmitic acid

Palmitic acid (16:0) is present in human and bovine milk at 22.6% and 26.3% of milk fat, respectively. Palmitic acid in triacylglycerols in human milk is predominantly esterified in the sn-2 position of the molecule. Feeding human infants a formula containing triacylglycerols similar to those in human milk (16% palmitic acid esterified predominantly in the sn-2 position) has significant effects on fatty acid intestinal absorption (91, 92). Myristic, palmitic, and stearic acids are better absorbed from human-like milk than from standard formula, without a change in total fat fecal excretion. Mineral balance is improved in comparison with a conventional formula, as shown by lower fecal calcium excretion, higher urinary calcium, and lower urinary phosphate. The specific distribution of the fatty acids in the triacylglycerol is known to play a key role in lipid digestion and absorption. Because pancreatic lipase selectively hydrolyzes triacylglycerols at the sn-1 and sn-3 positions, free fatty acids and 2-monoacylglyceriols are produced. Free palmitic acid, but not 2-monopalmitin (which is efficiently absorbed), may be lost as a calcium-fatty acid soap in the feces. A comparison between the effects of dietary laurate-myristate and the effects of palmitic acid in normolipemic humans showed that palmitic acid lowers serum cholesterol (93). In humans, replacement of dietary laurate-myristate with palmitate-oleate has a beneficial effect on an important index of thrombogenesis, ie, the ratio of thromboxane to prostacyclin in plasma (94).

 

Stearic acid

Dietary stearic acid (18:0) is derived primarily from bovine meat and dairy products. Stearic acid is present in human and bovine milk at 7.7% and 13.2% of milk fat, respectively. In relation to the question of their effects on serum cholesterol, stearic acid and saturated fatty acids with <12 carbon atoms are thought not to increase cholesterol concentrations (95). Dietary stearic acid decreases plasma and liver cholesterol concentrations by reducing intestinal cholesterol absorption. Recent data from studies with hamsters, which have a lipoprotein cholesterol response to dietary saturated fat that is similar to that of humans, suggest that reduced cholesterol absorption by dietary stearic acid is due, at least in part, to reduced cholesterol solubility and further suggest that stearic acid may alter the microflora populations that synthesize secondary bile acids (96).

 

The absorption of stearic acid from triacylglycerols containing only oleate and stearate depends on the position of esterification. 2-Monstearin is well absorbed if the stearic acid is esterified at the sn-2 position of the triacylglycerol. If the triacylglycerol is esterified at the sn-1 or the sn-3 position, it is released as free stearic acid, and in the presence of calcium and magnesium, it is poorly absorbed (97). In a study of the effects of dietary fat on serum lipid and lipoporoteion concentrations, the absorption of dietary oleic acid, palmitic acid, and stearic acid was similar, which indicates that differential effects of these fatty acids on plasma lipoprotein cholesterol are not due to differential absorption (98). Another study in humans also indicated that, even though stearic acid appears to have different metabolic effects with respect to its effect on the risk of cardiovascular disease than do other saturated fatty acids (95), reduced stearic acid absorption does not appear to be responsible for the differences in plasma lipoprotein responses (99).

 

Compared with consumption of dietary palmitic acid, consumption of dietary stearic acid (19 g/d) for 4 wk by healthy males produced beneficial effects on thrombogenic and atherogenic risk factors (100). Mean platelet volume, coagulation factor VII activity, and plasma lipid concentrations decreased significantly with consumption of the stearic acid diet, whereas platelet aggregation increased significantly with consumption of the palmitic acid diet. A subsequent study showed no alteration in plasma lipids, platelet aggregation, or platelet activation in short-term (3 wk) feeding trials when stearic acid and palmitic acid were provided in commercially available foods (101). An interesting finding in a study of the association between the composition of serum free fatty acids and the risk of a first myocardial infarction was that the percentage content of both very-long-chain n–3 fatty acids and stearic acid is inversely associated with the risk of myocardial infarction. The investigators speculated that the very-long-chain n–3 fatty acids might reflect diet but also that these 2 free fatty acids might in some way be related to the pathogenetic process and not just reflect their content in adipose tissue (102).

 

EFFECTS OF SATURATED FATTY ACIDS ON LIPOPROTEIN CHOLESTEROL

 

A causal relation between total and LDL cholesterol in blood and CAD has long been accepted. However, despite the strength of the relation between circulating concentrations of LDL cholesterol and heart disease, one should not assume that the relation between saturated fatty acid intake and heart disease is equally strong. Recommendations to decrease the intake of saturated and trans unsaturated fat and cholesterol have as a goal the prevention of CAD. However, in the Framingham study, 80% of the subjects who went on to have CAD had the same total cholesterol concentrations as those who did not (103). The metabolic contributor to coronary disease is the atherogenic lipoprotein profile, and there has been widespread use of a coronary risk lipid profile that uses the ratio of total to HDL cholesterol and the ratio of LDL to HDL cholesterol for predicting the risk of vascular disease. Abnormal lipid and lipoprotein cholesterol concentrations are an LDL-cholesterol concentration ≥ 4.1 mmol/L, an HDL-cholesterol concentration < 1.0 mmol/L, a triacylglycerol concentration ≥ 1.7 mmol/L, and a lipoprotein(a) concentration ≥ 3 g/L (104). It has been pointed out that assessment of the effects of diet on CAD should include consideration of the concomitant changes in both HDL and triacylglycerols (105).

 

Considerable evidence indicates that dietary saturated fats support the enhancement of HDL metabolism. In a study of the effects of reduced dietary intakes of total and saturated fat on HDL subpopulations in a group of multiracial, young and elderly men and women, subjects consumed each of the following 3 diets for 8 wk: an average American diet (34.3% of energy from total fat and 15.0% of energy from saturated fat), the American Heart Association Step I diet (28.6% of energy from total fat and 9.0% of energy from saturated fat), and a diet low in saturated fat (25.3% of energy from total fat and 6.1% of energy from saturated fat) (25). HDL2-cholesterol concentrations decreased in a stepwise fashion after the reduction of total and saturated fat. A reduction in dietary total and saturated fat decreased both large (HDL2 and HDL2b) and small, dense HDL subpopulations, although the decreases in HDL2 and HDL2b were most pronounced. Serum triacylglycerol concentrations were negatively correlated with changes in HDL2 and HDL2b cholesterol. In children fed a diet in which total fat was substituted with carbohydrate but in which total energy was held constant, total fat and saturated fat were positively associated with total cholesterol and HDL cholesterol (106). Perhaps it is ironic that diets enriched in saturated fat and cholesterol increase LDL-cholesterol concentrations but also increase HDL-cholesterol concentrations. The lack of a scientific, mechanistic understanding of these relations should be a warning that population-wide recommendations for all persons at all ages and circumstances to reduce their intake of saturated fats may be premature. For persons with low LDL and low HDL, is a recommendation to decrease saturated fatty acid intake to the maximum extent possible warranted?

 

The consumption by humans of a diet low in total fat, saturated fat, and cholesterol (National Cholesterol Education Program Step II diet) decreases both HDL-cholesterol and apo A-I concentrations, which parallels reductions in apo A-I secretion rate (11). An important finding is that persons differ in their response to dietary fat (12). We must recognize not only that individual responses to types of dietary fat vary but also that different fats have markedly different effects on serum lipids and lipoprotein concentrations. Evidence indicates that postprandial triacylglycerol-rich lipoproteins are related to atherogenic risk; however, few investigations of the effects of individual saturated fatty acids on plasma lipoproteins have been conducted. An investigation of the effect of stearic acid and myristic acid on postpranidal and 24-h fasting plasma lipoprotein triacylglycerol and cholesterol concentrations showed that fasting HDL cholesterol was affected within 24 h in healthy young men. HDL-cholesterol concentrations were higher after subjects consumed myristic acid than after they consumed stearic acid. Dietary myristic acid also caused a greater increase in postprandial HDL triacylglycerol than did dietary stearic acid (107). On the basis of the hypothesis that hypertriacylglycerolemia may represent a procoagulant state involving disturbances to the hemostatic system, the effects of individual dietary fatty acids (1 g/kg body wt; 43% from the test fatty acid) on the promotion of factor VII activation were tested (108). The test diets were rich in either stearic acid, palmitic acid, palmitic acid plus myristic acid, oleic acid, trans 18:1, or linoleic acid, and the postprandial lipid and hemostatic profiles were measured in young men 2, 4, 6, and 8 h after consumption of the diets. Although all of the diets increased factor VII activation, saturated fatty acids—especially stearic acid—resulted in less of an increase than did the unsaturated fatty acid diets that were tested.

 

The effects of fatty acids in the diet were examined in another study comparing women who consumed a high-saturated fatty acid diet with those who consumed a diet low in total fat or a diet with a high content of monounsaturated fatty acids and PUFAs (109). This study showed that total and LDL cholesterol and apo B were lowest in the women who consumed the diet high in unsaturated fatty acids. HDL-cholesterol and apo A-I concentrations in the women who consumed the diet high in saturated fatty acids were 15% and 11% higher, respectively, than those in the women who consumed the diet low in saturated fatty acids but were lower than those in the women who consumed the diet with high unsaturated fatty acids. The investigators concluded that to influence the ratio of LDL to HDL cholesterol, changing the proportions of dietary fatty acids may be more important than limiting the percentage of energy from total or saturated fat, at least when the diets contain high amounts of fats derived mainly from lauric and myristic acids, both of which increase HDL cholesterol.

 

A review was made of 27 controlled studies of the effect of carbohydrate and fatty acid intake on serum lipid and lipoprotein concentrations. When data were analyzed by using multiple regression analysis with isocaloric exchanges of saturated, monounsaturated, and polyunsaturated fatty acids for carbohydrates as the independent variables, all fatty acids elevated HDL cholesterol when they were substituted for carbohydrates, but the effect diminished with increasing unsaturation of the fatty acids (110). A recent meta-analysis of 60 controlled trials of the effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins found that lauric acid greatly increases total cholesterol, but the effect is to decrease the ratio of total to HDL cholesterol. Myristic acid and palmitic acid have little effect on the ratio, whereas stearic acid reduces the ratio slightly (111). Another study (112) showed that plasma phospholipid stearic acid concentrations are strongly positively correlated with plasma total cholesterol, LDL-cholesterol, and triacylglycerol concentrations regardless of the intake of saturated fat (vegan, moderate meat intake, and high meat intake). The author suggested that a reduction in total saturated fatty acid intake would be more appropriate than replacement of other saturated fatty acids with stearic acid, as suggested by the investigators in a study cited above (100). Because the effects of individual fatty acids on the ratio of total to HDL cholesterol may be different from their effects on LDL, these biomarkers may not directly reflect the risk of CAD.

 

Although elevated LDL cholesterol is associated with the endpoints of atherosclerotic disease, including heart disease and stroke, this association should not be extrapolated to suggest that there are equally compelling associations between plasma lipoproteins and other phenotypic outcomes. Lipoproteins in plasma are not a simple artifact of a modern Western diet. Lipoproteins play a wide variety of physiologic and pathophysiologic functions, and the multiple roles of lipoproteins in mediating the response to infectious and toxic agents are only now being recognized. Plasma HDL-cholesterol concentrations were recently associated with protection against the risk of infections (113). Acute infections in children seem to be accompanied by enhanced oxidative modification of LDL and by a decrease in HDL cholesterol (114), and circulating HDL protects against endotoxin toxicity (114, 115; for review see reference 116).

 

Lipopolysaccharide (LPS) is the major glycolipid component of the outer membranes of gram-negative bacteria. This endotoxin, which is responsible for pathophysiologic symptoms characteristic of infection, is associated with plasma lipoproteins, which suggests that sequestering of LPS by lipid particles may form an integral part of a humoral detoxification mechanism. The binding of LPS to lipoproteins is highly specific under simulated physiologic conditions, and HDL has the highest binding capacity for LPS (117, 118). Although lipoprotein-binding protein circulates in association with LDL and VLDL in healthy persons (119), chylomicrons, which carry lipids from the intestines into other body tissues, exceed other lipoproteins in LPS-inactivating capacity (120). Thus, lipoprotein-binding protein-lipoprotein complexes may be part of a local defense mechanism of the intestine against translocated bacterial toxin. Because saturated fats enhance HDL concentrations, saturated fats are potentially important in protecting against bacterial LPS toxicity.

 

 

 

Link til hele greia finner du her:Den gir et fint innblikk i historie rundt mettet fett, kontroverser og utdyper enda mer med en konklusjon.

 

 

[discostu]

Når man er inne på temaet transfett. Finnes det noen oversikt over matvarer som inneholder transfett? Burde vært bannlyst å selge mat i norge med transfett imo.

[storken]

Når man er inne på temaet transfett. Finnes det noen oversikt over matvarer som inneholder transfett? Burde vært bannlyst å selge mat i norge med transfett imo.

 

Dårlig med det. Den danske og sveitsiske regjeringen har bannlyst salg av prosseserte matvarer med trans-fett.

 

 

Selv har jeg gjort disse endringene:

Smør >Olivenolje > Margarin (hydrolyserte vetegabilske oljer + vann)

Kuttet ut kjeks og hyllevarer med kjempelang holdbarhetsdato.

 

Så det er sagt: det er forskjellige typer trans fett også. Du hører ofte om transfett i sammenheng med kjøtt og melk, men disse har faktisk positive virkninger i kroppen. Typen du finner i animalske kilder går under "CLA", søk det opp - så fins det masse stoff rundt det.

 

Jeg kunne snakka meg ekstremt bort her, men jeg liker å teste ut ting på meg selv før jeg bjeffer om det. Nå var jeg til blodprøve hos legen på mandag, venter bare på svaret fra den nå. Er litt spent på hvordan den kommer tilbake hva blodverdier angår Skal sies at blodtrykket mitt lå på 51/139, noe som må karakteriseres som utenfor normalen, men pappa har også så lavt blodtrykk.

 

 

 

[AndyPanda]

Hva er det dere ser etter når dere ser etter godt/ bra innhold i proteinpulver?

 

1. At råvaren er isolater, ikke konsentrat (google litt hvis du ikke vet forskjellen)

2. At proteininnholdet er høyt (over 80 %)

3. At fett- og karbohydratinnholdet er lavt

 

I tillegg pleier jeg å se litt på fordelingen av myse(whey) og kasein, siden jeg foretrekker litt blanda pulver, gjerne 50/50.

 

Så for deg er denne helt perfekt? http://www.norkost.n...ver_3000g/P_186

 

Det er noe som er aktuelt ja. Og som sagt så vurderer jeg å kjøpe den når jeg går tom for det jeg har nå. Nå har jo kvaliteten på selve råvaren også litt å si, men jeg tror ikke den der er så mye værre enn de av absolutt ypperste kvalitet. Det holder for min del hvertfall

[geil]

Jeg kunne snakka meg ekstremt bort her, men jeg liker å teste ut ting på meg selv før jeg bjeffer om det. Nå var jeg til blodprøve hos legen på mandag, venter bare på svaret fra den nå. Er litt spent på hvordan den kommer tilbake hva blodverdier angår Skal sies at blodtrykket mitt lå på 51/139, noe som må karakteriseres som utenfor normalen, men pappa har også så lavt blodtrykk.

 

Medfører det noen problemer for deg ifm trening? Har forholdsvist lavt blodtrykk selv - 110/60, hvilepuls på 37 ved sist måling. Blir veldig fort svimmel om jeg reiser meg raskt i perioder med mye trening, men merker ingen konsekvenser ellers.

[Thor - God Of Thunder]

AKTIV STATUS på myrevolution!

 

hehe, måtte bare. Fekk forresten symja 900m i dag!

(update i trenings-loggen)

[discostu]

Aktiv status?

[Thor - God Of Thunder]

= gratis frakt på det eg måtte ynskje

 

Om eg ska gå for fettklype, er denne å anbefale?

http://myrevolution.no/nettbutikk/slim-guide

Endret 10. mars 2011 av Ondskap