What you didn’t know about how your diet can effect cholesterol!
Hypercholesterolemia (high cholesterol) is typically due to a combination of environmental and genetic factors. Environmental factors include such things as obesity and dietary choices. Genetic contributions are usually due to the additive effects of multiple genes however occasionally may be due to a single gene defect such as in the case of familial hypercholesterolaemia.
A number of secondary causes exist including: type 2 diabetes mellitus, alcohol, monoclonal gammopathy, dialysis, nephrotic syndrome, obstructive jaundice, hypothyroidism, Cushing’s syndrome, anorexia nervosa and medications.
There is a substantial amount of research on this topic, below is a snippet of what is available with the corresponding rational.
Oats: Clinical trials indicate that dietary oats reduce total cholesterol levels by altering bile acid metabolism by as much as 5.4% and LDL by 8.5%[i]. The exact dose required is unknown but it’s hypothesized that 3g/d would generate clinically relevant decreases in total cholesterol levels[ii],[iii].
Mechanism of action (MOA): β-glucan increases the viscosity of the contents, which slows the rate and alters the site of lipid and carbohydrate absorption thereby reducing cholesterol absorption[iv],ii.
Apple pectin: contains both soluble and insoluble fibre, which lowers fat absorption and cholesterol, and reduces the risk of heart disease.
MOA: The insoluble fibre in pectin binds to cholesterol, and helps remove it from the body.
2.Garlic: A few in vitro and in vivo studies suggest high dose supplemental garlic decreases susceptibility of LDL oxidation[v]. Research results show conflicting evidence as to the efficacy of garlic to decrease cholesterol; it is believed that the effect would be from the inhibition of hepatic cholesterol synthesis[vi].
3.Chromium: Clinical trials have demonstrated a reduction in total cholesterol levels when supplemented with 1.6 mg chromium tripicolinate[vii]; despite inconsistent results, research implies chromium may decrease LDL and total triglycerides, chromium deficient individuals appear to benefit.
MOA: increases HDL which acts as a scavenger to move LDLs back to the liver, acting more as a cholesterol normaliser then a reducervii.
4.Fish oils: Research demonstrates fish oils may reduce cholesterol, improve endothelial function, reduce and reverse atherogenesis by beneficially modulating lipid profiles[viii],iii.
MOA: inhibition of hepatic fatty acid synthesis via DHA, EPA and impaired tricylglycerol synthesisvi. Incorporation of EPA and DHA into the erythrocyte membrane increases the clearance of circulating triglyceride through the activity of endothelial lipases[ix].
5.Nicotinic acid: Clinical trials found that, high doses, together with statins demonstrate a possibility to regress stenosis and decrease VLDL, LDL and increase HDL[x],[xi]. Studies also show an increase in vitamin A levels after 2 years of therapy, therefore supplementation should be avoided.
MOA: antilipolytic effect inhibits cyclic AMP accumulation in adipose tissue through a G protein-coupled receptor mediated inhibition of adenylate cyclase.
Alternatively Inositol hexaniacinate can be used.
MOA: Increases HDL levels through decreasing its fibrinolysis and catabolism, reduces free fatty acid mobilization and hepatic VLDL synthesis; this decreases LDL and total cholesterol[xii].
6.Plant sterols: Additive effects can be seen in conjunction with statins (Stipanuk 2006, p.25). Studies show inconsistency in LDL responsiveness with individuals of certain heterogeneity. Treatment with plant sterols should be targeted at clients with low basal cholesterol synthesis[xiii].
MOA: plant sterols are compounds that are structurally similar to cholesterol (Stipanuk 2006, p.25). May inhibit cholesterol absorption by competing with dietary and bile cholesterol for incorporation into the bile micellar phase at a dose of 2 g/d ii[xiv].
7. Carnitine: This supplement may provide a synergistic lipid-lowering property when combined with statins. A study on aged rats showed a decrease in age-related total cholesterol when supplemented with acetyl-L-carnitine[xv].
MOA: transports fatty acids into mitochondria xi.
8.Policosanol is a purified mixture of primary alcohols isolated from wheat germ and/or sugar cane that helps prevent LDL oxidation. Also helps lower total and LDL cholesterol by inhibiting hepatic cholesterol synthesis; helps reduce the cholesterol content of liver, heart, and fatty tissues[xvi] [xvii]. Policosanol helps reduce platelet aggregation by altering prostaglandin synthesis. Policosanol also helps prevent and reverse atherosclerotic lesions and thrombosis.
Policosanol administered orally for 54 weeks brought about a persistent reduction in blood cholesterol levels and was safe and well tolerated during long-term administration [xviii].
9.Vitamin C: Decreases LDL, triglycerides and lipid peroxidation. Studies show the higher the vitamin C content in blood the lower the cholesterol.
MOA is unknown; it may interfere with HDL elevating activity of statin niacin combination; or via CYP450 converting cholesterol to α-hydroxy cholesterol.
MOA: Not fully understood, however a HMG-CoA reductase inhibitor named monacolin K is thought be responsible. It also contains many other monacolins that have unknown effectsxxi.
Supplementation may interfere with Lipitor absorption[xxii] but may reduce cholesterol levels as deficiency may raise LDL levels.
MOA: Rosanoff & Seelig (2004) state that “Magnesium has effects that parallel those of statins”. Magnesium acts as a cofactor in the enzyme that deactivates HMG-CoA reductase, making it a reductase controller; activates lecithin cholesterol acyl transferase which lowers LDL and triglyceride levels and raises HDL levels and activates desaturase enzymexxii [xxiii].
Found in legumes. Important for bile, fat and cholesterol metabolism and acts as an emulsifying agent by joining water to fat. May reduce atherosclerosis by allowing cholesterol to pass through arterial walls[xxiv].
Black tea contains theaflavins which compare equally to green tea catechins as antioxidants[xxv]. Theaflavins have been shown to be more effective than catechins in preventing LDL oxidation[xxvi]. Furthermore, studies reveal a reduction in total and LDL cholesterol in adults with mildly high cholesterol levels[xxvii], as well as effectively lowering cholesterol in patients with mild to moderately high cholesterol levels when added as a component to green tea[xxviii]. Hence the combination of green and black tea may have greater cardiovascular benefit than just green tea alone.
[i] Anderson, J.W & Gilliland, S.E (1999) Effect of Fermented Milk (Yogurt) Containing Lactobacillus Acidophilus L1 on Serum Cholesterol in Hypercholesterolemic Humans. J of the American College of Nutr;18(1):43-50.
[ii] Varady, K.A & Jones, P.J.H (2005) Combination Diet and Exercise Interventions for the Treatment of Dyslipidemia: an Effective Preliminary Strategy to Lower Cholesterol Levels? The American Society for Nutr Sci;135:1829-1835.
[iii] Lōpez-Varela, S, Gonza´lez-Gross, M & Marcos, A (2002) Functional Foods and the Immune System: A Review, European Journal of Clinical Nutrition;56(3):29-33.
[iv] Burton-Freeman, B, Davis, P.A & Schneeman, B.O (2002) Plasma cholecystokinin is associated with subjective measures of satiety in women, The American journal of Clinical Nutrition;76(3):659-667.
[v] Lau, B.H.S (2001) Suppression of LDL Oxidation by Garlic. J of Nutr;131:985-988.
[vi] Adler, A.J & Holub, B.J (1997) Effect of Garlic and Fish-Oil Supplementation on Serum Lipid and Lipoprotein Concentrations in Hypercholesterolemic Men, American Journal of Clinical Nutrition;65:445-450.
[vii] Press, R.I, Geller, J & Evans, G.W (1990) The Effect of Chromium Picolinate on Serum Cholesterol and Apolipoprotein Fractions in Human Subjects. Western J of Med;152:41-45.
[viii] Artham, S.M, Lavie, C.J, (2008) Fish Oil in Primary and Secondary Cardiovascular Prevention. The Ochsner Journal;8:.49-60.
[x] Brown, B.G, Zhao, X.Q, et al (2001) Simvastatin and Niacin, Antioxidant Vitamins, or the Combination for the Prevention of Coronary Disease. The New England Journal Of Medicine;345(22).
[xi] Ames, B.N, Elson-Schwab, I & Silver, E.A (2002) High-Dose Vitamin Therapy Stimulates Variant Enzymes With Decreased Coenzyme Binding Affinity (Increased Km): Relevance to Genetic Disease And Polymorphisms. American Journal of Clinical Nutrition;75 (4):616-658.
[xii] Head, K.A (1996) Inositol Hexaniacinate: a Safer Alternative to Niacin, Alternative Medicine Review;1:176-84.
[xiii] Rideout, T.C, Harding, S.V, Mackay,D, Abumweis, S.S & Jones P.J.H (2010) High Basal Fractional Cholesterol Synthesis is Associated With Nonresponse of Plasma LDL Cholesterol to Plant Sterol Therapy, American Society for Clinical Nutrition.
[xiv] Sanchez-Muniz, F.J, Maki, K.C, et al (2009) Serum Lipid and Antioxidant Responses in Hypercholesterolemic Men and Women Receiving Plant Sterol Esters Vary by Apolipoprotein E Genotype. Journal of Nutrition; 1:13-19.
[xv] Tanaka,Y, Sasaki, R, et al (2004) Acetyl-L-Carnitine Supplementation Restores Decreased Tissue Carnitine Levels and Impaired Lipid Metabolism in aged rats. Journal of Lipid Research; 45:729–735.
[xvi] Crespo, N, Alvarez, R, et al (1997) Effect of Policosanol on Patients With Non-Insulin-Dependent Diabetes Mellitus and Hypercholesterolemia: A Pilot Study. Current Therapeutic Research;58(1).
[xvii] Gouni-Berthold, I & Berthold HK (2002) Policosanol: Clinical Pharmacology and Therapeutic Significance of a New Lipid-Lowering Agent. American Heart J;143:.356-365.
[xviii] Rodriguez-Echenique C, Mesa, R, et al (1994) Effects of Policosanol Chronically Administered in Male Monkeys. Food Chemistry Toxicology ;32(6):565-75.
[xix] Becker, D.J, Gordon, R.Y, et al (2009) Red Yeast Rice for Dyslipidemia in Statin-Intolerant Patients. Annals of Internal Med;150:830-839.
[xx] Bogsrud, M.P, Ose, L, et al (2010) HypoCol (red yeast rice) Lowers Plasma Cholesterol – A Randomized Placebo Controlled Study. Scandinavian Cardiovascular J ;44:197-200.
[xxi] Borden, W.B 2010, Red Yeast Rice for Dyslipidemia in Statin-Intolerant Patients. Current Atherosclerosis Reports, Springerlink;12:11-13.
[xxii] Rosanoff, A & Seelig, M.S (2004) Comparison of Mechanism and Functional Effects of Magnesium and Statin Pharmaceuticals, J of the American College of Nutr;23(5):501-505.
[xxiii] Das, U.N (2010) Lipoxins, Resolvins, Protectins, Maresins, and Nitrolipids: Connecting Lipids, Inflammation, and Cardiovascular Disease Risk. Current Cardiovascular Risk Reports;4(1):24-31.
[xxiv] Cohn, J.S, Kamilia, A, et al (2010) Reduction in Intestinal Cholesterol Absorption by Various Food Components: Mechanisms and Implications. Sci Direct;11(1):45-48.
[xxv] Leung, L.K, Su, Y, et al (2001) Theaflavins in Black Tea and Catechins in Green Tea Are Equally Effective Antioxidants, The Journal of Nutr; 131:2248-2251.
[xxvi] Ishikawa T, Suzukawa M, Ito T, et al (1997) Effect of Tea Flavonoid Supplementation on The Susceptibility of Low-Density Lipoprotein to Oxidative Modification. American J of Clinical Nutr;66:261-266.
[xxvii] Davies, M.J, Judd, J.T, (2003) Black tea consumption reduces total and LDL cholesterol in mildly hypercholesterolemic adults. The J of Nutr;133(10):3298-3302.
[xxviii] Maron, D.J, Lu, G.P, et al (2003) Cholesterol-lowering Effect of a Theaflvin-Enriched Green Tea Extract: A Randomized Controlled Trial. Archives of internal med;163:1448-1453.