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Drugs affecting lipid metabolism. Medications that lead to pathological changes in lipid metabolism. Consequences and complications

It's time to move on to fine-tuning the athlete's nutrition. Understanding all the nuances of metabolism is the key to athletic achievements. Fine-tuning will allow you to move away from classic dietary formulas and adjust nutrition individually to your own needs, achieving the fastest and most lasting results in training and competitions. So, let's study the most controversial aspect of modern dietetics - fat metabolism.

General information

Scientific fact: fats are absorbed and broken down in our body very selectively. So, in digestive tract humans simply do not have enzymes capable of digesting trans fats. The liver infiltrate simply seeks to remove them from the body in the shortest possible way. Perhaps everyone knows that if you eat a lot fatty foods, it causes nausea.

Constant excess fat leads to consequences such as:

On the other hand, balance fatty acids in the body is extremely important for achieving sports results- in particular in terms of increasing endurance and strength. In the process of lipid metabolism, regulation of all body systems occurs, including hormonal and genetic ones.

Let's take a closer look at what fats are good for our body, and how to consume them so that they help achieve the desired result.

Types of fats

The main types of fatty acids entering our body:

simple;
complex;
arbitrary.

According to another classification, fats are divided into monounsaturated and polyunsaturated (for example, here in detail) fatty acids. These are healthy fats for humans. There are also saturated fatty acids, as well as trans fats: these are harmful compounds that interfere with the absorption of essential fatty acids, complicate the transport of amino acids, and stimulate catabolic processes. In other words, neither athletes nor ordinary people need such fats.

Simple

First, let's look at the most dangerous but, at the same time, – The most common fats that enter our body are simple fatty acids.

What is their peculiarity: they disintegrate under the influence of any external acid, including gastric juice, into ethanol and unsaturated fatty acids.

In addition, it is these fats that become a source of cheap energy in the body. They are formed as a result of the conversion of carbohydrates in the liver. This process develops in two directions - either towards the synthesis of glycogen, or towards the growth of adipose tissue. Such tissue consists almost entirely of oxidized glucose, so that in a critical situation the body can quickly synthesize energy from it.

Simple fats are the most dangerous for an athlete:

The simple structure of fats practically does not burden the gastrointestinal tract and hormonal system. As a result, a person easily receives an excess caloric load, which leads to excess weight gain.
When they decay, alcohol, which is poisonous to the body, is released, which is difficult to metabolize and leads to a deterioration in overall health.
They are transported without the help of additional transport proteins, which means they can stick to the walls of blood vessels, which is fraught with the formation cholesterol plaques.

For more information about foods that are metabolized into simple fats, see the Food Table section.

Complex

Complex fats of animal origin proper nutrition are included in the composition muscle tissue. Unlike their predecessors, these are multimolecular compounds.

Let us list the main features of complex fats in terms of their effect on the athlete’s body:

Complex fats are practically not metabolized without the help of free transport proteins.
At correct observance fat balance in the body, complex fats are metabolized to release healthy cholesterol.
They are practically not deposited in the form of cholesterol plaques on the walls of blood vessels.
With complex fats, it is impossible to get an excess of calories - if complex fats are metabolized in the body without insulin opening the transport depot, which causes a decrease in blood glucose.
Complex fats burden liver cells, which can lead to intestinal imbalance and dysbiosis.
The process of breaking down complex fats leads to an increase in acidity, which negatively affects general condition Gastrointestinal tract and is fraught with the development of gastritis and peptic ulcers.

At the same time, fatty acids with a multimolecular structure contain radicals bound by lipid bonds, which means they can denature to the state of free radicals under the influence of temperature. In moderation, complex fats are beneficial for an athlete, but they should not be subjected to heat treatment. In this case, they are metabolized into simple fats, releasing huge amounts of free radicals (potential carcinogens).

free

Free fats are fats with a hybrid structure. For an athlete, these are the most beneficial fats.

In most cases, the body is able to independently convert complex fats into arbitrary fats. However, during the lipid change process, the formula releases alcohols and free radicals.

Consumption of arbitrary fats:

reduces the likelihood of free radical formation;
reduces the likelihood of cholesterol plaques;
has a positive effect on the synthesis of beneficial hormones;
practically does not burden the digestive system;
does not lead to excess calories;
do not cause an influx of additional acid.

Despite the many useful properties, polyunsaturated acids(in fact, these are arbitrary fats) are easily metabolized into simple fats, and complex structures that have a lack of molecules are easily metabolized into free radicals, obtaining a complete structure from glucose molecules.

What does an athlete need to know?

Now let’s move on to what an athlete needs to know about lipid metabolism in the body from the entire biochemistry course:

Paragraph 1. Classic nutrition, not adapted for sports needs, contains many simple fatty acid molecules. This is bad. Conclusion: radically reduce your fatty acid intake and stop frying in oil.

Point 2. Under influence heat treatment polyunsaturated acids break down into simple fats. Conclusion: replace fried foods with baked ones. The main source of fats should be vegetable oils- Dress salads with them.

Point 3. Avoid eating fatty acids with carbohydrates. Under the influence of insulin, fats, practically without the influence of transport proteins, enter the lipid depot in their complete structure. In the future, even during fat burning processes, they will release ethyl alcohol, and this is an additional blow to metabolism.

And now about the benefits of fats:

Fats must be consumed, as they lubricate joints and ligaments.
In the process of fat metabolism, the synthesis of basic hormones occurs.
To create a positive anabolic background, you need to maintain a balance of polyunsaturated omega 3, omega 6 and omega 9 fats in the body.

To achieve the right balance, you need to limit your total calorie intake from fat to 20% of your total fat intake. overall plan nutrition. It is important to take them in combination with protein foods, and not carbohydrates. In this case, the transport ones that will be synthesized in acidic environment gastric juice, will be able to almost immediately metabolize excess fat, removing it from circulatory system and digesting until final product vital activity of the body.

Product table

Product	Omega-3	Omega-6	Omega-3: Omega-6
Spinach (cooked)	—	0.1
Spinach	—	0.1	Residual moments, less than a milligram
fresh	1.058	0.114	1: 0.11
Oysters	0.840	0.041	1: 0.04
	0.144 - 1.554	0.010 — 0.058	1: 0.005 – 1: 0.40
Pacific cod	0.111	0.008	1: 0.04
Pacific mackerel fresh	1.514	0.115	1: 0.08
Fresh Atlantic mackerel	1.580	0.1111	1: 0. 08
Pacific fresh	1.418	0.1111	1: 0.08
Beet tops. poached	—	Residual moments, less than a milligram	Residual moments, less than a milligram
Atlantic sardines	1.480	0.110	1: 0.08
Swordfish	0.815	0.040	1: 0.04
Rapeseed liquid fat in the form of oil	14.504	11.148	1: 1.8
Palm liquid fat in the form of oil	11.100	0.100	1: 45
Fresh halibut	0.5511	0.048	1: 0.05
Olive liquid fat in the form of oil	11.854	0.851	1: 14
Atlantic eel fresh	0.554	0.1115	1: 0.40
Atlantic scallop	0.4115	0.004	1: 0.01
Sea shellfish	0.4115	0.041	1: 0.08
Liquid fat in the form of macadamia oil	1.400	0	No Omega-3
Liquid fat in the form of flaxseed oil	11.801	54.400	1: 0.1
Liquid fat in the form of hazelnut oil	10.101	0	No Omega-3
Liquid fat in the form of avocado oil	11.541	0.1158	1: 14
Canned salmon	1.414	0.151	1: 0.11
Atlantic salmon. farm raised	1.505	0.1181	1: 0.411
Atlantic salmon	1.585	0.181	1: 0.05
Turnip leaf elements. stewed	—	Residual moments, less than a milligram	Residual moments, less than a milligram
Dandelion leaf elements. stewed	—	0.1	Residual moments, less than a milligram
Stewed chard leaves	—	0.0	Residual moments, less than a milligram
Fresh red lettuce leaf elements	—	Residual moments, less than a milligram	Residual moments, less than a milligram
	—	Residual moments, less than a milligram	Residual moments, less than a milligram
Fresh leafy elements of yellow lettuce	—	Residual moments, less than a milligram	Residual moments, less than a milligram
Collard kale. stewed	—	0.1	0.1
Kuban sunflower liquid fat in the form of oil (oleic acid content 80% or higher)	4.505	0.1111	1: 111
Shrimps	0.501	0.018	1: 0.05
Coconut liquid fat in the form of oil	1.800	0	No Omega-3
Cale. stewed	—	0.1	0.1
Flounder	0.554	0.008	1: 0.1
Cocoa liquid fat in the form of butter	1.800	0.100	1: 18
Black caviar and	5.8811	0.081	1: 0.01
Mustard leaf elements. stewed	—	Residual moments, less than a milligram	Residual moments, less than a milligram
Fresh Boston salad	—	Residual moments, less than a milligram	Residual moments, less than a milligram

Bottom line

So, the recommendation of all times and peoples to “eat less fat” is only partly true. Some fatty acids are simply irreplaceable and must be included in an athlete’s diet. To correctly understand how an athlete should consume fats, here is the following story:

A young athlete approaches the coach and asks: how to eat fats correctly? The coach answers: don’t eat fat. After this, the athlete understands that fats are harmful to the body and learns to plan his meals without lipids. He then finds loopholes where the use of lipids is justified. He learns how to create the perfect meal plan with variable fats. And when he himself becomes a coach, and a young athlete comes up to him and asks how to eat fats correctly, he also answers: don’t eat fats.

Unfortunately, modern conditions life, poor ecology, poor quality nutrition, physical inactivity, neuroses and stress cause a number of ailments, the causes of which are not known to everyone. And in most cases they lie in a violation of lipid (fat) metabolism. The fact is that our body is constantly working to process the substances that enter it. nutrients and the energy necessary to maintain life processes. When these functions are disrupted, diseases such as:

vascular atherosclerosis;
diabetes and other endocrine disruptions;
obesity.

In addition, lipid metabolism disorders affect the condition of the skin, causing not only cosmetic defects such as cellulite, but also a number of dermatological diseases.

Meanwhile, impaired fat metabolism is difficult to correct, since it directly depends on sex hormones, insulin, triglin, adrenaline and others.

What is a lipid metabolism disorder?

To understand what this disorder is, we need to look at some of the body's functions.

The fact is that various substances come to us with food, these are fats, carbohydrates, proteins, as well as amino acids, vitamins, and mineral salts. To process them into energy, the body performs a number of functions:

Assimilation, which consists of synthesizing organic substances and storing energy. The process is called anabolism.
Dissimilation, which is the breakdown of organic compounds and the release of energy. This is catabolism.

Both processes should normally be in a state of balance. When it is violated, patients begin to pathologically lose weight when dissimilation predominates. And, on the contrary, a shift towards assimilation stimulates a rapid gain of extra pounds.

Before starting treatment for lipid metabolism, let’s establish the reasons, find out why this happens?

The performance of these functions depends on the balance of calories consumed and their expenditure.

However, the metabolic process is also influenced by factors such as:

Genetic predisposition.
Poor nutrition, overeating, eating the same type of fatty foods.
Insufficient physical activity.
Psycho-emotional stress and stress.

However, not only fats cause lipid metabolism disorders. Carbohydrates and proteins take part in the process of generating and releasing energy, so it is extremely important that the diet is balanced.

To understand that the body needs correction, you need to find out how the disorder manifests itself metabolic processes.

Symptoms

First of all, lipid metabolism disorder is expressed in the accumulation of subcutaneous fat. This not only manifests itself in intense weight gain, but also entails the development of diabetes mellitus, atherosclerosis, infertility, heart disease, obstructive apnea and other ailments that require urgent intervention and lipid-lowering therapy. This method Treatment involves taking medications and following a diet.

However, obesity can manifest itself as an accumulation of lipids in subcutaneous tissue, and an excess in the blood. Then atherosclerotic plaques form in the vessels.

A metabolic disorder can be accompanied by severe, causeless weight loss that occurs without changes in diet.

In addition, the following signs may indicate pathology:

The complexion becomes painful.
A rash appears on the skin.
Hair loses its shine, becomes dull and brittle, and increases dryness.
The thermoregulatory function of the body is disrupted.
Sleep becomes shallow and restless.

In addition, pockets of swelling appear on the body, and muscle and joint pain bothers them.

Complications

Metabolic disorders can lead to the development various diseases. As mentioned above, excess lipids cause obesity with the ensuing consequences. A lack of proteins is fraught with dystrophy, and an excess can lead to disruption of the liver and kidneys and the development of neuroses.

Angle disorder water balance causes diabetes mellitus.

Mineral metabolism is also important, since diseases develop with a lack of iodine thyroid gland, and a lack of fluoride provokes caries. With calcium deficiency, the musculoskeletal system suffers. Excess salts lead to the development of gout.

Often, noticing symptoms of metabolic disorders, people begin to self-treat. This approach is extremely undesirable, because the reasons may lie in the disruption of metabolic processes associated with the processing and assimilation of various substances. Before starting treatment, it is necessary to undergo an examination. This will allow you to make a diagnosis and correctly select a treatment method. In addition, the consequences also have to be treated, so seeing a doctor is extremely important.

Treatment with folk remedies

In advanced conditions and the presence of complications, it is not possible to do without drug therapy. However, on initial stages correction of nutrition, exercise, normalization of work and rest schedules, and stabilization of the psycho-emotional background will help.

The diet requires:

Reduce your consumption of fats, especially animal fats.
Increase your intake of vegetables and fruits with high content fiber.
Enrichment of the diet with vitamins.

However, it is not recommended to develop diets on your own, since poor nutrition can provoke the opposite effect.

Physical activity will help you lose weight.

For centuries, remedies have been successfully used traditional medicine to restore metabolic processes. Healers and herbalists used plants for healing various ailments. Violation is no exception fat metabolism. Modern doctors do not rule out treatment folk remedies, as an addition to complex therapy.

The most effective herbs in the fight against metabolic disorders are plantain, chamomile, St. John's wort, immortelle, fireweed, hawthorn, dandelion leaves, viburnum, strawberries, and birch buds.

However, the use of folk remedies must be coordinated with a doctor, who will recommend the desired composition herbal collection for each specific patient and will offer The right way their applications.

Normal functioning of everything human body due, among other things, to the processes that make up lipid metabolism. It is difficult to overestimate its importance. After all, lipid metabolism disorders are almost always a signal of certain pathologies. These are also symptoms of many unpleasant diseases. In general, lipids in the specialized literature are fats that are synthesized in the liver or enter the human body with food. Since lipids are of fatty origin, this determines their high hydrophobicity, that is, their ability to not dissolve in water.

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The importance of the process in the body

Actually, lipid metabolism is a variety of complex processes:

fat transport from the intestines;
process of individual species exchanges;
catabolism of fatty acids;
mutual processes of transformation of fatty acids and ketone bodies.

Here are just some examples of such processes. The main groups of lipids include:

phospholipids;
cholesterol;
triglycerides;
fatty acid.

These organic compounds are an important component of the membranes of absolutely all cells of the human body; they play important role in the processes of energy production and storage.

What is dyslipidermia?

A lipid metabolism disorder is a failure in the production of some lipids due to increased synthesis of others, which ends in their excess. The following symptoms of the disorder manifest themselves in the form of severe pathological processes. Without proper treatment, they progress into acute and chronic phases.

Dyslipidemia, as such disorders are also called, has a primary and secondary nature. In the first case, hereditary-genetic reasons play a role, in the second, it’s all to blame bad habits, unhealthy lifestyle, availability certain diseases and/or pathological processes.

Signs and etiology of disorders

In all the variety of manifestations of dyslipidemia, there are signs that should alert a person:

appearance on the skin different places various changes and manifestations, which are also called xanthomas;
excess weight;
fat deposits are visible in the inner corners of the eyes;
enlarged liver and spleen;
various pathological processes in the kidneys;
development of a number of endocrine diseases.

The most striking symptoms of such a disorder are increased content blood cholesterol and triglycerides. It is with the analysis of their level that various diagnostic measures.

Signs may vary depending on what is observed in a particular patient - an excess or lack of lipids. Excess is very often a consequence of malfunctions endocrine system and indicates a number of diseases, among which one of the first places is diabetes mellitus. In case of excess, a person experiences:

high cholesterol levels in the blood;
high pressure;
obesity;
atherosclerotic symptoms.

Lack of lipids can make itself felt:

general exhaustion of the body;
violation menstrual cycle and problems with reproductive functions;
eczema and/or other inflammatory processes skin;
hair loss

Violation of lipid metabolism is, in this case, a consequence of an improper diet or severe starvation, as well as serious disorders gastrointestinal organs. IN in rare cases The cause may be congenital genetic abnormalities.

Separately, it is necessary to mention diabetic dyslipidemia. Despite the fact that carbohydrate metabolism is impaired in this pathology, lipid metabolism is also often devoid of stability. There is increased breakdown of lipids. Lipolysis is insufficient, that is, fats are not broken down enough and accumulate in the body.

The main thing is not to harm yourself

However, these are not the only reasons for such a violation. Even a completely healthy person can harm himself:

unbalanced diet that contains a large number of fats and cholesterol. We are talking primarily about fast food;
sedentary, unsportsmanlike lifestyle;
smoking, alcohol abuse, drug use;
all kinds of diets that are not agreed upon with a specialist in this field.

Other objective reasons include the presence of diseases such as pancreatitis or hepatitis in people ( different types), uremic diseases, complications during pregnancy. Alas, an imbalance of fats in the body can sometimes be caused by banal human aging.

In turn, a disorder of lipid metabolism is the first step towards atherosclerosis, heart attack, stroke, destruction of the general hormonal levels. That is why the treatment of such pathologies is multifaceted. First of all, it is necessary to carry out a number of diagnostic measures, and then strictly adhere to preventive programs, which may be individual in nature.

Problems of diagnosis and treatment

In order to verify the presence/absence of this pathology, specialists perform a detailed lipid profile. It clearly shows all levels of the desired lipid classes. In addition, it is mandatory to carry out general analysis blood for cholesterol. These diagnostic measures should be carried out regularly for people with diabetes. Patients should also see a therapist, who, if necessary, will refer them to to the right specialist. If during diagnostic procedures it is revealed accompanying illnesses or pathology, treatment measures are immediately taken to eliminate them.

Special drug treatment Lipid metabolism disorders include taking:

statins;
drugs nicotinic acid and its derivatives;
fibrates;
antioxidants;
bile acid sequestrants;
dietary supplements.

If this one drug therapy did not bring success, such therapeutic measures as apheresis, plasmapheresis, shunting are indicated small intestine.

Application of diet therapy

However, taking medications alone is unlikely to be effective without changing the patient’s lifestyle, sometimes in the most dramatic way. Diet therapy is one of the key points in complex therapeutic measures. This treatment involves eating foods low in calories. The consumption of animal fats, so-called light carbohydrates, should also be sharply reduced. Should be excluded or at least, sharply limit the consumption of flour, sweet, smoked, salty foods, marinades, sweet carbonated drinks, hot seasonings and sauces. Preference should be given fresh vegetables and fruits, herbs, natural juices, compotes and fruit drinks. You should drink more mineral or well-purified water. Of course, tobacco and alcohol, narcotic and psychotropic drugs are completely excluded.

Additional measures

In parallel with the diet, you should give yourself regular physical activity, albeit small. In some cases, you may need the help of a specialist who will help you write it down and calculate it correctly so that various exercises do not have an impact negative influence for one or another internal organs. At first, light but regular exercise will be enough. hiking on fresh air, morning exercises, small exercises for different parts bodies. Subsequently, light jogging, swimming, cycling, etc. can be added to them.

Many experts draw certain parallels between lipid metabolism and the functioning of the central nervous system. This is why it is very important for people with similar problems to regularly restore their peace of mind. Regular short sessions of meditation and relaxation are suitable, but taking various medications such as antidepressants, on the contrary, can only do more harm. Not to mention the fact that only an appropriate specialist can prescribe them.

A unique novelty is the scientifically proven fact of increased cholesterol levels due to destabilization of the water balance in the body. Therefore, experts recommend that such people drink 150-200 g of purified or boiled water before every meal.

Treatment with folk remedies is additional, but not primary. In case of such pathology, you can use natural honey, which is mixed with freshly squeezed apple juice and drink a glass a day on an empty stomach. The positive effect of this composition is due to the powerful antioxidant properties of honey.

Alternatively, you can use freshly squeezed potato or red beet juice. Potato juice You should consume ½ glass three times a day, and beetroot, a third of a glass, after mixing it with purified or boiled water.

Oats have good hepaprotective and antioxidant properties. It can be consumed in the form of various porridges, or you can prepare infusions from it. For people with impaired lipid metabolism, it is a good idea to periodically take courses of herbal remedies based on milk thistle. In addition to juices, you can drink green tea, herbal infusions, but it is best to avoid coffee, cocoa and black tea.

Dyslipidemia can be primary or secondary and is characterized only by an increase in cholesterol (isolated hypercholesterolemia), triglycerides (isolated hypertriglyceridemia), triglycerides and cholesterol (mixed hyperlipidemia).

WHO Friederickson classification of dyslipidemias

Type of dyslipidemia	Increased lipoprotein content	Increased lipid content	Risk of developing atherosclerosis
I	Chylomicrons	Triglycerides, cholesterol	Not promoted
IIa	LDL	Cholesterol (may be normal)	Sharply increased, especially coronary arteries
IIb	LDL and VLDL	Triglycerides, cholesterol	Same
III	VLDL and chylomicron remnants	Triglycerides, cholesterol	Significantly increased, especially for coronary and peripheral arteries
IV	VLDL	Triglycerides, cholesterol (may be normal)	Likely elevated for coronary atherosclerosis
V	Chylomicrons and VLDL	Triglycerides, cholesterol	Dont clear

Primary dyslipidemias are determined by single or multiple mutations of the corresponding genes, as a result of which there is overproduction or impaired utilization of triglycerides and LDL cholesterol or overproduction and impaired clearance of HDL.

Primary dyslipidemias can be diagnosed in patients with clinical symptoms these violations, with early start atherosclerosis (up to 60 years), in persons with a family history of atherosclerosis or with an increase in serum cholesterol > 240 mg/dL (> 6.2 mmol/L).

Secondary dyslipidemias usually occur in the population of developed countries as a result of sedentary lifestyle life, consumption of food containing large amounts of cholesterol, saturated fatty acids.

Other causes of secondary dyslipidemia may include
1. Diabetes.
2. Alcohol abuse.
3. Chronic renal failure.
4. Hyperthyroidism.
5. Primary biliary cirrhosis.
6. Taking certain medications (beta blockers, antiretroviral drugs, estrogens, progestins, glucocorticoids).

Dyslipidaemias lead to symptoms cardiovascular diseases (coronary disease heart disease, peripheral arterial disease). High triglycerides (> 1000 mg/dL (> 11.3 mmol/L)) may cause symptoms acute pancreatitis. High levels of LDL lead to the appearance of xanthomas (subcutaneous cholesterol deposits) and xanthelasmas (small pale yellow formations in the area upper eyelid caused by the deposition of lipids in them). Severe hypertriglyceridemia (>2000 mg/dL (22.6 mmol/L)) may produce a creamy color to the retinal vessels (lipemia retinalis).

Diagnosis of dyslipidemia
Diagnosis of dyslipidemia is made based on determination of total cholesterol, triglycerides, HDL and LDL. During the day, even healthy people there are fluctuations in cholesterol levels by 10%; triglyceride parameters - by 25%. The determination of these indicators is carried out on an empty stomach.

LDL = cholesterol – (HDL + triglycerides/5).

Based on the fact that LDL is the amount of cholesterol minus the cholesterol contained in VLDL and HDL. The amount of cholesterol in VLDL is equal to triglycerides/5, since the concentration of cholesterol in VLDL is approximately 1/5 of the total amount of lipids.

This formula is used in cases where the fasting patient's triglyceride levels are
The obtained LDL parameters include cholesterol contained in LDLP and lipoprotein (A).

In addition, the LDL content can be determined by a direct method, after centrifugation of the plasma, as a result of which it is possible to separate different lipid fractions.

Measurement lipid profile on an empty stomach is performed in persons over 20 years of age every 5 years. In this case, it is necessary to identify other risk factors for the development of cardiovascular diseases (diabetes mellitus, smoking, arterial hypertension, family history of the development of coronary artery disease in first-degree relatives, which developed in men under the age of 55 years, in women under the age of 65 years). It is advisable to carry out these activities before patients reach the age of 80 years.

The main indications for screening persons over the age of 20 years are risk factors for the development of atherosclerosis (diabetes mellitus, arterial hypertension, smoking, obesity, coronary artery disease in relatives, cholesterol levels > 240 mg/dl (> 6.2 mmol/l) or the presence of dyslipidemia in one of the parents.

In patients with atherosclerosis of the coronary arteries, cardiovascular pathology, a history aggravated with respect to the development of cardiovascular diseases, but with normal indicators lipid fractions; in persons with borderline values of LDL parameters (to decide on the advisability of appropriate therapy); and in individuals with high LDL levels who are resistant to treatment, lipoprotein(a) measurement is necessary. In patients of the same groups, it is necessary to determine the values of C-reactive protein and homocysteine.

In addition, for atherogenesis great importance has a plasma content of high-density lipoproteins (HDL), which have antiatherogenic properties. Their content is inversely proportional to the rate of development of early atherosclerosis. The lower the plasma concentration of HDL, the higher the risk of developing atherosclerosis. In general, the risk of developing atherosclerosis is largely determined by the ratio of atherogenic and non-atherogenic lipoproteins (LP) in the blood.

For an approximate quantitative assessment of the degree of risk of atherosclerosis A.N. Klimov in 1977 the so-called cholesterol atherogenicity coefficient Kcs was proposed, which is the ratio of cholesterol (C) of atherogenic and cholesterol of non-atherogenic drugs:

K xc = LDL cholesterol + VLDL cholesterol/HDL cholesterol

HDL cholesterol is high-density lipoprotein cholesterol.

LDL cholesterol is low density lipoprotein cholesterol.

VLDL cholesterol is very low-density lipid cholesterol.

Since the total amount of atherogenic and non-atherogenic lipoprotein cholesterol (LDL and VLDL) can be represented as the difference between total cholesterol (total cholesterol) and HDL cholesterol, the atherogenic coefficient can be calculated based on the determination of only two indicators - total cholesterol and HDL cholesterol.

K xc = total cholesterol - HDL cholesterol / HDL cholesterol in order to establish the causes of secondary dyslipidemia (in patients with a newly diagnosed disease or suddenly worsened lipid profile parameters), it is necessary to evaluate glucose, liver enzymes, creatinine, thyrotropin, urine protein. ()

Prognosis and treatment

The prognosis and treatment of dyslipidemia depend on lipid levels and the presence of risk factors for the development of cardiovascular diseases.

Gradation of lipid profile indicators in the blood

Index	Interpretation of the result
Total cholesterol mg/dl (mmol/l)
	Desired content
200-239 (5,17 – 6,18)	Limit values
≥ 240 (6,20)	High content
LDL mg/dl (mmol/l)
	Optimal content
100–129 (2,58–3,33)	Limit values
130–159 (3,36–4,11)	Higher normal values
160–189 (4,13–4,88)	High content
≥ 190 (4,91)	Very high
HDL mg/dl (mmol/l)
	Low content
≥ 60 (1,55)	High content
Triglycerides mg/dl (mmol/l)
	Desired content
150–199 (1,695–2,249)	Above normal values

Formally, hypercholesterolemia is diagnosed when the cholesterol content in the blood plasma (serum) is more than 6.2 mmol/l (240 mg/dl), and triglyceridemia is diagnosed when the triglyceride concentration is more than 2.3 mmol/l (200 mg/dl).

Conditions for the use of lipid-lowering drugs. (Link to hypolipidemia therapy).

Recommendations for the treatment of hyperlipidemia depending on the risk group
Risk group	Lifestyle changes required	Drug therapy required	Desired LDL content
High risk: coronary heart disease (CAD) or its equivalent (risk of mortality from CAD or myocardial infarction within 10 years > 20%)	LDL ≥ 100 mg/dL (2.58 mmol/L)	LDL ≥ 100 mg/dL (2.58 mmol/L) (therapy is not necessary if:
Moderately high risk: ≥ 2 risk factors (risk of mortality from coronary artery disease or myocardial infarction within 10 years 10 - 20%)*		LDL ≥ 130 mg/dL (3.36 mmol/L)
Moderate risk: ≥ 2 risk factors (risk of mortality from coronary artery disease or myocardial infarction within 10 years	LDL ≥ 130 mg/dL (3.36 mmol/L)
Low risk: 0–1 risk factors	LDL ≥ 160 mg/dL (4.13 mmol/L)	LDL ≥ 190 mg/dL (4.91 mmol/L) (therapy not necessary if: 160–189 mg/dL (4.13–4.88 mmol/L))

Risk factors include: smoking, arterial hypertension (BP ≥ 140/90 mm Hg); HDL cholesterol *To calculate the 10-year risk, Framingham tables are used to assess the risk of developing atherosclerosis (for men and women).

Framingham table for assessing the risk of cardiovascular events in men.

Age	20–34	35–39	40–44	45–49	50–54	55–59	60–64	65–69	70–74	75–79
Risk assessment (%)	-7	-3		3	6	8	10	11	14	16
Total cholesterol

160–199	4	4	3	3	2	2	1	1	1	1
200–239	8	8	6	6	4	4	2	2	1	1
240–279	11	11	8	8	5	5	3	3	2	2
≥280	13	13	10	10	7	7	4	4	2	2
Non-smokers
Smoking	9	9	7	7	4	4	2	2	1	1
LDL (mg/dl)
≥ 60	1
50–59
40–49	1
	2


120–129
130–139
140–159
≥160

Risk assessment (risk of myocardial infarction or coronary heart disease within 10 years)

0–4 = 1%
5–6 = 2%
7 = 3%
8 = 4%
9 = 5%
10 = 6%
11 = 8%
12 = 10%
13 = 12%
14 = 16%
15 = 20%
16 = 25%
>17 = >30%.

Framingham table for assessing the risk of cardiovascular events in women

Age	20–34	35–39	40–44	45–49	50–54	55–59	60–64	65–69	70–74	75–79
Risk assessment (%)	-7	-3		3	6	8	10	11	14	16
Total cholesterol

160–199	4	4	3	3	2	2	1	1	1	1
200–239	8	8	6	6	4	4	2	2	1	1
240–279	11	11	8	8	5	5	3	3	2	2
≥280	13	13	10	10	7	7	4	4	2	2
Non-smokers
Smoking	9	9	7	7	4	4	2	2	1	1
LDL (mg/dl)
≥ 60	1
50–59
40–49	1
	2
Systolic blood pressure (mm Hg)
	Without therapy – 0; during therapy - 0
120–129	Without therapy – 0; during therapy - 3
130–139	Without therapy – 2; during therapy - 4
140–159	Without therapy – 3; during therapy - 5
≥160	Without therapy – 4; during therapy - 6

Risk assessment (risk of myocardial infarction or coronary heart disease within 10 years):

9–12 =1%
13–14 = 2%
15 = 3%
16 = 4%
17 = 5%
18 = 6%
19 = 8%
20 = 11%
21 = 14%
22 = 17%
23 = 22%
24 = 27%
>25 = >30%.

Lipid metabolism is the metabolism of lipids; it is a complex physiological and biochemical process that occurs in the cells of living organisms. Neutral lipids such as cholesterol and triglycerides (TG) are insoluble in plasma. As a result, lipids circulating in the blood are bound to proteins that transport them to various fabrics for energy utilization, deposition in the form of adipose tissue, products steroid hormones and formation of bile acids.

A lipoprotein is composed of a lipid (the esterified or non-esterified form of cholesterol, triglycerides and phospholipids) and a protein. The protein components of lipoprotein are known as apolipoproteins and apoproteins.

Features of fat metabolism

Lipid metabolism is divided into two main metabolic pathways: endogenous and exogenous. This division is based on the origin of the lipids in question. If the source of lipids is food, then we're talking about about the exogenous metabolic pathway, and if the liver - about the endogenous one.

There are different classes of lipids, each of which is characterized separate function. There are chylomicrons (CM), (VLDL), medium-density lipoproteins (MDL), and density lipoproteins (HDL). The metabolism of individual classes of lipoproteins is not independent; they are all closely interrelated. Understanding lipid metabolism is important for an adequate understanding of the pathophysiology of cardiovascular diseases (CVD) and the mechanisms of action of drugs.

Cholesterol and triglycerides are essential peripheral tissues for a variety of aspects of homeostasis, including the maintenance of cell membranes, the synthesis of steroid hormones and bile acids, and energy utilization. Considering that lipids cannot dissolve in plasma, they are carried by various lipoproteins circulating in the circulatory system.

The basic structure of a lipoprotein usually includes a core consisting of esterified cholesterol and triglyceride, surrounded by a bilayer of phospholipids, as well as non-esterified cholesterol and various proteins called apolipoproteins. These lipoproteins differ in their size, density and composition of lipids, apolipoproteins and other characteristics. It is significant that lipoproteins have different functional qualities (Table 1).

Table 1. Indicators of lipid metabolism and physical characteristics of lipoproteins in plasma.

Lipoprotein	Lipid content	Apolipoproteins	Density (g/ml)	Diameter
Chylomicron (CM)	TG	A-l, A-ll, A-IV, B48, C-l, C-ll, C-IIL E	<0,95	800-5000
Residual chylomicron	TG, cholesterol ester	B48,E	<1,006	>500
VLDL	TG	B100, C-l, C-ll, C-IIL E	< 1,006	300-800
LPSP	Cholesterol ester, TG	B100, C-l, C-ll, C-l II, E	1,006-1,019	250-350
LDL	Cholesterol ester, TG	B100	1,019-1,063	180-280
HDL	Cholesterol ester, TG	A-l, A-ll, A-IV, C-l, C-ll, C-ll, D	1,063-1,21	50-120

The main classes of lipoproteins, ordered by decreasing particle size:

VLDL,
LPSP,
LDL,
HDL.

Dietary lipids enter the circulatory system by attaching to apolipoprotein (apo) B48, which contains chylomicrons synthesized in the intestine. The liver synthesizes VLDL1 and VLDL2 around apoB100, attracting lipids present in the circulatory system (free fatty acids) or in the diet (chylomicron remnants). VLDL1 and VLDL2 are then delipidated by lipoprotein lipase, releasing fatty acids for consumption by skeletal muscle and adipose tissue. VLDL1, releasing lipids, is converted into VLDL2, VLDL2 is further transformed into LPSP. Residual chylomicron, LPSP and LDL can be taken up by the liver through the receptor.

High-density lipoproteins are formed in the intercellular space, where apoAI contacts phospholipids, free cholesterol and forms a disc-shaped HDL particle. Next, this particle interacts with lecithin, and cholesterol esters are formed, forming the HDL core. Cholesterol is ultimately consumed by the liver, and apoAI is secreted by the intestine and liver.

The metabolic pathways of lipids and lipoproteins are closely interconnected. Despite the fact that there are a number of effective drugs that lower lipids in the body, their mechanism of action still remains poorly understood. Further clarification of the molecular mechanisms of action of these drugs is required to improve the quality of treatment of dyslipidemia.

Effect of drugs on lipid metabolism

Statins increase the rate of elimination of VLDL, LPSP and LDL, and also reduce the intensity of VLDL synthesis. This ultimately improves the lipoprotein profile.
Fibrates accelerate the clearance of apoB particles and intensify the production of apoAI.
Nicotinic acid reduces LDL and TG, and also increases HDL content.
Reducing body weight helps reduce the secretion of VLDL, which improves lipoprotein metabolism.
The regulation of lipid metabolism is optimized by omega-3 fatty acids.

Genetic disorders

Science knows a whole set of hereditary dyslipidemic diseases, in which the main defect is the regulation of lipid metabolism. The hereditary nature of these diseases is in some cases confirmed by genetic studies. These diseases are often identified through early lipid screening.

A short list of genetic forms of dyslipidemia.

Hypercholesterolemia: familial hypercholesterolemia, hereditary defective apoB100, polygenic hypercholesterolemia.
Hypertriglyceridemia: familial hypertriglyceridemia, familial hyperchylomicronemia, lipoprotein lipase deficiency.
Disturbances in HDL metabolism: familial hypoalphalipoproteinemia, LCAT deficiency, apoA-l point mutations, ABCA1 deficiency.
Combined forms of hyperlipidemia: familial combined hyperlipidemia, hyperapobetalipoproteinemia, familial disbetalipoproteinemia.

Hypercholesterolemia

Familial hypercholesterolemia is a monozygotic, autosomal, dominant disease involving defective expression and functional activity of the LDL receptor. Heterozygous expression of this disease among the population is observed in one case out of five hundred. Various phenotypes have been identified based on defects in receptor synthesis, trafficking, and binding. This type of familial hypercholesterolemia is associated with significant elevations in LDL cholesterol, the presence of xanthomas, and the premature development of diffuse atherosclerosis.

Clinical manifestations are more pronounced in patients with homozygous mutations. Diagnosis of lipid metabolism disorders is often made on the basis of severe hypercholesterolemia with normal TG and the presence of tendon xanthomas, as well as in the presence of a family history of early CVD. Genetic methods are used to confirm the diagnosis. Treatment uses high doses of statins in addition to medications. In some cases, LDL apheresis is required. Additional evidence from recent research supports the use of intensive care for children and adolescents at high risk. Additional therapeutic options for complex cases include liver transplantation and gene replacement therapy.

Hereditary defective apoB100

Inherited defects in the apoB100 gene are an autosomal disorder that results in lipid abnormalities reminiscent of familial hypercholesterolemia. The clinical severity and approach to treatment of this disease are similar to those for heterozygous familial hypercholesterolemia. Polygenic cholesterolemia is characterized by a moderate increase in LDL, normal TG, early atherosclerosis and the absence of xanthoma. Defects including increased apoB synthesis and decreased receptor expression can lead to elevated LDL cholesterol.

Hypertriglyceridemia

Familial hypertriglyceridemia is an autosomal dominant disorder characterized by elevated triglycerides combined with insulin resistance and failure to regulate blood pressure and uric acid levels. Mutations in the lipoprotein lipase gene that underlie this disease are responsible for the degree to which triglyceride levels rise.

Familial hyperchylomicronemia is an extensive form of lipoprotein lipase mutation leading to a more complex form of hypertriglyceridemia. Lipoprotein lipase deficiency is associated with hypertriglyceridemia and early atherosclerosis. This disease requires a reduction in fat intake and the use of drug therapy to reduce TG. It is also necessary to stop drinking alcohol, fight obesity and intensively treat diabetes.

Disturbances in the metabolism of high-density lipoproteins

Familial hypoalphalipoproteinemia is a rare autosomal disease involving mutations in the apoA-I gene and leading to a decrease in high-density lipoproteins and early atherosclerosis. Lecithin cholesterol acyltransferase deficiency is characterized by faulty esterification of cholesterol on the surface of HDL particles. The result is low HDL levels. Various genetic mutations of apoA-I involving single amino acid substitutions have been described in a number of cases.

Analphalipoproteinemia is characterized by the accumulation of cellular lipids and the presence of foam cells in peripheral tissues, as well as hepatosplenomegaly, peripheral neuropathy, low HDL levels and early atherosclerosis. This disease is caused by mutations in the ABCA1 gene, leading to cellular accumulation of cholesterol. Enhanced renal clearance of apoA-I contributes to the reduction of high-density lipoproteins.

Combined forms of hyperlipidemia

The incidence of familial combined hyperlipidemia can reach 2% in the population. It is characterized by elevated levels of apoB, LDL, and triglycerides. This disease is caused by excess synthesis of apoB100 in the liver. The severity of the disease in a particular individual is determined by the relative lack of lipoprotein lipase activity. Hyperbetalipoproteinemia is a type of familial hyperlipidemia. Statins are commonly used to treat this disease in combination with other drugs, including niacin, bile acid sequestrants, ezetimibe, and fibrates.

Familial dysbetalipoproteinemia is an autosomal recessive disorder characterized by the presence of two apoE2 alleles, as well as elevated LDL-C, xanthomas, and early development of CVD. Failure in the clearance of VLDL and residual chylomicrons leads to the formation of VLDL particles (beta-VLDL). Since this disease is dangerous for the development of CVD and acute pancreatitis, intensive therapy is required to reduce triglycerides.

Lipid metabolism disorders - general characteristics

Inherited diseases of lipoprotein homeostasis lead to hypercholesterolemia, hypertriglyceridemia and low HDL levels.
In most of these cases, there is an increased risk of early CVD.
Diagnosis of metabolic disorders includes early screening using lipidograms, which are an adequate measure for early detection of problems and initiation of therapy.
For close relatives of patients, screening using lipid profiles is recommended, starting in early childhood.

Secondary causes contributing to lipid metabolism disorders

A small number of cases of abnormal LDL, TG, and HDL levels are caused by underlying medical problems and medications. Treatment of these causes usually leads to normalization of lipid metabolism. Accordingly, for patients with dyslipidemia, examination is required for the presence of secondary causes of lipid metabolism disorders.

Assessment of secondary causes of lipid metabolism disorders should be made during the initial examination. Analysis of the initial condition of patients with dyslipidemia should include an assessment of the thyroid gland, as well as liver enzymes, blood sugar and urine biochemistry parameters.

Lipid metabolism disorders in diabetes mellitus

Diabetes is accompanied by hypertriglyceridemia, low HDL and the presence of small and dense LDL particles. In this case, insulin resistance, obesity, increased levels of glucose and free fatty acids and decreased lipoprotein lipase activity are noted. Intensive glycemic control and reduction of central obesity may have a positive effect on total lipid levels, especially in the presence of hypertriglyceridemia.

Disturbances in glucose homeostasis observed in diabetes are accompanied by high blood pressure and dyslipidemia, which leads to atherosclerotic phenomena in the body. Coronary heart disease is the most important factor in mortality in patients with diabetes mellitus. The incidence of this disease is 3–4 times higher in patients with non-insulin-dependent diabetes than in the norm. LDL-lowering drug therapy, especially statins, is effective in reducing the severity of CVD in diabetics.

Biliary obstruction

Chronic cholelithiasis and primary biliary cirrhosis are associated with hypercholesterolemia through the development of xanthomas and increased blood viscosity. Treatment of bile duct obstruction can help normalize lipid metabolism. Although standard lipid-lowering medications can usually be used for biliary obstruction, statins are generally contraindicated in patients with chronic liver disease or cholelithiasis. Plasmaphoresis can also be used to treat symptomatic xanthoma and hyperviscosity.

Kidney diseases

Hypertriglyceridemia is common in patients suffering from chronic renal failure. This is largely due to decreased lipoprotein lipase and hepatic lipase activity. Abnormal triglyceride levels are commonly observed in individuals undergoing peritoneal dialysis treatment.

It has been suggested that a reduced rate of elimination of potential lipase inhibitors plays a key role in the development of this process. There is also an increased level of lipoprotein (a) and a low level of HDL, which leads to accelerated development of CVD. Secondary reasons contributing to the development of hypertriglyceridemia include:

An attempt was made through clinical trials to elucidate the effects of lipid-lowering therapy in patients with end-stage renal disease. These studies showed that atorvastatin did not reduce the composite endpoint of CVD, myocardial infarction and stroke. It was also noted that rosuvastatin did not reduce the incidence of CVD in patients on regular hemodialysis.

Nephrotic syndrome is associated with increased TG and lipoprotein (a), which is caused by increased synthesis of apoB by the liver. Treatment of nephrotic syndrome is based on eliminating the underlying problems, as well as normalizing lipid levels. The use of standard lipid-lowering therapy can be effective, but constant monitoring for possible side effects is required.

Thyroid diseases

Hypothyroidism is accompanied by elevated levels of LDL and triglycerides, and the degree to which they deviate from normal depends on the extent of the problems with the thyroid gland. The reason for this is a decrease in the expression and activity of the LDL receptor, as well as a decrease in lipoprotein lipase activity. Hyperthyroidism usually manifests as low LDL and TG.

Obesity

Central obesity is accompanied by increased levels of VLDL and triglycerides, as well as low HDL. Weight loss, as well as dietary adjustments, lead to positive effects on triglyceride and HDL levels.

Medications

Many concomitant medications cause the development of dyslipidemia. For this reason, the initial evaluation of patients with lipid abnormalities should be accompanied by careful consideration of medications.
Table 2. Drugs that affect lipid levels.

A drug	Increased LDL	Increased triglycerides	Decrease in HDL
Thiazide diuretics	+
Cyclosporine	+
Amiodarone	+
Rosiglitazone	+
Bile acid sequestrants		+
Proteinase inhibitors		+
Retinoids		+
Glucocorticoids		+
Anabolic steroid		+
Sirolimus		+
Beta blockers		+	+
Progestins			+
Androgens			+

Thiazide diuretics and beta blockers, when taken, often cause hypertriglyceridemia and low HDL. Exogenous estrogen and progesterone, which are part of the components of hormone replacement therapy and oral contraceptives, cause hypertriglyceridemia and a decrease in HDL. Antiretroviral drugs for HIV patients are accompanied by hypertriglyceridemia, increased LDL, insulin resistance and lipodystrophy. Anabolic steroids, corticosteroids, cyclosporine, tamoxifen and retinoids also lead to lipid metabolism abnormalities when used.

Treatment of lipid metabolism disorders

Correction of lipid metabolism

The role of lipids in the pathogenesis of atherosclerotic CVD has been well studied and substantiated. This has led to an active search for ways to reduce the level of atherogenic lipids and enhance the protective properties of HDL. The past five decades have been characterized by the development of a wide range of dietary and pharmacological approaches to correct lipid metabolism. A number of these approaches have contributed to reducing the risk of CVD, which has led to the widespread introduction of these drugs into practice (Table 3).
Table 3. Main classes of drugs used to treat lipid metabolism disorders.

Pharmaceutical group	LDL	Triglycerides	HDL