Natural Medicine Approaches to Lower Cholesterol

Olive oil

Cholesterol is a fat that is manufactured in the liver or intestines. It is used to produce hormones & cell membranes & is transported in the blood. Natural medicine approaches to maintain & lower cholesterol.

There are now 900 studies proving the adverse effects of the popularly prescribed statins drugs, including muscle problems, diabetes, birth defects, exercise-related muscle damage and increased cancer risk. Herbal, supplements and diet can lower cholesterol without harmful side effects, and at a saving to the states of overstretched countries.

Cholesterol is also an involved in the manufacture of bile acids, steroid hormones and Vitamin D. Whilst cholesterol is essential, high levels of cholesterol damage arteries and are potentially linked to cardiovascular disease primarily by causing atherosclerosis.

Pathophysiology of cholesterol

Our bodies, make approximately 1 g of cholesterol a day. Depending on how cholesterol is transported, within either LDL or HDL lipoproteins, determines whether high levels of cholesterol in the blood are associated with atherosclerosis and heart diseases. The more cholesterol we eat the less cholesterol our bodies synthesise.

Cholesterol is recycled in our bodies

Cholesterol is excreted by the liver via the bile into the digestive tract and into the stool. Typically about 50% of the excreted cholesterol is reabsorbed by the small intestine back into the bloodstream. Phytosterols from plants, compete with cholesterol reabsorption in the intestinal tract, thus reducing cholesterol reabsorption. Read more in naturopathic treatment of high cholesterol below.

Function of cholesterol

  • Cholesterol is required to build and maintain cell membranes where it modulates membrane fluidity.
  • Within the cell membrane, cholesterol also functions in intracellular transport, cell signaling and nerve conduction.
  • The myelin sheath of neurons that provides insulation for conduction of impulses. Myelin is rich in cholesterol.
  • Within cells, cholesterol is the precursor molecule in several biochemical pathways.
  • In the liver, cholesterol is converted to bile, which is then stored in the gallbladder.
  • Bile contains bile salts, which emulsify fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat-soluble vitamins, Vitamin A, Vitamin D, Vitamin E, and Vitamin K.
  • Cholesterol is an important precursor molecule for the synthesis of Vitamin D and the steroid hormones, including the adrenal gland hormones cortisol and aldosterone as well as the sex hormones progesterone, oestrogens, and testosterone.
  • Some research indicates that cholesterol may act as an antioxidant.

Food sources of cholesterol

Animal fats are a mixture of triglycerides, phospholipids and cholesterol. As a consequence, all foods containing animal fat contain cholesterol to varying extents. Major dietary sources of cholesterol include cheese, egg yolks, beef, pork, poultry, and shrimp. Human breast milk also contains significant quantities of cholesterol.

Plant foods are generally much lower in cholesterol than animal foods. In addition, plant products such as flax seeds contain cholesterol-like compounds called phytosterols, which inhibit cholesterol absorption and lower cholesterol levels.

Saturated fats and trans fats

Total fat intake, especially saturated fat and trans fat, plays a larger role in blood cholesterol than the intake of cholesterol itself. Saturated fat is present in full fat dairy products, animal fats, several types of oil and chocolate.

Trans fats are typically derived from the partial hydrogenation of unsaturated fats. Trans fats are strongly linked with the pathogenesis of atherosclerosis and heart disease. Trans fat is most often found in margarine and hydrogenated vegetable fat, and consequently in many fast foods, snack foods, and fried or baked goods.

A change in diet in addition to other lifestyle modifications may help reduce blood cholesterol. Avoiding animal products may decrease the cholesterol levels in the body not only by reducing the quantity of cholesterol consumed but also by reducing the quantity of cholesterol synthesised by the body.

Cholesterol Synthesis

About 20–25% of daily cholesterol production occurs in the liver. Other sites of cholesterol synthesis are the adrenal glands and the reproductive organs. Cholesterol is made from acetyl CoA which is converted to 3-hydroxy-3-methylglutaryl CoA (HMG-CoA). This molecule is then reduced to mevalonate by the enzyme HMG-CoA reductase. Statins are HMG-CoA reductase inhibitors. Unfortunatley HMG-CoA is also involved in the synthesis of the vitamin CoQ10 so a side effect of statins is CoQ10 deficiency.

Lipoproteins and transport and absorption of cholesterol in the blood

As cholesterol is insoluble in blood, it is transported in the blood within lipoproteins. Triglycerides and cholesterol is carried inside lipoproteins. Lipoproteins assist cholesterol transport and absorption as they have exterior amphiphilic proteins and lipids whose outward-facing surfaces are water-soluble and inward-facing surfaces and are lipid-soluble, therefore allowing insoluble cholesterol to become soluble in the body for transport and absorption.

Lipoproteins have cell-targeting signals that direct the fats they carry to certain tissues. For this reason, there are several types of lipoproteins within blood called, in order of increasing density.

Types of lipoproteins


Chylomicrons, the least dense type of cholesterol transport molecules. Chylomicrons are the transporters that carry fats from the intestine to muscle and other tissues that need fatty acids for energy or fat production. Cholesterol which is not used by muscles remains in more cholesterol-rich chylomicron remnants, which are taken up from the bloodstream by the liver.

Very-low-density lipoprotein (VLDL)

VLDL molecules are produced by the liver and contain excess cholesterol that is not required by the liver for synthesis of bile acids. They become LDL molecules.

Intermediate-density lipoprotein (IDL)

Low-density lipoprotein (LDL)

LDL molecules are the major carriers of cholesterol in the blood. LDL particles carry cholesterol to the peripheral tissues whereby, if in excess, this can oxidise and contribute to atherosclerosis. LDL, especially higher LDL particle concentrations and smaller LDL particle size, contribute to this process more than the cholesterol content of the LDL particles.

LDL and the formation of atherosclerosis

LDL particles are called "bad cholesterol" because they have been linked to atheroma formation (plaque in the arteries). When the cell has abundant cholesterol, LDL receptor synthesis is blocked so that new cholesterol in the form of LDL molecules cannot be taken up. On the other hand, however, more LDL receptors are made when the cell is deficient in cholesterol.

When this system is deregulated, many LDL molecules appear in the blood without receptors on the peripheral tissues. These LDL molecules are oxidised and taken up by macrophages, which become engorged and form foam cells. These cells often become trapped in the walls of blood vessels and contribute to atherosclerotic plaque formation. These plaques are the main causes of heart attacks, strokes, and other serious medical problems, leading to the association of so-called LDL cholesterol (actually a lipoprotein) with "bad" cholesterol. Having large numbers of large LDL particles correlates with a high risk of atherosclerosis.

High-density lipoprotein (HDL)

HDL particles are described as “good cholesterol” because they transport cholesterol back to the liver. In the liver, it is excreted to other tissues that use cholesterol to synthesise hormones in a process known as reverse cholesterol transport (RCT). Having large numbers of large HDL particles means less risk of heart disease. Having small numbers of large HDL is associated with atheromatous disease progression within the arteries.

Metabolism, recycling and excretion of cholesterol

The enterohepatic circulation

Cholesterol is oxidised by the liver into a variety of bile acids. Approximately 95% of the bile acids are reabsorbed from the intestines and the remainder are lost in the faeces (stool). The excretion and reabsorption of bile acids form the basis of what is known as the enterohepatic circulation, which is essential for the digestion and absorption of dietary fats. Under certain circumstances, when more concentrated, as in the gallbladder, cholesterol crystallises and is the major constituent of most gallstones.

From a naturopathic perspective, high cholesterol is as much to do, if not more, with poor enterohepatic clearance of cholesterol as it is to do with excess. dietary intake.

Hypercholesterolemia / High cholesterol

Hypercholesterolemia is abnormal cholesterol levels. Higher concentrations of LDL and lower concentrations of functional HDL are strongly associated with cardiovascular disease because these promote atheroma development in arteries (atherosclerosis). This disease process leads to myocardial infarction (heart attack), stroke, and peripheral vascular disease. Elevated concentrations of oxidised LDL particles, especially "small dense LDL" (sdLDL such as LDL, IDL and VLD) particles, are associated with atheroma formation in the walls of arteries, or atherosclerosis.

In contrast, HDL particles (especially large HDL) have been identified as a mechanism by which cholesterol and inflammatory mediators can be removed from atheroma to take back to the liver for excretion Increased concentrations of HDL correlate with not only lower rates of atheroma but even regression.

The ratio of LDL:HDL

It is the ratio of LDL:HDL rather than the total cholesterol level, that is an indicator of correlating the extent and progress of atherosclerosis. Total cholesterol can be within normal limits, yet if the there are high levels of small LDL and low levels of HDL particles then the risk for atherosclerosis is high. In contrast, however, if LDL is low (mostly large particles) and a HDL is high then atheroma risk is low.

Ideal Cholesterol Levels

The desirable LDL level is considered to be less than 100mg/dL (2.6 mmol/L). A ratio of total cholesterol to HDL, a far more useful measure, of far less than 5:1 is thought to be healthier.

Western Medical Treatment

Elevated cholesterol levels are treated with a strict diet consisting of low-saturated fat, trans-fat free, low cholesterol foods, often followed by one of the various hypolipidemic agents such as statins, fibrates, cholesterol absorption inhibitors, nicotinic acid derivatives or bile acid sequestrants.

Cholesterol testing

It is recommended to test cholesterol every 5 years for people aged 20 years or older. A blood sample after 12-hour fasting is taken by a doctor or a home cholesterol-monitoring device to determine a lipoprotein profile. This measures total cholesterol, LDL (bad) cholesterol, HDL (good) cholesterol, and triglycerides.

Atherosclerosis (Plaque in the Arteries)

Atherosclerosis is commonly referred to as a hardening of the arteries. It is a condition in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol. It is a syndrome affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries, caused largely by the accumulation of macrophage white blood cells and promoted by LDL as they do not clear macrophages and cholesterol from the lining of the arteries. The atheromatous plaque is divided into three distinct components:

  1. 1. The atheroma, which is the nodular accumulation of a soft, flaky, yellowish material at the centre of large plaques, composed of macrophages nearest the lumen of the artery
  2. 2. Underlying areas of cholesterol crystals
  3. 3. Calcification at the outer base of older/more advanced lesions.

Atherosclerosis compared to arteriosclerosis

Arteriosclerosis and atherosclerosis are similar terms but distinct in both spelling and meaning. Arteriosclerosis describes any hardening (and loss of elasticity) of medium or large arteries. Atherosclerosis, on the other hand, is a hardening of an artery specifically due to an atheromatous plaque.

Development of atherosclerosis

Atherogenesis is the developmental process of atheromatous plaques. It is characterised by a remodeling of arteries leading to subendothelial accumulation of fatty substances called plaques. The build up of an atheromatous plaque is a slow process, developed over a period of several years.

Injury to the artery

Atherosclerosis develops from low-density lipoprotein molecules (LDL) becoming oxidised (ldl-ox) by free radicals ( a molecule with an unpaired electron). When oxidised LDL comes in contact with an artery wall, a series of reactions occur to repair the damaged artery wall. Other factors including high blood pressure due to increased blood turbulence, obesity, diabetes, smoking and sedentary lifestyle due to increased blood lipids, and free radicals due to their attack on healthy cells in the intima, all cause injury to the inside of the artery in the form of “scratches”. These “scratches” attract and trap lipids.

Oxidisation of LDL

Low Density Lipoprotein (LDL) particles invade the endothelium and become oxidised. This causes the first stages of the atherosclerotic process known as atherogenesis.

Monocytes are attracted to the area of insult

The body's immune system responds to the damage to the artery wall caused by oxidised LDL by sending specialised white blood cells (macrophages and T-lymphocytes) to absorb the oxidised-LDL forming specialised foam cells. These white blood cells are not able to process the oxidised-LDL, and ultimately grow then rupture, depositing a greater amount of oxidised cholesterol into the artery wall. This triggers more white blood cells, continuing the cycle. These monocytes begin to attack the endothelium of the artery lumen in cardiac muscle causing inflammation, leading to the formation of atheromatous plaques in the lining of the artery.

The formation of a fatty streak

The initial damage to the blood vessel wall results in an inflammatory response. Monocytes (a type of white blood cell) enter the artery wall (endothelium/inner lining) of the artery from the bloodstream, with platelets adhering to the area of insult. The monocytes differentiate into macrophages, which ingest oxidised LDL, slowly turning into large "foam cells". Under the microscope, the lesion now appears as a fatty streak. Foam cells eventually die, and further propagate the inflammatory process. Upper normal or elevated concentrations of blood glucose also play a major role.

Fibrous cap formation or the atheroma

There is smooth muscle proliferation and migration from tunica media to intima responding to cytokines secreted by damaged endothelial cells. This causes the formation of a fibrous capsule covering the fatty streak. The process is worsened if there is insufficient high-density lipoprotein (HDL) to remove cholesterol from tissues and carry it back to the liver. The foam cells and platelets also encourage the migration and proliferation of smooth muscle cells, which in turn ingest lipids, become replaced by collagen and transform into foam cells themselves. The protective fibrous cap normally forms between the fatty deposits and the artery lining (the intima).


Stenosis is a late event, which may never occur and is often the result of repeated plaque rupture and healing responses, not just the atherosclerotic process by itself. These capped fatty deposits (now called 'atheromas') produce enzymes that cause the artery to enlarge over time. As long as the artery enlarges sufficiently to compensate for the extra thickness of the atheroma, then no narrowing ("stenosis") of the opening ("lumen") occurs. If the enlargement is beyond proportion to the atheroma thickness, then an aneurysm is created.

Summary of the development of atherosclerosis

  • Injury to the artery due to free radical damage, smoking, obesity, diabetes, hypertension, inflammation due to excess glucose and/or excess inflammatory forming diet.
  • Monocytes are attracted to the injury in an attempt to heal it.
  • Monocytes become macrophages then soak up oxidised LDL cholesterol to become foam cells. This is now known as a fatty streak and is the beginning of atherogenesis.
  • Smooth muscle cells of the artery wall lining infiltrate the fatty streak to form a fibrous cap.
  • As the foam cells and muscle cells die this results in calcification.
  • Smooth muscle cells ingest lipids and become replaced by collagen and transform into foam cells, forming a protective fibrous cap between the fatty deposits and the artery lining (the intima). These capped fatty deposits are now called atheroma.
  • This leads to stenosis and narrowing of the artery or predisposes the artery to developing aneurysms.

Complications of atherosclerosis 

Rupture and stenosis

Although the disease process tends to be slowly progressive over decades, it usually remains asymptomatic until an atheroma ulcerates, leading to immediate blood clotting at the site of atheroma ulcer, which can quickly obstruct the flow of blood. Though any artery in the body can be involved, usually only severe narrowing or obstruction of some arteries, those that supply more critically important organs are recognised.

Obstruction of arteries supplying the heart muscle result in a heart attack. Obstruction of arteries supplying the brain result in a stroke. These events are life-changing, and often result in irreversible loss of function because lost heart muscle and brain cells do not grow back to any significant extent. Plaque rupture can lead to artery lumen occlusion within seconds to minutes, and potential permanent debility and sometimes sudden death.


Ruptures of the fibrous cap, expose thrombogenic material, such as collagen to the circulation and eventually induce thrombus formation in the lumen. Upon formation, intraluminal thrombi can occlude arteries outright (i.e. When one obstruct the artery to the heart it is known as a coronary occlusion). Interestingly, chronically expanding lesions are often asymptomatic until lumen stenosis is so severe that blood supply to downstream tissue(s) is insufficient resulting in ischemia.


More often the fibrous cap ruptures and move into the circulation eventually occlude smaller downstream branches. This is known as a thromboembolism (i.e. Stroke is often caused by thrombus formation in the carotid arteries).

Infarction- Mainly heart attack and stroke

These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures, causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately 5 minutes. This catastrophic event is called an infarction.

One of the most common recognised scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction (a heart attack). The same process in an artery to the brain is commonly called stroke. Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs, typically caused by a combination of both stenosis and aneurysmal segments narrowed with clots. Since atherosclerosis is a body-wide process, similar events occur also in the arteries to the brain, intestines, and kidney.

Diagnosis of atherosclerosis

Areas of severe narrowing, stenosis, detectable by angiography, and to a lesser extent "stress testing" have long been the focus of human diagnostic techniques for cardiovascular disease, in general. However, these methods focus on detecting only severe narrowing, not the underlying atherosclerosis disease. Over the last couple of decades, methods other than angiography and stress-testing have been increasingly developed as ways to better detect atherosclerotic disease before it becomes symptomatic.

These have included both;

  • anatomic detection methods
  • physiologic measurement methods

Examples of anatomic methods include:

(1) coronary calcium scoring by CT

(2) carotid IMT (intimal media thickness) measurement by ultrasound

(3) intravascular ultrasound (IVUS)

Examples of physiologic methods include:

(1) lipoprotein subclass analysis

(2) HbA1c

(3) hs-CRP

(4) homocysteine

The example of the metabolic syndrome combines both anatomic (abdominal girth) and physiologic (blood pressure, elevated blood glucose) methods.

Western Medical Treatment

If atherosclerosis leads to symptoms, some symptoms such as angina pectoris can be treated. Non-pharmaceutical means are usually the first method of treatment, such as cessation of smoking and practicing regular exercise. If these methods do not work, medicines are usually the next step in treating cardiovascular diseases, and, with improvements, have increasingly become the most effective method over the long term.


In general, the group of medications referred to as statins has been the most popular and are widely prescribed for treating atherosclerosis. They have relatively few short-term or longer-term undesirable side-effects, and several clinical trials comparing statin treatment with placebo have fairly consistently shown strong effects in reducing atherosclerotic disease 'events' and generally ~25% comparative mortality reduction. Combinations of statins, niacin, intestinal cholesterol absorption-inhibiting supplements (ezetimibe and others, and to a much lesser extent fibrates) have been the most successful in changing common but sub-optimal lipoprotein patterns and group outcomes.

Side effects of statins

Satins cause Co Q 10 deficiency. CoQ10 is an essential nutrient involved in energy production in the mitochondria. Since coenzyme Q10 (CoQ10) and cholesterol are both synthesised from the same substance, mevalonate, statin drugs (Lipitor, Zocor, etc) also inhibit the body's synthesis of coenzyme Q10. This is not a "side effect," of statins, but a direct, inherent function of the drugs. In fact, the use of statins can decrease the body's synthesis of coenzyme Q10 by as much as 40%.

Researchers looked at data from more than two million 30-84 year-olds from GP practices in England and Wales over a six-year period. Adverse effects identified in the study, published in the British Medical Journal, include liver problems, acute kidney failure, muscle weakness and cataracts. For kidney failure and liver dysfunction, higher doses of the drugs seemed to be associated with greater risk. Risks of side-effects were greatest in the first year of use.

Healthy people may derive no benefit from taking cholesterol-lowering statins, according to a review of previous studies and in fact statins may damage the health of people who aren't at high risk of a heart attack. The study concluded there is no evidence to justify their use in people at low risk of developing heart disease.

Natural medicine causes & treatment of hypercholesterolemia

  1. Excess dietary intake of high GI carbohydrates, sat fats, trans fat and rancid fats
  2. Diabetes or Impaired glucose tolerance (IGT) + / Elevated serum insulin levels or Metabolic Syndrome
  3. Dyslipoproteinemia- High serum concentration of LDL, and/or VLDL particles and low HDL
  4. Elevated serum levels of triglycerides
  5. Having hypertension on its own increasing risk by 60%
  6. Elevated serum C-reactive protein concentrations or excess inflammation
  7. Central obesity /sedentary lifestyle
  8. Hypercoagulability / thrombophilia (abnormality of blood coagulation)
  9. Postmenopausal oestrogen deficiency
  10. Elevated serum levels of homocysteine
  11. Chronic systemic inflammation as reflected by upper normal WBC concentrations
  12. Nutritional deficiencies B6, B12, CoQ10
  13. Poor enterohepatic function ie sluggish liver
  14. Tobacco smoking increases risk by 200% after several pack years

Naturopathic treatment principles for high cholesterol

  1.  Reduce intake of saturated fats, trans fats and rancid fats
  2.  Improving insulin sensitivity
  3.  Eat a Diet to Lower LDL, raise HDL and thin the blood
  4.  Lower C Reactive Protein and reduce inflammation
  5.  Replace oestrogen deficiency in postmenopausal women
  6.  Lower homocysteine
  7.  Replace nutritional deficiencies
  8.  Improve enterohepatic circulation

1. Reduce intake of saturated fats, trans fats and rancid fats

Saturated fats

Medical, heart-health, and governmental authorities advise that saturated fat is a risk factor for cardiovascular disease (CVD). Examples of foods containing a high proportion of saturated fat include animal fats such as cream, cheese, butter, and ghee; suet, tallow, lard, and fatty meats; as well as certain vegetable products such as coconut oil, cottonseed oil, palm kernel oil, chocolate, and many prepared foods. Lauric and myristic acid are most commonly found in "tropical" oils (e.g., palm kernel, coconut) and dairy products. The saturated fat in meat, eggs, chocolate, and nuts is primarily the triglycerides of palmitic and stearic acid.

Trans fat

Trans fat is the common name for unsaturated fat that undergoes a process called hydrogenation. No trans fats are essential fatty acids; indeed, the consumption of trans fats increases the risk of coronary heart disease by raising levels of "bad" LDL cholesterol and lowering levels of "good" HDL cholesterol. Health authorities worldwide recommend that consumption of trans fat be reduced to trace amounts. Trans fats from partially hydrogenated oils are more harmful than naturally occurring oils.

Some studies have shown natural trans fats in beef and dairy products can have the opposite health effect and can actually be beneficial, e.g. lowering total and LDL cholesterol and triglyceride levels.

Rancid fats

The role of dietary oxidised fats/lipid peroxidation (rancid fats) in humans is not clear. People should theoretically avoid eating rancid fats and oils taste very bad even in small amounts. The majority of oils consumed often hidden in foods however are refined, bleached, deodorised and degummed leaving them colourless, odourless, tasteless to give them a longer shelf life.This extensive processing serves to make peroxidated, rancid oils much more elusive to detection via the various human senses than the unprocessed oils.

Controversy - Does reducing fat in the diet lower cholesterol?

From a naturopapathic perspective, dietary changes such as reducing saturated fats may be less effective. The belief that high fat and cholesterol consumption causes atherosclerosis has been questioned. Because fat and cholesterol are the substances that consist plaque, they are both considered to be contributors to the cause of atherosclerosis, though this remains to be verified. Inflammation is considered to be a cause of atherosclerosis rather than fat and cholesterol.

One key reason for this is that most cholesterol, typically 80-90%, within the body is created and controlled by internal production by all cells in the body (true of all animals), with typically slightly greater relative production by hepatic/liver cells. (Cell structure relies on fat membranes to separate and organise intracellular water, proteins and nucleic acids and cholesterol is one of the components of all animal cell membranes.

2. Improve insulin sensitivity and balance the blood sugar

Insulin resistance is a condition in which the body produces insulin but does not use it properly. When people are insulin resistant, their muscle, fat, and liver cells do not respond properly to insulin. As a result, their bodies need more insulin to help glucose enter cells. The pancreas tries to keep up with this increased demand for insulin by producing more. Eventually, the pancreas fails to keep up with the body's need for insulin. Excess glucose builds up in the bloodstream, setting the stage for diabetes. Many people with insulin resistance have high levels of both glucose and insulin circulating in their blood at the same time. Insulin resistance increases the chance of developing type 2 diabetes and heart disease.

Insulin resistance and metabolic syndrome

Many people with insulin resistance and high blood glucose have other conditions that increase the risk of developing type 2 diabetes and cardiovascular disease. These conditions include having excess weight around the waist, high blood pressure, and abnormal levels of cholesterol and triglycerides in the blood. Having several of these problems is called metabolic syndrome or insulin resistance syndrome, formerly called syndrome X.

Metabolic syndrome is defined as the presence of any three of the following conditions:

  • Central obesity (defined as waist circumference# with ethnicity specific values)

AND any two of the following:

  • Raised triglycerides: > 150mg/dL (1.7mmol/L), or specific treatment for this lipid abnormality
  • Reduced HDL cholesterol: < 40mg/dL (1.03mmol/L) in males, < 50mg/dL (1.29mmol/L) in females, or specific treatment for this lipid abnormality
  • Raised blood pressure: systolic BP > 130 or diastolic BP >85mm Hg, or treatment of previously diagnosed hypertension.

Raised fasting plasma glucose:(FPG)>100mg/dL (5.6mmol/L), or previously diagnosed type 2 diabetes. If FPG >5.6mmol/L or 10mg/dL, OGTT Glucose tolerance test is strongly recommended but is not necessary to define the presence of the Syndrome.

Nutritional therapy to improve insulin sensitivity

Diet to improve insulin sensitivity

Increase Fibre

Fibre reduces insulin production.

Eat Low-Glycemic Index Foods

A low-glycemic-index diet improves insulin sensitivity and improves the regulation of glucose metabolism.

Insulin Levels and Vitamin K

Vitamin K a nutrient found in Brussels sprouts, broccoli, and dark leafy greens regulates insulin levels.

Chromium rich foods

Chromium is involved in Glucose Tolerance Factor (GTF) and insulin production. The highest food sources of chromium are barley, raw onions, ripe tomatoes and romaine lettuce and whole grain cereals.

Supplements to improve insulin sensitivity


Alpha-Lipoic Acid (ALA) plays a fundamental role in converting glucose to energy. Stephan Jacob, MD, of the University of Tübingen, Germany, described his recent study of 74 diabetics given at least 600 mg of ALA supplements daily. The ALA stimulated insulin activity, which safely lowered and stabilised glucose levels. The best food source of ALA are green leafy vegetables like spinach, kale and cabbage.


Chromium mineral helps to escort the glucose from the bloodstream and into the cells of the body and improves insulin sensitivity. High intensity exercise Only 15 minutes of high-intensity exercise, three days a week for at least two week reduces blood-sugar levels and risk of diabetes.

3. Diet to Lower LDL, raise HDL and thin the blood

Many plant compounds are capable of lowering plasma levels of glucose and cholesterol and blood pressure, as well as compounds inhibiting atherosclerosis and thrombosis. Hypoglycemic natural products comprise flavonoids, xanthones, triterpenoids, alkaloids, glycosides, alkyldisulfides, aminobutyric acid derivatives, guanidine, polysaccharides and peptides.

Among natural products with hypocholesterolemic activity are β-carotene, lycopene, cycloartenol, βsitosterol, sitostanol, saponin, soybean protein, indoles, dietary fibre, propionate, mevinolin (β-hydroxy-β-methylglutaryl coenzyme A reductase inhibitor) and polysaccharides. Heparins, flavonoids, tocotrienols, β-hydroxy-β-methylglutaryl coenzyme A reductase inhibitors (statins), garlic compounds and fungal proteases exert antithrombotic action. Statins and garlic compounds also possess antiatherosclerotic activity.

Phytosterols and cholesterol metabolism

Phytosterols are plant sterols structurally similar to cholesterol that act in the intestine to lower cholesterol absorption. This help to control body total cholesterol levels, as well as improves the ration of HDL:LDL.

Food list of phytosterols

  • Flaxseed
  • Wheat germ
  • Oats
  • Rye bread
  • Nuts
  • Almonds
  • Walnuts
  • Pistachios
  • Macadamias
  • Pecans
  • Broccoli
  • Red onion
  • Carrot
  • Potato
  • Brussels sprouts
  • Spinach
  • Strawberry
  • Blueberry
  • Raspberry
  • Lingonberry


The fibre in oats binds to the cholesterol molecules and carry it out of the body. Oatmeal is most effective in lowering LDL cholesterol levels. According to the studies in adults, LDL cholesterol may be lowered by 10 percent in some cases. In these studies, anywhere between 40 and 60 grams, roughly one bowl, of oatmeal was consumed by each subject per day. The cholesterol lowering benefits of oatmeal is also dose-dependent. That is, the more oatmeal you eat, the lower your cholesterol will go.

Fish and Cardiovascular Benefits

The fish-oil-derived EPA and DHA, garlic, and proteolytic enzymes also have been shown to have anticoagulant properties. Intake of fish rich in omega-3 fat (including salmon) is associated with decreased risk of numerous cardiovascular problems including heart attack, stroke, heart arrhythmia, high blood pressure and high triglycerides in the blood. Most of the benefits, however, start to show up in research studies with somewhat higher fish intake, along the lines of 2-3 times per week.

The Oily Fish

  • Mackerel
  • Lake trout
  • Herring
  • Sardines
  • Albacore tuna
  • Salmon
  • Halibut

Thin the bloood

Coagulation is the process of blood cells clumping together to form a clot. Coagulation occurs when blood platelets stick together. This is known as platelet aggregation and Platelet Aggregating Factor(PAF) is involved. As beneficial as this process may be to the healing of wounds, platelet aggregation can be lethal when it occurs in the circulatory system and increases the risk of atherosclerotic plaques develop, heart attacks and stroke. Excess platelet aggregation or abnormal blood clotting is also called hypercoagulability and can be reduced by consuming foods that act as natural PAF inhibitors.

PAF inhibiting foods

PAF inhibiting foods keep the blood thin and decrease the risk of atherosclerosis.

Garlic and onions

Sulphur compounds in onions have also been shown to be anti-inflammatory both by inhibiting the formation of thromboxanes and by inhibiting the action of platelet-activating factor (PAF).


A recent study indicates that ginger (Zingiber officinale) and its compound gingerol is a potent anticoagulant. Platelet aggregation is triggered by an inflammatory substance produced in the body known as arachidonic acid. Ginger constituents inhibit arachidonic acid-induced platelet activation in human whole blood. The components of ginger indeed stop platelets from sticking together, possibly by inhibiting the enzyme COX-1. Gingerol compounds and their derivatives are more potent antiplatelet agents than aspirin under the conditions described in this study


Turmeric exhibits powerful anticoagulant properties due to its ability to inhibit the formation of fibrinogen, a plasma protein that plays a key final role in the cascade that results in blood clotting. Elevated fibrinogen blood levels have been identified in a number of studies to be a major risk factor for coronary heart disease and cerebrovascular disease (strokes), exceeding the contributions of homocysteine, cholesterol and other lipid parameters in the pathogenesis of these diseases. Turmeric can reduce fibrinogen levels, thereby inhibiting blood clotting. Other research shows that turmeric-derived curcumin can directly inhibit arachidonic acid-induced platelet aggregation, possibly by its ability to inhibit the clotting factor known as thromboxane A2.5

Vitamin E

Vitamin E also is a key player in the inhibition of platelet aggregation. Platelets aggregate because arachidonic acid is converted into pro-aggregatory thromboxanes-an oxidative process. As an antioxidant, vitamin E can prevent free radicals causing this conversion.

Salicylates foods are natural blood thinners

Aspirin, also known as salicylate, is a naturally occurring product that reduces inflammation and reduces the risk of stroke and heart attack. Salicylates, interfere with platelet adhesion, which makes it harder for the platelets to aggregate and form a blood clot.

Many foods contain salicylates, which mimic the effects of aspirin and have the potential to make it harder for blood to clot. Spices such as cinnamon, oregano, peppermint, cayenne and curry powder and most fruits are high in salicylates. Honey, vinegar, broccoli, cauliflower, lettuce, apples and nuts are also rich in salicylates.

Fruits and vegetables, in general, are high in salicylates. Salicylates from the diet have the potential to have many of the beneficial effects of aspirin. According to a 2003 article in "The Journal of Clinical Pathology," people who eat more fruits and vegetables are less likely to die from cardiovascular disease and cancer, in part due to the consumption of more salicylates, which can help prevent blood clots and can reduce inflammation throughout the body.

4. Lower C-Reactive Protein and reduce inflammation

C-reactive protein (CRP) is an inflammatory biomarker. Based on the results of several prospective epidemiologic studies, C-reactive protein has emerged as one of the most powerful predictors of cardiovascular disease. High levels of this compound may be a sign of a future risk for heart attacks, stroke and cancer, though it does not seem to be a direct cause.

C reactive protein blood test

A simple blood test for C-reactive protein CRP can be done at the same time as a cholesterol screening. The high-sensitivity C-reactive protein (hs-CRP) test, helps determine heart disease risk and is widely available. It is important to remember that the usefulness of knowing hs-CRP levels in a particular individual is still unknown.

Mediterranean Diet and C Reactive Protein

Levels of C-reactive protein can be decreased by increasing consumption of fruits and vegetables and by taking certain supplements such as vitamin C. Sticking to a Mediterranean diet, high in fruits and vegetables and low in saturated fats, lowers levels of inflammation as reflected by lower levels of C-reactive protein. This effect should, in turn, lead to a lower risk of cardiovascular disease that has been associated with this type of diet.

Fibre and C Reactive Protein

Foods high in fibre lower C reactive protein. In a study of 524 healthy adults, investigators found that those with the highest fibre intake had lower blood levels of C-reactive protein CRP than those who ate the least fibre. The findings support the general recommendation that adults get 20 to 35 grams of fibre per day in the form of fruits, vegetables, beans and whole grains. It's not clear why fibre reduces inflammation, but it lowers cholesterol and blood sugar, both of which can contribute to inflammation.

Both of the main forms of fibre, soluble and insoluble, were related to lower CRP levels. Soluble fibre is found in oatmeal, beans, berries and apples, while whole grains and many vegetables are good sources of insoluble fibre. American Journal of Clinical Nutrition, April 2006.

Flavonoids and C reactive protein

intake of dietary flavonoids is inversely associated with serum c reactive protein concentrations in U.S. adults. Intake of flavonoid-rich foods reduces inflammation-mediated chronic diseases

Vitamin C and C Reactive Protein

Vitamin C treatment significantly reduces C-reactive protein.

Omega-3 fatty acids and C Reactive Protein

Higher intake of n–3 polyunsaturated fatty acids from marine or fish is inversely associated with serum C-reactive protein (CRP) concentrations. Therefore, eating more fish or taking fish oil capsules can reduce C reactive protein levels.

Dark chocolate and C Reactive Protein

Consuming dark chocolate can reduce c reactive protein levels.

General Anti-inflammatory Diet

Certain foods contain compounds which are naturally anti-inflammatory. Examples of such compounds are omega 3, curcumin, resveratrol and flavanoids.

  • Eat plenty of berries and cherries and fruits and vegetables.
  • Minimise saturated and trans fats.
  • Eat a good source of omega-3 fatty acids, such as fish or fish oil supplements, walnuts and flax. #
  • Reduce intake of refined carbohydrates such as pasta and white rice.
  • Eat plenty of whole grains such as oats, brown rice and bulgur wheat.
  • Cut back on red meat and full-fat dairy foods.
  • Eat lean protein sources such as chicken.
  • Avoid refined foods and processed foods.
  • Ginger, curry, and turmeric have an anti-inflammatory effect.
  • Green tea and tea are rich in flavanoids.

5. Replace oestrogen deficiency in postmenopausal women

Post menopause, a woman’s risk of heart disease becomes the same as a man’s. This is because oestrogen has a protective effect on the cardiovascular system. Specifically oestrogen;

Oestrogen and coagulation

  • increase circulating level of factors 2, 7, 9, 10, plasminogen
  • decrease antithrombin III
  • increase platelet adhesiveness

Oestrogen and Lipids

  • increase HDL, triglyceride decrease LDL, fat deposition

Try Carahealth Menopause Support

6. Lower Homocysteine

Homocysteine is a measurable marker for heart disease. Increased levels of homocysteine are linked to high concentrations of endothelial asymmetric dimethylarginine and therefore low levels of nitric oxide otherwise known as endothelial derived relaxing factor (EDRF). EDRF helps relax artery walls to reduce blood pressure.

Homocysteine degrades and inhibits the formation of the three main structural components of the artery, collagen, elastin and the proteoglycans. Homocysteine permanently degrades cysteine disulfide bridges and lysine amino acid residues in proteins, resulting in a breakdown of the collagen matrix. Simply put, high homocysteine results in a breakdown of the itegrity of the arterial walls themselves.

Deficiencies of the vitamins folic acid (B9), pyridoxine (B6), or B12 (cobalamin) can lead to high homocysteine levels. Supplementation with pyridoxine, folic acid, B12 or trimethylglycine (betaine) reduces the concentration of homocysteine in the bloodstream.

7. Replace Nutritional Deficiencies

Niacin (vitamin B3)

Niacin (vitamin B3), in pharmacologic doses, (generally 1,000 to 3,000 mg/day, but starting with much lower doses increased over several weeks, to avoid side-effects) can; Raise HDL levels. Niacin has HDL raising effects (by 10 - 30%) Shift LDL particle distribution to larger particle size Lower lipoprotein(a), atherosclerosis promoting genetic variant of LDL. Individual responses to daily niacin, while mostly evident after a month at effective doses, tend to continue to slowly improve further over time.

Vitamin C

Vitamin C deficiency has been confirmed as an important role in the development of hypercholesterolemia and atherosclerosis, Vitamin C acts as an antioxidant in vessels and inhibits inflammatory process. It has therapeutic properties on high blood pressure and its fluctuation and arterial stiffness in diabetes. Vitamin C is also a natural regulator of cholesterol and higher doses (over 150mg/kg daily) may protect against atherosclerosis even in the situation of elevated cholesterol levels.

B 6

Vitamin B6, also known as pyridoxine, is not credited with lowering cholesterol. It does, however, play a role in lowering your risk of heart disease and stroke by reducing the levels of homocysteine in your system. An amino acid, high levels of homocysteine can cause heart disease and stroke. Food Sources of vitamin B6, eat more brown rice, spinach, carrots, salmon, turkey, chicken, liver, tuna, salmon, sunflower seeds, bran and wheat germ.

Lower blood pressure

8. Improve enterohepatic circulation

Herbal medicine is the best therapy to improve liver function as bitter herbs have a physiological function to promote bile flow and move the stool to encourage elimination of cholesterol via the bowel.

Try Carahealth Heart Tonic

This tincture contains hypocholesterolaemic herbs that specifically lower cholesterol in the blood. The liver and bowel are responsible for the breakdown of fats in the diet and the excretion of cholesterol via the bowel so herbal bitters, which increase the secretion and flow of bile from the liver and gall-bladder are used to assist the breakdown and elimination of cholesterol. The herbs specifically lower cholesterol and triglyceride levels and regulate the ratio of HDL:LDL.

There is evidence from randomised clinical trials that fenugreek (Trigonella foenumgraecum), artichoke (Cynara scolymus), and yarrow (Achillea millefolium) reduce serum cholesterol. Actions Lowers cholesterol Lowers triglycerides Increases HDL (good cholesterol) Lowers LDL (bad cholesterol).


Beetroot is a powerful antioxidant

Beetroot contains pigments called betalains. There are two types of betalains:

  1. Betacyanins (Betacyanins are pigments are red-violet)
  2. Betaxanthins (Betaxanthins are yellowish)

The betalains function both as antioxidants and anti-inflammatory molecules and promote Phase 2 detoxification. (Phase 2 is the second step in the detoxification process). Beetroot also contains antioxidant carotenoids called lutein and zeaxanthin, vitamin C and another antioxidant manganese.

Beetroot is anti-inflammatory

The compounds betanin, isobetanin and vulgaxanthin show anti-inflammatory effects. They inhibit the activity of cyclo-oxygenase enzymes (including both COX-1 and COX-2). The COX enzymes are widely used by cells to produce messaging molecules that trigger inflammation. Several types of heart disease, including atherosclerosis and cancer and diabetes are characterised by excess COX activity. Betaine also lowers levels of several inflammatory markers, including C reactive protein, interleukin-6, and tumor necrosis factor alpha. Beetroot lowers homocysteine as they contain betaine. Elevated levels of homocysteine are associated with excess inflammation and risk of cardiovascular problems like atherosclerosis.

Beetroot assists detoxification processes

Betalin pigments supports phase 2 detoxification process. Phase 2 involves an enzyme called glutathione-S-transferase (GSTs). GSTs attach toxins with glutathione to neutralise them and makes them water-soluble for excretion in the urine. The betalains found in beetroots promote GST activity to aid in the elimination of toxins that require glutathione for excretion.

Beetroot prevents colon cancer and heart disease

Lab studies on human tumour cells have confirmed this possibility for colon, stomach, nerve, lung, breast, prostate and testicular cancers. Beetroots are high in fibre called pectin polysaccharides, which prevents of colon cancer and benefits the cardiovascular system. Beetroot specifically lowers CD8 cells which are responsible for colon cancer.

For further details contact Carina Harkin BHSc.Nat.BHSc.Hom.BHSc.Acu. This email address is being protected from spambots. You need JavaScript enabled to view it.

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