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| | From: taka00381 (Original Message) | Sent: 4/8/2008 4:01 PM |
An interesting study posted on the other group where most of the pro-omega-3 crowd is wondering how it is possible that mice on Omega-3 rich oil diet live shorter than on an Omega-6 rich oil diet. Too bad that these kinds of studies don't include a saturated fat or Omega-9 control diet:
J Nutr. 2000 Feb;130(2):221-7.
Serum lipid concentrations and mean life span are modulated by dietary polyunsaturated fatty acids in the senescence-accelerated mouse.
Umezawa M, Takeda T, Kogishi K, Higuchi K, Matushita T, Wang J, Chiba T, Hosokawa M.
Department of Nutrition, Koshien University, Hyogo, Japan.
The senescence-accelerated mouse (SAMP8) is an animal model used in studies of aging. This study was undertaken to investigate the effects of dietary PUFA on longevity (Experiment 1) and serum lipid concentrations (Experiment 2) in SAMP8 mice. Male mice were fed either an (n-3) PUFA-rich (9 g/100 g perilla oil) or an (n-6) PUFA-rich (9 g/100 g safflower oil) diet beginning at 6 wk of age. Experiment 1: The groups did not differ in body weight gain, but those fed perilla oil had significantly lower scores of senescence relative to those fed safflower oil (P<0.05). The mean life span of mice fed perilla oil was 357+/-21 d and of those fed safflower oil, 426+/-24 d (P<0.05). Pathological studies revealed that the incidence of tumors was significantly lower in the perilla oil group than in the safflower oil group (P<0.05). Approximately half the mice fed perilla oil had died after 10 mo, and the direct causes closely connected with death could not be specified. Experiment 2: The serum total cholesterol, HDL cholesterol, triglyceride and phospholipid concentrations were significantly lower in the perilla oil group than in the safflower oil group (P<0.01). A marked decrease of serum HDL cholesterol and apolipoprotein A-II (ApoA-II)concentrations in advanced age were observed in the mice fed perilla oil (P<0.01). Ten-month-old mice fed perilla oil had a significantly greater ratio of apolipoprotein A-I(ApoA-I) to ApoA-II than those fed safflower oil. Separation of HDL subfractions revealed that the smaller HDL species were much more abundant than the larger HDL species in both dietary oil groups. These findings suggest that dietary (n-3) and (n-6) PUFA differ in their effects on serum lipid metabolism which may modulate the mean life span of SAMP8 mice fed each dietary oil. PMID: 10720173 |
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Hans, I was wondering if you could interpret the results of Experiment 2. Ive just recently been learning about biochem and have no idea what the second experiment is telling me.
-Drew |
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Well, it's all about "markers," which are contextual, so it really doesn't mean much to you or me specifically. I suggest you read the essays on this site, along with the posts in the forums that interest you, and then ask questions you may have at that point. It's very easy to "drive yourself crazy" if you fixate on one study or a small number of them. Instead, they key is to keep an open mind and gradually "fill in the blanks" in your understanding. If you "get stuck," you can ask me questions at that point. You will learn a lot more by struggling to conceptualize things, rather than have someone explain some minor point that may be irrelevant or impossible to determine the significance of, given the limited amount of evidence in some areas.
In general, I'll say that many studies today focus on the LDL-lowering effects of this or that substance. This is only relevant in the heart disease context if your cells are loaded with arachidonic acid and your diet/lifestyle is oxidizing. If not, as is the case with myself, you want your LDL to be "high" according to typical standards in the USA. If it is "off the charts" high, that would be an indication that something is wrong, but today marginally "high" means healthy, not unhealthy, especially as you get older (again, if you avoid oxidizing issues). |
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Drew, I'll try to give you the answer I think you're looking for. In Experiment 2, the total cholesterol, HDL, triglycerides, and phospholipids were all low. While total cholesterol and triglycerides need to be kept within a normal range, the HDL cholesterol should be kept on the high side, and LDL cholesterol should be low. HDL is considered "good" cholesterol, and LDL is considered "bad" cholesterol. Here is an explanation of cholesterol: So what this experiment is showing is that the omega 3 group had low HDL, as well as low apolipoprotein A-11. The HDL and apolipoprotein A-11 cholesterol fractions are thought to confer protection from atherosclerosis and heart disease. Therefore it is desirable to keep them on the high side, and LDL and apolipoprotein A-11 fractions at low levels, as they are believed to be responsible for the build up of plaque. For an explanation of the lipoproteins, see this page: Therefore this study would seem to prove that omega 3 fatty acids are delererious to ones coronary health, which is in opposition to all the proponents of omega 3 supplementation. Combine that with the greatly shortened life span, 69 days shorter than the 426 days for the omega 6 group in experiment 1. My comments: While it says that the "direct" cause of death was undetermined, omega 3 fatty acids are highly unstable and oxidize within the body, causing high amounts of free radicals, which hasten cell death, and therefore could be the cause of early death in that group. Also it is a known fact that eskimo tribes who consume high fish diets, die from a higher percentage of strokes than any other group of people, which is likely due to the blood thinning effects of omega 3 fatty acids. |
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