What are the essential functions of cholesterol in the human body. How is cholesterol tested and measured in clinical settings. Why is maintaining healthy cholesterol levels crucial for cardiovascular health.

The Vital Role of Cholesterol in Human Physiology

Cholesterol, a lipophilic molecule, plays a crucial role in maintaining various bodily functions. Despite its often negative reputation, cholesterol is essential for human life and contributes significantly to cellular health and overall well-being.

Key Functions of Cholesterol

• Cell membrane structure and fluidity
• Precursor for vitamin D synthesis
• Production of steroid hormones (cortisol, aldosterone)
• Synthesis of sex hormones (testosterone, estrogen, progesterone)
• Component of bile salts for fat-soluble vitamin absorption

Is cholesterol solely harmful to the body. No, cholesterol is essential for many healthy cell functions. However, when LDL-cholesterol levels become too high, a condition known as hypercholesterolemia, it can increase the risk of premature atherosclerotic cardiovascular diseases (ASCVD).

Cholesterol Transport: Lipoproteins and Their Functions

Due to its lipophilic nature, cholesterol doesn’t dissolve well in blood. To overcome this challenge, the body packages cholesterol in lipoproteins, which are composed of a lipid core and a hydrophilic outer membrane.

Types of Lipoproteins

1. High-density lipoproteins (HDL)
2. Intermediate-density lipoproteins (IDL)
3. Low-density lipoproteins (LDL)
4. Very-low-density lipoproteins (VLDL)
5. Chylomicrons (present only in non-fasting plasma)

Which lipoproteins are most significant in clinical settings. LDL and HDL are particularly important. LDL particles act as major cholesterol transporters to peripheral tissues, while HDL molecules remove excess cholesterol and return it to the liver for excretion. High LDL and low HDL levels increase the risk of atherosclerotic vascular diseases.

Cellular Synthesis and Metabolism of Cholesterol

While cholesterol can be obtained through dietary sources, the body is also capable of synthesizing it. The liver is the primary site for de novo cholesterol synthesis, accounting for the majority of cholesterol production in the body.

Cholesterol Synthesis Process

The synthesis of cholesterol begins with Acetyl-CoA and involves a series of complex reactions. This process allows cells to maintain adequate cholesterol levels for various physiological functions.

How does cellular cholesterol synthesis impact overall cholesterol levels. The body’s ability to synthesize cholesterol means that dietary intake is not the sole determinant of blood cholesterol levels. This fact underscores the importance of considering both dietary and genetic factors in managing cholesterol-related health issues.

Cholesterol’s Role in Cell Membrane Function

At the cellular level, cholesterol plays a vital role in maintaining the structure and function of cell membranes. Its presence in the membrane contributes to both stability and fluidity.

Impact on Membrane Properties

• Regulates membrane fluidity
• Influences small molecule diffusion
• Affects internal cell environment
• Contributes to intracellular transportation

How does cholesterol affect membrane permeability. Cholesterol’s presence in the cell membrane can influence the ability of small molecules to diffuse through it, ultimately altering the internal environment of the cell. This property is crucial for maintaining cellular homeostasis and proper function.

Clinical Assessment of Cholesterol Levels

To assess a patient’s cholesterol status, physicians typically order a lipid panel or lipid profile. This comprehensive test provides valuable information about various lipid components in the blood.

Components of a Lipid Panel

1. High-density lipoprotein (HDL) cholesterol
2. Low-density lipoprotein (LDL) cholesterol
3. Triglycerides
4. Total cholesterol

Why is a lipid panel important for health assessment. The results of a lipid panel help screen patients for abnormalities in cholesterol and triglyceride blood levels, which are critical factors in assessing cardiovascular health risks.

Managing Cholesterol Levels: Lifestyle and Medical Interventions

When cholesterol levels are found to be high, various interventions can be implemented to bring them back to a healthy range. These interventions typically start with lifestyle modifications and may progress to medication if necessary.

Lifestyle Modifications for Cholesterol Management

• Dietary changes (reducing saturated and trans fats, increasing fiber intake)
• Weight management for obese individuals
• Regular exercise
• Smoking cessation
• Supplementation with plant stanols

Are lifestyle changes always sufficient to manage high cholesterol. While lifestyle modifications are often the first line of defense against high cholesterol, some cases may be refractory to these changes. In such situations, cholesterol-lowering drugs, such as statins, may be prescribed by healthcare providers.

Cholesterol and Cardiovascular Health: Understanding the Connection

The relationship between cholesterol levels and cardiovascular health is well-established in medical literature. High levels of LDL cholesterol, in particular, are associated with an increased risk of atherosclerotic cardiovascular diseases (ASCVD).

Cholesterol’s Role in Atherosclerosis

Excess LDL cholesterol can accumulate in the walls of arteries, leading to the formation of plaques. These plaques can narrow blood vessels and increase the risk of heart attacks and strokes.

Why is maintaining a balance between LDL and HDL cholesterol important. While high LDL levels are associated with increased cardiovascular risk, HDL cholesterol plays a protective role by removing excess cholesterol from the bloodstream. Maintaining a healthy balance between these two types of cholesterol is crucial for cardiovascular health.

Emerging Research and Future Directions in Cholesterol Studies

As our understanding of cholesterol metabolism and its impact on health continues to evolve, researchers are exploring new avenues for managing cholesterol-related disorders and improving cardiovascular outcomes.

Areas of Ongoing Research

• Novel cholesterol-lowering therapies
• Genetic factors influencing cholesterol metabolism
• Role of inflammation in cholesterol-related diseases
• Personalized approaches to cholesterol management

How might future research change our approach to cholesterol management. Advances in genetic testing and personalized medicine may lead to more tailored strategies for managing cholesterol levels, taking into account individual genetic predispositions and lifestyle factors.

Understanding cholesterol’s complex role in human physiology is crucial for maintaining overall health and preventing cardiovascular diseases. By recognizing both the essential functions of cholesterol and the risks associated with imbalanced levels, individuals and healthcare providers can work together to implement effective strategies for cholesterol management and improved health outcomes.

As research in this field continues to progress, we can anticipate more refined approaches to cholesterol assessment and management, potentially leading to better prevention and treatment of cholesterol-related disorders. The ongoing exploration of cholesterol’s multifaceted role in human health underscores its significance as a key component of medical research and public health initiatives.

In conclusion, cholesterol remains a fascinating and critical subject in human physiology and medicine. Its dual nature as both an essential molecule for cellular function and a potential risk factor for cardiovascular disease highlights the importance of maintaining a balanced approach to cholesterol management. By staying informed about the latest research and guidelines, individuals can make informed decisions about their health and work effectively with healthcare providers to maintain optimal cholesterol levels.

The field of cholesterol research continues to evolve, promising new insights and innovative approaches to managing cholesterol-related health issues. As we look to the future, it’s clear that our understanding of cholesterol will play a pivotal role in shaping strategies for disease prevention and promoting overall health and longevity.

Physiology, Cholesterol – StatPearls – NCBI Bookshelf

Trevor Huff; Brandon Boyd; Ishwarlal Jialal.

Author Information and Affiliations

Last Update: March 6, 2023.

Introduction

Cholesterol is a lipophilic molecule that is essential for human life. It has many roles that contribute to normally functioning cells. For example, cholesterol is an important component of the cell membrane. It contributes to the structural makeup of the membrane as well as modulates its fluidity. Cholesterol functions as a precursor molecule in the synthesis of vitamin D, steroid hormones (e.g., cortisol and aldosterone and adrenal androgens), and sex hormones (e.g., testosterone, estrogens, and progesterone). Cholesterol is also a constituent of bile salt used in digestion to facilitate absorption of fat-soluble vitamins A, D, E, and K.[1]

Since cholesterol is mostly lipophilic, it is transported through the blood, along with triglycerides, inside lipoprotein particles (HDL, IDL, LDL, VLDL, and chylomicrons). These lipoproteins can be detected in the clinical setting to estimate the amount of cholesterol in the blood. Chylomicrons are not present in non-fasting plasma.

Issues of Concern

While cholesterol is central to many healthy cell functions, it also can harm the body if it is allowed to reach abnormal blood concentrations. Interestingly, when LDL-cholesterol levels are too high, the condition referred to as hypercholesterolemia, the risk for premature atherosclerotic cardiovascular diseases (ASCVD) increases.[2] Particular care is necessary to educate patients about the harmful effects of high cholesterol and how to reduce their serum cholesterol levels. Patient lifestyle changes like diet (reduction in saturated fat and trans fat with an increase in fiber and total calories if obese and supplementation with plant stanols), smoking cessation, and exercise are often a favorable approach to cholesterol reduction. However, in cases that are refractory to these behavioral modifications, cholesterol-lowering drugs, such as statins, should be used.

Cellular Level

Cholesterol can be introduced into the blood through the digestion of dietary fat via chylomicrons. However, since cholesterol has an important role in cellular function, it can also be directly synthesized by each cell in the body. The synthesis of cholesterol begins from Acetyl-CoA and follows a series of complex reactions that will not be covered in this article. A primary location for this process is the liver, which accounts for most de-novo cholesterol synthesis.

Since cholesterol is mostly a lipophilic molecule, it does not dissolve well in the blood. For this reason, it is packaged in lipoproteins that have phospholipid and apolipoprotein.[3] Lipoproteins are made up of a lipid core (which can contain cholesterol esters and triglycerides) and a hydrophilic outer membrane comprising phospholipid, apolipoprotein, and free cholesterol. This allows the lipid molecules to move around the body through the blood and be transported to cells that need them. There are several types of lipoproteins that travel through the blood, and they each have different purposes. There are high-density lipoproteins (HDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and very-low-density lipoproteins (VLDL). Notably, LDL particles are thought to act as a major transporter of cholesterol; at least two-thirds of circulating cholesterol resides in LDL to the peripheral tissues. Conversely, HDL molecules are thought to do the opposite. They take excess cholesterol and return it to the liver for excretion. Clinically, these two lipoproteins are significant since high LDL and low HDL increase patients’ risk of atherosclerotic vascular diseases.[4][5]

Within the cell, cholesterol has several vital functions. Some of the primary uses for cholesterol are related to the cell membrane. It is required for the normal structure of the membrane; it contributes to its fluidity.[6] This fluidity can influence the ability of some small molecules to diffuse through the membrane, which ultimately changes the internal environment of the cell. [7] Also, within the membrane, cholesterol plays a role in intracellular transportation. Beyond its place in the cell membrane, cholesterol has several other biological functions. Of note, cholesterol is known to be an important precursor molecule for the synthesis of vitamin D, cortisol, aldosterone, progesterone, estrogen, testosterone, bile salts, among others.[8]

Related Testing

Physicians can order a lipid panel (lipid profile) to determine the cholesterol concentrations in a patient’s blood. A typical test result will include the concentrations of high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides, and total cholesterol. These values are used to screen patients for abnormalities in cholesterol and triglyceride blood levels. With this information, physicians can estimate a patient’s risk for certain health problems such as coronary artery disease, peripheral arterial disease (PAD), and stroke. Most laboratories report both LDL-cholesterol and non-HDL cholesterol, which is a secondary target for treatment.

Pathophysiology

Hypercholesterolemia (high LDL-cholesterol) is one of the major risk factors contributing to the formation of atherosclerotic plaques. These plaques lead to an increased possibility of various negative clinical outcomes, including, but not limited to, coronary artery disease. PAD, aortic aneurysms,  and stroke. A major contributor to the increased risk of atherosclerotic lesion formation is high levels of low-density lipoprotein (LDL) in the blood. Also, it has been shown that an elevated high-density lipoprotein (HDL) blood concentration is correlated with a decreased risk in epidemiological studies, but clinical trials with therapies that elevate HDL-cholesterol have yielded null results. For this reason, a major focus of patient care is primarily to decrease LDL levels.

The process through which atherosclerotic plaques develop begins with endothelial damage. Endothelial damage leads to the dysfunction of endothelial cells, increasing the number of LDL particles that can permeate through the vascular wall. Lipoproteins, especially LDL, can then accumulate within the vessel wall trapped by the cellular matrix in the intima. LDL is then modified and taken up via scavenger receptors on macrophages resulting in foam-cell formation. As more lipid accumulates within the vessel wall, smooth muscle cells begin to migrate into the lesion. Ultimately, these smooth muscle cells encapsulate the newly formed plaque forming the fibrous plaque, the protector of the lesion, preventing the lipid core from being exposed to the lumen of the vessel. Atherosclerotic plaques can lead to occlusion of the vessel (decreasing blood flow distally and causing ischemia)  or, more commonly because of abundant lipid and macrophages (vulnerable plaque) rupture, inducing the formation of a thrombus which can completely block the flow of blood (as occurs in acute myocardial infarctions, unstable angina).

Clinical Significance

Hypercholesterolemia refers to the condition in which a patient has elevated blood concentrations of LDL-cholesterol. High LDL is of particular clinical importance, but it should be noted that hypercholesterolemia can also include very-low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL), i.e., non-HDL-cholesterol. High LDL levels have been associated with an increased risk of atherosclerosis, potentially leading to several other conditions such as coronary artery disease, stroke, and peripheral arterial disease. Several factors can lead to increased LDL levels. Some of these factors include genetics, diet, stress, sedentary lifestyle, medications, and other disorders such as nephrotic syndrome and hypothyroidism.

On clinical examination, looking for absent pulses, bruits, arcus senilis (younger than 50 years of age), tendon xanthoma, xanthelasma, and aortic stenosis are all stigmata of very high cholesterol levels as in familial hypercholesterolemia.

Genetic defects that lead to increased LDL levels in the blood include genes that regulate LDL receptors in the liver. LDL receptors mediate the uptake of LDL into the liver. Endocytosis of LDL is the primary way that the body decreases cholesterol levels, so it follows that a decrease in LDL receptor function would also increase LDL concentrations in the blood. Patients with a genetic disposition for high cholesterol can be placed on cholesterol-lowering medications like statins to decrease their risk.

Diet has a variable effect on cholesterol levels among individuals.[9] However, it has been shown that diets high in saturated fats and trans fats can increase cholesterol in the blood.[10] Dietary cholesterol has not been shown to contribute significantly to LDL concentrations, but its role is still in question.[11][12][13] Lifestyle changes such as regular aerobic exercise can also help control cholesterol levels. Saturated fats should not comprise any more than 7% to 10% of the diet.

Hypercholesterolemia is often treated medically with lifestyle modification and medications. The goal of lifestyle changes is typically for the patient to increase physical activity, lose weight, and follow a heart-healthy diet. For patients with higher risk, a lipid-lowering drug (often a statin) will be used in conjunction with these behavioral changes. Statins have been shown to reduce ASCVD in patients and are the favored drugs because there are now generic formulations that make them cost-effective.[14][15][16][17]

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• Access free multiple choice questions on this topic.

• Comment on this article.

Figure

The molecular structure of cholesterol. Contributed by Boris T.M. (Public Domain, https://commons.wikimedia.org/w/index.php?curid=645994)

References

1.

Di Ciaula A, Garruti G, Lunardi Baccetto R, Molina-Molina E, Bonfrate L, Wang DQ, Portincasa P. Bile Acid Physiology. Ann Hepatol. 2017 Nov;16(Suppl. 1: s3-105.):s4-s14. [PubMed: 29080336]

2.

Ibrahim MA, Asuka E, Jialal I. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Apr 23, 2023. Hypercholesterolemia. [PubMed: 29083750]

3.

Wang HH, Garruti G, Liu M, Portincasa P, Wang DQ. Cholesterol and Lipoprotein Metabolism and Atherosclerosis: Recent Advances In reverse Cholesterol Transport. Ann Hepatol. 2017 Nov;16(Suppl. 1: s3-105.):s27-s42. [PubMed: 29080338]

4.

Sacks FM, Lichtenstein AH, Wu JHY, Appel LJ, Creager MA, Kris-Etherton PM, Miller M, Rimm EB, Rudel LL, Robinson JG, Stone NJ, Van Horn LV., American Heart Association. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. Circulation. 2017 Jul 18;136(3):e1-e23. [PubMed: 28620111]

5.

Karney A, Brągoszewska H, Soluch L, Ołtarzewski M. [Risk factors for atherosclerosis in obese children aged 6-12 years]. Dev Period Med. 2017;21(3):259-265. [PMC free article: PMC8522952] [PubMed: 29077565]

6.

Yeagle PL. Modulation of membrane function by cholesterol. Biochimie. 1991 Oct;73(10):1303-10. [PubMed: 1664240]

7.

Dotson RJ, Smith CR, Bueche K, Angles G, Pias SC. Influence of Cholesterol on the Oxygen Permeability of Membranes: Insight from Atomistic Simulations. Biophys J. 2017 Jun 06;112(11):2336-2347. [PMC free article: PMC5474842] [PubMed: 28591606]

8.

Javitt NB. Bile acid synthesis from cholesterol: regulatory and auxiliary pathways. FASEB J. 1994 Dec;8(15):1308-11. [PubMed: 8001744]

9.

Stone NJ, Lloyd-Jones DM. Lowering LDL cholesterol is good, but how and in whom? N Engl J Med. 2015 Apr 16;372(16):1564-5. [PubMed: 25773740]

10.

Stefanick ML, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD. Effects of diet and exercise in men and postmenopausal women with low levels of HDL cholesterol and high levels of LDL cholesterol. N Engl J Med. 1998 Jul 02;339(1):12-20. [PubMed: 9647874]

11.

Denke MA, Adams-Huet B, Nguyen AT. Individual cholesterol variation in response to a margarine- or butter-based diet: A study in families. JAMA. 2000 Dec 06;284(21):2740-7. [PubMed: 11105179]

12.

Lecerf JM, de Lorgeril M. Dietary cholesterol: from physiology to cardiovascular risk. Br J Nutr. 2011 Jul;106(1):6-14. [PubMed: 21385506]

13.

Dubois C, Armand M, Mekki N, Portugal H, Pauli AM, Bernard PM, Lafont H, Lairon D. Effects of increasing amounts of dietary cholesterol on postprandial lipemia and lipoproteins in human subjects. J Lipid Res. 1994 Nov;35(11):1993-2007. [PubMed: 7868978]

14.

Lloyd-Jones DM, Goff DC, Stone NJ. Treatment of Blood Cholesterol to Reduce Risk for Atherosclerotic Cardiovascular Disease. Ann Intern Med. 2016 Jan 19;164(2):135-6. [PubMed: 26784486]

15.

Hendrani AD, Adesiyun T, Quispe R, Jones SR, Stone NJ, Blumenthal RS, Martin SS. Dyslipidemia management in primary prevention of cardiovascular disease: Current guidelines and strategies. World J Cardiol. 2016 Feb 26;8(2):201-10. [PMC free article: PMC4766270] [PubMed: 26981215]

16.

Blum CB, Stone NJ. New Strategies to Treat High Cholesterol. JAMA. 2016 Mar 15;315(11):1169. [PubMed: 26978218]

17.

Cholesterol Treatment Trialists’ (CTT) Collaborators. Mihaylova B, Emberson J, Blackwell L, Keech A, Simes J, Barnes EH, Voysey M, Gray A, Collins R, Baigent C. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet. 2012 Aug 11;380(9841):581-90. [PMC free article: PMC3437972] [PubMed: 22607822]

Disclosure: Trevor Huff declares no relevant financial relationships with ineligible companies.

Disclosure: Brandon Boyd declares no relevant financial relationships with ineligible companies.

Disclosure: Ishwarlal Jialal declares no relevant financial relationships with ineligible companies.

Long term effects of ketogenic diet in obese subjects with high cholesterol level

Clinical Trial

. 2006 Jun;286(1-2):1-9.

doi: 10.1007/s11010-005-9001-x.

Epub 2006 Apr 21.

Hussein M Dashti 
¹
, Naji S Al-Zaid, Thazhumpal C Mathew, Mahdi Al-Mousawi, Hussain Talib, Sami K Asfar, Abdulla I Behbahani

Affiliations

Affiliation

• ¹ Department of Surgery, Kuwait University, Safat, Kuwait. [email protected]

• PMID:

  16652223

• DOI:

  10.1007/s11010-005-9001-x

Clinical Trial

Hussein M Dashti et al.

Mol Cell Biochem.

2006 Jun.

. 2006 Jun;286(1-2):1-9.

doi: 10.1007/s11010-005-9001-x.

Epub 2006 Apr 21.

Authors

Hussein M Dashti 
¹
, Naji S Al-Zaid, Thazhumpal C Mathew, Mahdi Al-Mousawi, Hussain Talib, Sami K Asfar, Abdulla I Behbahani

Affiliation

• ¹ Department of Surgery, Kuwait University, Safat, Kuwait. [email protected]

• PMID:

  16652223

• DOI:

  10.1007/s11010-005-9001-x

Abstract

Objective:

Various studies have convincingly shown the beneficial effect of ketogenic diet (in which the daily consumption of carbohydrate is less than 20 grams, regardless of fat, protein and caloric intake) in reducing weight in obese subjects. However, its long term effect on obese subjects with high total cholesterol (as compared to obese subjects with normal cholesterol level is lacking. It is believed that ketogenic diet may have adverse effect on the lipid profile. Therefore, in this study the effect of ketogenic diet in obese subjects with high cholesterol level above 6 mmol/L is compared to those with normocholesterolemia for a period of 56 weeks.

Materials and methods:

In this study, 66 healthy obese subjects with body mass index (BMI) greater than 30, having high cholesterol level (Group I; n = 35) and those subjects with normal cholesterol level (Group II; n = 31) were selected. The body weight, body mass index, total cholesterol, LDL-cholesterol, HDL-cholesterol, urea, creatinine, glucose and triglycerides were determined before and after the administration of the ketogenic diet. Changes in these parameters were monitored at 8, 16, 24, 32, 40, 48 and 56 weeks of the treatment.

Results:

The body weight and body mass index of both groups decreased significantly (P < 0.0001). The level of total cholesterol, LDL cholesterol, triglycerides and blood glucose level decreased significantly (P < 0.0001), whereas HDL cholesterol increased significantly (P < 0.0001) after the treatment in both groups.

Conclusion:

This study shows the beneficial effects of ketogenic diet following its long term administration in obese subjects with a high level of total cholesterol. Moreover, this study demonstrates that low carbohydrate diet is safe to use for a longer period of time in obese subjects with a high total cholesterol level and those with normocholesterolemia.

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References

1. 1. JAMA. 2003 Aug 20;290(7):912-20

      –

      PubMed

2. 1. Am J Clin Nutr. 1992 Aug;56(2):320-8

      –

      PubMed

3. 1. Am J Cardiol. 1990 Sep 4;66(6):20A-23A

      –

      PubMed

4. 1. Ann Intern Med. 1993 Oct 1;119(7 Pt 2):655-60

      –

      PubMed

5. 1. ScientificWorldJournal. 2004 Sep 24;4:853-8

      –

      PubMed

Publication types

MeSH terms

Substances

Blood test for HDL cholesterol (high density)

Test method

• Colorimetric

High-density lipoproteins (HDL) are considered an anti-atherogenic fraction of lipoproteins, they are involved in the transport of cholesterol from peripheral tissues to the liver (reverse or afferent transport of cholesterol). The main HDL proteins are apolipoproteins A-I and A-II. It is in the composition of HDL that excess cholesterol is removed from the body. Therefore, HDL cholesterol is considered “good” cholesterol.

Main structural components of HDL

• Diagnosis of the risk of atherosclerosis and cardiovascular diseases.

Reference values ​​(standard version):

Age, years	Men	Women	Units
<1	0.36 – 1. 62	0.49 – 1.78	mmol/l
15	0.64 – 1.90	0.64 – 1.9
5 – 10	0.99 – 1.94	0.93 – 1.89
10 – 15	0.96 – 1.92	0.96 – 1.82
15 – 20	0.78 – 1.63	0.91 – 1.92
20 – 25	0.78 – 1.63	0.86 – 2.05
25 – 30	0.81 – 1.63	0.96 – 2.15
30 – 35	0.73 – 1.63	0.94 – 2.00
35 – 40	0.75 – 1.61	0.88 – 2.13
40 – 45	0.7 – 1.74	0.88 – 2.28
45 – 50	0.78 – 1.66	0.88 – 2.26
50 – 55	0.73 – 1.63	0.96 – 2.39
55 – 60	0. 73 – 1.84	0.96 – 2.36
60 – 65	0.78 – 1.92	0.99 – 2.39
65 – 70	0.78 – 1.95	0.91 – 2.49
> 70	0.80 – 1.95	0.86 – 2.39

In accordance with the following international and domestic recommendations:

Cardiovascular Prevention 2017. Russian national guidelines Russian Society of Cardiology, National Society of Preventive Cardiology, Russian Society for the Prevention of Noncommunicable Diseases

Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents, 2012

National Cholesterol Education Program. ATP III Guidelines At-A-Glance. Quick Desk Reference, 2002 Public Health Service National Institutes of Health National Heart, Lung, and Blood Institute.

Provided comments on the HDL-cholesterol test.

Optimal values ​​- more than 1.55; low values ​​(increased risk of cardiovascular diseases) – less than 1.04 mmol / l.

Sample result:

We draw your attention to the fact that the interpretation of the results of studies, the establishment of a diagnosis, as well as the appointment of treatment, in accordance with the Federal Law No. 323-FZ “On the Fundamentals of Protecting the Health of Citizens in the Russian Federation” dated November 21, 2011, must be carried out by a doctor of the appropriate specialization.

Prices for biochemical research Kurkino, Khimki, Planernaya

The cost of blood sampling is 180 rubles;

The cost of taking a scraping/smear is 390 rubles;

Download full price list

No.	BIOCHEMICAL BLOOD TESTS
		Analysis name		Deadline		Price
1	Total protein		up to 1 q.d.		292 rubles
2	Albumin		up to 1 q. d.		341 rubles
3	Creatinine		up to 1 q.d.		286 rubles
4	Urea		up to 1 q.d.		286 rubles
5	Uric acid		up to 1 q.d.		297 rubles
6	Total bilirubin		up to 1 q.d.		286 rubles
7	Bilirubin direct		up to 1 q. d.		286 rubles
8	Total cholesterol		up to 1 q.d.		286 rubles
9	HDL cholesterol		up to 1 q.d.		$3.99
10	LDL cholesterol		up to 1 q.d.		$3.99
11	Triglycerides		up to 1 q.d.		303 rubles
12	Glucose		up to 1 q. d.		270 rubles
13	Lactate		up to 1 q.d.		803 rubles
14	Glycosylated hemoglobin		up to 1 q.d.		682 rubles
15	Alanine aminotransferase ALT		up to 1 q.d.		275 rubles
16	Aspartate aminotransferase AST		to 1 k.d.		275 rubles
17	Gamma-glutamine transferase GGT		up to 1 q. d.		286 rubles
18	Alkaline Phosphatase ALP		up to 1 q.d.		286 rubles
19	Cholinesterase ChE		up to 1 q.d.		391 rubles
20	Alpha-amylase		up to 1 q.d.		$3.99
21	Pancreatic amylase		up to 1 q.d.		413 rubles
22	Lactate dehydrogenase LDH		up to 1 q. d.		286 rubles
23	Creatine kinase KK		up to 1 q.d.		418 rubles
24	C-reactive protein highly sensitive method		up to 1 q.d.		550 rubles
25	Rheumatoid factor		up to 1 q.d.		550 rubles
26	Antistreptolysin-0 ASL-0		up to 1 q.d.		550 rubles
27	Total iron-binding capacity of serum		up to 1 q. d.		396 p.
28	Unsaturated iron-binding capacity of serum		up to 1 q.d.		352 rubles
29	Calcium (Ca2+), Sodium (Na+), Potassium (K+), Chlorine (Cl-)		up to 1 q.d.		693 rubles
HEMOSTASIOLOGICAL STUDIES
30	Fibrinogen		up to 1 q.d.		380 rubles
31	Quick prothrombin + INR		up to 1 q. d.		385 rubles
32	Antithrombin III		up to 1 q.d.		528 rubles
33	Activated partial thromboplastin time		up to 1 q.d.		297 rubles
34	Thrombin time		up to 1 q.d.		385 rubles
35	Lupus anticoagulant		up to 1 q.d.		1056 rubles
36	D – dimer		up to 1 q. Leave a Reply Cancel reply Your email address will not be published. Required fields are marked * Comment * Name * Email * Website