Evolving worldwide approaches to lipid management (2022)

Guidelines on assessing and managing lipid disorders are constantly evolving as new knowledge and treatments emerge to help health professionals andpatients decide the best course of disease management.

As the point of first contact with the health system, general practitioners (GPs) are uniquely placed to see, assess and prevent disease in the early stages of development.1 The care provided by GPs can extend to families and communities and involves contact across multiple generations, yielding opportunities for unique insights into the family histories and the biopsychosocial dynamics affecting individual patient risk and disease presentations.2

Lipid disorders are commonly managed in general practice but their severity and optimum treatment options may not always be appreciated or updated. As patients progressively age, many develop multiple chronic conditions, with multimorbidity the norm as people progress beyond their middle years.3,4

Younger people gain most if signs and risk factors of cardiovascular disease (CVD) are detected early and preventive actions tailored to their overall risk are enacted.5 Lower-risk patients can be advised of diet and other lifestyle strategies to maintain their status quo while those with lipid disorders often need additional strategies.6,7

CVD accounted for 14% of Australia’s total burden of disease in 2015, with 27% of deaths attributed to CVD in 2017.8 Raised blood lipids are just one of multiple modifiable risk factors for CVD, all of which deserve appropriate consideration for treatment.9

The aim of this article is to review international lipid management guidelines focusing on recommendations of relevance to the primary care management of lipid disorders.

Lipid disorders

Lipid disorders are increasingly prevalent in the modern world, due primarily to poor diet and unhealthy, sedentary lifestyles; they can also be secondary to other disease conditions and treatments. Left untreated, lipid disorders can progress to severe CVD and predispose to other conditions such as diabetes, non-alcoholic fatty liver disease, chronic kidney disease (CKD) and pancreatitis.

Lipids are a component of plasma lipoproteins and can be subject to abnormalities in their metabolism due to genetic and environmental factors resulting in elevated levels of cholesterol or triglycerides. Such abnormalities can occur at any stage of the continuum, from synthesis through processing and clearance, resulting over time in increased risk of CVD.10

Cholesterol and triglyceride are the two major forms of lipid found in the body. Both are carried in lipoproteins in the blood. Cholesterol is used mainly in cell membrane formation as well as in bile acids and in steroid hormones.

Hypertriglyceridaemia has strong environmental and genetic causes. High triglyceride levels can lead to increased CVD risk, pancreatitis and hepatic steatosis.11 Levels up to 1.7 mmol/L are normal while >10 mmol/L increases risk of pancreatitis and hepatic steatosis. It is important that fasting blood levels are taken, as levels are highest after meals. After a trial period of diet and exercise, it is recommended that a fasting triglyceride test is repeated.11

Common causes are sugary foods, inactivity, excess alcohol/binge drinking, smoking, certain conditions (egdiabetes, kidney and thyroid disorders), medications such as thiazide diuretics, steroids, oestrogen and tamoxifen, and inheritance. Obesity and the metabolic syndrome are other complicating factors that need to be considered.11,12

Among the inherited hypercholesterolaemias, heterozygous familial hypercholesterolaemia (HeFH) is an often-missed, autosomal dominant, hereditary disorder with high phenotypic penetrance that is present in approximately 1:250 people in the general population.5,13,14 Dominant forms of familial hypercholesterolaemia are also caused by APOB mutations and proprotein convertase subtilisin/kexin type 9 (PCSK9) gain-of-function mutations causing markedly elevated low-density lipoprotein cholesterol (LDL-C) levels related to defective LDL receptor activity in liver cells, leading to premature CVD and death if untreated.13–16 HeFH is recognised worldwide as a major public health problem13,14 with 50% of first-degree relatives harbouring the disease.

Homozygous familial hypercholesterolaemia (HoFH) is a much more serious condition affecting 1:300,000 people. It results from the union of two HeFH carriers, with 25% of their offspring inheriting the homozygous form.13,14 Such children have markedly elevated LDL-C from birth and rarely survive beyond teenage years unless aggressively treated from infancy.5,13,14

Elevated lipoprotein(a) is a dominantly inherited disorder leading to accumulation in plasma of lipoprotein(a) particles17,18 affecting 20% of the population. A high level (>50 mg/dL) increases the risk of coronary and peripheral artery disease, calcific aortic stenosis and strokes. Testing is not listed on the Medical Benefits Schedule in Australia and is currently undertaken mostly by lipid specialists if there is a family history of heart disease.

Up to 30% of patients with HeFH have elevated lipoprotein(a).17 There is currently no specific treatment other than lipoprotein(a) apheresis but RNA-based therapies that target the hepatic over-production of apolipoprotein(a) and the formation of lipoprotein(a) particles are under investigation.17,18

A comparison of heritable lipid disorders, including prevalence, mutations and epidemiology, is presented in Table1.

Table 1. Summary of inherited lipid disorders
(Homozygous familial hypercholesterolaemia)
Lipoprotein(a)Familial combined hyperlipidaemiaFamilial hypertri-glyceridaemiaType III familial dysbetalipo-proteinaemiaFamilial chylomicronaemia syndrome
InheritanceMonogenic co-dominantPolygenic with variable penetrance and secondary causes, environmental factorsMonogenic,
Prevalence1 in 250
(1 in 300,000)
1 in 51 in 1001 in 5001 in 500013 per million
Effect on lipidsElevated LDLElevated lipoprotein(a)Elevated LDL-C, triglyceride, ApoBElevated
Elevated intermediate densitylipoproteinElevated
Clinical featuresPremature CADCADPremature CADCAD, acute
CADRecurrent acute pancreatitis
Gene variantsLDLR, APOB, PCSK9APOASeveral gene
APOE2/E2Deficiency lipoprotein lipase orAPOC-11
APO, apolipoprotein; CAD, coronary artery disease; LDL, low-density lipoprotein; LDL-C, low-density lipoprotein cholesterol; LDLR, low-density lipoprotein receptor; PCSK9, proprotein convertase subtilisin/kexin type 9; VLDL, very low-density lipoprotein

Cardiovascular disease risk assessment

Approaches to assessing cardiovascular risk have moved from determining individual risk factors to a more global perspective involving absolute risk calculations.6,19 Absolute risk determines the percentage probability of an individual having a major cardiovascular event in the next 5–10 years. The target group are those with no known or overt CVD and usually in the 45–74 years age range.

Risk calculators were originally developed using specific variables based on Framingham data to estimate 10-year risk of developing coronary heart disease.20 The original cohort involved patients to age 70 years, but other versions have been developed to cater for different population and ethnic groups.21,22

(Video) Lipid Management in 2019: From Inclisaran to ANGPTL3- Evolution or Revolution? - Dr. Robert Rosenson

Apart from patients with known high-risk conditions, the absolute cardiovascular risk assessment tool found at www.cvdcheck.org.au23,24 should be used for Australian patients aged over 45years (35–75 years if Aboriginal or Torres Strait Islander) to assess the individual’s overall risk. Young Aboriginal patients may need clinical CVD assessment from age 18years.25

Absolute risk assessment uses an algorithm to evaluate the probable impact on CVD events of multiple risk factors.22 While an absolute risk assessment is more accurate than clinician or patient judgement,26 relying on the outcome may cause high-risk patients to be mislabelled if an accurate family history is not considered.2

Young patients are not accurately assessed with CVD risk calculators developed from patient cohorts aged over 40 while inherited risk (eg familial hypercholesterolaemia) may exist but remain undetected. Postmenopausal women are also at increased risk.12

The risk calculator is not appropriate for assessing patients with already known high CVD risk (eg familial hypercholesterolaemia) for absolute CVD risk.5,13 Their relative risk from the pre-existing condition immediately places them in the highest risk category with atherosclerosis risk present from birth.5,13,15,16

Risk enhancers

The role of coronary artery calcium scores (CACs) is receiving increasing attention in guidelines9,15,16,22,26,27 and can help patient–doctor understanding of an individual’s risk. The Cardiac Society of Australia and New Zealand acknowledges a role for CACs in guiding decisions for patients at intermediate risk where a high CAC score re-classifies them at higher risk, whereas a zero score reflects low disease probability.28

As well as elevated LDL-C, lipid disorders (apolipoprotein B and lipoprotein(a)) are attracting increasing attention in overall risk estimation and treatment approaches due to synergistic effects on CVD risk.9,15,16,26

Inherited factors and secondary causes

It is important to consider the risk of serious hereditary conditions (egfamilial hypercholesterolaemia) in patients with a total cholesterol level above 7.5mmol/L, especially those with a family history of premature coronary artery disease and death.5,13 An unexpected high total cholesterol level is a prompt for further exploration of the patient’s family history.2,29

It is important to exclude potential secondary causes of raised cholesterol levels such as hypothyroidism, uncontrolled diabetes, excess alcohol intake, liver disease and nephrotic syndrome.13,15,16

A family history of premature CVD or death in a younger patient (age <45years) should alert the treating doctor to the potential for hereditary factors16,30 and prompt consideration of random lipid profile (total cholesterol, LDL-C and triglyceride) to assess future CVD risk. Fasting lipids are not required, but it is recommended that a repeat check be fasted if initial results are high.

International approaches to risk assessment

A summary of lipid risk assessment approaches for Australia,6,7 New Zealand,27 Canada,26 UK,31,32 USA9,16 and Europe15 ispresented (Appendix 1).

Evidence from human Mendelian randomisation studies,33 the Cholesterol Treatment Trialists Collaboration analysis,34 the Improve-IT35 and the PCSK9-mAb trials (FOURIER and ODYSSEY)36,37 on the role of LDL-C in atherogenesis, plaque formation and future cardiovascular events now influences dosage and timing oftreatment.

The risk of CVD is no longer seen as an ‘LDL-hypothesis’ as the evidence increasingly shows LDL-C values are causally related to CVD, and the lower the LDL-C level achieved, the better the outcome.15,38,39 For each 1 mmol/L reduction in LDL-C achieved, there is a 22% relative risk reduction in cardiovascular events over five years.34

In the UK, the National Institute for Health and Care Excellence (NICE) CVD risk guidelines recommend 50% lowering of total cholesterol levels. This is aligned with average fall in large trials.40 The NICE guidelines,31 which formerly recommended ‘fire and forget’, now emphasise more precise clinical practice.

European guidelines originally proposed their target should be to a specific cholesterol level (in other words ‘treat to target’) based on evidence that the lower the cholesterol levels, the better the health outcomes.41 More recently, there has been discussion of individualising treatment on the basis of the person’s riskstatus.40

While many countries, including Australia, previously favoured a percentage reduction approach, there has been a debate about what cholesterol target should be achieved with lipid lowering treatment. The targets were originally based on LDL-C (<2.6mmol/L and <1.8 mmol/L for primary and secondary prevention, respectively), but increasingly non-HDL has gained favour.31,32

It is important that intensity of treatment reflects the patient’s total cardiovascular risk. Increasing age is the most potent driver representing the individual’s exposure over time to multiple risk factors. This inherent limitation in CVD risk estimation means that older patients progressively move into high risk categories irrespective of other risk factors.15,16 Younger people have greater cumulative risk over time5,15,19 but this may not become manifest until later in life when their CVD may have progressed.

Any lowering of LDL-C brings benefit, even if targets are not reached.15 Duration of treatment brings cumulative benefit, especially when started early in life.5,15,42,43 Future medications that target PCSK944 are expected to facilitate LDL-C levels <1.0 mmol/L and this may provide additional cardiovascular benefits.

Risk communication

Risk communication is seen as the critical element in allowing for shared decisions between clinician and patient about future risk management.9,15,26,27 Itis vital that results of risk assessments are delivered to patients and their families/carers at a level appropriate to their circumstances. It is important to stress heart-healthy lifestyle interventions and compliance reinforcement throughout all recommendations.7,9,26,27 This is enhanced by opportunistic health promotion by GPs at routine consultations.1

Increasing age, sex and inheritance are key immutable risk factors.15,19 Patients aged >75 years who are already on statins should continue.15,45 It is recommended that children with HeFH commence lifelong treatment from the age of 8–10years,5 while statins should be avoided in pregnancy.13 High-risk adults with HeFH should commence maximally tolerated doses of high potency statins on diagnosis and continue for life.15,43 Itis recommended that relevant specialist advice is sought for the care of children and pregnant women.5,13

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Other important and potentially modifiable risk factors include smoking; obesity, especially central obesity; poor diet; lack of exercise; social deprivation and isolation; raised blood pressure; diabetes; and lipid disorders.9,46

Chronic kidney disease (eGFR <45mL/min/m2),47 severe mental illness (depression, bipolar affective disorder and schizophrenia), use of antipsychotic medications or steroids, obstructive sleep apnoea, atrial fibrillation, heart failure and non-alcoholic fatty liver disease are also important risk factors.27


Risk assessment approach

Most patients without overt CVD can have risk assessment undertaken using a global risk calculator. Those with known CVD are already at increased risk and benefit from management with aggressive treatment. In Australia, all patients with absolute risk >15% for a CVD event in the next five years should be similarly treated, while those with absolute risk of 10–15% plus additional risk factors should also betargeted.6,7

Secondary causes for increased lipid levels (hypothyroidism, CKD, poorly controlled diabetes, alcohol abuse and liver disease) require individual assessment and management.

Lifestyle modifications

A healthy lifestyle is encouraged for all patients for both primary and secondary prevention. This includes regular physical exercise, a heart-healthy diet, avoidance ofobesity and smoking cessation.7

It is important that support for smoking cessation be central to lifestyle modification. All guidelines recognise smoking as a key risk factor in CVD minimisation,5–7,9,15,26,27,31 particularly for young patients with hereditary disorders, HeFH and HoFH.5

A key dietary approach is the use of mono- and poly-unsaturated fats and wholegrains instead of saturated fats and refined carbohydrates to help reduce LDL-C levels. A Mediterranean-style diet,48 which includes nuts and olive oil, can complement medication in achieving treatment goals.

Exercise recommendations consist of 150 minutes per week of moderate exercise or 75 minutes of more vigorous exercise together with muscle strengthening exercises twice weekly. Joining group classes or clubs to encourage swimming, walking, cycling, dancing or gym attendance can be helpful.2,6,7

Weight management targets body mass index of 25 kg/m2 with waist circumferences of <94 cm in men and <80cm in women.

Alcohol intake should be a maximum of two standard drinks per day, with two to three alcohol-free days per week encouraged.

The active support of GPs can be critical to ensure patients adhere to agreed treatment plans and help to guarantee the sustainability of the approach.2,6,49

Cholesterol targets and pharmacotherapies

A summary of international approaches to treating elevated cholesterol levels is shown (Appendix 2). A comparison of medications and their effects is also included (Table2).

Table 2. Comparison of lipid-lowering drugs
Medication/classTypical effect on lipidsTolerabilityDose frequencyComments
StatinsReduce LDL 25–55%

Reduce triglycerides 10–20%

Well toleratedOnce dailyMedications of choice; most effective oral LDL-lowering agents with best supporting evidence

Reduce risk of MI, stroke and mortality in patients at high risk of cardiovascular disease (with or without coronary heart disease)

A 1 mmol/L decrease in LDL reduces rates of coronary death by 20% and non-fatal MI by 27%

Colestyramine (bile acid binding resin)Reduces LDL 15–25%

May increase triglycerides

GI disturbances common

Poorly tolerated

1–4 times dailyMay be used in combination treatment (in low dose), for example when a statin alone is inadequate
EzetimibeReduces LDL 15–25%Well toleratedOnce dailyOption when statins are contraindicated or nottolerated

May be added to a statin when statin alone isinsufficient

FibratesReduce LDL 5–15% (>25% with fenofibrate)

Increase HDL 10–30%

(Video) Webinar | Lipid lowering landscape: New and emerging treatment approaches | Heart Foundation

Decrease triglycerides 40–80%

GI disturbances common


1–2 times


Used in severe hypertriglyceridaemia (triglycerides >10 mmol/L) to prevent pancreatitis

LDL may increase in pure hypertriglyceridaemia

Fish oils (omega-3 fattyacids)Lower triglycerides when taken daily in doses containing 2–4 g omega-3 fatty acids

Do not reduce LDL

Few adverse effects

High doses may increase bleeding time

1–3 times dailyUsed in hypertriglyceridaemia or with LDL-lowering medications in mixed hyperlipidaemia

Content varies between products

To obtain 2–5 g omega-3 fatty acids daily may require >6 capsules daily

Nicotinic acidReduces LDL 15–30%

Reduces triglycerides 25–40%

Increases HDL 20–35%

Poorly tolerated


3 times dailyMay be used for hypertriglyceridaemia or in combination therapy for mixed hyperlipidaemia (if tolerated)
PCSK9 inhibitorsReduce LDL 60% (alone or withstatins)

Evolocumab reduces LDL 20–30% in homozygous familial hypercholesterolaemia

Increase HDL

Appear well tolerated

Injection site reactions may occur

Once every 2–4 weeksSC injection, reduce ischaemic cardiovascular events (when used with statins) in patients with cardiovascular disease

Option in familial hypercholesterolaemia, usually in combination with maximally tolerated statins

Use is limited by high cost

Long-term safety data are lacking

GI, gastrointestinal; HDL, high-density lipoprotein; LDL, low-density lipoprotein; MI, myocardial infarction; PCSK9, proprotein convertase subtilisin/kexin type 9; SC, subcutaneous
Reproduced with permission from Australian Medicines Handbook, Adelaide, SA, Australian Medicines Handbook Pty Ltd, 2020.

Patients requiring help with raised lipids can be advised that statin treatment has the most powerful evidence from robust clinical trials based on outcomes research.50,51


Statins have been for decades the main primary prevention treatment for CVD in patients with significant hypercholesterolaemia as well as for patients aged 40–75 years with diabetes or higher CVD risk.6,7,9,13,15,16,26,27,32 LDL-C is the dominant form of atherogenic cholesterol and the mainstay of treatment.

(Video) Reduce LDL Cholesterol Naturally (IN JUST 10 DAYS)!!!

Lipid management for secondary prevention of CVD will involve pharmacotherapy with high intensity statins at doses higher than used for primary prevention.13,15–16

There is increasing evidence that high intensity statins (atorvastatin 80 mg and rosuvastatin 40 mg) are capable of more substantial lowering of LDL-C levels, resulting in greater reductions in CVD.39 The new approach from European and American guidelines is the lower the LDL-C level, the better the outcome for thepatient.9,15,16,34


Patient resistance to statins can occur but major side effects, especially in randomised trials, are rare.13,15,34 Potential statin adverse effects include myopathy, mild elevation of alanine aminotransferase and some medication interactions involving cytochrome P450 pathways. It is important to avoid statins in combination with gemfibrozil, while combination with fenofibrate carries very low myopathy risk.15 Statin treatment can precipitate new-onset diabetes mellitus, linked to medication potency and concomitant obesity and insulin resistance.9 For patients with an adverse reaction to statin, 70% will tolerate an alternative regimen.13


Non-statin lipid-lowering medications include ezetimibe and PCSK9 inhibitors.52 Ezetimibe, which inhibits cholesterol absorption from the gut, has a low incidence of side effects and can be used in combination with a statin13,35 or alone to achieve a 13–20% LDL-C lowering. Patients resistant to statin treatment can try ezetimibe prior to re-introducing a low dose statin later.9,13,16

PCSK9 inhibitors evolocumab and alirocumab have been registered in Australia with evolocumab on the Pharmaceutical Benefits Scheme53 according to strict revised criteria for bothfamilial hypercholesterolaemia and non–familial hypercholesterolaemia patients from 1 May 2020.

If PCSK9 inhibitors are added to a statin, the overall effect can produce reductions of 43–64% in LDL-C levels.36,37 Because PCSK9 inhibitors cross the placenta, they are not suitable for use in pregnancy and are not licensed for use in children. A downside to their use is cost plus 2–4-weekly injections. No adverse effects for diabetes or neurocognition have been found.54

Some newer medications undergoing clinical trials include inclisiran, which targets PCSK9 via small interfering RNA.44 These medications offer considerable hope for the future, especially potential reduced costs and twice annual dosage requirements.

Bile acid sequestrants act indirectly by binding to bile acids in the intestine to prevent the reabsorption of both the medication and cholesterol into the blood.15 They can reduce LDL-C by 15–30% but cause constipation and risk increasing triglyceride levels if baseline levels are raised.15

Fibrates produce small reductions in LDL-C levels among patients with normal triglycerides and have benefits for some patients with severe hypertriglyceridemia.16 Triglyceride levels >10 mmol/L are associated with increased risk of pancreatitis11 with levels <1.7 mmol/L advised. In addition to dietary and lifestyle advice, statins are the optimum medication treatment and can be combined with fenofibrate15 to reduce hepatic production of very low-density lipoproteins and hasten removal of hypertriglyceridaemia from the blood.

Fish oil supplements15 (2–4 g daily) can lower hypertriglyceridemia. They do not reduce LDL-C and have few side effects but may require more than six capsules daily to achieve effective dose levels (Table2).

Niacin is now rarely used26 because of adverse effects including liver damage andstrokes.

Other areas of interest

Nutraceuticals are food-type products that may have potential as fourth-line adjuncts to standard lipid pharmacotherapy or in patients with statin resistance or statin-associated muscle symptoms55,56 but to date there is no evidence they reduce atherosclerotic CVD events. Their mode of action is not well defined.

Apheresis is used in specialist lipid centres for difficult-to-manage, high-risk patients (eg HoFH, severe HeFH or those with high lipoprotein(a) levels) to separate disease-provoking components from their plasma, with the remaining blood then returned to the patient.14,17

Bempedoic acid is a novel therapy to inhibit cholesterol synthesis that recently completed phase 3 trials. It has been approved by the US Food and Drug Administration for LDL-C reduction therapy for established atherosclerotic CVD and HeFH and is expected to help statin-resistant patients.57


Adherence to optimum management can be problematic, and a patient-centred approach addressing concerns about medications and potential side effects is recommended. Statin adherence and persistence is often poor, lacking patient benefit if not taken.42 Initial patient–doctor discussion should seek consensus on treatment need, stratification of risk involved as well as planned approach involving diet, regular exercise, lifestyle changes and potential pharmacotherapy. Supportive counselling from pharmacists as well as new electronic reminder devices, including texting, can also help adherence.15

Understanding patient and family health literacy is essential because reinforcement in follow-up visits about the nature of the underlying problem plays a critical part in management outcomes.


Evolving worldwide guidelines and research on lipid management and CVD mitigation show consensus towards tighter control of LDL-C with higher-risk patients requiring earlier diagnosis and more aggressive treatments. Close adherence to diet, lifestyle and medications is underscored and remains a challenge in practice. New lipid treatment targets beyond LDL-C for which specific therapies are being tested are triglyceride-risk, lipoprotein remnants and lipoprotein(a).

Future directions in primary healthcare delivery will need to focus on increasing awareness of how to improve CVD risk assessment among GPs, practice nurses and their patients; early identification of those at highest risk; plus an ability to adjust and meet management strategies as newer, more focused and personalised treatments become available. The new findings presented in this article can positively influence GP clinical decision making and provide a foundation for developing new lipid management guidelines for Australia.

Competing interests: TB, JR and GFW are Chief Investigators and JP is an Associate Investigator on the National Health and Medical Research Council Partnership Grant ‘to improve the detection and management of familial hypercholesterolaemia in primary care’ and Pharmaceutical companies Amgen and Sanofi-Aventis are industry partners in the study. TB, JR and GFW have also received presentation honoraria and travel re-imbursement for the familial hypercholesterolaemia summit from Amgen. Neither company had any involvement in the commissioning or writing of the submitted article. NQ reports honoraria and travel costs from Amgen, outside the submitted work. GFW has received honoraria for lectures, advisory boards and research projects from Amgen, Sanofi, Regeneron, Kowa, AstraZeneca, Arrowhead and Novartis.

(Video) Dr. Peter Attia: Exercise, Nutrition, Hormones for Vitality & Longevity | Huberman Lab Podcast #85

Provenance and peer review: Not commissioned, externally peer reviewed.

Funding: None.Correspondence to:


How does HDL and LDL levels reflect the risk and progression of atherosclerosis? ›

HDL helps prevent atherosclerosis. It has long been recognized that the cholesterol concentrations in the blood are indicators of the probability that a plaque will develop: higher LDL and lower HDL concentrations indicate a higher probability of plaque development.

What is the role of cholesterol in the development of atherosclerosis? ›

Over time, high cholesterol leads to plaque buildup inside your blood vessels. This plaque buildup is called atherosclerosis. People with atherosclerosis face a higher risk of many different medical conditions. That's because your blood vessels do important work all throughout your body.

How do lipids contribute to atherosclerosis? ›

Role of lipids in the pathophysiology of atherosclerosis

Because lipids are insoluble in plasma, circulating lipids are bound to lipoproteins and transported to various tissues where they are used for various functions including energy utilisation, synthesis of steroid hormones, and bile acid formation.

Which of the following lipids are thought to decrease heart disease? ›

HDL (high-density lipoprotein), or “good” cholesterol, absorbs cholesterol and carries it back to the liver. The liver then flushes it from the body. High levels of HDL cholesterol can lower your risk for heart disease and stroke.

What kind of blood protein can cause atherosclerosis? ›

We have demonstrated that plaque formation in atherosclerosis is accompanied by protein 3-nitrotyrosine accumulation in organs that are distal to the atherosclerotic lesion (Upmacis et al., 2007).

Which lipid type is associated with the highest risk of atherosclerosis development? ›

High serum lipid levels, especially the elevated level of low-density lipoprotein (LDL), have been shown to be strongly related to the development of atherosclerosis.

What type of cholesterol causes atherosclerosis? ›

Population studies have demonstrated that elevated levels of LDL cholesterol and apolipoprotein B (apoB) 100, the main structural protein of LDL, are directly associated with risk for atherosclerotic cardiovascular events (ASCVE).

What is the main cause of high cholesterol? ›

High cholesterol is when you have too much of a fatty substance called cholesterol in your blood. It's mainly caused by eating fatty food, not exercising enough, being overweight, smoking and drinking alcohol. It can also run in families. You can lower your cholesterol by eating healthily and getting more exercise.

What foods cause your cholesterol to be high? ›

High-cholesterol foods to avoid
  • Full-fat dairy. Whole milk, butter and full-fat yogurt and cheese are high in saturated fat. ...
  • Red meat. Steak, beef roast, ribs, pork chops and ground beef tend to have high saturated fat and cholesterol content. ...
  • Processed meat. ...
  • Fried foods. ...
  • Baked goods and sweets. ...
  • Eggs. ...
  • Shellfish. ...
  • Lean meat.
13 Oct 2021

Which lipids can cause heart disease? ›

High levels of LDL cholesterol and triglycerides, and low levels of HDL cholesterol are linked to heart disease. High levels of LDL cholesterol, often called the “bad” cholesterol, are associated with heart disease.

Is lipid structure linked to heart disease? ›

Lipids and lipoprotein particles crucially contribute to atherosclerosis as underlying pathology of cardiovascular disease and influence inflammatory processes as well as function of leukocytes, vascular and cardiac cells, thereby impacting on vessels and heart.

Which lipid is associated with coronary heart disease? ›

Higher concentrations of LDL, IDL, and VLDL cholesterol (the apolipoprotein B-100–containing lipoproteins) and lower concentrations of HDL cholesterol are generally considered to be important lipid CHD risk factors.

Which 2 lipids are responsible for increasing the risk of developing heart disease? ›

Elevated LDL (>190 mg/dL) and triglycerides are risk factors for coronary heart disease; see Desirable Blood Lipid Levels.

How do lipids affect the heart? ›

Lipids and lipoprotein particles crucially contribute to atherosclerosis as underlying pathology of cardiovascular disease and influence inflammatory processes as well as function of leukocytes, vascular and cardiac cells, thereby impacting on vessels and heart.

What is the difference between a lipid and cholesterol? ›

The main difference between lipids and cholesterol is that lipids are one of the three main constituents of the living cells together with carbohydrates and proteins whereas cholesterol is a waxy substance, which is an essential component of the cell membrane.

Can you reverse plaque buildup in your arteries? ›

The key is lowering LDL and making lifestyle changes.

"Making plaque disappear is not possible, but we can shrink and stabilize it," says cardiologist Dr. Christopher Cannon, a Harvard Medical School professor. Plaque forms when cholesterol (above, in yellow) lodges in the wall of the artery.

What can remove plaque from arteries? ›

To remove plaque from arteries, the following procedures are performed:
  1. Angioplasty. ...
  2. Coronary Artery Bypass Graft. ...
  3. Coronary Stent. ...
  4. Rotational Atherectomy.

How can I lower my cholesterol and triglycerides without medication? ›

  1. Eat heart-healthy foods. A few changes in your diet can reduce cholesterol and improve your heart health: ...
  2. Exercise on most days of the week and increase your physical activity. Exercise can improve cholesterol. ...
  3. Quit smoking. ...
  4. Lose weight. ...
  5. Drink alcohol only in moderation.

Can high cholesterol be treated without statins? ›

There are many non-statin medications your doctor might prescribe: Bile acid-binding resins, like cholestyramine (Locholest, Prevalite, Questran), colesevelam (WelChol), and colestipol (Colestid) stick to cholesterol-rich bile acids in your intestines and lower your LDL levels.

When should I start lipid treatment? ›

Dietary therapy should be initiated in patients who have borderline-high LDL cholesterol levels (130 to 159 mg per dL [3.35 to 4.10 mmol per L]) and two or more risk factors for coronary heart disease and in patients who have LDL levels of 160 mg per dL (4.15 mmol per L) or greater.

What foods unclog your arteries naturally? ›

Top Foods That Unclog Arteries Naturally
  • Berries. Strawberries, blueberries, cranberries, blackberries, and raspberries are best. ...
  • Tomatoes. ...
  • Onions. ...
  • Citrus Fruits. ...
  • Cruciferous Vegetables. ...
  • Leafy Greens. ...
  • Beans. ...
  • Fish.
21 Jul 2021

Does oatmeal remove plaque arteries? ›

Oats. Oats are an excellent choice for those who have atherosclerosis or are trying to prevent clogged arteries. Eating oats can help significantly reduce atherosclerosis risk factors, including high levels of total and LDL (bad) cholesterol ( 39 ).

What are the signs of high cholesterol on face? ›

It can also lead to a host of skin conditions. If you notice fatty deposits under your skin, yellowish bumps, patches around your eyes, or mild to severe skin discoloration, you might have a skin condition related to high cholesterol.

Does stress make cholesterol high? ›

Is stress linked to high cholesterol? The short is yes. Feeling under pressure for a long time can raise your risk of high cholesterol and even heart disease. But you can take steps to get your stress under control and protect your heart.

Do eggs raise your cholesterol? ›

Chicken eggs are an affordable source of protein and other nutrients. They're also naturally high in cholesterol. But the cholesterol in eggs doesn't seem to raise cholesterol levels the way some other foods, such as those high in trans fats and saturated fats, do.

What is a normal cholesterol level? ›

Here are the ranges for total cholesterol in adults: Normal: Less than 200 mg/dL. Borderline high: 200 to 239 mg/dL. High: At or above 240 mg/dL.

What reduces cholesterol quickly naturally? ›

Foods that make up a low cholesterol diet can help reduce high levels
  • Oats. ...
  • Barley and other whole grains. ...
  • Beans. ...
  • Eggplant and okra. ...
  • Nuts. ...
  • Vegetable oils. ...
  • Apples, grapes, strawberries, citrus fruits. ...
  • Foods fortified with sterols and stanols.

Are bananas good for cholesterol? ›

The fiber and potassium in bananas can reduce the level of cholesterol and blood pressure. Banana is especially known as a good source of soluble fibre which will gives one a healthy body and good immune system.

What drinks are good for cholesterol? ›

Best drinks to improve cholesterol
  • Green tea. Green tea contains catechins and other antioxidant compounds that seem to help lower “bad” LDL and total cholesterol levels. ...
  • Soy milk. Soy is low in saturated fat. ...
  • Oat drinks. ...
  • Tomato juice. ...
  • Berry smoothies. ...
  • Drinks containing sterols and stanols. ...
  • Cocoa drinks. ...
  • Plant milk smoothies.

What is dangerously high cholesterol? ›

A person is considered at high risk for developing heart disease if their total cholesterol level is higher than 240 mg/dL, LDL levels are higher than 160 mg/dL (190 mg/dL is even higher risk), and if the HDL level is below 40 mg/dL.

What is a healthy cholesterol level by age? ›

Optimal ranges
Age and sexTotal serum cholesterolTriglycerides
all aged 19 years and younger170 mg/dl at mostless than 150 mg/dl
females aged 20 years and older125–200 mg/dlless than 150 mg/dl
males aged 20 years and older125–200 mg/dlless than 150 mg/dl

Can high cholesterol be cured? ›

Lifestyle changes such as exercising and eating a healthy diet are the first line of defense against high cholesterol. But, if you've made these important lifestyle changes and your cholesterol levels remain high, your doctor might recommend medication.

What are three important functions of cholesterol in the body? ›

Cholesterol facts

In our bodies, cholesterol serves three main purposes: It aids in the production of sex hormones. It's a building block for human tissues. It assists in bile production in the liver.

How are lipids involved in obesity? ›

The lipid abnormalities in patients who are obese include elevated serum triglyceride, VLDL, apolipoprotein B, and non-HDL-C levels. The increase in serum triglycerides is due to increased hepatic production of VLDL particles and a decrease in the clearance of triglyceride rich lipoproteins.

What vitamin does cholesterol help to synthesize? ›

In the skin vitamin D3 is synthesized from cholesterol, which leaves the question whether a feedback mechanism controlling the level of blood cholesterol exists.

Can lipid profile detect heart blockage? ›

A cholesterol test, also called a lipid panel or lipid profile, measures the fats in the blood. The measurements can help determine the risk of having a heart attack or other heart disease.

What is the effect of diabetes on blood lipids? ›

Abnormal blood lipids in diabetic patients include elevated very low-density lipoproteins (VLDL) and triglyceride and reduced levels of high-density lipoproteins (HDL). These are associated with obesity and precede the onset of diabetes.

Does the heart get stronger with exercise? ›

Your heart is a muscle. Just like your bicep, the more you work your heart, the bigger and stronger it gets. During moderate- to high-intensity exercise, your muscles and tissues demand more nutrients and oxygen, which means that your heart must work harder and pump faster to meet those needs, says Dr. Cho.

How do you normalize a lipid profile? ›

Lifestyle Modifications for Lipid Disorders
  1. Eat Healthfully. Consuming a diet low in saturated and trans fats is key for reducing cholesterol and triglyceride levels. ...
  2. Exercise Regularly. ...
  3. Maintain a Healthy Weight. ...
  4. Consume Omega-3 Fatty Acids. ...
  5. Avoid Alcohol.

What are the food sources of lipids? ›

Food Sources of Lipids

Commonly consumed oils are canola, corn, olive, peanut, safflower, soy, and sunflower oil. Foods rich in oils include salad dressing, olives, avocados, peanut butter, nuts, seeds, and some fish. Fats are found in animal meat, dairy products, and cocoa butter.

Which of the following lipids are thought to decrease heart disease? ›

HDL (high-density lipoprotein), or “good” cholesterol, absorbs cholesterol and carries it back to the liver. The liver then flushes it from the body. High levels of HDL cholesterol can lower your risk for heart disease and stroke.

What can cause high lipids? ›

High lipid levels may also be caused by medical conditions such as diabetes, hypothyroidism, alcoholism, kidney disease, liver disease and stress. In some people, certain medicines, such as birth control pills, steroids and blood pressure medicines, can cause high lipid levels.

What are four examples of lipids? ›

Examples of lipids include fats, oils, waxes, certain vitamins (such as A, D, E and K), hormones and most of the cell membrane that is not made up of protein.

Is it important to regulate lipid metabolism? ›

In conclusion, lipid metabolism plays an essential role in regulating the aging process. Experimental evidence shows that lipid metabolism is changed during aging and lipid-related interventions can modulate age-related diseases and aging in various model organisms.

Which is the most important component of lipid profile? ›

Cholesterol: Predictor of Heart Attack

They combine to give you a "lipid profile" score, but the three individual scores are most important.

What are the 4 major results of a lipid panel? ›

A standard lipid panel typically measures four different types of lipids:
  • Total cholesterol (TC)
  • Low-density lipoprotein cholesterol (LDL-C)
  • High-density lipoprotein cholesterol (HDL-C)
  • Triglycerides (TG)
19 Jan 2021

What are the 3 types of cholesterol? ›

The types of cholesterol and lipoproteins include:
  • Low-Density Lipoprotein (LDL) or Bad Cholesterol — Plaque Builder. ...
  • High-Density Lipoprotein (HDL) or Good Cholesterol — The Bad Cholesterol Eater. ...
  • Triglycerides — Blood Fats. ...
  • Lp(a) Cholesterol.
1 Jul 2019

How does HDL affect atherosclerosis? ›

High-density lipoproteins (HDLs) oppose atherosclerosis directly, by removing cholesterol from foam cells, by inhibiting the oxidation of LDLs, and by limiting the inflammatory processes that underlie atherosclerosis. HDLs also have antithrombotic properties.

How does LDL cholesterol contribute to the development of atherosclerosis quizlet? ›

Increased LDL cholesterol levels present a health risk because LDL carries cholesterol to the tissues to be deposited as fat and can contribute to the development of atherosclerosis.

How are the concentrations of LDL and HDL associated with the risk for heart disease and associated disorders? ›

The fact is, elevated low-density lipoprotein (LDL), the bad cholesterol, is a major cause of heart disease. LDL causes the build-up of fatty deposits within your arteries, reducing or blocking the flow of blood and oxygen your heart needs. This can lead to chest pain and heart attack.

What is the relationship between HDL cholesterol and risk of coronary artery disease? ›

Epidemiological studies clearly show that levels of high-density lipoprotein cholesterol (HDL-C) are inversely associated with the risk of coronary artery disease and its thrombotic complications.

What type of cholesterol causes atherosclerosis? ›

Population studies have demonstrated that elevated levels of LDL cholesterol and apolipoprotein B (apoB) 100, the main structural protein of LDL, are directly associated with risk for atherosclerotic cardiovascular events (ASCVE).

How can I raise my good cholesterol and lower my cholesterol? ›

  1. Reduce saturated fats. Saturated fats, found primarily in red meat and full-fat dairy products, raise your total cholesterol. ...
  2. Eliminate trans fats. ...
  3. Eat foods rich in omega-3 fatty acids. ...
  4. Increase soluble fiber. ...
  5. Add whey protein.

Does High HDL cause plaque? ›

Whereas LDL particles deposit cholesterol into plaques of atherosclerosis, some high-density lipoprotein (HDL) particles help remove cholesterol from plaques. That's why it's often referred to as "good" cholesterol.

What is a function of cholesterol that does not harm health? ›

Its main function is to maintain the integrity and fluidity of cell membranes and to serve as a precursor for the synthesis of substances that are vital for the organism including steroid hormones, bile acids, and vitamin D.

Which of the following is a risk factor for the formation of atherosclerosis? ›

Risk factors may include high cholesterol and triglyceride levels, high blood pressure, smoking, diabetes, obesity, physical activity, and eating saturated fats.

Which type of lipid serves as fuel for the body when energy is needed quizlet? ›

Triglycerides are a lipid type that is the major form of fat in foods and a key source of energy from the body. Triglycerides are composed of 3 fatty acids attached to a glycerol molecule.

What are the new guidelines for cholesterol levels 2021? ›

Reduce LDL-C levels ≥50% and LDL-C goal ≥1.8 mmol/L (≥70 mg/dL). LDL-C <2.6 mmol/L (<100 mg/dL). Reduce levels ≥50% in patients with DM and LDL-C ≥1.8 mmol/L (≥70 mg/dL). LDL-C <2.6 mmol/L (<100 mg/dL).

What level of LDL requires medication? ›

Your health care provider may prescribe medicine if: You have already had a heart attack or stroke, or you have peripheral arterial disease. Your LDL cholesterol level is 190 mg/dL or higher.

Does fasting raise LDL levels? ›

Fasting increases serum total cholesterol, LDL cholesterol and apolipoprotein B in healthy, nonobese humans. J Nutr.

What is the best way to raise HDL cholesterol? ›

5 Ways to Raise Your HDL Cholesterol
  1. Get active. Physical activity can boost your HDL level. ...
  2. Lose extra weight. If you're overweight, losing extra pounds can help raise your HDL levels, as well as cut your LDL ("bad") cholesterol levels.
  3. Choose better fats. ...
  4. Alcohol in moderation. ...
  5. Stop smoking.
16 Mar 2022

Can high HDL lead to heart disease? ›

Higher levels of HDL have been associated with a lower risk of cardiovascular disease. However, pharmaceutical approaches to reduce heart disease risk by raising HDL levels have had disappointing results.

What level of HDL is considered higher risk for heart disease? ›

The total cholesterol/HDL ratio is an indicator of your potential for developing blockages in the arteries of your heart. A ratio greater than 4.5 is considered a high risk for coronary heart disease.


1. Lower Cholesterol with These 3 Foods
(Zonya Foco, RDN)
2. Multidisciplinary Approach on Lipid Management: Beyond "Ordinary" LDL Target
(Kardiologi UNPAD)
3. Prof. Scott Gilbert: The new evolutionary medicine - an eco-devo approach to health and disease
(Biosynteesi Biosynthesis)
4. Dr. Robert Cywes reviews our lab results | Is high cholesterol safe on keto? | Is Keto safe?
5. How to stay calm when you know you'll be stressed | Daniel Levitin
6. What Should We Really Be Eating? | The Perfect Human Diet (Full Documentary) | Tonic

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