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School of Dietetics and Human Nutrition, McGill University, Ste. Anne de Bellevue, QC, Canada
1To whom correspondence should be addressed. E-mail: peter.jones{at}mcgill.ca.
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ABSTRACT |
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 TOP ABSTRACT LITERATURE CITED |
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KEY WORDS: • dyslipidemia • diet • exercise • cholesterol • coronary heart disease
Evidence from human clinical as well as epidemiologic trials indicate that dyslipidemia is one of the most important modifiable risk factors for coronary heart disease (CHD)2 (1–3). Dyslipidemia is generally characterized by increased fasting concentrations of total cholesterol (TC), LDL cholesterol (LDL-C), and triglycerides (TG), in conjunction with decreased concentrations of HDL cholesterol (HDL-C) (4). At present, these lipid imbalances are most routinely treated with pharmacological therapy. Certain commonly prescribed pharmacological agents include: 3-hydroxy-3-methylglutaryl CoA reductase inhibitors (statins), bile acid sequestrants, nicotinic acid, fibric acids, as well as the cholesterol absorption inhibitor, ezetimibe. These cholesterol-lowering agents were shown to decrease LDL-C levels up to 55%, increase HDL-C levels up to 35%, and decrease TG levels as much as 50%, depending on the drug and dose (4). Although these drugs produce desirable shifts in lipid levels within a short period of time, several safety concerns have surfaced regarding the long-term use of these pharmacological agents (5–10). In particular, evidence suggests that the use of statins may result, although infrequently, in certain forms of myopathy, i.e., mild muscle aches to severe pain, restriction in mobility, as well as grossly elevated levels of creatine kinase (5). Additionally, liver toxicity, characterized by increases in hepatic transaminases, was also shown to result from prolonged use of statins at high doses (5,7). Safety concerns regarding the use of bile acid sequestrants and fibric acids were also reported (8–10).
In view of these safety issues, the implementation of nonpharmacological therapies that beneficially modulate lipid profiles without the risk of adverse affects would be highly advantageous. The Third Report of the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) recommends lifestyle therapies in place of drug therapies for patients who fall into an intermediate range of CHD risk (4). The level of risk at which to implement lifestyle therapy is dependent on the individual’s fasting LDL-C concentration as well as the number and type of CHD risk factors they possess (4). The specific dietary and lifestyle modifications outlined in the NCEP report are termed Therapeutic Lifestyle Changes (TLC). The essential features of the ATP III TLC approach include: decreasing total fat intake to 25–35% of daily energy, lowering saturated fat consumption to 7% of daily energy, reducing cholesterol intake to 200 mg/d, as well as consuming certain nutritional supplements that enhance lipid lowering (4). In accordance with these dietary guidelines, moderate physical activity is also encouraged as an adjunctive therapy (4). Although the effect of diet and exercise therapies on lipid levels, when applied individually, has been thoroughly reported (11–15), the effect of these therapies when applied in combination has yet to be summarized. Certain questions that arise include: What effect do combination diet and exercise therapies have on plasma lipid profiles in patients diagnosed with dyslipidemia? How do lipid alterations resulting from combination lifestyle therapies compare with drug treatment? Are lifestyle therapies still relevant forms of treatment in the age of cholesterol-lowering drugs? Thus, to address these questions, the goal of this review was to examine the cholesterol-lowering efficacy of the following 2 commonly prescribed combination diet and exercise 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 nondiabetic, dyslipidemia.
Low saturated fat diets combined with exercise
In a clinical setting, when lifestyle modifications are prescribed to hypercholesterolemic patients, the most common recommendations include decreasing fat intake, in particular, saturated fat intake, with or without increasing daily physical activity. The individual effects of these 2 lifestyle therapies, low saturated fat diets and exercise, on plasma lipid profiles were carefully assessed in several recent reports (11–15). In a meta-analysis by Yu-Poth et al. (11), the effects of low saturated fat diets on plasma lipid levels were examined systematically. From this report, it was concluded that decreases in total and saturated fat intakes affect primarily TC and LDL-C concentrations, whereas they have little or no effect on HDL-C or TG levels (11). More specifically, it was shown that when dietary fat intake was limited to 30% of energy, with concurrent saturated fat and cholesterol restrictions of <10% of energy and 300 mg/d, respectively, TC levels were reduced by 10%, whereas LDL-C levels decreased by 12% (11). Moreover, when saturated fat and cholesterol intakes were further decreased to <7% of energy and 200 mg/d, respectively, with total fat intake remaining at a constant level of 30% of energy, subjects experienced decreases of 13 and 16% in TC and LDL-C concentrations (11). In contrast to the effects of dietary modifications on lipid levels, the most common alterations observed with aerobic training involved changes in HDL-C and TG concentrations (13–15). In a study by Fahlman et al. (13), the effect of aerobic exercise on lipid levels was examined in 45 hypercholesterolemic, elderly women. After a 10-wk intervention period, subjects assigned to the aerobic exercise intervention experienced a 20% increase in HDL-C levels, and a 14% decrease in TG concentrations (13). These changes in HDL-C and TG levels were obtained without any change in body weight or dietary intake (13). Changes in TC and LDL-C concentrations, as a result of endurance training, are observed less frequently (14). In a meta-analysis by Leon and Sanchez (14), it was reported that exercise training, in the absence of dietary modifications, caused mean reductions of 5% in LDL-C concentrations. These authors, however, were unable to find any sufficient effect of exercise training on TC levels (14). In addition, it must be noted that the evidence linking exercise-induced HDL-C increases to decreased cardiovascular disease risk has yet to be firmly established.
In considering the complementary effects that low saturated fat diets and exercise have on cholesterol levels, we hypothesized that combining these 2 interventions would yield highly favorable alterations in all 4 lipid variables. Seven studies examined this combination therapy (Table 1) (16–22). For the most part, the diet interventions implemented in these trials limited total fat intake to 20–30% of energy and limited saturated fat intake to 6–10% of energy; the exercise programs consisted of moderate intensity training, 3–7 times/wk, for a 30- to 60-min duration. Results of these interventions on fasting lipid profiles varied. Total and LDL-C level reductions ranged from 7 to 18%, and 7 to 15%, respectively (16–22). Similar reductions were noted for TG concentrations (4–18%) (16–22). The effect of the combination therapy on HDL-C levels, however, is less clear. Although some of the trials showed significant increases ranging from 5 to 14%, a majority of the trials showed no significant effect, and some indicated that HDL-C levels may even decrease as a result of lifestyle therapy (16–22).
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The large variability between studies in treatment-induced lipid lowering may be due in part to the different trial durations. When the trials were ordered according to study length, it became apparent that the studies that achieved the greatest lipid altering effects were long-term trials (16–22). For instance, in a study conducted by Niebauer et al. (22), men with diagnosed coronary artery disease experienced declines of 18 and 7% in TC and LDL-C, respectively, and an increase of 14% in HDL-C concentrations after a 6-y combination diet and exercise program. Similarly, in a trial performed by Stefanick et al. (20), after 52 wk of treatment, TC and LDL-C concentrations decreased by 18 and 15%, respectively. In comparison, studies with slightly shorter trial periods have also demonstrated favorable lipid modifications (16,17,19). For instance, when Andersen et al. (17) applied a combination therapy for 16 wk, significant reductions in TC and LDL-C levels of 11 and 10%, respectively, were noted. Thus, these findings suggest that LDL lowering resulting from these lifestyle interventions may be achieved after 16 wk of treatment; however, for maximal LDL lowering to occur, the intervention should be applied for 1 y. These results also imply that, as demonstrated by the 6-y follow-up study, the degree of lipid lowering reached after 1 y of therapy may be maintained if the lifestyle intervention is continued.
The different diet interventions applied may also account for the discrepancies in cholesterol lowering noted between trials. The diet therapies implemented varied considerably in their percentage of allowances for total fat and saturated fat (16–22). Nevertheless, no clear positive or negative associations could be established for the effect of percentage of fat, i.e., total fat or saturated fat, on individual lipid variables. Although it is not evident from the present findings, it is postulated that very low fat diets, i.e., diets with <20% energy from fat, would potentially adversely affect lipid profiles (27–30). This could potentially occur as a result of an increased percentage of carbohydrate in the diet to compensate for the lack of fat. As demonstrated by several recent studies (27–30), increases in carbohydrate intake could potentially raise TG levels in the blood, resulting in less favorable lipid profiles. This relation, however, was not noted in any of the combination diet and exercise trials currently under review.
The weight loss noted in 6 of the 7 studies reviewed (16–21), could also potentially account for the lipid-lowering inconsistencies observed among trials. The weight reduction observed in these studies, expressed as a post-treatment percentage of change from initial body mass, ranged from 2 to 10% (16–21). Although no clear dose-response relation between weight loss and lipid modulations could be determined, it would appear that those trials that experienced a weight reduction >5% of initial body weight, observed the most significant changes in TC and LDL-C concentrations. For instance, in the study by Andersen et al. (17), in which the subjects experienced a 10% decrease in body mass, TC and LDL-C levels decreased by 10.9 and 10.7%, respectively. Similarly, in the study by Williams et al. (21), in which body mass decreased by 7% over the course of the 52-wk trial, LDL-C levels decreased by 15.2%. In contrast, no clear associations between weight loss and HDL-C or TG modulations could be determined. In examining separately the study by Niebauer et al. (22), in which significant weight loss was not observed, interesting relations among study design, lack of weight loss, and lipid alterations were noted. In this study, subjects were randomized either to a supervised combination diet and exercise group, or a nonsupervised combination diet and exercise group for a 6-y trial period. Throughout the study, the subjects exercised every day for 30–60 min, and consumed a diet consisting of <20% of energy as total fat. Surprisingly, although the supervised combination group did not experience any significant weight reduction, this group witnessed significant reductions in TC, LDL-C, and TG concentrations of 17.6, 6.9, and 17.5%, respectively, whereas HDL-C levels increased by 14.0%. In comparison, in the nonsupervised combination group, which experienced a nonsignificant body mass reduction of 5%, TC concentrations decreased by 4%, LDL-C levels increased by 1%, and HDL-C and TG levels were modulated to an extent similar to that in the supervised group. The unclear association between diet/exercise-induced weight loss and lipid lowering observed in this review was also summarized in other recent reports (14). Although it has been shown consistently that decreases in body weight beneficially modulate cholesterol profiles (31–34), a clear dose-response relation between decreased body mass and degree of cholesterol lowering has yet to be established (14). Establishing this dose-response relation has been difficult because isolating the effect of body weight reduction vs. treatment effect on lipid profiles is practically impossible. Accordingly, as an attempt to isolate the effect of this confounder, a trial should be conducted that examines the effect of a combination diet and exercise therapy on lipid levels, with and without energy restriction. Only if such a study were performed, might the independent effects of treatment vs. treatment-induced weight loss on lipid concentrations be determined.
Nutritional supplementation combined with exercise
Some hypercholesterolemic patients may find it difficult to adhere to a tightly regimented low saturated fat diet; thus, compliance with the lipid-lowering therapy may be compensated (35,36). For these patients, supplementing the diet with certain functional foods or nutraceuticals known to enhance lipid lowering, i.e., fish oil, oat bran, or plant sterols, may be a more appropriate strategy (37). Randomized clinical trials examining lifestyle therapies that combine nutritional supplementation with exercise training are listed in Table 2 (38–42).
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4 allele, whereas no adverse shifts were noted in those possessing the 3 allele (50,51). Thus, in future clinical practice, it may be necessary to screen for such diet-gene interactions before certain nutritional therapies, such as fish oil, may be recommended to individuals diagnosed with dyslipidemia. The potential synergistic or additive effect of fish oil supplementation when combined with exercise on lipid levels was examined in only 2 randomized control trials (38,39). In a study conducted by Hermann et al. (38), 12 g/d of fish oil supplementation in conjunction with swimming 6 times/wk for a period of 4 wk lowered TC and LDL-C concentrations by 12 and 16%, respectively. In addition, HDL-C levels increased by 8%, whereas TG concentrations decreased by 20% (38). Similar results were noted in a study by Warner et al. (39), which tested the effect of fish oil (45 g/d) alone or in combination with exercise, on lipid profiles. After a 12-wk intervention period, LDL-C levels were significantly decreased in the combination group, whereas HDL-C concentrations increased in both the fish oil and combination group (39). Thus, although there are only a few studies from which to draw conclusions, these results suggest that when combined, fish oil and exercise may help to lower the risk of CHD by favorably modulating all 4 lipid variables. In particular, combining these 2 interventions results in a beneficial, additive effect on TG concentrations, while in some way producing a positive, synergistic effect on LDL-C concentrations. The reason for these significant reductions in LDL-C levels, however, remains unclear. Because neither fish oil supplementation nor exercise therapy was shown to positively modulate LDL-C concentrations when applied alone, it is unusual that the combinatory effect of these 2 treatments would synergistically produce such favorable alterations. Nevertheless, on the basis of the present findings, combining fish oil supplementation with a regular exercise program could be recommended in clinical practice as an effective strategy to beneficially alter lipid profiles in those at risk for CHD. Future research should aim to examine the mechanisms of action underlying the synergistic relationship of this combination therapy on lipid levels, and in addition, the role that diet-gene interactions may play in modulating this effect.
Oat bran supplementation combined with exercise. Evidence suggests that viscous, soluble fibers, such as oat bran, may have a substantial hypocholesterolemic effect (52–54). In particular, supplementing the diet with oat products was shown to produce significant reductions in both TC and LDL-C concentrations, while having little effect on either HDL-C or TG levels (52–54). In a study that supplemented mildly hypercholesterolemic men and women for 5 wk with 50–75 g oat fiber extract/d, LDL-C concentrations were shown to decrease by 21% (55). Recent evidence indicates that the lipid-lowering effect of oat products may be attributed to their main soluble fiber component, ß-glucan (56). To elucidate the specific mechanism of action, it was suggested that ß-glucan decreases the absorption of ingested nutrients and bile acids by increasing the viscosity of intestinal contents (56). The precise dose of ß-glucan required to elicit such lipid-lowering effects, however, remains unclear (56). In a study by Davidson et al. (57), it was shown that supplementing the diet with 3.6, 4.0, and 6.0 g of ß-glucan from oatmeal resulted in LDL-C concentration reductions of 10, 16, and 12%, respectively. As such, this study was not able to establish a dose-response relation because the highest dose of ß-glucan produced an intermediate hypocholesterolemic response (57). Although solid conclusions regarding ß-glucan dose have yet to be made, it would appear that a minimal dose of 3 g/d is required to produce clinically relevant reductions in both TC and LDL-C concentrations (56).
In studies that have combined oat bran supplementation with exercise, consistent and substantial plasma lipid decreases were demonstrated (40,41). After 4 wk of supplementing with 35–50 g oat bran/d combined with supervised endurance training for 60 min/d, Berg et al. (41) demonstrated reductions in TC and LDL-C of 26 and 30%, respectively. Similarly, in a 4-wk study by Kelley et al. (40), which combined 100 g/d of oat bran supplementation with nonsupervised training for 40–60 min/d, TC and LDL-C concentrations decreased by 8 and 9%, respectively. HDL-C and TG concentrations, however, were not significantly affected in either study (40,41). The lack of effect on HDL-C levels could potentially be due to the short-term duration of the study. Recent evidence suggests that regular exercise must be performed for a minimum period of 8 wk to promote HDL-C elevations (14). In view of this, future studies should be conducted that implement this combination therapy for longer trial durations, to determine whether further LDL-C reductions, as well as potential HDL-C–raising effects occur. The large discrepancy in TC and LDL-C lowering seen between the 2 studies is most likely due to the different diet and exercise regimens prescribed. In the study by Berg et al. (41), a diet that had a 4190 kJ/d deficit, was implemented in combination with a supervised daily exercise program. In contrast, in the study by Kelley et al. (40), neither energy intake nor exercise compliance was controlled. Thus, in considering the dietary energy deficit as well as the tightly controlled training protocol imposed in the study by Berg et al. (41), it is not surprising that these subjects experienced much greater lipid reductions than those participating in the study by Kelley et al. (40). Interestingly, neither study reported the dose of ß-glucan contained in the quantity of oat bran prescribed. Because levels of ß-glucan vary among different oat products (56), it is not possible to approximate the daily dose of ß-glucan implemented in these supplementation regimens. However, because significant reductions were noted in both TC and LDL-C levels, it can be assumed that the minimal dose of 3 g/d of ß-glucan was consumed. Thus, from the present findings, combining oat bran supplementation, containing a minimal dose of 3 g ß-glucan/d, with daily exercise would appear to be an effective natural therapy to decrease both TC and LDL-C levels in hypercholesterolemic individuals.
Plant sterols combined with exercise. Plant sterols, plant compounds that are structurally similar to cholesterol, were shown to lower lipid levels in humans by inhibiting cholesterol absorption from the intestine (58–60). Food sources of plant sterols include vegetable oils, seeds, and nuts (60). Increasing the dietary intake of these compounds is also possible through the consumption of certain products that have been supplemented with plant sterols, such as margarines, yogurts, cereal bars, and fruit juices (58). In a meta-analysis of 21 trials of plant sterol supplementation (58), it was shown that a near-maximum effect of a 10% reduction in LDL-C occurs at a dose of 2 g/d. Total cholesterol levels were shown to be reduced to a similar extent (58). Although plant sterols consistently lower TC and LDL-C concentrations, evidence suggests that these nutritional supplements have no effect on HDL-C or TG levels (58–60). Thus, to achieve the most advantageous lipid alterations, combining this supplement with a therapy that beneficially modulates both HDL-C and TG levels, such as exercise, would be highly favorable. Only 1 trial (42) to date tested the effects of this combination strategy on cholesterol concentrations. After an 8-wk trial period in which the individual vs. combined effects of plant sterols and exercise were compared, it was shown that the combination group experienced the most beneficial alterations in lipid profiles because each lipid variable was shifted in a favorable direction (42). More specifically, TC, LDL-C, and TG levels decreased by 7.7, 8.3, and 11.8%, respectively, whereas HDL-C concentrations increased by 7.5% (42). These favorable alterations were achieved by consuming 1.8 g/d of plant sterols, while performing endurance training 3 times/wk for a period of 25–40 min (42). In considering the degree to which this combination therapy was able to favorably alter all 4 lipid variables without having to change dietary patterns, this lifestyle strategy could be considered a practical method for lowering cholesterol levels in hypercholesterolemic patients.
In summary, it is clear that lifestyle therapies that combine diet and exercise interventions are efficacious, nonpharmacological strategies for the treatment of dyslipidemia. Combination lifestyle treatments are particularly advantageous because diet and exercise elicit complementary effects on lipid profiles. More specifically, diet therapies, with some exceptions, act primarily to lower TC and LDL-C concentrations, and exercise interventions increase HDL-C while decreasing TG levels. Thus, when combined, favorable shifts in all 4 lipid variables are demonstrated. In this review, 2 combination lifestyle therapies outlined in the ATP III TLC guidelines, i.e., low saturated fat diets combined with exercise as well as nutritional supplements combined with exercise, were examined. Results revealed that therapies involving 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%. When nutritional supplements, i.e., fish oil, oat bran, and plant sterols, were combined with exercise, these combination lifestyle therapies decreased TC, LDL-C, and TG concentrations by 8–26, 8–30, and 12–39%, respectively, while increasing HDL-C concentrations 2–8%. Additionally, it was also noted that in trials in which the combination intervention induced weight loss >5% of initial body weight, TC and LDL-C concentrations were decreased more than in those trials that did not experience this degree of weight loss. In contrast, no clear associations between treatment-induced weight loss and HDL-C or TG level modulations could be determined.
Thus, in considering the degree to which cholesterol levels were favorably altered, it is evident that these nonpharmacological interventions remain valuable strategies in the treatment of dyslipidemia. In particular, these lifestyle therapies are an efficacious means of lowering cholesterol levels in those individuals whose LDL-C levels fall just above the normal range. For these individuals, who require only a 5–25% decrease in LDL-C concentrations, combination interventions that elicit this degree of cholesterol lowering should be implemented as a preliminary measure. Furthermore, implementing lifestyle therapies as a first line of treatment is particularly important in view of drug-induced adverse events that are occasionally observed with pharmacological treatment. Additionally, applying combination lifestyle interventions as an adjunctive therapy to drug treatment may help to decrease the dose of the lipid-lowering drug required to meet treatment goals. Moreover, combination lifestyle therapies are cost effective, and may further benefit the overall health of the individual, whether they are hypercholesterolemic or within the normal range, by supporting weight control, lowering blood pressure, and improving glucose tolerance. In conclusion, combination lifestyle therapies are an efficacious means of improving cholesterol levels in those diagnosed with dyslipidemia, and should be implemented over and above drug therapy when cholesterol levels fall just above the normal range.
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FOOTNOTES |
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Manuscript received 13 February 2005. Initial review completed 20 March 2005. Revision accepted 5 May 2005.
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