**1. Introduction**

**Definition**: Hyperlipidemia is a heterogeneous group of disorders characterized by high level of lipids (fats) in the bloodstream. These lipids include cholesterol, cholesterol esters, phos‐ pholipids, and triglycerides. Lipids are transported in the blood as large 'lipoproteins'. Alternatively, the disease refers to elevated levels of lipids and cholesterol in the blood, or the manifestations of different disorders of lipoprotein metabolism (dyslipidemia).

**Causes**: Hyperlipidemia could be caused by: (i) Familial combined hypercholesterolemia (ii) Familial hypertriglyceridemia (iii) other disease states such as *insulin and non-insulin dependent diabetes mellitus*, *hypothyroidism*, *Cushing's syndrome*, dysproteinemias, *nephrotic syndrome* and *renal failure*, cholestatic disorders and low thyroid (iv) drugs such as anabolic steroids, betablockers, birth control pills and estrogens, corticosteroids, protease inhibitors, retinoids, thiazide diuretics (v) diets like cholesterol intake greater than 300 mg per day, fat intake per total calories greater than 40 %, saturated fat intake per total calories greater than 10 % (vi) life style involving habitual excessive alcohol use, lack of exercise, smoking (vii) risk factors such as advancing age, sex (male), stress and postmenopause.

**Classification**: Lipoproteins are divided into five major classes, based on density and they include: (i) chylomicrons (ii) very low-density lipoproteins (VLDL) (iii) intermediate-density lipoproteins (IDL) (iv) low-density lipoproteins (LDL) and (v) high-density lipoproteins (HDL). Most triglyceride is transported in chylomicrons or VLDL, while most cholesterol is carried in LDL and HDL. Hyperlipidemia, a major, modifiable risk factor for atherosclerosis and cardiovascular disease, including coronary heart disease (CHD) is classified under (1) Primary hyperlipidemias - are probably genetically based, but the genetic defects are known for only a minority of patients. Examples are (i) primary chylomicronemia- recessive traits of deficiency of lipoprotein lipase or its cofactor (ii) familial hypercholesterolemia- an autosomal

© 2014 Nwodo et al.; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

dominant trait, although levels of LDL tend to increase with normal VLDL; familial combined (mixed) hyperlipoproteinemia- elevated levels of VLDL, LDL (iii) familial dysbetalipoprotei‐ nemia-increased LDL with increased TG and cholesterol levels (iv) familial hypertriglyceri‐ demia-increased VLDL production with normal or decreased LDL (v) familial mixed hypertriglyceridemia-serum VLDL and chylomicrons are increased. (2) Secondary hyperlipi‐ demia- results from disease states such as Cushing's syndrome, diabetes, liver disorders, renal disorders, thyroid disease, obesity, as well as alcohol consumption, estrogen administration, and other drug-associated changes in lipid metabolism.

triglycerides are lower and HDL-C levels tend to be higher in the African-American popula‐ tion. Asian-Indians have the highest risk, Europeans have an intermediate risk while Chinese have the lowest risk (race factor) (ix) familial combined hyperlipidemia inheritance is autoso‐ mal dominant and likely to involve one of multiple enetic defects, familial hypertriglyceride‐ mia is most likely inherited as an autosomal dominant defect, lipoprotein lipase deficiency and hepatic lipase deficiency are very rare autosomal recessive conditions hypercholesterole‐ mia in the majority of the general public is attributed to high-fat diets and poorly understood susceptibility and modifier genes (genetics factor). Published data on the prevalence of lipid abnormalities in Nigeria are scanty. This could be attributed to low prevalence of hyperlipi‐ demia in Nigeria prior to occidental lifestyle. Osuji et al, 2012, reported that the current state of dyslipidemia in Nigeria clearly contradicts the previous perceptions. In their report, dsylipidemia was found to be highly prevalent in Nigeria with consistent low HDL-cholesterol and high LDL-c especially amongst the upper social class and people with other risk factors. Other studies reported low HDL-c, with TC/HDL-c to be prevalent in the Northern part of the country while high prevalence of TC, TG and low HDL were observed in the Southern part of

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243

**Dietary intervention**: is the primary treatment strategy, but drug therapy may often be added later to augment treatment. The main component of a "heart-healthy" diet is a food pattern that is low in saturated fat and dietary cholesterol and provides adequate energy to support growth and maintain an appropriate weight. Specific dietary recommendations include: (i) decreased intakes of saturated fat- most effective in lowering LDL. Sources include stick margarine, partially hydrogenated oils and fats, hydrogenated peanut butters, commercial bakery products, commercial fried food (e.g., French fries) and high fat animal products (ii) decreased intakes of trans-fatty acids- trans-fatty acids are thought to increase LDL levels nearly as much as saturated fat and appear to lower HDL. (iii) decreased intakes of dietary cholesterol- lead to LDL reduction. Diabetic patients tend to be more sensitive to dietary cholesterol intake, which is only found in animal products (iv) balance the fatty acid compo‐ sition of diet- polyunsaturated and monounsaturated fatty acids can lower LDL and could be good substitutes for saturated fats (v) increased fiber intakes- soluble fiber can contribute to LDL reduction and is now a formal part of hyperlipidemia dietary recommendations. Com‐ mon sources of fiber include oats, psyllium, guar gum, pectin, barley, dried beans, fruits, vegetables, cereals, whole grains, and legumes are good sources of soluble fiber (vi) encourage antioxidant food sources such as carotenoids, vitamins C and E and antioxidant-rich foods such as whole grains, citrus fruits, melons, berries and leafy green vegetables rather than supplements (vii) reduce serum homocysteine levels- adequate intakes of folate and vitamins B6 and B12 as well as total fat restriction may keep homocysteine levels low. Food sources of these nutrients include fruits, dark green and leafy vegetables, fortified cereals, whole grains,

the country amongst people of upper social class.

**2. Treatment**

lean meats and poultry.

Symptoms: Hyperlipidemia usually does not cause symptoms. Very high levels of lipids or triglycerides can cause yellowish nodules of fat in the skin beneath eyes, elbows and knees, and in tendons (xanthomas). Sometimes pain, swelling of organs such as the liver, spleen or pancreas (pancreatitis) or whitish rings around the eye's iris occur. **Diagnosis**: Diagnosis is typically based on medical history, physical examination and most importantly blood test done after overnight fasting. The blood test, measure the levels of lipids in the blood and consist of, a fasting blood test for total cholesterol (TC), LDL (bad cholesterol), HDL (good cholesterol), triglycerides (TG). American Cholesterol Education Program advises that lipids be checked at least once every five years, starting at age 20. However, more frequent or earlier testing is recommended if family history of hyperlipidemia; risk factor or disease that may cause hyperlipidemia; complication that may result from hyperlipidemia exist. Also, the American Academy of Pediatrics recommends lipid screening for children at risk (example, a family history of hyperlipidemia and/or diabetes). Table 1 provides specifications for making a determination.


**Table 1.** Classification of cholesterol level

**Prevalence**: (i) A significant percentage of world population has an increased plasma lipid level, resulting in increased risk of coronary heart disease (ii) Ethnic groups adopting a 'western' lifestyle tend to have higher levels of plasma lipids (iii) Men >30 years and women >55 years (in the U.S.) have10 % rise in fasting triglyceride level >200 mg/dl (iv) Severe hypertriglyceridemia (>2000 mg/dl) higher in diabetic patients or patients suffering alcoholism (iv) Lipoprotein lipase deficiency prevalence is much higher in Quebec, Canada. (v) total C and LDL-C rise steadily about 20% in men aged 20 to 50 years, 30% in women aged 20 to 60 years and younger women have lower levels than men while homozygous familial hypercho‐ lesterolemia manifests itself from birth (vii) hyperlipidermia is higher among men than women (gender factor) (viii) total cholesterol and LDL-C levels are similar in whites and blacks, triglycerides are lower and HDL-C levels tend to be higher in the African-American popula‐ tion. Asian-Indians have the highest risk, Europeans have an intermediate risk while Chinese have the lowest risk (race factor) (ix) familial combined hyperlipidemia inheritance is autoso‐ mal dominant and likely to involve one of multiple enetic defects, familial hypertriglyceride‐ mia is most likely inherited as an autosomal dominant defect, lipoprotein lipase deficiency and hepatic lipase deficiency are very rare autosomal recessive conditions hypercholesterole‐ mia in the majority of the general public is attributed to high-fat diets and poorly understood susceptibility and modifier genes (genetics factor). Published data on the prevalence of lipid abnormalities in Nigeria are scanty. This could be attributed to low prevalence of hyperlipi‐ demia in Nigeria prior to occidental lifestyle. Osuji et al, 2012, reported that the current state of dyslipidemia in Nigeria clearly contradicts the previous perceptions. In their report, dsylipidemia was found to be highly prevalent in Nigeria with consistent low HDL-cholesterol and high LDL-c especially amongst the upper social class and people with other risk factors. Other studies reported low HDL-c, with TC/HDL-c to be prevalent in the Northern part of the country while high prevalence of TC, TG and low HDL were observed in the Southern part of the country amongst people of upper social class.

### **2. Treatment**

dominant trait, although levels of LDL tend to increase with normal VLDL; familial combined (mixed) hyperlipoproteinemia- elevated levels of VLDL, LDL (iii) familial dysbetalipoprotei‐ nemia-increased LDL with increased TG and cholesterol levels (iv) familial hypertriglyceri‐ demia-increased VLDL production with normal or decreased LDL (v) familial mixed hypertriglyceridemia-serum VLDL and chylomicrons are increased. (2) Secondary hyperlipi‐ demia- results from disease states such as Cushing's syndrome, diabetes, liver disorders, renal disorders, thyroid disease, obesity, as well as alcohol consumption, estrogen administration,

Symptoms: Hyperlipidemia usually does not cause symptoms. Very high levels of lipids or triglycerides can cause yellowish nodules of fat in the skin beneath eyes, elbows and knees, and in tendons (xanthomas). Sometimes pain, swelling of organs such as the liver, spleen or pancreas (pancreatitis) or whitish rings around the eye's iris occur. **Diagnosis**: Diagnosis is typically based on medical history, physical examination and most importantly blood test done after overnight fasting. The blood test, measure the levels of lipids in the blood and consist of, a fasting blood test for total cholesterol (TC), LDL (bad cholesterol), HDL (good cholesterol), triglycerides (TG). American Cholesterol Education Program advises that lipids be checked at least once every five years, starting at age 20. However, more frequent or earlier testing is recommended if family history of hyperlipidemia; risk factor or disease that may cause hyperlipidemia; complication that may result from hyperlipidemia exist. Also, the American Academy of Pediatrics recommends lipid screening for children at risk (example, a family history of hyperlipidemia and/or diabetes). Table 1 provides specifications for making a

**Cholesterol level Acceptable Borderline High** Total Cholesterol (mg/dl) <170 170 – 199 ≥ 200 LDL Cholesterol (mg/dl) <110 110 – 129 ≥ 130 HDL Cholesterol (mg/dl) <40 40-59 ≥ 60 Total glycerides (mg/dl) <150 150-200 ≥ 200

**Prevalence**: (i) A significant percentage of world population has an increased plasma lipid level, resulting in increased risk of coronary heart disease (ii) Ethnic groups adopting a 'western' lifestyle tend to have higher levels of plasma lipids (iii) Men >30 years and women >55 years (in the U.S.) have10 % rise in fasting triglyceride level >200 mg/dl (iv) Severe hypertriglyceridemia (>2000 mg/dl) higher in diabetic patients or patients suffering alcoholism (iv) Lipoprotein lipase deficiency prevalence is much higher in Quebec, Canada. (v) total C and LDL-C rise steadily about 20% in men aged 20 to 50 years, 30% in women aged 20 to 60 years and younger women have lower levels than men while homozygous familial hypercho‐ lesterolemia manifests itself from birth (vii) hyperlipidermia is higher among men than women (gender factor) (viii) total cholesterol and LDL-C levels are similar in whites and blacks,

and other drug-associated changes in lipid metabolism.

242 Antioxidant-Antidiabetic Agents and Human Health

determination.

**Table 1.** Classification of cholesterol level

**Dietary intervention**: is the primary treatment strategy, but drug therapy may often be added later to augment treatment. The main component of a "heart-healthy" diet is a food pattern that is low in saturated fat and dietary cholesterol and provides adequate energy to support growth and maintain an appropriate weight. Specific dietary recommendations include: (i) decreased intakes of saturated fat- most effective in lowering LDL. Sources include stick margarine, partially hydrogenated oils and fats, hydrogenated peanut butters, commercial bakery products, commercial fried food (e.g., French fries) and high fat animal products (ii) decreased intakes of trans-fatty acids- trans-fatty acids are thought to increase LDL levels nearly as much as saturated fat and appear to lower HDL. (iii) decreased intakes of dietary cholesterol- lead to LDL reduction. Diabetic patients tend to be more sensitive to dietary cholesterol intake, which is only found in animal products (iv) balance the fatty acid compo‐ sition of diet- polyunsaturated and monounsaturated fatty acids can lower LDL and could be good substitutes for saturated fats (v) increased fiber intakes- soluble fiber can contribute to LDL reduction and is now a formal part of hyperlipidemia dietary recommendations. Com‐ mon sources of fiber include oats, psyllium, guar gum, pectin, barley, dried beans, fruits, vegetables, cereals, whole grains, and legumes are good sources of soluble fiber (vi) encourage antioxidant food sources such as carotenoids, vitamins C and E and antioxidant-rich foods such as whole grains, citrus fruits, melons, berries and leafy green vegetables rather than supplements (vii) reduce serum homocysteine levels- adequate intakes of folate and vitamins B6 and B12 as well as total fat restriction may keep homocysteine levels low. Food sources of these nutrients include fruits, dark green and leafy vegetables, fortified cereals, whole grains, lean meats and poultry.

**Drug Therapy**: Currently, there are many classes of medications that may be utilized in the pharmacologic management of hyperlipidemia. They are (1) HMG-CoA (3-hydroxy-3 methylglutaryl-coenzyme A) reductase inhibitors (statins). The cornerstone of the lipidlowering therapy in adults has rested with the HMG CoA reductase inhibitors or statins. The use of these drugs has resulted in important reductions in overall cardiovascular morbidity and mortality. Mechanism of action- reduction of cholesterol synthesis in liver; inhibiting the rate-limiting step in endogenous cholesterol synthesis; compensatory increase in synthesis of LDL receptors on hepatic and extra hepatic tissues; increase in hepatic uptake of circulating LDL which decreases plasma LDL cholesterol; increase in HDL, decrease in TGs and vasodi‐ latation and decrease in atherosclerosis. Pharmacological indication: Clinically used in the treatment of all types of hyperlipidemia except those who are homozygous for familial hypercholesterolemia (lack of LDL receptors). Table 2 summarizes the statins and their clinically applications.

related phytosterol absorption; decrease in concentration of intrahepatic cholesterol; increase in uptake of circulating LDL; decrease in serum LDL cholesterol levels and compensatory increase in LDL receptors. Pharmacological indication: Effective in hypercholesterolemia together with statins and diet regulation; utilization of ezetimibe along with a statin allows for lower doses of the statin to be used, therefore reducing the likelihood of dose-related side effects of the statin. (4) Nicotinic acid; Niacin (Inhibitor of lipolysis): Mechanism of action- a potent inhibitor of lipolysis in adipose tissues; decreases mobilization of FFAs (major precursor of TGs) to the liver; increases HDL levels; decreases LDL, decreases endothelial dysfunction and thrombosis. Pharmacological indication- Used in the treatment of familial hyperlipide‐ mias (type IIB) (increase in VLDL and LDL); combined with fibrates or cholestyramine in the treatment of hypercholesterolemia (5) Bile acids- Sequestrants(resins): The bile acid binding resins have been felt to be preferred in the pediatric age group as they are not systemically absorbed. Mechanism of action- are anion exchange resins; bind bile acids in the intestine forming complex that leads to loss of bile acids in the stools; increase the conversion of cholesterol into bile acids in the liver; compensatory increase in LDL receptors leading to decreased concentration of intrahepatic cholesterol; increase hepatic uptake of circulating LDL and decrease serum LDL cholesterol levels. Pharmacological indication: Effective in the treatment of type IIA and IIB hyperlipidemias (along with statins when response to statins is inadequate or they are contraindicated); treatment of pruritus in biliary obstruction (as rising from increase in bile acids). Typical examples are cholestyramine, colestipol and colesevelam. (6) Lovaza (Omega-3-acid ethyl ester): Mechanism of action: is unclear; however, proposed mechanisms include decreasing lipogenesis in the liver, increasing plasma lipoprotein lipase activity, and increasing mitochondrial and perixosomal lipase activity. The drug may increase aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and has also been known to prolong bleeding time. Pharmacological indication: is indicated as adjunct therapy to diet in patients with triglyceride levels greater than or equal to 500 mg/dl (hypertriglyceri‐ demia). It provides significant reduction in triglycerides, of approximately 44.9%, making it an ideal drug choice in patients with high triglycerides (7) Fish oil is another common overthe-counter (OTC) product that provides an alternative to the prescription product Lovaza (8) OTC herbal product: (i) Red yeast rice (RYR)- herbal supplements used for lipid-lowering effects. RYR is obtained by fermenting *Monascus purpureus*, a form of yeast, on rice, which is then dried, pulverized, and encapsulated. This process leads to the formation of 14 monacolins, which are compounds that inhibit HMG-CoA reductase. One of the mona-colins, monacolin K (lovastatin or mev-inolin) was the first synthesized HMG-CoA reductase inhibitor. RYR is commercially available in 600-mg capsules (ii) Plant sterols and stanols also assist in the reduction of LDL-C. Plant sterols reduce cholesterol absorption by competing with cholesterol for space within bile salt micelles in the intestinal lumen. The plant stanols, which are the result of the hydrogenation of sterols, are not absorbed as well as sterols. Ingestion of about 2 g per day of plant sterols or stanols, produces LDL-C reduction of 6% to 15%. Prevention: Cardio‐ vascular disease (CVD) is the leading cause of mortality in advance countries, with hyperli‐ pidemia a common risk factor for CVD, in adults having abnormal cholesterol values and elevated low-density lipoprotein (LDL) cholesterol levels. Prevention could be subdivided

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**Table 2.** HMG-CoA INHIBITORS

(2) Fibrates (activators of lipoprotein lipase): Mechanism of action- agonists at peroxisome proliferator-activated receptor (PPAR); hydrolysis of VLDL and chylomicrons; decrease in serum TGs; increase clearance of LDL by liver and increase in HDL and expression of genes responsible for increased activity of plasma lipoprotein lipase enzyme. Pharmacological indication: most effective in reduction TGs (hypertriglyceridemia); combined hyperlipidemia (type III) if statins are contraindicated. Typical examples are fenofibrate(prodrug) and gemfibrozil (lopid) (3) Ezetimibe: Mechanism of action- inhibits intestinal cholesterol and related phytosterol absorption; decrease in concentration of intrahepatic cholesterol; increase in uptake of circulating LDL; decrease in serum LDL cholesterol levels and compensatory increase in LDL receptors. Pharmacological indication: Effective in hypercholesterolemia together with statins and diet regulation; utilization of ezetimibe along with a statin allows for lower doses of the statin to be used, therefore reducing the likelihood of dose-related side effects of the statin. (4) Nicotinic acid; Niacin (Inhibitor of lipolysis): Mechanism of action- a potent inhibitor of lipolysis in adipose tissues; decreases mobilization of FFAs (major precursor of TGs) to the liver; increases HDL levels; decreases LDL, decreases endothelial dysfunction and thrombosis. Pharmacological indication- Used in the treatment of familial hyperlipide‐ mias (type IIB) (increase in VLDL and LDL); combined with fibrates or cholestyramine in the treatment of hypercholesterolemia (5) Bile acids- Sequestrants(resins): The bile acid binding resins have been felt to be preferred in the pediatric age group as they are not systemically absorbed. Mechanism of action- are anion exchange resins; bind bile acids in the intestine forming complex that leads to loss of bile acids in the stools; increase the conversion of cholesterol into bile acids in the liver; compensatory increase in LDL receptors leading to decreased concentration of intrahepatic cholesterol; increase hepatic uptake of circulating LDL and decrease serum LDL cholesterol levels. Pharmacological indication: Effective in the treatment of type IIA and IIB hyperlipidemias (along with statins when response to statins is inadequate or they are contraindicated); treatment of pruritus in biliary obstruction (as rising from increase in bile acids). Typical examples are cholestyramine, colestipol and colesevelam. (6) Lovaza (Omega-3-acid ethyl ester): Mechanism of action: is unclear; however, proposed mechanisms include decreasing lipogenesis in the liver, increasing plasma lipoprotein lipase activity, and increasing mitochondrial and perixosomal lipase activity. The drug may increase aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and has also been known to prolong bleeding time. Pharmacological indication: is indicated as adjunct therapy to diet in patients with triglyceride levels greater than or equal to 500 mg/dl (hypertriglyceri‐ demia). It provides significant reduction in triglycerides, of approximately 44.9%, making it an ideal drug choice in patients with high triglycerides (7) Fish oil is another common overthe-counter (OTC) product that provides an alternative to the prescription product Lovaza (8) OTC herbal product: (i) Red yeast rice (RYR)- herbal supplements used for lipid-lowering effects. RYR is obtained by fermenting *Monascus purpureus*, a form of yeast, on rice, which is then dried, pulverized, and encapsulated. This process leads to the formation of 14 monacolins, which are compounds that inhibit HMG-CoA reductase. One of the mona-colins, monacolin K (lovastatin or mev-inolin) was the first synthesized HMG-CoA reductase inhibitor. RYR is commercially available in 600-mg capsules (ii) Plant sterols and stanols also assist in the reduction of LDL-C. Plant sterols reduce cholesterol absorption by competing with cholesterol for space within bile salt micelles in the intestinal lumen. The plant stanols, which are the result of the hydrogenation of sterols, are not absorbed as well as sterols. Ingestion of about 2 g per day of plant sterols or stanols, produces LDL-C reduction of 6% to 15%. Prevention: Cardio‐ vascular disease (CVD) is the leading cause of mortality in advance countries, with hyperli‐ pidemia a common risk factor for CVD, in adults having abnormal cholesterol values and elevated low-density lipoprotein (LDL) cholesterol levels. Prevention could be subdivided

**Drug Therapy**: Currently, there are many classes of medications that may be utilized in the pharmacologic management of hyperlipidemia. They are (1) HMG-CoA (3-hydroxy-3 methylglutaryl-coenzyme A) reductase inhibitors (statins). The cornerstone of the lipidlowering therapy in adults has rested with the HMG CoA reductase inhibitors or statins. The use of these drugs has resulted in important reductions in overall cardiovascular morbidity and mortality. Mechanism of action- reduction of cholesterol synthesis in liver; inhibiting the rate-limiting step in endogenous cholesterol synthesis; compensatory increase in synthesis of LDL receptors on hepatic and extra hepatic tissues; increase in hepatic uptake of circulating LDL which decreases plasma LDL cholesterol; increase in HDL, decrease in TGs and vasodi‐ latation and decrease in atherosclerosis. Pharmacological indication: Clinically used in the treatment of all types of hyperlipidemia except those who are homozygous for familial hypercholesterolemia (lack of LDL receptors). Table 2 summarizes the statins and their

> **FDA-Approved Maximum (mg)**

**Half-life (hours)**

**Average Decrease in LDL-C Per Dose (mg:%)**

20:43 80:60

80:35

4:43

80:37

10:52 40:63

80:36-47

10/40:55

clinically applications.

244 Antioxidant-Antidiabetic Agents and Human Health

**Table 2.** HMG-CoA INHIBITORS

S**tarting Dose (mg)**

Atorvastatin (lipitor) 10-20 80 14 or 20-30 10:39

Fluvastatin (Lescol) 20 80 3 20:22

Lovastatin (Mevacor) 20 80 2 20:28 Pitavastatin (Livalo) 2 4 12 2:36

Pravastatin (Pravachol) 40 80 2 40:34

Rosuvastatin (Crestor) 5-10 40 19 5:45

Simvastatin (Zocor) 20 80 4 20:38

Simvastatin/Ezetimibe (Vytorin) 10/10 10/40 22 10/10:45

(2) Fibrates (activators of lipoprotein lipase): Mechanism of action- agonists at peroxisome proliferator-activated receptor (PPAR); hydrolysis of VLDL and chylomicrons; decrease in serum TGs; increase clearance of LDL by liver and increase in HDL and expression of genes responsible for increased activity of plasma lipoprotein lipase enzyme. Pharmacological indication: most effective in reduction TGs (hypertriglyceridemia); combined hyperlipidemia (type III) if statins are contraindicated. Typical examples are fenofibrate(prodrug) and gemfibrozil (lopid) (3) Ezetimibe: Mechanism of action- inhibits intestinal cholesterol and

**Drug**

into: Primary prevention- (i) initial treatment is diet/exercise and should be given three to six months on dietary therapy prior to beginning medication and longer if lipids are improving and nearing LDL thresholds (ii) obtain cholesterol tests starting at the age of 20 (iii) eat a diet low in total fat, saturated fat, and cholesterol namely eat poultry without the skin, fish, vegetables, most fruits, whole grains, and skim milk (iv) reduce sugar intake (v) eat foods high in soluble fiber (vi) eat more cold water fish and soy products (vii) avoid cigarette smoking (viii) drink alcohol in moderation (two drinks per day for men, one drink per day for women) (ix) avoid overweight (x) exercise regularly and control blood sugar if diabetes is implicated (xi) increase physical activity (xii) consume a diet that contains adequate potassium, calcium, and magnesium to facilitate blood pressure control. Secondary prevention: Measuring lipids in adolescents that have strong family history of two or more coronary heart disease risk factors. In summary, US National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III in its guidelines has communicated the importance of early identification of risk, lifestyle modification, and pharmacologic treatment as the mainstay of therapy for hyperlipidemia and in the prevention of cardiovascular-related death.

**Sources Morphological parts Comments References**

*Emilapraetermissa* Leaves, aqueous extract Hypolipidemic activity Anaka *et al*.*,* 2013

Fruit, aqueous extract Hypolipidemic activity at

Leaves, aqueous extract Hypolipidemic activity at

Leaves, methanolic extract Hypolipidemic activity at 40 mg/kg

> Hypolipidemic activity at 300-900 mg/kg

> Hypolipidemic activity at 50-100 mg/kg

100-400 mg/kg

400-600 mg/kg

20-100 mg/kg

100-200 mg/kg

Hypolipidemic activity Hypolipidemic activity at 100-200 mg/kg

mg/kg

mg/g

100-800 mg/kg

30-60 mg/kg

100-600 mg/kg

125-500 mg/kg

100-300 mg/kg

ml/kg

*Stachytarphelaaugustifolia* Aerial part, methanolic extractHypolipidemic activity Garba *et al*., 2013 *Vitexdoniana* Leaves, ethanolic extract Hypolipidemic activity Oche *et al*., 2012

Hypolipidemic activity at

Hypolipidemic activity at 100-150 mg/kg

Kolawole *et al*., 2012

http://dx.doi.org/10.5772/57181

247

Plants with Hypolipidaemic Effects from Nigerian Flora

Udenze *et al*., 2012

Udem *et al*., 2011

Odey *et al*., 2013

Nnodim *et al*, 2011

Mohammed *et al*., 2012

Oluwatosin *et al*., 2008 Igbakin 2009, Owen *et al*.,

Ghasi *et al*., 2000

Adenaya *et al*., 2008

Odetola *et al*., 2006

Adeneye & Agbaje, 2007

Antia & Okokon, 2005

Saidu *et al*., 2010

Adeneye, 2008

Hypolipidemic activity Adeyemi *et al*., 2009

Hypolipidemic activity Orhue and Nwanze, 2006

2011

Elekofehiniti *et al*. 2012; Sodipo *et al*., 2011

Oluwatosin *et al*.*,* 2012

Nwangwa and Ekhoye 2013

*PerseaAmerican* (Avocado

*Solanumanguivi*, *S*. *macrocarpum*

*Acalypha* torta A. capitata

*Vernonia* amygdalina Vernonia amygdalina

*Garciniakola* Root and seed, normal saline extracts

extract

extract

*Nauclealatifolia* Root and stem bark, ethanolic extract

*Scopariadulcis* Plant (herb) parts, methanolic extract

extract

extract

*Parkiabiglobosa* Plant parts, methanolic

*Caricapapaya* Seed, aqueous extract Hypolipidemic activity at

Cleistopholis patens Leaves, aqueous extract Hypolipidemic activity at

*Alchorneacordifolia* Leaves, butanolic extract Hypolipidemic activity at 800

Plant parts, methanolic extract; Leaves, ethanolic extract; root, normal saline

Moringa oleifera Leaves, aqueous extract Hypolipidemic activity at 1

*Clerodendrumcapitalum* Leaves, aqueous extract Hypolipidemic activity at

*Citrusparadisi* Seed, methanolic extract Hypolipidemic activity at

*Cymbopogoncitrates* Leaves, aqueous extract Hypolipidemic activity at

*Catharanthusroseus* Leaves, aqueous extract Hypolipidemic activity at1

*Albizziachevalieri* Root, aqueous extract Hypolipidemic activity at

*Viscumalbum* Plant parts, methanolic

*Annonamuricata* Plant parts, methanolic

pea)

**The Promise of Nigeria Natural Products**: Since the recognition of hyperlipiermia, a large number of plant species have been identified as having antihyperlipidermic properties and natural products are part of the current therapy for hyperlipidermia. Numerous natural products with antihyperlipidemic effect have been described in the literature. The objective of this chapter is to summarize the role of Nigeria natural products in the treatment and preven‐ tion of hyperlipidermia to date and to highlight specific classes of compounds that possess a requisite level of activity that would be considered worthy of further investigation as potential drug candidate.
