How to Lower Triglyceride Levels Naturally

How can diet lower triglyceride levels?

Triglycerides are a type of fat found in the blood.
High triglyceride levels can be a risk factor for various health conditions. Therefore, your doctor may advise changing your diet to try to reduce their levels. Certain health conditions, genetics, medications, and lifestyle choices are risk factors for high blood triglyceride levels. For example, a diet high in refined carbohydrates, added sugars, saturated fats, and excessive alcohol can increase triglyceride levels in the body.

By changing your diet, you can regulate the level of triglycerides in your blood.

This article explains what triglycerides are and what levels are considered normal. It discusses which foods can lower triglyceride levels and which foods to avoid. It also provides a sample meal plan and describes other options your doctor may recommend.

Causes of “high” and “low” triglycerides

Most often, hypertriglyceridemia develops with an unhealthy diet. Health conditions are aggravated by inactivity, smoking, alcohol abuse, and excess weight. However, an increase in triglyceride levels is typical for some diseases that are not always associated with an unhealthy lifestyle:

• diabetes mellitus;
• congenital disorder of lipid metabolism;
• thyroid insufficiency;
• chronic renal failure;
• nephrotic syndrome;
• inflammation of the pancreas;
• some liver diseases;
• Down syndrome;
• myocardial infarction;
• glycogenosis;
• anorexia nervosa.

What are triglycerides?

Triglycerides are a type of fat or lipid in the body. They are the most common form of body fat because the body stores most fat as triglycerides.

Triglycerides circulate in the blood and their levels can be measured using a blood test.

A triglyceride is made up of three fatty acid molecules combined with a glycerol molecule, which is a form of glucose. We consume triglycerides as fats in our diet. The human body can also convert glucose from foods into triglycerides.

Triglycerides serve as one of the main sources of energy in the body. If the body does not need energy immediately, it stores triglycerides as fat.

Spherical particles known as lipoproteins package triglycerides and pass through the bloodstream, delivering them throughout the body.

According to the American Heart Association (AHA), high levels of triglycerides in the blood are a risk factor for cardiovascular disease. Research also shows that there is a link between high triglyceride levels and the following conditions:

• obesity
• insulin resistance
• type 2 diabetes
• pancreatitis

Hyperlipidemia syndrome in children and adolescents: pathogenesis, clinical picture, treatment

Lipids are organic substances that, together with proteins and carbohydrates, make up the bulk of the body's organic substances. They accumulate in adipose tissue in the form of triglycerides (TG), being the main energy substance. Lipids are part of cell membranes and participate in the synthesis of steroid hormones.

Physiology of lipid metabolism

Lipids without a protein connection are insoluble or poorly soluble in water, but as part of lipoprotein complexes consisting of lipids and proteins, they easily go into solution. In this state, they provide transport of lipids in the plasma for delivery of the latter to the body tissues.

The components of lipids are fatty acids (saturated, monounsaturated, polyunsaturated), triglycerides, free cholesterol (CS), cholesteryl esters (CE), phospholipids (PL, complex lipids).

TG are chemical compounds of glycerol with three molecules of fatty acids. In everyday life they are called fats. When TG is hydrolyzed in adipocytes in the presence of lipoprotein lipase (LPL), fatty acids are released from them, which are used by the body for energy purposes.

Cholesterol (chole - bile, sterol - fatty) is produced in the liver and is used for the construction of cell membranes, the synthesis of steroid hormones and bile acids. In the intestine, bile acids are necessary for the emulsification and absorption of exogenous fat.

The main form of cholesterol circulating in plasma is its esters (cholesterol bound to a fatty acid). They are in the form of highly soluble complexes with transporter proteins. Their formation requires the enzyme lecithin cholesterol acyltransferase (LCAT).

PL are lipids that contain glycerol, fatty acids, phosphoric acid, and nitrogen-containing compounds. They are an integral part of cell membranes.

In the blood, TG, cholesterol, and PL are transformed in the form of lipoproteins (LP), and free, non-fat, non-esterified fatty acids (NEFA) are transformed in the form of complexes with albumin [1].

In the process of ultracentrifugation, individual fractions of drugs are isolated: chylomicrons (CM) - the lightest particles, very low-density lipoproteins (VLDL), transition-density lipoproteins (TDLP), low-density lipoproteins (LDL), high-density lipoproteins (HDL).

The proteins that make up the drug are referred to as apolipoproteins (apo). They are necessary for the transport of various lipids (mainly triglycerides and cholesteryl esters) from sites of synthesis to the cells of peripheral tissues, as well as for the reverse transport of cholesterol to the liver. Apoproteins regulate the activity of enzymes - LCAT, LPL, hepatic triglyceride lipase (TGL).

There are six main classes of apolipoproteins, designated by letters (A, B, C, E, D, H). Their synthesis occurs mainly in the liver and intestines.

The main lipids of chylomicrons are TG, and their structural apoprotein is B48. VLDL consists of 55% TG, 20% cholesterol, and the transport protein is apo-B100.

DILI is formed from VLDL, contains 35% cholesterol and 25% TG and is transported by apo-B100. The LDLP fraction is an intermediate product, a precursor to LDL, which is formed during the conversion of VLDL with the participation of hepatic lipase. It is characterized by a short plasma lifetime and is rapidly metabolized into LDL.

LDL is the end product of VLDL hydrolysis. They are the main carriers of cholesterol to tissues. The half-life is 3–4 days. Approximately 70% of total cholesterol is associated with LDL. LDL catabolism occurs predominantly in peripheral tissues. In humans, 70–80% of LDL is removed from the plasma every day by receptor-mediated pathways. The rest is captured by phagocytic cells of the reticulohistiocytic system. It is believed that this is the main atherogenic lipoprotein. Apo-B100 makes up more than 95% of total LDL protein.

HDL is formed mainly in the liver, but also in the intestine from exogenous lipids. It is a heterogeneous group of molecules with distinct metabolic roles. HDL absorbs free PL cholesterol, which is formed in plasma under the influence of LCAT. High levels of HDL have a protective effect against atherosclerosis. HDL consists of 50% protein apo-A1, apo-E, apo-C, 25% PL, 20% cholesterol and 5% TG.

The formation of a lipid-protein complex occurs through many receptors. Changes in genes encoding apoprotein receptors can disrupt lipoprotein function [2].

A variety of fatty acids in the composition of chemicals are supplied with food, which are processed with the participation of hepatic lipase. The main lipids found in blood plasma are NEFA, PL, TG, cholesterol and EC. In a healthy person, CMs after consuming fats disappear from the blood 12 hours after eating.

An important source of fatty acid formation is carbohydrates. A significant portion of essential fatty acids is synthesized in the liver, less in adipocytes from acetyl-coenzyme A, formed during the conversion of glucose.

Insulin is a potent inhibitor of the activity of hormone-sensitive LPL and, consequently, lipolysis in the liver and adipose tissue. In adipocytes, high levels of glucose and insulin promote the deposition of FFAs in the form of TG. Insulin and glucose also stimulate the biosynthesis of FFAs in the liver when consumed in excess. FFAs are converted into TG with subsequent formation of VLDL. FFAs are captured by various cells and used as energy material, and when in excess they are deposited in the form of triglycerides in tissue.

Energy expenditure (lipolysis) occurs under the control of adrenaline, norepinephrine, glucagon, and adrenocorticotropic hormone (ACTH). The resulting FFAs capture working organs.

The content of cholesterol and TG in the blood plasma can be used to judge the nature of lipoprotein particles. An isolated increase in TG levels indicates an increase in the concentration of cholesterol or VLDL. On the other hand, an isolated increase in cholesterol levels almost always indicates an increase in LDL concentrations. TG and cholesterol levels often increase simultaneously. This may reflect a sharp increase in the concentration of cholesterol and VLDL [1, 2].

Hyperlipidemia

Plasma lipid levels vary among children due to genetic and dietary factors. Hyperlipoproteinemia (dyslipidemia) is a syndrome complex accompanied by excessive levels of lipids and/or lipids in the blood plasma.

Hyperlipidemia (HLP) occurs in 2–10% of children and 40–60% of adults [2]. HLP is an important factor in the development of cardiovascular diseases. LPs of one or more classes may accumulate in the blood due to increased formation or secretion or increased administration of exogenous lipid components or decreased excretion from the body. In some cases, all of these processes take place.

Disturbances in fat metabolism may be associated with changes in proteins involved in fat metabolism (LP, apoproteins) and in the LP receptor apparatus. The mechanism of these disorders may be due to a deficiency or block of apoproteins and LP receptors, which are the most important cofactors of LPL activity and endocytosis by macrophages. The synthesis of LDL receptors is inhibited by glucocorticoids.

GLP is divided into primary (1/3) and secondary (2/3). According to the mechanism of development, HLPs are grouped into nutritional, retention, and transport. In most cases they are combined.

According to the WHO classification, various combinations of drugs, the level of which is elevated in pathology, are divided into six types or categories. Most of them can be caused by various genetic diseases. Types of hyperlipoproteinemia should be considered as evidence of a disorder of lipid metabolism, and not as the name of a specific disease.

Primary SDP

Primary HLP type 1 (familial lipoprotein lipase deficiency) occurs in 1% of cases with autosomal recessive inheritance resulting from a mutation in the LPL gene. The defect is associated with congenital or acquired LPL deficiency. As a result of this disorder, the metabolism of CMs is blocked, which leads to their extreme accumulation in the plasma. With insufficient blood LPL activity, the transition of fatty acids from blood plasma chylomicrons to fat depots is disrupted (TGs are not broken down). The excretion of TG-rich drugs is blocked. Severe triglyceridemia develops.

The pathology usually manifests itself in early childhood with recurrent attacks of abdominal pain. They are caused by pancreatitis, which develops due to the formation of toxic products during the partial hydrolysis of TG and PL of chylomicrons. Excess CM can cause microthrombosis in various organs.

In the clinic, patients are found to have yellow papules with an erythematous rim in different areas of the skin and xanthoma as a result of the deposition of large quantities of chylomicron triglycerides in histiocytes. THs are also deposited in phagocytes of the reticulohistiocytic system, causing hepatomegaly, splenomegaly and bone marrow infiltration by foam cells. When examined with an ophthalmoscope, a whitish retina and white vessels in it can be detected, allowing the diagnosis of retinal lipemia. Despite the sharp increase in plasma TG levels, the development of atherosclerosis does not accelerate.

The diagnosis of familial lipoprotein lipase deficiency should be assumed when milky yellow, creamy blood plasma is detected upon standing. The diagnosis is confirmed by the absence of an increase in plasma lipoprotein lipase activity after heparin administration and a sharp increase in the levels of cholesterol and triglycerides.

Symptoms become less pronounced if the patient is switched to a low-fat diet. Since medium-chain TGs are not included in HM, these are the fats that should be used in the diet to ensure its normal calorie content. The patient must also receive fat-soluble vitamins.

HLP type 2 (familial hypercholesterolemia) is the most common form. It is an autosomal dominant disorder caused by a mutation in the gene for apo B100, a protein that binds LDL to the LDL receptor.

Due to the reduced activity of LDL receptors, the catabolism of these drugs is blocked, and their amount in the plasma increases in proportion to the decrease in receptor function. The liver is unable to effectively capture LDLP, which should be converted into LDL. This leads to impaired uptake, impaired LDL excretion and accumulation of total cholesterol in the blood plasma. As a result, their concentration increases by 2–6 times.

This form of HLP is divided into subtypes 2a and 2b. The first is characterized, along with an increase in LDL and cholesterol, by normal levels of VLDL and TG. With subtype 2b, described in 1973, combined lipidemia is typical: increased LDL, VLDL, TG, cholesterol.

Heterozygous familial hypercholesterolemia type 2a should be assumed when an isolated increase in plasma cholesterol levels is detected in children against the background of unchanged triglyceride concentrations. An isolated increase in cholesterol levels is usually caused by an increase in the concentration of LDL cholesterol only. In familial hypercholesterolemia, only half of first-degree relatives have elevated plasma cholesterol levels. The presence of skin xanthomas helps in diagnosis. When collecting anamnesis from relatives, early manifestations of coronary heart disease can be identified.

HLP type 2b is much more common in children. High levels of cholesterol, TG, LDL, and VLDL are detected. Excess LDL infiltrates the vascular wall, leads to unregulated accumulation of cholesterol in cells, their foamy transformation, and contributes to the development and early progression of atherosclerosis and coronary heart disease.

Relatives are often diagnosed with hyperinsulinism, insulin resistance, arterial hypertension, uricemia, and early development of atherosclerosis. With familial hypercholesterolemia, the incidence of obesity and diabetes mellitus does not increase. In patients, body weight, as a rule, is even less than normal.

This form of HLP occurs already in newborns. With homozygous carriage, such patients die in childhood from myocardial infarction. In cases where very high levels of cholesterol in the blood plasma are detected, parents should be examined to exclude familial hypercholesterolemia.

Since atherosclerosis in this disease is caused by a prolonged increase in plasma LDL levels, patients should be switched to a diet low in cholesterol and saturated fat and high in polyunsaturated fat. You should exclude butter, cheese, chocolate, fatty meats and add polyunsaturated oils (corn, olive, fish oil, etc.). In this case, the plasma cholesterol level in heterozygotes decreases by 10–15% [1].

Familial HLP type 3 is a rare form. In this congenital disease, plasma levels of both cholesterol and TG are elevated. This is due to the accumulation of residues in the plasma resulting from the partial destruction of VLDL. The mutation that determines the disease affects the gene encoding the structure of apoprotein E, a protein that is normally found in DILI and remnants of chylomicrons. It binds both the chylomicron remnant receptor and the DILI receptor with very high affinity. VLDL, LPPP, and TG increase in the blood plasma. The conversion of VLDL to LDL is disrupted, and the level of HDL decreases. These drugs accumulate in large quantities in plasma and tissues, causing xanthomatosis and atherosclerosis.

HLP manifests itself after 20 years. In the clinic, accelerated sclerosis of the vessels of the heart, carotid arteries, and vessels of the lower extremities is typical, and, consequently, early myocardial infarctions, strokes, intermittent claudication and gangrene of the legs.

The disease may be accompanied by obesity, type 2 diabetes mellitus, and hepatosis. Tuberous xanthomas, which are localized in the area of ​​the elbow and knee joints, are considered pathognomonic. The plasma becomes cloudy when standing.

Primary type 4 HLP, or familial triglyceridemia, is characterized by high TG concentrations with normal or slightly elevated fasting cholesterol levels. It is a common (17–37%) autosomal dominant disorder. It appears in various periods of childhood, but more often in older years.

The pathogenesis of primary triglyceridemia is not entirely clear. It is believed that there is excess production of TG in the presence of normal levels of apo-B lipoproteins, causing the formation of TG-rich VLDL in the liver. There is not enough data on the atherogenicity of these lipoproteins [2].

Familial triglyceridemia can be suspected if the patient has high levels of TG, VLDL and a normal amount of cholesterol. The disease should be confirmed by studying the lipid profile of close relatives. When the blood taken is left standing for 8 hours, flakes can be detected in the plasma. In some patients, HDL is elevated, which may be due to the low atherogenicity of this form of HLP. Xanthomas are not typical for familial hypertriglyceridemia.

This variant of secondary HLP occurs in metabolic syndrome, type 2 diabetes mellitus and other endocrinopathies.

HLP type 5, or familial combined HLP, is inherited as an autosomal dominant trait. This form, combining an increase in TG and CM, has signs of types 1 and 4 of HLP. Close relatives may have only a mild form of the disease with moderate hypertriglyceridemia without hyperchylomicronemia, hypercholesterolemia, i.e., it may be characterized by hyperlipidemia of various types. When standing, the plasma forms a cloudy layer. The mutant gene is unknown.

Increases in plasma cholesterol and/or triglyceride levels are detected at puberty and persist throughout the patient's life. The increase in lipid and lipid levels is not constant: during different periods of the examination, high indicators may decrease, while others, on the contrary, may increase significantly.

Family history often suggests early coronary artery disease. Mixed type HLP is found in approximately 10% of all patients with myocardial infarction. The incidence of obesity, hyperuricemia and impaired glucose tolerance is increased [1].

Mild or moderate hypertriglyceridemia can sharply increase under the influence of various provoking factors (decompensated diabetes mellitus, hypothyroidism, taking medications containing estrogens). Plasma triglyceride levels may increase. During periods of exacerbations, patients develop mixed hyperlipidemia, i.e., the concentration of both VLDL and CM increases. After eliminating the provoking factors, chylomicron-like particles disappear from the plasma and the concentration of triglycerides returns to the original level.

Secondary SLP

There are basal and induced HLP. Basal HLP is detected in fasting blood tests and is more severe and indicates profound disturbances in fat metabolism. Induced (postprandial) HLP are detected after taking carbohydrates, fats, hormonal drugs, and severe physical activity. These include nutritional HF, which develop after excessive consumption of fats in food.

Secondary HLP are often manifested by increased levels of several classes of drugs in the blood plasma. The change in lipid spectrum may be similar to the primary types of HLP. Clinical changes are determined by the underlying disease. Often (primarily at the beginning of the development of the pathological process), quantitative and qualitative changes in the composition of drugs in the blood plasma are adaptive in nature [3].

Diabetes mellitus type 1

Insulin-dependent diabetes mellitus (DM) significantly affects lipid metabolism. Hypertriglyceridemia occurs in most patients. It is associated with the role of insulin in the formation and removal of lipid-rich drugs from plasma [1, 3].

With insulin deficiency, the synthesis of TG and the content of apo-B lipoproteins increase. Due to impaired LPL activity, the excretion of TG-rich particles is reduced. Insulin deficiency increases lipolysis in adipose tissue, resulting in a high flow of FFA to the liver. It enhances the synthesis and secretion of TG into the blood as part of VLDL as a secondary reaction to the increased mobilization of free fatty acids from adipose tissue.

The cholesterol content of LDL increases, but to a lesser extent. In decompensated diabetes, the plasma concentration of FFA is increased and correlates with the level of glucose in the blood.

As the duration of hypoinsulinemia increases, the rate of removal of VLDL and cholesterol from the blood decreases due to a decrease in lipoprotein lipase activity, since insulin is necessary for the synthesis of LPL in adipocytes. Diabetic lipimia develops. This is facilitated by glucagon, which increases sharply during decompensation, increasing the release of FFA into the blood.

Some of the FFA is metabolized to acetyl-CoA, which is then converted into acetoacetic and B-hydroxybutyric acids. These lipid metabolism disorders resemble the phenotype characteristic of primary type 4 or 5 HLP.

Severe lipidemia leads to fatty liver and pancreas, creamy appearance of retinal vessels, and abdominal pain.

According to V.M. Delyagin et al. In children with type 1 diabetes, dyslipidemic disorders were manifested by changes in the pattern of the liver parenchyma, thickening of the vascular walls, changes in the media/intima ratio, and a decrease in vascular elasticity [4].

The blood has a milky color and a creamy layer appears when standing. This is due to acquired LPL deficiency. But, given the prevalence of diabetes, a combination of primary hereditary disorders of lipid metabolism and HLP associated with absolute insulin deficiency is possible. Hormone replacement therapy quickly reduces the severity of lipoproteinemia.

So, hypertriglyceridemia, increased VLDL cholesterol levels, and non-enzymatic glycosylation of apoproteins are risk factors for the development of atherosclerosis in patients with type 1 diabetes and type 2 diabetes. Compensation of diabetes reduces the severity of HLP and, therefore, inhibits the development of atherosclerosis.

Obesity

Among all forms of obesity in childhood, a simple form occurs (85–90%). The constitutional factor is leading in the genesis of this form of the disease. Genetic predisposition to obesity may be associated with central dysregulation of energy balance, with an increase in the number of adipocytes and increased metabolic activity of the latter.

In adipose tissue, the synthesis and hydrolysis of lipids, the synthesis of fatty acids, including from carbohydrates, their esterification into neutral fats (TG), their deposition and breakdown with the formation of fatty acids, and their use for energy purposes constantly occur.

LPL activity in adipose tissue is regulated by insulin, i.e. insulin stimulates the uptake and accumulation of circulating FFAs in adipocytes.

Another mechanism for lipid deposition in adipose tissue involves the conversion of glucose and other carbohydrates into fats, which is controlled by insulin. Under physiological conditions, one third of dietary glucose is used for the synthesis of endogenous fat, in obese patients up to two thirds.

In the blood of obese patients, increased levels of cholesterol, TG, LDL and decreased HDL are detected. Such patients have reduced tolerance to exogenous lipids—in response to a fat load, they experience a pronounced prolonged hyperlipidemic reaction. CMs in these patients are broken down slowly, and lipolytic activity appears late [3].

Hyperinsulinemia is important in the pathogenesis of obesity. Increased insulin secretion causes increased appetite. The liver begins to synthesize more TG.

Metabolic syndrome

Obesity with excess visceral fat, accompanied by insulin resistance (IR) and hyperinsulinemia (HI), disorders of carbohydrate, lipid, purine metabolism, and arterial hypertension, is systematized under the term “metabolic syndrome (MS)” [5].

Abdominal obesity increases the release of FFAs from adipocytes into the blood plasma and their uptake by the liver. The synthesis of TG and apo-B lipoproteins increases in it, and small LDL particles dominate. The production of HDL decreases, the removal of excess cholesterol from the body is impaired, the level of glucose in the blood increases, and the tendency to blood clots and inflammation increases. Conditions are created for the formation of the atherosclerotic process. This is predisposed by glycation of apoproteins, which impairs their binding to lipids. Glycated VLDL cholesterol and LDL cholesterol circulate in the blood longer. The risk of developing cardiovascular diseases increases.

The pathogenetic cause of MS is still unknown, but a close relationship has been noted between increased body weight and IR and GI. Abdominal obesity contributes to increased IR, causing an increased influx of FFA from adipocytes to the liver. Adipocytes of visceral adipose tissue, having increased sensitivity to the lipolytic action of catecholamines and low sensitivity to the antilipidic action of insulin, secrete FFAs, which prevent the binding of insulin to the hepatocyte, which leads to HI [6].

Risk factors for metabolic syndrome in a child are the presence of abdominal obesity, type 2 diabetes, arterial hypertension, myocardial infarction, stroke and other vascular disorders in relatives [2].

To diagnose MS, it is necessary to evaluate anthropometric measurements, blood pressure, determination of glucose, insulin, fasting C-peptide levels, and lipid spectrum. A simple indicator is the IR ratio of fasting TG concentration to HDL cholesterol level. If this index is 3.5 or more, then this indicates IR.

Hypothyroidism

Dyslipidemia accompanying hypothyroidism is accompanied by an increase in atherogenic drugs and a decrease in the content of antiatherogenic drugs.

Thyroid hormones influence all stages of lipid metabolism. They promote the uptake and synthesis of lipids in the liver, the oxidation of TG from adipose tissue, the transport of FFAs, the absorption and excretion of cholesterol in the composition of bile acids, and an increase in the activity of hepatic lipase.

Apparently, thyroid hormones exert their effects by stimulating genes responsible for the synthesis and lipolysis of lipids and lipids. With a deficiency of thyroid hormones, the amount of apo-B and apo-E proteins and LDL receptors in the liver decreases, the excretion of cholesterol is impaired, and the level of VLDL and LDL in the blood increases. A decrease in hepatic lipase activity disrupts the conversion of VLDL into LDLP, and from the latter the formation of HDL. A decrease in the activity of cholesterol transport protein leads to disruption of the reverse transport of cholesterol to the liver.

A high level of LDL cholesterol with a reduced concentration of HDL is associated with a high risk of atherosclerosis [7].

If hypothyroidism is detected, levothyroxine is prescribed. This treatment is accompanied by normalization of the patient's lipid levels within a month.

In subclinical hypothyroidism, the presence of atherogenic dyslipidemia is also indicated, which requires corrective therapy. Opinions are divided on thyroid hormone replacement therapy for subclinical hypothyroidism [7, 8]. Some authors believe that the administration of L-thyroxine more often normalizes the lipid spectrum in such patients. Others believe that the administration of lipid-lowering drugs is sufficient to correct dyslipidemia.

Somatotropic insufficiency

Growth hormone (GH) plays an active role in the regulation of basal metabolism. It is an anabolic hormone and has lipolytic activity. In adipose tissue, GH increases the number of preadipocytes and suppresses the activity of LPL, an enzyme that hydrolyzes TG in lipoproteins to NEFA, which are re-esterified in the liver and deposited in adipocytes [9].

Most patients with somatotropic insufficiency (STI) exhibit excess adipose tissue, decreased muscle mass and strength, osteoporosis, and early atherosclerosis. GH deficiency in adults increases the risk of death from cardiovascular diseases (myocardial infarction, stroke, etc.). One of the factors that provoke changes in blood vessels during STN is a disorder of lipid metabolism. An increase in the level of total cholesterol, LDL, and apoprotein B is detected. Other studies have revealed an increase in TG levels and a decrease in HDL [10]. More significant changes in lipid metabolism were observed in patients with multiple pituitary hormone deficiency.

Long-term replacement therapy with recombinant growth hormone led to a decrease in the levels of total cholesterol and LDL, but did not affect the content of HDL and TG [11].

Cushing's syndrome

Glucocorticoids (GCs) play important roles in energy homeostasis and have complex but unclear effects on lipid metabolism. GCs modulate the expression of about 10% of human genes. They regulate the differentiation, function and distribution of adipose tissue.

Under the influence of GCs, FFAs in the blood increase, since these hormones accelerate lipolysis, disrupt the formation of glycerol, and reduce glucose utilization. The effect of GC on fat metabolism depends on the localization of subcutaneous fat. With an excess of HA, the fat layer on the extremities is reduced, and on the face and torso it is overdeveloped.

With an excess of glucocorticoids in the blood, total cholesterol and TG increase, while the level of HDL may vary. Insulin resistance plays a key role in this dyslipidemia. In vitro, cortisol increases lipoprotein lipase levels in adipose tissue, especially visceral fat, where lipolysis is activated and FFAs are released into the circulation.

Impaired glucose tolerance or steroid diabetes, IR, hypercoagulation determine an increased risk of cardiovascular pathology in this group of patients. However, the degree of dyslipidemia in the clinic is very variable in patients with exogenous and endogenous excess GC [1, 2].

A study of 15,004 patients found that GC use was not directly associated with an unfavorable lipid profile. In Cushing's syndrome, there is an increase in VLDL, but not HDL, with a subsequent increase in triglycerides and total cholesterol. The prevalence of hepatic steatosis among patients receiving GCs and patients with Cushing's syndrome is not the same. In the latter, it primarily depends on the volume of abdominal and visceral fat [12].

These changes are normalized or significantly improved after correction of hypercortisolism.

Kidney diseases

HLP in renal diseases is common. Changes in the spectrum of lipids occur already in the early stages of glomerulonephritis and are aggravated during chronic course. In the acute period of the disease, an increase in TG, represented by cholesterol and VLDL, is characteristic, i.e., dyslipidemia develops, similar to primary type 4 HLP. The cholesterol content in VLDL also increases with a relative decrease in TG. Opposite ratios are typical in LDL.

In chronic kidney disease, dyslipidemia is manifested by an increase in TG. This is due to an increase in the content and decrease in clearance of VLDL and accumulation of LDL [13]. The experiment showed that in case of renal failure, the formation of receptors for VLDL in adipose tissue is disrupted, which increases their concentration and, consequently, maintains hypertriglyceridemia. This is facilitated by a decrease in LPL activity in adipose tissue. Deficiency of hepatic lipase impairs the hydrolysis of TG in LDLP with the formation of LDL and HDL phospholipids.

With renal failure, the content of the most atherogenic LDPP increases, which accelerates the atherosclerotic process.

With nephritic syndrome, a mixed form of HF is often detected with an increase in both cholesterol and TG, which is similar to type 2 of HF. The concentration of LDL increases with normal or decreased amount of HDL. HLP is associated with hypoalbuminemia. Remission of the disease is accompanied by normalization of lipidemia.

Treatment

Etiological treatment for primary HLP has not yet been developed. Some forms of secondary HLP are well corrected by replacement therapy (type 1 diabetes, hypothyroidism, somatotropic insufficiency).

Pathogenetic treatment of HF is primarily aimed at reducing plasma cholesterol levels. A diet low in cholesterol and saturated fat and high in polyunsaturated fat. Exclude butter, cheese, chocolate, pork. The diet uses corn and sunflower oil.

When metabolic syndrome is detected, it is recommended to limit or eliminate easily digestible carbohydrates. The amount of fat is reduced by up to 70%, mainly due to animals, which are replaced by 50% with vegetable ones.

Physical activity along with diet for HLP is the most important factor in treatment. Physical activity increases metabolism and accelerates the mobilization of fat from the depot.

The use of lipid-lowering drugs in childhood is limited due to many side effects [14].

Literature

1. Kronenberg G. M. et al. Obesity and lipid metabolism disorders / Trans. from English edited by I. I. Dedova, G. F. Melnichenko. M.: Read Elsiver LLC, 2010. 264 p.
2. Endocrinology and metabolism. T. 2. Per. from English / Under. ed. F. Fehling, J. Baxter, A. E. Broadus, L. A. Fromen. M.: Med., 1985. 416 p.
3. Turkina T.I., Shcherbakova V.Yu. Features of dyslipidemia in children // Rational pharmacotherapy in cardiology. 2011, no. 7 (1), 65–69.
4. Delyagin V.M., Melnikova M.B., Serik G.I. Dyslipidemia syndrome in children with chronic diseases // Practical Medicine. 2014, No. 9 (85), p. 7–10.
5. Bokova T. A. Metabolic syndrome in children. Tutorial. M., 2013. 21 p.
6. Gurina A. E., Mikaelyan N. P., Kulaeva et al. The relationship between the activity of insulin receptors and blood ATP against the background of dyslipidemia in children with diabetes mellitus // Fundamental Research. 2013, no. 12–1, p. 30–34.
7. Biondi B., Klein I. Cardiovascular abnormalities in subclinical and overt hypothyroidism/The Thyroid and cardiovascular risk. Stuttgart; New York, 2005. 30–35.
8. Budievsky A.V., Kravchenko A.Ya., Feskova A.A., Drobysheva E.S. Dyslipidemia in subclinical hypofunction of the thyroid gland and the effectiveness of its correction with L-thyroxine replacement therapy // Young scientist. 2014, 17, p. 138–141.
9. Dedov I. I., Tyulpakov A. N., Peterkova V. A. Somatotropic insufficiency. M.: Index Print, 1998. 312 p.
10. Volevodz N. N. Systemic and metabolic effects of growth hormone in children with various types of short stature. Diss. Doctor of Medical Sciences 2005.
11. Volevodz N. N., Shiryaeva T. Yu., Nagaeva E. V., Peterkova V. A. The state of the lipid profile in patients with somatotropic insufficiency and the effectiveness of correction of dyslipidemia during treatment with the domestic recombinant growth hormone “Rastan”. https://umedp.ru |articles|sostoyanie_lipidnogo_profilya.
12. Arnaldi G., Scandali VM, Trementino L., Cardinaletti M., Appolloni G., Boscaro M. Pathophysiology of Dyslipidemia in Cushing's Syndrome // Neuroendocrinology. 2010; 92(suppl 1): 86–90.
13. Rudenko T. E., Kutyrina I. M., Shvetsov M. Yu. State of lipid metabolism in chronic kidney disease. Clinical nephrology. 2012, no. 2, p. 14–21.
14. Vasyukova O. V. Federal clinical guidelines for the diagnosis and treatment of obesity in children and adolescents. M.: Institute of Pediatric Endocrinology ENC, 2013. 18 p.

V. V. Smirnov1, Doctor of Medical Sciences, Professor A. A. Nakula

State Budgetary Educational Institution of Higher Professional Education Russian National Research Medical University named after N. I. Pirogov Ministry of Health of the Russian Federation, Moscow

1 Contact information

Healthy triglyceride levels

According to the National Heart, Lung, and Blood Institute, normal fasting blood triglyceride levels are:

• less than 75 milligrams per deciliter (mg/dL) for children under 10 years of age
• less than 90 mg/dL for children aged 10 years and older and adults

Doctors call elevated levels of triglycerides in the blood hypertriglyceridemia. You can be diagnosed with hypertriglyceridemia if your fasting blood triglyceride level is consistently 150 mg/dL or higher.

However, different clinical guidelines may classify high triglycerides at different levels.

Research shows that blood triglyceride levels are higher in men and increase with age in both men and women.

Some also have a genetic predisposition to high triglyceride levels, and doctors call this familial hypertriglyceridemia.

Examples of Triglyceride Lowering Products

The AHA recommends focusing on certain foods to help manage triglyceride levels. Foods that may help lower triglyceride levels include:

• Low fructose vegetables: These include leafy greens, squash, pumpkin, green beans and eggplant.
• Low fructose fruits: such as berries, kiwis and citrus fruits.
• Fiber-rich whole grains: brown rice, whole grain bread, quinoa, oats, barley and buckwheat.
• Fatty fish : salmon, herring and sardines.
• Low-fat dairy products: These include milk, yogurt and cheese.

Additionally, the AHA advises:

• limit added sugar to no more than 10% of total daily calories
• limit carbohydrate intake to 50–60% of daily calories
• keep the fat content in the diet to 25–35% of the total diet
• reduce or avoid alcohol intake

Limit carbohydrates

You should limit your total carbohydrate intake to less than 60% of your recommended daily calorie intake. If you consume more carbohydrates than you need, your body will store them as fat. There are many ways to avoid carbs, such as eating lean burgers with lettuce instead of a sweet cream bun. Some carbohydrate foods, including some grains, may be beneficial in the diet. However, refined carbohydrates such as white bread provide few nutrients and add calories to the diet.

To get more healthy carbohydrates, choose whole grains, oatmeal and vegetables such as carrots. For dessert, choose fresh or frozen blueberries, blackberries or raspberries instead of sweet baked goods. These fruits can reduce sugar cravings and also provide healthy carbohydrates. Not only are unrefined carbohydrates a source of dietary fiber, but they also provide faster and longer-lasting satiety than refined carbohydrates because they release their energy more slowly.

Sample meal plan

Below is a sample meal plan that may help lower your triglyceride levels.

Other Triglyceride Lowering Options

In addition to dietary changes, your doctor may also recommend the following to lower triglyceride levels:

• Physical Activity: The AHA recommends at least 30 minutes of moderate-intensity physical activity at least 5 days per week for a total of at least 150 minutes per week.
• Achieving a moderate weight: According to the AHA, losing 5 to 10% weight results in a 20% reduction in triglyceride levels.
• Taking omega-3 fatty acids : Research suggests that omega-3s may prevent and treat hypertriglyceridemia.
• Taking niacin: Studies have shown that niacin, also known as niacin, may help lower triglyceride levels.
• Taking fibrates: Evidence also suggests that fibrates are effective in lowering triglyceride levels.

Conclusion

You can lower your triglyceride levels by changing your diet, maintaining a moderate weight, and exercising regularly.

You should also avoid refined carbohydrates, added sugars and saturated fats. Replacing them with low-sugar fruits and vegetables, whole grains and fatty fish can reduce triglyceride levels and the risk of obesity and cardiovascular disease.

It is important for the doctor to decide whether this approach is enough to make a difference or whether medications will be necessary. You should definitely contact your doctor to find out which approach is most appropriate.

Indications for the purpose of analysis

1. Atherosclerosis and related diseases of the cardiovascular system, in particular coronary heart disease (prognosis, assessment of the risk of complications, diagnosis).
2. Liver and kidney diseases.
3. Endocrine pathology (hypothyroidism, diabetes mellitus).
4. Screening examinations.

Preparation It is recommended to donate blood in the morning, between 8 and 11 am. Blood is drawn on an empty stomach, after 10-12 hours of fasting. It is allowed to drink water without gas and sugar. On the eve of the examination, food overload should be avoided.