Flaxseed reverses atherosclerotic lesion formation and lowers lipoprotein (a) in ovarianhormone deficiency

January 1, 2013 Human Health and Nutrition Data 0 Comments

Flaxseed reverses atherosclerotic lesion formation and lowers lipoprotein (a) in ovarianhormone deficiency

Year: 2013
Authors: Campbell, S.C. Bakhshalian, N. Sadaat, R.L. Lerner, M.R. Lightfoot, S.A. Brackett, D. Arjmandi, B.H.
Publication Name: J. NA Menopause Soc.
Publication Details: Volume 20; Number 11. PAGE 5.


Objective: The incidence of cardiovascular disease dramatically increases during menopause, and postmenopausal women seek natural alternatives to hormone therapy. Flaxseed can slow the progression of atherosclerotic lesion formation; however, it is not known whether it can reverse formation that has already occurred. Methods: Seventy-two female Golden Syrian hamsters were randomly divided into six groups, shamoperated (sham) or ovariectomized (ovx), and kept on the same diet for 120 days to allow for atherosclerotic lesion development. After this 120-day period, whole flaxseed was introduced to the diets of hamsters in three of the groups: group 1 (sham + casein); group 2 (ovx + casein); group 3 (ovx + 7.5percent flaxseed); group 4 (ovx + 15percentflaxseed); group 5 (ovx + 22.5percent flaxseed); and group 6 (ovx + 17A-estradiol). This diet was maintained for an additional 120 days. Lesion regression was examined histologically, and serum was analyzed for total cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, Apo A, Apo B, and lipoprotein(a).
Results: Results showed that 15percent and 22.5percent flaxseed, compared with ovx animals, significantly reduced lipoprotein(a) (4.4 mg/dL [ovx] vs 2.15 mg/dL [15percent flaxseed] and 0.3 mg/dL [22.5percent flaxseed]; P G 0.05) and Apo B (2.8 mg/dL [ovx] vs 2.4 mg/dL [15percent flaxseed] and 2.5 mg/dL [22.5percent flaxseed]). Flax reduced by 67percent the number of animals with aortic arch lesions. Conclusions: All three doses of flax reduce the severity of lesion formation compared with ovx controls. These results support the efficacy of flaxseed in reducing cardiovascular disease risk. (Authors abstract)
Although hormone therapy (HT) has been shown to improve lipid profile and to relieve symptoms associated with menopause, its cardiovascular benefits have recently been questioned.   Recent studies have shown no benefit  for V or even an increased rate of CVD events among V women receiving HT. In addition, HT may be accompanied by increased risks for endometrial cancer,breast cancer,ovarian cancer,systemic lupus erythematosus, and thromboembolism. The use of cholesterol-lowering pharmacological agents has also been associated with a number of adverse effects or contraindications.   Although flaxseed is known to reduce serum cholesterol in both humans and animal models, including ovariectomized (ovx) hamsters, its antiatherogenicity may be independent of its cholesterol-lowering properties.  Studies examining flaxseed and its ability to prevent atherosclerotic lesion formation have been successful.   In our recent animal trial, we showed that all doses of flaxseed (7.5percent, 15percent, and 22.5percent) decreased aortic fatty streak area to that seen in sham-operated (sham) animals, whereas 17A-estradiol (E2) had a modest effect.  Flaxseed, on average, reduced fatty streak area by 80percent (compared with 60percent with E2); furthermore, lesions in  ovx hamsters were at more advanced stages compared with flaxseed, which inhibited progression. Other findings indicate that postmenopausal women benefit from consuming flaxseed. Our clinical studies showed that flaxseed significantly lowered TC, nonY high-density lipoprotein cholesterol (HDLC), lipoprotein(a) (Lp(a)), and Apo B concentrations without altering HDLC in postmenopausal women.  In addition to clinical studies, the authors have also shown the hypocholesterolemic effects of flaxseed on ovx hamsters, an animal model suitable for studying lipid changes that occur in women after menopause. Other animal investigation yielded results showing that flaxseed is capable of preventing atherosclerotic lesion formation by decreasing fatty streak area and the severity of atheromatous plaques.   Based on these findings, this study was designed to examine whether flaxseed can reverse lesions that have already formed. As such, the hypothesis of this study is that whole flaxseed reverses atherosclerotic lesions and reduces the risk of CVD. The findings confirm that flaxseed is effective in lowering serum Lp(a), Apo B, and TG, as well as reversing atherosclerotic lesion formation, as indicated by the decreased severity of lesions and number of animals with lesions in the heart and aorta. To date, our laboratory’s flaxseed related studies suggest that this functional food is effective in reducing cholesterol in both ovx animal models  and postmenopausal women; decreasing Lp(a), an independent atherogenic factor in ovx animals models (current study) and postmenopausal women; preventing the formation of atherosclerotic lesions in an ovx hamster model of postmenopausal hyperlipidemia; and reversing atherosclerotic lesions in an ovx model of postmenopausal women (current study).
These findings support the efficacy of flaxseed in helping modify CVD-related risk factors in postmenopausal women. Although flaxseed and its components seem to slow atherosclerotic lesion progression, there is a great need for natural products that aid regression because of the large number of individuals seeking treatment of already developed atherosclerosis.
With the similarities between human and animal trials thus far, it is critical to investigate flaxseed’s effect on postmenopausal women with established atherosclerosis. Flaxseed is a safe and efficacious functional food, and this study’s preliminary evidence clearly showing regression of atherosclerotic lesion formation provides a potential valuable treatment option for postmenopausal women. Finally, direct mechanisms by which flaxseed regresses lesion formation should be addressed to understand its pathways of action. (Editors comments)

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