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Dyslipidaemia and Cystic Fibrosis


What is it?

The term dyslipidaemiaidentifies an elevated level of lipids (cholesterol, triglycerides or both) carried in the blood by lipoproteins.

This situation includes hyper-lipoproteinemia (hyperlipidemia), i.e. extremely high levels of total low-density cholesterol (LDL), i.e. ‘bad’ cholesterol, and extremely low levels of high-density cholesterol (HDL), i.e. ‘good’ cholesterol.


This condition is caused by the individual’s lifestyle (e.g. diet too rich in animal fats and proteins), genetics (polygenic hypercholesterolaemia, familial hypercholesterolaemia and familial hypertriglyceridaemia), the presence of certain diseases (diabetes mellitus, obesity, hypothyroidism, kidney and liver disease), the intake of certain drugs or a combination of some of these factors.

Lipoprotein and therefore lipid levels, especially LDL-cholesterol, increase slightly with age. Generally, men have slightly higher levels than women, but in women the increase in levels occurs after the menopause. This can result in atherosclerosis, leading to angina, heart attacks, strokes and peripheral artery disease.


Physical activity, proper nutrition and drug therapy can be effective.

In particular, the intake of omega-3 LCPUFA fatty acids showed cardioprotective effects. The cardiovascular health outcomes attributed to LCPUFA-3, would be the consequences of the following mechanisms:

  • decrease in plasma cholesterol levels by inhibiting the biosynthesis of very low density lipoproteins (VLDL) and TG in the liver, without affecting the biosynthesis of high density lipoproteins (HDL);
  • lower blood pressure due to reduced platelet aggregation and reduced inflammation;
  • decreased incidence of arrhythmias.

Thus, EPA and DHA can act both directly and indirectly, in the form of other biologically active compounds, by reducing the frequency and preventing certain dangerous irregularities in heart rhythm, controlling triglyceride levels in the blood and regulating processes leading to thrombosis and inflammation.mie.

Cystic fibrosis

What is it?

Cystic fibrosis is the most common autosomal recessive genetic disease in the Caucasian population, affecting about 1 in every 2,500 individuals. The condition is caused by a defect in the CFTR gene, which encodes a protein whose function is to transport chlorine through epithelial cells. Under normal conditions, particular cells lining the airways secrete mucus along with a watery fluid that decreases its density. In cystic fibrosis, secretion of aqueous fluid is greatly reduced, so mucus becomes very thick and difficult to remove from the airways even with the most vigorous coughing.with the risk of obstruction of the respiratory, pancreatic and biliary tracts, with progressive damage to the organs involved (bronchi, lungs, pancreas, liver). The disease may manifest itself more or less early on with respiratory impairment (pertussis cough, persistent catarrhal cough, recurrent bronchitis and bronchopneumonia, chronic bronchopneumopathy) and/or with digestive disorders secondary to pancreatic insufficiency (malabsorption syndrome, stunted growth). Less frequently, and depending on the age of the patients, other clinical pictures may also be present (meconium ileus, hepatopathy, diabetes, sinusitis, nasal polyposis, osteoporosis). The advanced stages of the disease can be characterised by the onset of serious complications (cardio-respiratory failure, pneumothorax, haemoptysis, biliary cirrhosis). The diagnosis can be suspected at birth by various methods, but the most common is the trypsin assay in blood taken on the fourth day of life. Diagnostic certainty is provided by the sweat test, which shows a high concentration of chlorine and sodium in the sweat itself, and/or by the identification of gene mutations. In families at risk, prenatal diagnosis is possible in the first trimester of pregnancy with chorionic villus sampling.


Since cysticfibrosis is a hereditary disease that is transmitted in an autosomal recessive manner, it is important to consider the family history of the future parents. The parents of a child with cystic fibrosis both have a defective CFTR gene and a functioning CFTR gene. The parent is not ill, because the functioning gene allows the enzyme to be produced and to function regularly; the parent is called a ‘healthy carrier’. Children with cystic fibrosis have inherited both defective CFTR genes.


The treatment of cystic fibrosis is aimed at counteracting the evolution of the disease and is essentially based on:

  • respiratory physiotherapyto help remove mucus from the bronchi;
  • administration of pancreatic enzymes;
  • balanced, high-calorie diet;
  • antibiotic therapy of respiratory infections targeting germs isolated from bronchial secretions;
  • medical and/or surgical treatment of complications.

Cystic fibrosis patients have altered levels of fatty acids in their blood and tissues. Specifically, they have low levels of omega 3 long-chain polyunsaturated essential fatty acids, and one of these fatty acids, docosahexaenoic acid or DHA is lower than arachidonic acid (an omega 6), which is increased instead. This imbalance would create a condition conducive to inflammation, which is known to be accentuated in this disease, especially in the lungs. This led to suggestions, confirmed by some preliminary clinical studies, for a diet rich in omega-3 fatty acids to raise omega-3 levels and counteract the inflammatory process resulting from higher omega-6 levels.

Information sites

LIFC – Italian Cystic Fibrosis League: www.fibrosicistica.it

SIFC – Italian Society for the Study of Cystic Fibrosis: www.sifc.it

Foodar Solutions

Our Richoil™ line of products are a valuable aid in reducing the inflammatory state and increasing proinflammatory and neutrophil formation in people with cystic fibrosis.