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#1 |
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Homocysteine is a moderate and independent risk factor of heart disease. In
a new study high intake of saturated fatty acids was associated with higher plasma homocysteine. Fish oils were associated with reduced levels. ------------------------------------------------------------------------------------------------- Dietary fat and plasma total homocysteine concentrations in 2 adult age groups: the Hordaland Homocysteine Study Paula Berstad, Svetlana V Konstantinova, Helga Refsum, Eha Nurk, Stein Emil Vollset, Grethe S Tell, Per M Ueland, Christian A Drevon and Giske Ursin Background: The intake of n-3 (formerly called omega-3) fatty acids (FAs) may be inversely associated with plasma total homocysteine (tHcy) concentrations, but the epidemiologic data are sparse. Objective: We examined the association between dietary fat and tHcy in a Norwegian population. Design: A cross-sectional, population-based study of 5917 subjects in 2 age groups (47-49 and 71-74 y old) was conducted with the use of food-frequency questionnaires and measurement of plasma tHcy concentrations. Results: The intake of saturated FAs (SFAs) was positively and significantly (P for trend < 0.001) associated with tHcy concentrations; the difference in plasma tHcy concentrations between the highest and lowest quartiles of SFAs was 8.8%. The intake of marine very-long-chain n-3 FAs was inversely associated with tHcy concentrations; the difference in plasma tHcy concentrations between the lowest and the highest quartiles was -5.0% (P for trend < 0.001). Intakes of total and monounsaturated fat also were positively associated with plasma tHcy concentrations (P for trend < 0.001 and < 0.005, respectively), whereas the intake of polyunsaturated fat was positively associated with tHcy concentrations only in the younger subjects (P for trend = 0.03). The associations were weakened by additional adjustment for B vitamin intake but remained significant for SFA intake (P < 0.001). When stratified for total B vitamin intake, the inverse association between tHcy concentrations and very-long-chain n-3 FAs was significant only in the highest quartile of B vitamin intake (P for trend = 0.001), regardless of supplement use. Conclusions: High intakes of SFAs are associated with high plasma concentrations of tHcy. The inverse association between dietary intakes of very-long-chain n-3 FAs and plasma tHcy concentrations is apparent only at high B vitamin intakes. http://www.ajcn.org/cgi/content/abstract/85/6/1598 -- Juhana |
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#2 |
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Juhana Harju wrote: > Homocysteine is a moderate and independent risk factor of heart disease. No, it isn't. Susan |
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#3 |
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Juhana Harju wrote: No link has ever stood up to further scrutiny. Lowering homocysteine resulted in increased mortality. Clearly, whatever it's a marker for, it isn't causal itself. Susan |
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#4 |
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Susan wrote:
> Juhana Harju wrote: > > Lowering homocysteine resulted in increased mortality. Not always, and now the question was not about lowering it by supplements. The orginal posting was about having a diet lower in saturated fats and higher in long-chain omega-3 fatty acids. That is a completely different thing. > Clearly, whatever it's a marker for, it isn't causal itself. I did not say anything about causality. -- Juhana |
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#5 |
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Juhana Harju wrote: > Susan wrote: > >> Juhana Harju wrote: >> >> Lowering homocysteine resulted in increased mortality. > > > Not always, and now the question was not about lowering it by > supplements. The orginal posting was about having a diet lower in > saturated fats and higher in long-chain omega-3 fatty acids. That is a > completely different thing. > >> Clearly, whatever it's a marker for, it isn't causal itself. > > > I did not say anything about causality. > Such studies are useless wrt saturated fats unless they control for grass fed vs. feedlot animal products. Susan |
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#6 |
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Susan wrote:
> Juhana Harju wrote: >> Susan wrote: >>> Juhana Harju wrote: >>> >>> Lowering homocysteine resulted in increased mortality. >> >> Not always, and now the question was not about lowering it by >> supplements. The orginal posting was about having a diet lower in >> saturated fats and higher in long-chain omega-3 fatty acids. That is >> a completely different thing. >> >>> Clearly, whatever it's a marker for, it isn't causal itself. >> >> I did not say anything about causality. > > Such studies are useless wrt saturated fats unless they control for > grass fed vs. feedlot animal products. That is just a way to evade the topic. -- Juhana |
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#7 |
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Juhana Harju wrote: > That is just a way to evade the topic. > It IS the topic. There is no good evidence for any increased health risks from saturated fats. Further, the fat profiles from grass fed meat and dairy is extremely heart healthy, much more so than that from feedlot beef. All we have so far is research on feedlot animal fat which is much less healthy, and still, it's what you eat with the fat, not the fat that has been proven to cause the risks. Susan |
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#8 |
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It's not the SFAs, except in terms of "associations," "links," or
"correlations." If SFAs were so bad, where is all the "associated" disease amongst those who consume SFA-rich, but PUFA-poor diets? They are studying SFAs in the context of typical Western diets, where people don't eat much coconut, but do eat plenty of meat. There is no biochemical connection between homocysteine and SFAs. The reason they don't understand is because they are not isolating the various molecules and determining which are dangerous. More insightful researchers have demonstrated that a PUFA-rich diet and the HCAs generated in cooked meat are a very dangerous combination. To see these kinds of studies, go to my free site and read the essay about saturated fatty acids being the solution, not the problem: http://groups.msn.com/TheScientificDebateForum- |
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#9 |
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On Jul 5, 4:50 pm, Susan <neverm...@nomail.com> wrote:
> x-no-archive: yes > > Juhana Harju wrote: > > That is just a way to evade the topic. > There is no good evidence for any increased health risks from saturated > fats. There's plenty of evidence. > Further, the fat profiles from grass fed meat and dairy is extremely > heart healthy, much more so than that from feedlot beef. http://www.csuchico.edu/agr/grassfe...fits/index.html shows that it's better, but not extremely better. The reason its better is because of increased omega 3 fatty acid content. > All we have so far is research on feedlot animal fat which is much less > healthy, and still, it's what you eat with the fat, not the fat that has > been proven to cause the risks. What nutrition component do you think can lead to CVD? -- Ron |
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#10 |
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Ron Peterson wrote: > http://www.csuchico.edu/agr/grassfe...fits/index.html > shows that it's better, but not extremely better. The reason its > better is because of increased omega 3 fatty acid content. That's not the only reason. It's also has higher CLA and lower arachidonic acid. > > >>All we have so far is research on feedlot animal fat which is much less >>healthy, and still, it's what you eat with the fat, not the fat that has >>been proven to cause the risks. > > > What nutrition component do you think can lead to CVD? High glycemic load; starch and sugar and the resultant oxidative stress. Susan |
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#11 |
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Susan wrote:
> Juhana Harju wrote: > >> That is just a way to evade the topic. > > It IS the topic. > > There is no good evidence for any increased health risks from > saturated fats. I just provided some further evidence by posting two studies but you are evading the subject because you are denying that which is evident. However, I completely understand the reasons you are so evasive. Because of your health reasons you are a low-carber who is favouring animal fats, saturated fats among them. So you have hard time when you see any contrary evidence. You should notice that I am not denying the obvious health benefits of low-carbing in achieving better glycemic control. But the subject is different now. -- Juhana |
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#12 |
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In 2000 I had my blood lipids checked. For a several of days prior
I had been eating raw coconut. My HDL was 70 and the Doc said even though my total cholesterol was ~ 230 my blood lipids were excellent. The next time I was tested the HDL was down to 38 and I had been eating somewhat more conventionally. Granted at the time I was very stressed so there were other factors. I also have suspect heated polyunsaturated fats are worse than the same fats if unheated. For example a raw sesame or sunflower seed versus sesame oil or sunflower oil. Butter is thought of as saturated but it tends to go rancid rather rapidly. Certainly frying with butter, would be a way to up one's toxic oxysterol exposure. I've tried coconut oil for cooking and wasn't overly impressed. It seems to disappear into the food more than other fats. I keep aiming to cook a pie and try it in the crust, it would have to be better than hydrogenated lard. On Jul 5, 3:26 pm, monty1...@lycos.com wrote: > It's not the SFAs, except in terms of "associations," "links," or > "correlations." If SFAs were so bad, where is all the "associated" > disease amongst those who consume SFA-rich, but PUFA-poor diets? They > are studying SFAs in the context of typical Western diets, where > people don't eat much coconut, but do eat plenty of meat. There is no > biochemical connection between homocysteine and SFAs. The reason they > don't understand is because they are not isolating the various > molecules and determining which are dangerous. More insightful > researchers have demonstrated that a PUFA-rich diet and the HCAs > generated in cooked meat are a very dangerous combination. To see > these kinds of studies, go to my free site and read the essay about > saturated fatty acids being the solution, not the problem: > > http://groups.msn.com/TheScientificDebateForum- |
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#13 |
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Yes, it is.
Now that is my equally rich response :-) On Jul 5, 11:18 am, Susan <neverm...@nomail.com> wrote: > x-no-archive: yes > > Juhana Harju wrote: > > Homocysteine is a moderate and independent risk factor of heart disease. > > No, it isn't. > > Susan |
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#14 |
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I see that as an unwarrented conclusion for the bulk of the population. Most people will be eating feed lot animals and their fat whatever it is seems less than optimal. On Jul 5, 2:10 pm, Susan <neverm...@nomail.com> wrote: > x-no-archive: yes > > > > Juhana Harju wrote: > > Susan wrote: > > >> Juhana Harju wrote: > > >> Lowering homocysteine resulted in increased mortality. > > > Not always, and now the question was not about lowering it by > > supplements. The orginal posting was about having a diet lower in > > saturated fats and higher in long-chain omega-3 fatty acids. That is a > > completely different thing. > > >> Clearly, whatever it's a marker for, it isn't causal itself. > > > I did not say anything about causality. > > Such studies are useless wrt saturated fats unless they control for > grass fed vs. feedlot animal products. > > Susan |
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#15 |
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x-no-archive: yes
betaine_hcl@yahoo.com wrote: > I see that as an unwarrented conclusion for the bulk of the > population. > Most people will be eating feed lot animals and their fat whatever it > is > seems less than optimal. So what? That doesn't suggest that saturated fat is bad. only that feedlot animal foods are bad. Susan |