General information

Body fats provide the human organism with energy (fuel).  They are structural components of the basic unit of life—the cell—and form initial chemical unions from which human hormones are biosynthesized.

Α) Cholesterol is a sterol located in the membrane of cells of all body tissues and in the blood plasma of all animals. It binds to proteins and lipoproteins and is found in its highest concentrations in tissues that either produce it or that have dense membranes, for example the liver, the spine and the brain, as well as in atheromas (or plaque). Edible cholesterol is not sufficient for the body’s needs, the result being that most of it is produced by the liver. The lipids (i.e. both liquid and solid fats) in our body are from both an exogenous source via the intake of food and from an endogenous source, which is their synthesis by the liver.  Lipids (mainly cholesterol and triglycerides) are solubilized and transported to and from the liver within the aqueous blood environment of the human organism by means of carriers named lipoproteins.  Of major importance are the LDL (low-density) lipoproteins whose main role is the transportation of cholesterol from the liver to the tissues and thus to the arteries, where, should the cholesterol build up, this results in atheromata—that is to say, the formation of plaque that narrows the artery channel and restricts the flow of blood. The latter explains the term applied to this type of cholesterol of “bad cholesterol”, whereas HDL (high-density) cholesterol, which carries cholesterol away from the arteries and back to the liver thus preventing the formation of atheromata / plaque, is called “good cholesterol”.

Β) Triglycerides are among the basic lipids that are to be found in food. Triglycerides in foodstuffs are dispersed in the intestine and, subsequently, are transported by means of chylomicrons to peripheral tissues where they undergo intense processing before reaching the liver.  Specifically, they release free fatty acids into the bloodstream, which are used for energy production and finally are stored as fat in the body.


  • Cholesterol and triglycerides serve as the basis of the structure of cell membranes.
  • Cholesterol has a role in allowing nerve cells (neurons) of the brain to communicate, while it also helps in the formation and protection of neurons and the creation of tissue cells.
  • It is involved in the synthesis of hormones, e.g. testosterone, oestrogen.
  • It is involved in the synthesis of vitamin D.
  • It comprises a component of the salts of cholic acid which, in their turn, contribute to the digestion of fats.

1) Dyslipidaemia

  • Dyslipidaemia means an abnormal amount of lipids (cholesterol and/or fat) in the blood (i.e. dys-lipid-aemia). It is specifically both the increase in whole-body cholesterol, LDL and triglycerides as well as the reduction of HDL, this causing damage to body functioning.
  • Dyslipidaemia is categorized into primary, when it is of genetic (inherited) aetiology, and secondary, when it is caused by other pathological conditions or an unhealthy diet and sedentary lifestyle.  In addition, according to the predominant disorder, it may be characterized as hypercholesterolaemia (elevated cholesterol), hypertriglyceridaemia (elevated triglycerides) and mixed dyslipidaemia (elevated cholesterol and triglycerides).
  • Primary dyslipidaemia is rarer than secondary: it is characterized by major disorders in the levels of lipids which usually manifest more frequently than those in secondary dyslipidaemia in clinical trials.  They are largely responsible for the development of ischaemic cardiovascular diseases among younger-aged individuals (3rd and 4th decades of life).
  • Secondary dyslipidaemias are associated with an unhealthy diet as well as with other accompanying diseases, such a diabetes mellitus, hypothyroidism, nephrotic syndrome, or obesity or certain medications (e.g. diuretics).

2) Distinguishing between the hyperlipidaemias

a) Hyperlipoproteinaemia type I

  • Cholesterol is normal, while the triglycerides are greatly increased (often exceeding 1,000 mg).
  • Symptoms often appear, although not always, before the age of 10. It may manifest as intense abdominal pain. The liver and spleen are enlarged. On ophthalmoscopy, the damaged arterioles appear yellowish.  Occasionally there is acute pancreatitis.  The disease is inherited as a recessive trait.
  • Other diseases that produce a similar laboratory profile (secondary hyperliproteinaemias) are diabetes mellitus, thyroid diseases, pancreatitis and the taking of oral contraceptives.

b) Hyperlipoproteinaemia type II

  • This is subdivided into subtypes IIa and IIb.
  • Type IIa is characterized by a big increase in LDL cholesterol. Plasma cholesterol values are high, but the triglycerides are normal.  The genetic defect that is associated with this picture is familial hypercholesterolaemia, which is inherited as an autosomal dominant trait.
  • Type IIb is relatively common and is characterized by elevated LDL as well as VLDL (very low-density).  Both cholesterol and triglycerides are increased.

In general, type II is a greater health risk.  Homozygotes exhibit a more severe and earlier clinical picture as compared with heterozygotes. There are reports of some homozygotes with type IIb suffering a heart attack during their childhood.
Most homozygotes do not live over the age of 40.  Heterozygotes usually experience angina or heart attack between the ages of 30 and 60. In most cases (particularly among homozygotes), xanthomas (visible yellowish-orange, lipid-filled nodules that are due to a deposition of fat in the tendons, especially the Achilles tendon, and large areas of the hands, the knees and the elbows) are observed.
Often also observed is gerontoxon (or arcus senilis:  an opaque circle around the cornea of the eye frequently seen in elderly people), and in other cases there is a yellowish deposit of fat under the skin usually on or around the eyelids which is called xanthelasma.

c) Hyperlipoproteinaemia type IIΙ

Cholesterol and triglycerides increase in roughly equal amounts.  It is relatively rare.

d) Hyperlipoproteinaemia type IV

  • This type includes familial combined hyperlipoproteinaemia and the lighter forms of familial hypertriglyceridaemia.
  • It is often observed secondary to diabetes, kidney failure, nephrotic syndrome, oestrogen administration, contraceptive use, hypothyroidism, and others. It is a fairly common state. It frequently occurs among middle-aged and older obese persons who often develop diabetes or simply reduced glucose tolerance and hyperuricaemia.  Excess intake of carbohydrates as well as of alcoholic drinks aggravates cases of hypertriglyceridaemia.

e) Hyperlipoproteinaemia type V

This is a rare condition.  It is characterized by a large increase in chylomicrons and VLDL. Both cholesterol and triglycerides are elevated.  It is worsened by fat- and carbohydrate-rich foods.  Symptoms vary (abdominal pains, pancreatitis, hepatosplenomegaly, obesity, diabetes, etc.).

3) Symptoms

Dyslipidaemia has justifiably been called a “silent killer”, a treacherous adversary since, more often than not, it has no symptoms and gives no warning, causing serious damage to the lumen, or inside space, of the arteries and narrowing them.  It thereby impairs the blood supply to the vital organs (heart, brain, kidneys, digestive system, etc.).  It is only when symptoms of ischaemia (i.e. reduced blood supply) manifest in the organ that dyslipidaemia will be detected, it then having completed its silent and destructive action.
More rarely, when serum lipid levels are particularly disrupted (as in primary dyslipidaemias), skin lipid aggregates (such as eyelid xanthomas or tendon xanthelasmas) may occur, gerontoxon (or arcus senilis, a whitish ring around the periphery of the iris) or, in pancreatitis, hypertriglyceridaemia which is usually intractable.

4) Treatment

Assessment of the normal lipids limits is individualized in accordance with the presence or not of other parameters that raise cardiovascular risk.  These parameters are:

  1. Arterial hypertension (>140/90 or taking antihypertensive medication)
  2. Smoking
  3. Low HDL levels
  4. Age (men of 45, women of 55)
  5. Having a first-degree relative who suffered coronary heart disease at a relatively young age (men < 55, women < 65)

If HDL levels are high (>60), this removes a major risk factor.
For all population groups, irrespective of cardiovascular risk, dyslipidaemia will exist when:
–    HDL is < 40 in men and < 50 in women
–    triglycerides are >150 (both genders)
Normal LDL levels are individualized and dyslipidaemia exists when:
–   among persons with 0 – 1 risk factors (as mentioned above) LDL is > 160
–   among persons with 2 or more risk factors LDL is > 130
–   among persons with coronary heart disease or comparable conditions (diabetes mellitus, abdominal aortic aneurysm, transient ischaemic attacks, stroke or 10-year absolute CVD risk of >20%) LDL is > 100
–   among persons with diabetes mellitus and concurrent symptomatic coronary disease LDL is > 70.

  • Treatment of dyslipidaemia requires a holistic approach, which incorporates correction of the cause of secondary dyslipidaemia (e.g. hypothyroidism); determination and treatment of concomitant diseases that exponentially increase cardiovascular risk (e.g. obesity, hypertension, smoking, heavy drinking, etc.).
  • Basic to the treatment of dyslipidaemia is a combination of diet and exercise interventions or modifications that will be determined and prescribed by the attending physician, along with administration of medication.

5) Who needs to do a screening test?

In Greece, 10,000 people die annually of coronary heart disease, and dyslipidaemia is a major risk factor for this disease. Thus, it is imperative for people to be screened when they have the following:

  • A family history of coronary heart disease, dyslipidaemia or premature death from CVD.
  • The presence of other factors, such as diabetes mellitus, smoking, arterial hypertension.
  • Diseases accompanied by dyslipidaemia, such as hypothyroidism, nephritic syndrome, excessive alcohol intake.
  • Proactive medical testing starts:

a. In childhood if there is a family history of primary dyslipidaemia;
b. At the age of 20 and, provided that lipid levels are normal, this will be repeated every 3-5 years.



Development of a tendon xanthoma. The hand
of a patient with dyslipidaemia
Development of an “arc” in the cornea in a
patient with elevated cholesterol
Development of a xanthelesma over the eyes
in a patient with elevated cholesterol.