Maintaining Healthy Lipid Profiles When On

Bilter, it seems that one can count on some strategies (from medicines to things like diet, exercise training, fish oil, etc.) that may help to balance blood lipids. We'll see some of them on the following posts.

Drug options:

Dunbar RL, Rader DJ. Current drug options for raising HDL cholesterol. Curr Treat Options Cardiovasc Med. 2005;7(1):15-23.

ABSTRACT

Although circumstantial evidence supports raising high-density lipoprotein cholesterol (HDLC) in patients with low levels of HDLC, the scarcity of event-based trials has led to uncertainty with regard to the benefit of high-density lipoprotein (HDL)-raising therapy. Based on the National Cholesterol Education Program guidelines, therapy for dyslipidemia is focused initially on targeting low-density lipoprotein cholesterol (LDLC), and in patients with hypertriglyceridemia, secondarily on targeting non-HDLC. When HDLC remains low, the decision to target HDLC depends on the assessment of risk of cardiovascular events. We often consider drug therapy specifically to raise HDLC in high-risk patients, such as those with established atherosclerotic vascular disease, type 2 diabetes, or a Framingham risk score of 20% or above. The majority of high-risk patients require drug therapy, usually a statin, to achieve aggressive LDLC and non-HDLC goals, and thus many patients with low HDLC are candidates for statin therapy. However, a second drug is often required to achieve substantial HDL raising. Although no formal goals for HDLC exist, reasonable goals are HDLC greater than 40 mg/dL in men and greater than 50 mg/dL in women. We often add either niacin or a fibrate to a statin in high-risk patients with low HDLC levels. Targeting HDLC with pharmacologic therapy is a more difficult decision in moderate-risk patients, in whom therapy must be highly individualized.

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Ito MK. Advances in the understanding and management of dyslipidemia: using niacin-based therapies. Am J Health Syst Pharm. 2003;60(13 Suppl 2):S15-21; quiz S25.

ABSTRACT

The use of niacin, alone and in combination, for the treatment of dyslipidemia in patients with or at risk for coronary heart disease (CHD), is discussed. Cardiovascular risk is independently predicted not only by high levels of low-density lipoprotein cholesterol (LDL-C), but also low levels of high-density lipoprotein cholesterol (HDL-C) and elevated triglycerides. Moreover, we now understand that LDL particle size and number are associated with differing levels of atherogenicity. Metabolic syndrome, increasingly being recognized as a marker for elevated cardiovascular risk, is associated with atherogenic dyslipidemia characterized by low HDL-C, high triglycerides, and small, dense LDL particles. Controlled clinical studies have shown that niacin therapy effectively increases HDL-C and lowers triglyceride and LDL-C levels while causing a shift toward larger, less atherogenic LDL particles. Niacin, alone or in combination, prevents progression and promotes regression of coronary atherogenic lesions and significantly reduces CHD-related morbidity and mortality. Statin monotherapy causes modest increases in HDL-C and decreases triglycerides, while more potently reducing LDL-C. Combinations of lipid-modifying agents may better address the full spectrum of lipoprotein abnormalities in some patients. Investigations have shown that combining statin therapy with niacin results in additive improvement in the major lipids and lipoproteins and improves clinical outcome. With recently broadened treatment recommendations, it seems likely that combination therapy will be increasingly deemed the appropriate choice for addressing a range of lipid abnormalities.

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Isles CG, Paterson JR. Identifying patients at risk for coronary heart disease: implications from trials of lipid-lowering drug therapy. QJM. 2000;93(9):567-74.

ABSTRACT

Abnormal lipid levels contribute significantly to the risk of coronary heart disease (CHD), which is increased further in the presence of other risk factors. The association between elevated low-density lipoprotein (LDL) cholesterol and CHD risk is well established, and large primary and secondary prevention studies of HMG-CoA reductase inhibitors (statins) have shown conclusively that lowering LDL cholesterol levels reduces CHD events and total mortality. Regardless of the intervention used (diet, surgery, drugs), reduction of plasma cholesterol has consistently produced a reduction in cardiovascular risk. Absolute benefit is greatest in those who are at highest risk initially, and trial results suggest that the lower the LDL cholesterol level achieved, at least down to LDL of 3.0 mmol/l, then the lower is the CHD event risk. Epidemiological data also point to the negative impact of other lipids on CHD risk. Low levels of high-density lipoprotein (HDL) and high levels of triglycerides (particularly in conjunction with an LDL/HDL ratio >5) are particularly strong risk factors for CHD. Thus, although prevention trials to date have primarily assessed the impact of LDL lowering on CHD events, the initial assessment of CHD risk should consider a more detailed atherogenic profile including HDL and triglyceride levels. A general approach to preventing cardiovascular disease should include strategies to reduce the overall CHD risk by lifestyle modification and management of modifiable risk factors such as smoking, hypertension and diabetes. Based on data from recent prevention studies, and because they are the most potent lipid-lowering agents available for lowering LDL cholesterol, statins have appropriately become the drug of choice for most patients with hyperlipidaemia who require drug therapy.

Exercise interventions:

Fahlman MM, Boardley D, Lambert CP, Flynn MG. Effects of endurance training and resistance training on plasma lipoprotein profiles in elderly women. J Gerontol A Biol Sci Med Sci. 2002;57(2):B54-60.

ABSTRACT

It has been shown that high levels of high-density lipoprotein (HDL) cholesterol and low levels of low-density lipoprotein (LDL) cholesterol are associated with health maintenance in older women, but the few studies that have examined the relationship between exercise and plasma lipoprotein levels in this elderly population have been equivocal. In addition, there are no studies that examine the plasma lipoprotein response of two different types of exercise in a group of active but nonexercising women. Thus, the effects of exercise training on plasma lipoprotein levels in elderly women remain unclear. The purpose of this research was to examine the effects of endurance and resistance exercise on plasma lipoprotein levels in elderly women who were active but nonexercising prior to the study. A total of 45 healthy, active women, aged 70-87 years, were randomly assigned to either an aerobic training (AT, 76 +/- 5 years, n = 15), resistance training (RT, 73 +/- 3 years, n = 15), or control (C, 74 +/- 5 years, n = 15) group. The AT group walked 3 days a week at 70% heart rate reserve. The duration on day 1 was 20 minutes, and it was increased by 5 minutes each day until subjects were walking for 50 minutes (week 3). The exercise training session for the RT group consisted of one to three sets of eight repetitions of eight different exercises at an eight repetition maximum; the C group maintained normal activity. Weight and diet were unchanged across groups. The exercise interventions lasted 10 weeks. Blood samples were obtained from all subjects at week 0 and week 11. Training resulted in a significant decrease in 1-mile walk times and heart rate at completion of the walk for the AT group and a significant increase in eight repetition maximum of all RT exercises. Both AT and RT groups experienced increased HDL cholesterol and decreased triglycerides at week 11 compared with week 0. There were no positive changes in control lipoproteins. Both triglycerides and the total cholesterol to HDL ratio increased significantly while total cholesterol, HDL cholesterol, and LDL cholesterol remained unchanged. The RT group also had significantly lower LDL cholesterol and total cholesterol compared with controls at week 11. Both RT and endurance training resulted in favorable changes to plasma lipoprotein levels for elderly women in only 10 weeks. The fact that this occurred without concurrent changes in weight or diet is an indication that high-intensity exercise alone can be used to modify lipoproteins in populations of healthy elderly women.

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Sgouraki E, Tsopanakis A, Tsopanakis C. Acute exercise: response of HDL-C, LDL-C lipoproteins and HDL-C subfractions levels in selected sport disciplines. J Sports Med Phys Fitness. 2001;41(3):386-91.

ABSTRACT

BACKGROUND: High HDL levels has been shown to be associated with high endurance capacity. The acute effects of maximal endurance exercise (of short duration) (15 min) on low density lipoproteins-cholesterol (LDL-C), high density lipoproteins - cholesterol (HDL-C) and HDL subfractions HDL2 and HDL3 were examined, in order to determine whether the magnitude of response can be affected by maximal intensity of exercise (incremental stress test). METHODS: Male athletes (n=78) of national level, from four sport disciplines, volunteered to participate in this cross-sectional study; basketball (n=10), swimming (n=9), long distance (LD) running (n=23) and wrestling (n=35); also a group of non athletes as controls (n=19). Participants trained at least 2 hrs/day for more than 3 years; they were healthy, non-smokers and fasted 12 hrs before blood sampling. The ergometric test was a test for the estimation of maximal oxygen uptake on a treadmill ergometer based on a stepwise stress protocol. RESULTS: Immediately after a maximal effort all groups (controls included) showed significant HDL-C increases (p<0.001) from rest values, while LD running showed the highest values. HDL2 levels increased in LD running (p<0.001), basketball and wrestling, while HDL3 ones in all groups and controls (p<0.001). The HDL2 of all athletes showed the highest correlation (R=0.37**, p<0.01) with VO2max, even higher than HDL itself. CONCLUSIONS: Acute maximal endurance exercise (100 percent VO2max) may induce acute modifications and intermolecular redistribution of HDL-C and subfractions. It is possible that the increased flux of lipids to HDL-C molecule may result from the regulatory action of lipoprotein lipase (LPL).

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Couillard C, Despres JP, Lamarche B, Bergeron J, Gagnon J, Leon AS, Rao DC, Skinner JS, Wilmore JH, Bouchard C. Effects of endurance exercise training on plasma HDL cholesterol levels depend on levels of triglycerides: evidence from men of the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study. Arterioscler Thromb Vasc Biol. 2001;21(7):1226-32.

ABSTRACT

High density lipoprotein (HDL) cholesterol concentrations have been shown to increase with regular endurance exercise and, therefore, can contribute to a lower risk of coronary heart disease in physically active individuals compared with sedentary subjects. Although low HDL cholesterol levels are frequently observed in combination with hypertriglyceridemia, some individuals may be characterized by isolated hypoalphalipoproteinemia, ie, low HDL cholesterol levels in the absence of elevated triglyceride (TG) concentrations. The present study compared the responses of numerous lipoprotein-lipid variables to a 20-week endurance exercise training program in men categorized on the basis of baseline TG and HDL cholesterol concentrations: (1) low TG and high HDL cholesterol (normolipidemia), (2) low TG and low HDL cholesterol (isolated low HDL cholesterol), (3) high TG and high HDL cholesterol (isolated high TGs), and (4) high TGs and low HDL cholesterol (high TG/low HDL cholesterol). A series of physical and metabolic variables was measured before and after the training program in a sample of 200 men enrolled in the Health, Risk Factors, Exercise Training and Genetics (HERITAGE) Family Study. At baseline, men with high TG/low HDL cholesterol had more visceral adipose tissue than did men with isolated low HDL cholesterol and men with normolipidemia. The 0.4% (not significant) exercise-induced increase in HDL cholesterol levels in men with isolated low HDL cholesterol suggests that they did not benefit from the "HDL-raising" effect of exercise. In contrast, men with high TG/low HDL cholesterol showed a significant increase in HDL cholesterol levels (4.9%, P<0.005). Whereas both subgroups of men with elevated TG levels showed reductions in plasma TGs (approximately -15.0%, P<0.005), only those with high TG/low HDL cholesterol showed significantly reduced apolipoprotein B levels at the end of the study (-6.0%, P<0.005). Multiple regression analyses revealed that the exercise-induced change in abdominal subcutaneous adipose tissue (10.6%, P<0.01) was the only significant correlate of the increase in plasma HDL cholesterol with training in men with high TG/low HDL cholesterol. Results of the present study suggest that regular endurance exercise training may be particularly helpful in men with low HDL cholesterol, elevated TGs, and abdominal obesity.

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Olchawa B, Kingwell BA, Hoang A, Schneider L, Miyazaki O, Nestel P, Sviridov D. Physical fitness and reverse cholesterol transport. Arterioscler Thromb Vasc Biol. 2004;24(6):1087-91.

ABSTRACT

BACKGROUND: Physical exercise is associated with a decreased risk of cardiovascular disease, which may be partly caused by the effect of exercise on the lipoprotein profile. The most consistent effect of exercise on lipoprotein metabolism is an increase in high-density lipoprotein (HDL). METHODS AND RESULTS: Parameters of reverse cholesterol transport (RCT) in 25 endurance-trained male athletes were compared with 33 age-matched males enjoying an active lifestyle. VO2max was higher in athletes than in controls (53.4+/-1.2 versus 38.8+/-1.0 mL/min per kg; P<0.01). The following differences in parameters of RCT were found: (1) plasma HDL cholesterol and apoA-I levels were higher in athletes compared with controls (1.7+/-0.1 versus 1.4+/-0.1 mmol/L; P<0.001; and 145+/-2 versus 128+/-3 mg/dL; P<0.001, respectively). Both correlated with VO2max up to the value of 51 mL/min per kg; (2) prebeta1-HDL was higher in athletes than in controls (54+/-4 versus 37+/-3 microg/mL; P<0.001) and correlated positively with VO2max; (3) lecithin cholesterol: acyltransferase activity was higher in athletes (29.8+/-1.2 versus 24.2+/-1.4 nmol/microL per hour; P<0.005); and (4) the capacity of plasma to promote cholesterol efflux from macrophages was higher in athletes (18.8%+/-0.8% versus 16.2%+/-0.3%; P<0.03). CONCLUSIONS: The likely reason for higher HDL concentration in physically fit people is increased formation of HDL from apoA-I and cellular lipids.

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Vuorimaa T, Ahotupa M, Irjala K, Vasankari T. Acute prolonged exercise reduces moderately oxidized LDL in healthy men. Int J Sports Med. 2005;26(6):420-5.

ABSTRACT

We studied the effects of a 2-day walk exercise (6 h+6 h) on the serum concentration of circulating moderately oxidized LDL (LDL baseline conjugated dienes), lipids (total cholesterol, LDL cholesterol, HDL cholesterol, and triglyceride), antioxidants (alpha-tocopherol, gamma-tocopherol, beta-carotene, and ubiquinol-10), and antioxidant potential in serum (S-TRAP) and LDL (LDL-TRAP) in healthy well-trained men. The exercise was performed twice with an interval of 14 days. While 6 h walking the subjects drank 6 cl . kg (-1) water which contained either carbohydrate (CHO trial) or placebo (PLA trial). During the 2-day exercise the level of oxidized LDL decreased by 25 % (p=0.001) in the PLA trial. At the same time serum gamma-tocopherol decreased by 20 % (p=0.049), while the other measured antioxidants remained unchanged and the serum antioxidant potential increased by 22 % (p=0.018). Serum total cholesterol decreased by 3 % (p=0.017), serum triglycerides by 22 % (p=0.001), and LDL-cholesterol by 14 % (p=0.045). HDL cholesterol increased by 9 % (p=0.001). The results in the carbohydrate trial were similar to the ones in the PLA trial. The findings suggest that exercise of long duration but of low, non-exhaustive intensity decreases the concentration of circulating oxidized LDL simultaneously with an increase in serum antioxidant potential in healthy trained men. Carbohydrate ingestion during the exercise does not have any further effect on these changes.

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Thompson PD, Crouse SF, Goodpaster B, Kelley D, Moyna N, Pescatello L. The acute versus the chronic response to exercise. Med Sci Sports Exerc. 2001;33(6 Suppl):S438-45; discussion S452-3.

ABSTRACT

PURPOSE: There is strong and consistent evidence that a single exercise session can acutely reduce triglycerides and increase high-density lipoprotein (HDL) cholesterol (HDL-C), reduce blood pressure, and improve insulin sensitivity and glucose homeostasis. Such observations suggest that at least some of the effects on atherosclerotic cardiovascular disease (ASCVD) risk factors attributed to exercise training may be the result of recent exercise. RESULTS: These acute and chronic exercise effects cannot be considered in isolation. Exercise training increases the capacity for exercise, thereby permitting more vigorous and/or more prolonged individual exercise sessions and a more significant acute effect. The intensity, duration, and energy expenditure required to produce these acute exercise effects are not clearly defined. The acute effect of exercise on triglycerides and HDL-C appears to increase with overall energy expenditure possibly because the effect maybe mediated by reductions in intramuscular triglycerides. Prolonged exercise appears necessary for an acute effect of exercise on low-density lipoprotein (LDL) cholesterol (LDL-C) levels. The acute effect of exercise on blood pressure is a low threshold phenomenon and has been observed after energy expenditures requiring only 40% maximal capacity. The acute effect of exercise on glucose metabolism appears to require exercise near 70% maximal, but this issue has not been carefully examined. CONCLUSIONS: Exercise has definite acute effects on blood lipids, blood pressure, and glucose homeostasis. Exercise also has acute effects on other factors related to atherosclerosis such as immunological function, vascular reactivity, and hemostasis. Considerable additional research is required to define the threshold of exercise required to produce these putatively beneficial effects.

I tend to maintain low lipids I take 6-10 grams of fish oil daill 500mgs of flush free niacin and often supplement with Nolvadex during the the year. My HDL's are also rather low but the overall ratio isn't bad.

Supplementation interventions:

Hill AM, Buckley JD, Murphy KJ, Saint DA, Morris AM, Howe PR. Combined effects of omega-3 supplementation and regular exercise on body composition and cardiovascular risk factors. Asia Pac J Clin Nutr. 2005;14 Suppl:S57.

ABSTRACT

Background - Regular exercise and inclusion of n3 fatty acids in the diet can improve cardiovascular (CV) health. Objectives - We examined whether the combination of both could reduce CV and metabolic risk factors more than either treatment alone. Design - Volunteers with metabolic syndrome characteristics (mean BMI=34 kg/m(2); TG=1.82 mM) were randomly assigned to take 6 g/day of HiDHA(R) tuna fish oil or sunflower oil (provided in blinded capsules by NuMega Ingredients) and to undertake regular exercise (walking for 45 min, 3 days/wk at 75% of age-predicted maximal heart rate) or remain relatively sedentary. Fasting plasma lipids, blood pressure and measures of arterial function and respiratory exchange ratio (RER) during exercise were assessed at baseline and after 6 and 12 weeks of intervention. Body composition was assessed by Dual Energy X-ray Absorptiometry at baseline and 12 weeks only. Outcomes - Fish oil supplementation lowered plasma triglycerides, increased HDL cholesterol and tended to improve endothelium dependent vasodilation (P =0.06), while exercise independently improved arterial compliance (P <0.01). The combined treatment, however, caused a 5% loss of body fat (P < 0.05) - a benefit not seen with either treatment alone. The loss of fat correlated with increased fat oxidation (RER) during exercise (P < 0.01). Conclusion - Fish oil and exercise appear to have a synergistic effect on body fat, indicating that omega-3 supplementation may be a useful adjunct to exercise programs aimed at improving body composition and CV risk.

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Lewis A, Lookinland S, Beckstrand RL, Tiedeman ME. Treatment of hypertriglyceridemia with omega-3 fatty acids: a systematic review. J Am Acad Nurse Pract. 2004;16(9):384-95.

ABSTRACT

PURPOSE: To (a) critically appraise available randomized controlled trials (RCTs) addressing the efficacy of long-chain omega-3 fatty acids as secondary agents for prevention of hypertriglyceridemia and (b) make recommendations for clinical practice. DATA SOURCES: Two independent reviewers examined all RCTs from 1994 to 2003 identified in several databases, extracted data from each study, and used the previously tested Boyack and Lookinland Methodological Quality Index (MQI) to determine study quality. CONCLUSIONS: Ten studies reported long-chain omega-3 fatty acids to be effective in the treatment of hypertriglyceridemia. The average decrease in triglycerides was 29%, total cholesterol 11.6%, very low density lipoprotein (VLDL) 30.2%, and low-density lipoprotein (LDL) 32.5%. One study found LDLs to increase by 25%. The average increase in high-density lipoprotein was 10%. The overall average MQI score was 36% (range = 26% to 54%). Many of the RCTs had serious shortcomings, including short duration, lack of a power analysis, no intention-to-treat analysis, no report of blind assessment of outcome, and lack of dietary control as a confounding variable. IMPLICATIONS FOR PRACTICE: Overall study methodology was weak. Although the evidence supporting use of long-chain omega-3 fatty acids in the secondary prevention of hypertriglyceridemia is reasonably strong, until there are larger RCTs of better methodological quality, it is not recommended that practitioners treat hypertriglyceridemia with omega-3 fatty acid supplementation in lieu of lipid-lowering medications.

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Moloney F, Yeow TP, Mullen A, Nolan JJ, Roche HM. Conjugated linoleic acid supplementation, insulin sensitivity, and lipoprotein metabolism in patients with type 2 diabetes mellitus. Am J Clin Nutr. 2004;80(4):887-95.

ABSTRACT

BACKGROUND: Some animal studies have suggested that conjugated linoleic acid (CLA) supplementation may have therapeutic potential with respect to insulin sensitivity and lipid metabolism, which are important cardiovascular disease (CVD) risk factors associated with type 2 diabetes mellitus. OBJECTIVE: We investigated the effect of CLA supplementation on markers of glucose and insulin metabolism, lipoprotein metabolism, and inflammatory markers of CVD in subjects with type 2 diabetes. DESIGN: The study was a randomized, double-blind, placebo-controlled trial. Thirty-two subjects with stable, diet-controlled type 2 diabetes received CLA (3.0 g/d; 50:50 blend of cis-9,trans-11 CLA and trans-10,cis-12 CLA) or control for 8 wk. A 3-h 75-g oral-glucose-tolerance test was performed, and fasting plasma lipid concentrations and inflammatory markers were measured before and after the intervention. RESULTS: CLA supplementation significantly increased fasting glucose concentrations (6.3%; P < 0.05) and reduced insulin sensitivity as measured by homeostasis model assessment, oral glucose insulin sensitivity, and the insulin sensitivity index (composite) (P = 0.05). Total HDL-cholesterol concentrations increased by 8% (P < 0.05), which was due to a significant increase in HDL(2)-cholesterol concentrations (P < 0.05). The ratio of LDL to HDL cholesterol was significantly reduced (P < 0.01). CLA supplementation reduced fibrinogen concentrations (P < 0.01) but had no effect on the inflammatory markers of CVD (C-reactive protein and interleukin 6). CONCLUSIONS: CLA supplementation had an adverse effect on insulin and glucose metabolism. Whereas CLA had positive effects on HDL metabolism and fibrinogen, a therapeutic nutrient should not be associated with potentially adverse effects on other clinical markers of type 2 diabetes.

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Salonen RM, Nyyssonen K, Kaikkonen J, Porkkala-Sarataho E, Voutilainen S, Rissanen TH, Tuomainen TP, Valkonen VP, Ristonmaa U, Lakka HM, Vanharanta M, Salonen JT, Poulsen HE; Antioxidant Supplementation in Atherosclerosis Prevention Study. Six-year effect of combined vitamin C and E supplementation on atherosclerotic progression: the Antioxidant Supplementation in Atherosclerosis Prevention (ASAP) Study. Circulation. 2003;107(7):947-53.

ABSTRACT

BACKGROUND: Self-selected supplementation of vitamin E has been associated with reduced coronary events and atherosclerotic progression, but the evidence from clinical trials is controversial. In the first 3 years of the ASAP trial, the supplementation with 136 IU of vitamin E plus 250 mg of slow-release vitamin C twice daily slowed down the progression of carotid atherosclerosis in men but not women. This article examines the 6-year effect of supplementation on common carotid artery (CCA) intima-media thickness (IMT). METHODS AND RESULTS: The subjects were 520 smoking and nonsmoking men and postmenopausal women aged 45 to 69 years with serum cholesterol > or =5.0 mmol/L (193 mg/dL), 440 (84.6%) of whom completed the study. Atherosclerotic progression was assessed ultrasonographically. In covariance analysis in both sexes, supplementation reduced the main study outcome, the slope of mean CCA-IMT, by 26% (95% CI, 5 to 46, P=0.014), in men by 33% (95% CI, 4 to 62, P=0.024) and in women by 14% (not significant). In both sexes combined, the average annual increase of the mean CCA-IMT was 0.014 mm in the unsupplemented and 0.010 mm in the supplemented group (25% treatment effect, 95% CI, 2 to 49, P=0.034). In men, this treatment effect was 37% (95 CI, 4 to 69, P=0.028). The effect was larger in subjects with either low baseline plasma vitamin C levels or CCA plaques. Vitamin E had no effect on HDL cholesterol. CONCLUSIONS: These data replicate our 3-year findings confirming that the supplementation with combination of vitamin E and slow-release vitamin C slows down atherosclerotic progression in hypercholesterolemic persons.

hey lifts, how does your alt/ast fair with the flush free? I kow it is not suppose to effect them but...... I have recently started a an intense course of polycosinol to see if i can bring up my hdl. Overall, it seems that with miniamal intervention you can control lipids while on with little to no problems.

jb

Combined interventions:

Carr TP, Weller CL, Schlegel VL, Cuppett SL, Guderian DM Jr, Johnson KR. Combination diet and exercise interventions for the treatment of dyslipidemia: an effective preliminary strategy to lower cholesterol levels? J Nutr. 2005;135(8):1829-35.

ABSTRACT

At present, dyslipidemia is most commonly treated with drug therapy. However, because safety concerns regarding the use of pharmaceutical agents have arisen, a need for alternative nonpharmacological therapies has become increasingly apparent. The National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) recommends lifestyle therapies, which include a combination of diet and exercise modifications, in place of drug treatment for patients who fall into an intermediate range of coronary heart disease (CHD) risk. This review examined the cholesterol lowering efficacy of the following 2 NCEP-recommended combination therapies: 1) low saturated fat diets combined with exercise, and 2) nutritional supplementation, i.e., fish oil, oat bran, or plant sterol supplementation, combined with exercise, in the treatment of dyslipidemia. Combination therapies are particularly advantageous because diet and exercise elicit complementary effects on lipid profiles. More specifically, diet therapies, with some exceptions, lower total (TC) and LDL cholesterol (LDL-C) concentrations, whereas exercise interventions increase HDL cholesterol (HDL-C) while decreasing triglyceride (TG) levels. With respect to specific interventions, low saturated fat diets combined with exercise lowered TC, LDL-C, and TG concentrations by 7-18, 7-15, and 4-18%, respectively, while increasing HDL-C levels by 5-14%. Alternatively, nutritional supplements combined with exercise, decreased TC, LDL-C, and TG concentrations by 8-26, 8-30, and 12-39%, respectively, while increasing HDL-C levels by 2-8%. These findings suggest that combination lifestyle therapies are an efficacious, preliminary means of improving cholesterol levels in those diagnosed with dyslipidemia, and should be implemented in place of drug therapy when cholesterol levels fall just above the normal range.

Great info. Thank you all for the responses.

Other misc. interventions:

Kiessling G, Schneider J, Jahreis G. Long-term consumption of fermented dairy products over 6 months increases HDL cholesterol. Eur J Clin Nutr. 2002;56(9):843-9.

ABSTRACT

OBJECTIVE: Assessment of the hypocholesterolaemic effect of yoghurt supplemented with Lactobacillus acidophilus 145 and Bifidobacterium longum 913 in women. DESIGN: The cross-over study consisted of three periods (7 weeks each): first period, control yoghurt for all 29 women; second period, probiotic yoghurt for 18 women, control yoghurt for 11 women; third period, the reverse of that in the second period. SETTING: Department of Nutritional Physiology, Institute of Nutritional Science, Friedrich Schiller University, Jena. SUBJECTS: Twenty-nine healthy women, aged 19-56 y. Fifteen of these were normocholesterolaemic and 14 women were hypercholesterolaemic. INTERVENTION: Yoghurt (300 g) daily containing 3.5% fat and starter cultures of Streptococcus thermophilus and L. lactis. Probiotic yoghurt was the control yoghurt enriched with L. acidophilus 145, B. longum 913 and 1% oligofructose (synbiotic). RESULTS: The mean serum concentration of total cholesterol and the LDL cholesterol was not influenced by the synbiotic (P>0.05). The HDL concentration increased significantly by 0.3 mmol/l (P=0.002). The ratio of LDL/HDL cholesterol decreased from 3.24 to 2.48 (P=0.001). CONCLUSIONS: The long-term daily consumption of 300 g yoghurt over a period of 21 weeks (control and synbiotic) increased the serum concentration of HDL cholesterol and lead to the desired improvement of the LDL/HDL cholesterol ratio.

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Singhal S, Gupta R, Goyle A. Comparison of antioxidant efficacy of vitamin E, vitamin C, vitamin A and fruits in coronary heart disease: a controlled trial. J Assoc Physicians India. 2001;49:327-31.

ABSTRACT

OBJECTIVE: To determine the efficacy of various antioxidant vitamins and a major dietary source of antioxidants (fruits) we performed a randomized controlled trial. METHODS: 175 successive patients with coronary heart disease (CHD) presenting to our centre were recruited and using a Latin-square design divided into five groups of 35 each. The groups were matched for age, lifestyle and dietary variables, clinical diagnosis and drug treatment status. None of the patients was on lipid-lowering drugs. Supplemental vitamins were stopped for one month before study began and American Heart Association Step II dietary advice was given to all. At baseline, total cholesterol, triglycerides, HDL and LDL cholesterol and lipid peroxide measured as thiobarbaturic acid reactive substances (TBARS) were determined. Group I received placebo capsules; Group II vitamin E 400 units/day; Group III vitamin C 1,000 mg; Group IV vitamin A 25,000 IU; Group V received 400 gm of fruit daily. Lipids and lipid peroxide levels were determined at 30 days follow-up. RESULTS: Response rate in various groups varied form 86% to 91%. No significant changes in total, HDL, LDL cholesterol and triglyceride levels were seen in Groups I, II, III and IV (paired t-test p > 0.05). In Group V there was a significant decrease in total cholesterol (-7.8 +/- 11.1%), and LDL cholesterol (-11.2 +/- 25.4%) and increase in HDL cholesterol (+12.9 +/- 20.1%) (paired t-test p < 0.01). Lipid peroxide levels decreased significantly in all the treatment groups (p < 0.01). This decrease was the highest in Group II (vitamin E; -36.4 +/- 17.7%) as compared to Group III (vitamin C -19.8 -/+ 10.8%); Group IV (vitamin A -5.4 +/- 17%) and Group V (fruits -13.1 +/- 12.0%). CONCLUSIONS: All the antioxidant vitamins and fruits significantly decrease lipid peroxide levels and oxidant load in CHD patients. However, fruits are the best choice as they also favourably modify the lipid profile.

Great read,thnx for the info guijr

now gj, summarize all that into a brief paragraph for all us short attention span types! a gold star coming.

jb

Okay Jb, there you go . In order to help to maintain our blood lipids on track, maybe we may combine several strategies, as follow:

1) Niacin and statin (maybe the drug of choice);
2) Exercise training (aerobic and resistance training);
3) Omega-3 supplementation;
4) CLA supplementation;
5) Vitamin E and vitamin C;
6) Low saturated fat diets;
7) Fermented dairy products (Yoghurt);
8) Fruits;
9) Oat bran (Poulter et al. Lipid profiles after the daily consumption of an oat-based cereal: a controlled crossover trial. Am J Clin Nutr. 1994;59(1):66-9; Robitaille et al. Effect of an oat bran-rich supplement on the metabolic profile of overweight premenopausal women. Ann Nutr Metab. 2005;49(3):141-8).

Guys, what else do you think that should have been included?

polycosinol and non-flush niacin. good job.

jb

Awesome!! Ever since I realized I am not imortal this subjest (which I consider to be one of the worst yet un talked about sides of aas use) has become of great interest to me. Great summary Quijr, I think this info will be of great use to many!
The only other things I will include in my regement are, Nolvadex 20mg PD throughout a cycle and a green tea suppliment. I always take one anyway but I have rad a study that suggests it too will help lower LDL