Causes of dyslipidemia: heredity, nutrition, diseases and medications

Dyslipidemia is a disorder of the quantity or composition of fat particles in the blood: low-density lipoproteins, high-density lipoproteins, triglycerides, non-high-density lipoprotein cholesterol, apolipoprotein B, and lipoprotein A. In modern clinical practice, it is not considered a single disease with a single cause: it is a laboratory and metabolic syndrome that can be influenced by heredity, nutrition, obesity, diabetes, thyroid disease, kidney disease, liver disease, medications, pregnancy, and chronic inflammation. [1]

The key to diagnosing the cause of dyslipidemia is to first understand which specific indicator is abnormal. Some causes more often increase low-density lipoproteins, others more often increase triglycerides, and still others produce a mixed picture, with both cholesterol and triglycerides elevated. Endotext emphasizes that when assessing a patient, it is necessary to separately consider elevated low-density lipoproteins, triglycerides, non-high-density lipoprotein cholesterol, and lipoprotein A, as well as decreased high-density lipoproteins. [2]

The causes of dyslipidemia are conventionally divided into primary and secondary. Primary causes are associated with genetic factors affecting lipid metabolism, such as familial hypercholesterolemia or a polygenic predisposition to high cholesterol. Secondary causes arise from diseases, diet, lifestyle, or medications; they are especially important to look for if lipids suddenly worsen in a person whose lipid levels were previously normal or stable. [3]

In practice, primary and secondary causes often overlap. A person may have a hereditary predisposition to high low-density lipoproteins, but severe dyslipidemia will only manifest after weight gain, the development of diabetes, hypothyroidism, chronic kidney disease, or the use of certain medications. Therefore, the correct question is not simply "what causes elevated cholesterol," but "what factors together formed this lipid profile?" [4]

The current 2026 guidelines from the American College of Cardiology and the American Heart Association emphasize a lifelong approach to dyslipidemia: lipids should be assessed not only in pre-existing heart disease but also earlier, when abnormalities can be used as a warning sign. These guidelines specifically highlight a family history of heart disease, obesity, diabetes, chronic kidney disease, chronic inflammatory diseases, early menopause, preeclampsia, gestational diabetes, lipoprotein A, apolipoprotein B, and triglycerides as risk-adjusting factors. [5]

Group of reasons	What is usually violated	Examples
Genetic causes	Most often, low-density lipoproteins or lipoprotein A	Familial hypercholesterolemia, polygenic hypercholesterolemia
Nutrition and lifestyle	Low-density lipoproteins, triglycerides, high-density lipoproteins	Excess saturated fat, alcohol, excess sugar, sedentary lifestyle
Endocrine causes	Low-density lipoproteins, triglycerides	Diabetes mellitus, hypothyroidism, Cushing's syndrome
Diseases of organs	Mixed violations	Chronic kidney disease, nephrotic syndrome, cholestatic liver disease
Medicines	Most often triglycerides, sometimes low-density lipoproteins	Glucocorticosteroids, estrogens, some diuretics, beta-blockers, immunosuppressants

Hereditary causes: when lipid metabolism is disrupted from birth

Hereditary dyslipidemia occurs when genetic variants alter the uptake, transport, processing, or removal of lipid particles from the blood. The most well-known example is familial hypercholesterolemia, in which low-density lipoproteins are elevated from childhood. This isn't a result of "poor nutrition from an early age," but rather a disruption in the mechanism for removing low-density lipoproteins from the bloodstream, leaving blood vessels exposed to increased cholesterol levels for years. [6]

In familial hypercholesterolemia, the genes most commonly affected are those associated with the low-density lipoprotein receptor, apolipoprotein B, and proprotein convertase subtilisin kexin type 9. Endotext reports that among individuals with the familial hypercholesterolemia phenotype, low-density lipoprotein receptor mutations occur in approximately 93%, apolipoprotein B mutations in approximately 5%, and proprotein convertase subtilisin kexin type 9 mutations in approximately 2%. [7]

However, not every low-density lipoprotein level above 190 mg per deciliter automatically indicates classic monogenic familial hypercholesterolemia. Endotext emphasizes that in some patients, high low-density lipoprotein levels are polygenic in nature: multiple common genetic variants, while individually having little effect, together significantly increase cholesterol levels. Therefore, diagnosis should take into account not only the blood test but also family history, age of onset, clinical features, and, if necessary, genetic testing. [8]

A genetic cause is especially likely if high cholesterol is diagnosed at a young age, if close relatives have had early heart attacks or strokes, if there are tendon xanthomas, a pronounced corneal arcus at a young age, or very high levels of low-density lipoproteins. In such situations, it is important to examine not only the individual patient but also relatives, because early detection of familial hypercholesterolemia allows for prevention before a vascular accident occurs. [9]

A separate hereditary cause is high lipoprotein A. This is a particle similar to low-density lipoprotein, but with an additional protein, apolipoprotein A; its level is largely genetically determined and varies little with diet or physical activity. The 2026 guidelines recommend measuring lipoprotein A at least once in adulthood, because high levels increase the lifelong risk of heart attack and stroke, even with a relatively good standard lipid profile. [10]

Hereditary cause	Typical lipid profile	Clinical clue
Familial hypercholesterolemia	Very high low-density lipoproteins	Early heart attacks in the family, xanthomas
Polygenic hypercholesterolemia	Moderately or significantly elevated low-density lipoproteins	There is no single identified mutation, but there is a familial predisposition
High lipoprotein A	High lipoprotein A, sometimes apparent elevation of low-density lipoproteins	Early atherosclerosis with "unexplained" risk
Familial hypertriglyceridemia	High triglycerides	Family history of pancreatitis or very high triglycerides
Combined hereditary forms	Elevated low-density lipoproteins and triglycerides	Several abnormal indicators in relatives

Diet, body weight, and lifestyle: the most common exacerbators of dyslipidemia

Diet affects lipids differently: saturated fats often increase low-density lipoproteins, excess sugar and fast carbohydrates often increase triglycerides, and alcohol is especially dangerous for those prone to hypertriglyceridemia. Therefore, the universal phrase "eat less fat" is too crude: for different types of dyslipidemia, doctors emphasize different dietary factors. [11]

Overweight and abdominal obesity often lead to atherogenic dyslipidemia: triglycerides increase, the number of particles containing apolipoprotein B increases, high-density lipoproteins decrease, and low-density lipoproteins become smaller and denser. This is particularly characteristic of insulin resistance, metabolic syndrome, and type 2 diabetes. [12]

Alcohol is a separate causative factor because it can sharply increase triglycerides in susceptible individuals. The American College of Cardiology's guidelines for hypertriglyceridemia emphasize that alcohol should be limited and, if triglycerides are significantly elevated, completely eliminated. This is especially important if the level approaches the range associated with the risk of pancreatitis. [13]

Sedentary lifestyle alone doesn't always dramatically increase LDL, but it does increase insulin resistance, promote weight gain, worsen glucose control, and maintain high triglyceride levels. The American Consensus on Hypertriglyceridemia recommends physical activity not only as a "general healthy habit" but also as part of basic treatment: approximately 150 minutes of moderate activity per week or 75 minutes of vigorous activity per week. [14]

Sleep, smoking, and overall cardiometabolic health are also important. The 2026 guidelines explicitly include healthy weight, regular physical activity, tobacco cessation, and healthy sleep habits among the key measures for early reduction of lifelong exposure to atherogenic lipids. This means that the causes of dyslipidemia cannot be reduced to a single food or test: it is often a combination of daily factors. [15]

Lifestyle factor	How does it affect lipids?	What is usually adjusted?
Excess saturated fat	Increases low-density lipoproteins	Replace with unsaturated fats, reduce processed foods
Excess sugar and fast carbohydrates	Increases triglycerides	Limiting sugary drinks, sweets, and excess starchy foods
Alcohol	May sharply increase triglycerides	Limit or completely stop if triglycerides are high
Abdominal obesity	Increases triglycerides and apolipoprotein B	Weight loss, physical activity
Sedentary lifestyle	Increases insulin resistance	Regular aerobic and strength training

Diabetes mellitus and insulin resistance: a cause of mixed dyslipidemia

Type 2 diabetes mellitus is one of the most common causes of secondary dyslipidemia. It often results in a combination of elevated triglycerides, reduced high-density lipoproteins, and increased atherogenic particles, even if low-density lipoproteins do not appear to be extremely high. Therefore, diabetes risk cannot be assessed solely by total cholesterol. [16]

The mechanism of diabetic dyslipidemia is linked to insulin resistance. When tissues respond less well to insulin, more free fatty acids enter the bloodstream, the liver actively produces very low-density lipoproteins, triglycerides rise, and particle metabolism becomes more atherogenic. As a result, a person may have a high concentration of particles capable of penetrating the arterial wall, even with a moderate increase in standard values. [17]

Poor glucose control can dramatically increase triglycerides. Endotext specifically notes that improving glycemic control in a patient with poorly controlled diabetes can significantly reduce triglyceride levels. Therefore, in patients with severe hypertriglyceridemia, glucose, glycated hemoglobin, and signs of diabetic decompensation should always be monitored. [18]

Type 1 diabetes mellitus can also be associated with lipid abnormalities, particularly in the presence of insulin deficiency, glucose fluctuations, or concomitant kidney disease. The Endocrine Society recommends assessing the lipid profile in adults with endocrine disorders and, in people with diabetes, considering not only lipids but also overall cardiovascular risk. [19]

In diabetes, it is important to assess not only low-density lipoproteins but also apolipoprotein B. The 2026 guidelines indicate that apolipoprotein B may more accurately reflect residual risk in people with type 2 diabetes, high triglycerides, cardiorenal-metabolic syndrome, or existing cardiovascular disease. [20]

State	Typical lipid profile	Why is this important?
Insulin resistance	High triglycerides, low high-density lipoproteins	Early marker of metabolic risk
Type 2 diabetes mellitus	Mixed atherogenic dyslipidemia	The risk is higher than total cholesterol suggests.
Poor glucose control	A sharp increase in triglycerides	There is a risk of pancreatitis at very high values.
Diabetic kidney disease	Mixed lipid disorders	Increases cardiovascular risk
High apolipoprotein B	Many atherogenic particles	May explain the risk in moderate low-density lipoproteins

Hypothyroidism and other endocrine causes

Hypothyroidism is a classic cause of secondary hypercholesterolemia. Thyroid hormone deficiency reduces the removal of low-density lipoproteins from the blood, leading to significant increases in LDL and total cholesterol levels. Endotext emphasizes that treatment of hypothyroidism often results in significant reductions in LDL, sometimes reaching normal levels. [21]

The Endocrine Society explicitly recommends ruling out hypothyroidism before initiating lipid-lowering therapy and re-evaluating the lipid profile once thyroid hormone levels have normalized. This is also important for safety: untreated hypothyroidism can increase the likelihood of muscle complaints with statins and create a false impression of treatment intolerance. [22]

Cushing's syndrome and long-term exposure to excess glucocorticosteroids can cause elevated low-density lipoprotein (LDL), triglycerides, weight gain, insulin resistance, and hypertension. The Endocrine Society classifies Cushing's syndrome as a condition in which lipids should be assessed and treated along with other cardiovascular risk factors. [23]

Menopause and early menopause can also alter lipid profiles and cardiovascular risk. The Endocrine Society guidelines recommend assessing and treating lipids and other risk factors in women who experience menopause early, before age 40–45. However, hormone therapy should not be used as a treatment for high cholesterol in postmenopausal women. [24]

Some endocrine diseases are not always a direct cause of high cholesterol, but they increase vascular risk and alter the threshold for treatment. Therefore, with dyslipidemia, it is important not just to "get a cholesterol test" but to check the context: body weight, glucose, blood pressure, thyroid function, signs of hypercortisolism, reproductive history, and family history. [25]

Endocrine cause	What increases more often?	Practical significance
Hypothyroidism	Low-density lipoproteins, total cholesterol	First, normalize the thyroid gland function.
Diabetes mellitus	Triglycerides, apolipoprotein B, remnant particles	Glucose and cardiovascular risk control is needed
Cushing's syndrome	Low-density lipoproteins and triglycerides	Treat the underlying endocrine disorder
Early menopause	May worsen lipid profile and risk	Active preventive assessment is required
Obesity as an endocrine-metabolic condition	Triglycerides, reduction of high-density lipoproteins	Weight loss and treatment of insulin resistance are important

Kidney disease, liver disease, inflammation and pregnancy

Chronic kidney disease is a significant cause and exacerbator of dyslipidemia. As kidney function declines, lipoprotein metabolism changes, cardiovascular risk increases, and lipid abnormalities are often associated with inflammation, impaired phosphorus-calcium metabolism, and hypertension. The 2026 guidelines classify chronic kidney disease as a condition requiring particular attention to lipid risk. [26]

Nephrotic syndrome can cause a marked increase in low-density lipoprotein and total cholesterol. This is due to protein loss in the urine, altered protein synthesis in the liver, and impaired lipoprotein metabolism. Therefore, if cholesterol levels are unexpectedly high, edema is present, or albumin or protein levels in the urine are decreased, it is important to investigate the underlying renal cause rather than dismissing the condition as mere dietary hypercholesterolemia. [27]

Liver diseases can affect lipids in different ways. The liver synthesizes, processes, and eliminates many lipid particles, so cholestatic liver diseases can be accompanied by markedly elevated cholesterol, while severe liver diseases sometimes result in very low cholesterol. Endotext notes that very low levels of low-density lipoproteins or triglycerides can also be a sign of other medical problems, including liver disease, chronic infections, malabsorption, or cancer. [28]

Chronic inflammatory diseases, such as rheumatoid arthritis or systemic lupus erythematosus, do not always cause the same increase in cholesterol, but they do increase cardiovascular risk and can alter the quality of lipoproteins. The 2026 guidelines include chronic inflammatory conditions as factors that help clarify the need for more active prevention, even if standard lipid levels do not appear catastrophic. [29]

Pregnancy physiologically alters lipid metabolism, but in predisposed women, it can provoke severe hypertriglyceridemia. The American consensus on hypertriglyceridemia includes pregnancy among the secondary causes of elevated triglycerides, and the 2026 guidelines additionally highlight preeclampsia and gestational diabetes as reproductive factors that predict future cardiovascular risk. [30]

State	Possible lipid effect	When to be especially suspicious
Chronic kidney disease	Mixed dyslipidemia, high cardiovascular risk	Decreased glomerular filtration rate, albuminuria
Nephrotic syndrome	High low-density lipoprotein and total cholesterol	Edema, protein in urine, low albumin
Cholestatic liver diseases	Cholesterol may increase	Itching, jaundice, increased alkaline phosphatase
Chronic inflammation	Increased vascular risk	Rheumatoid arthritis, systemic lupus erythematosus
Pregnancy	Increased triglycerides	Especially with an initial tendency to hypertriglyceridemia

Drugs as a cause of dyslipidemia

Drug-induced dyslipidemia is more common than thought. Some medications increase low-density lipoproteins, others increase triglycerides, and still others worsen several indicators simultaneously, especially in people with diabetes, obesity, chronic kidney disease, or a family history of diabetes. Therefore, if a new or sharply worsening lipid profile occurs, it is always necessary to review your medication list, including hormonal medications, immunosuppressants, and over-the-counter medications. [31]

The American College of Cardiology classifies medications that can increase triglycerides as beta-blockers, diuretics, bile acid sequestrants, glucocorticosteroids, estrogens, human immunodeficiency virus protease inhibitors, tamoxifen, cyclophosphamide, and immunosuppressants. This does not mean that all of these medications should be discontinued, but in cases of severe hypertriglyceridemia, their contribution must be assessed. [32]

Estrogens are especially important in women with a predisposition to high triglycerides. Endotext cites the example that in some postmenopausal women with hypertriglyceridemia, discontinuing oral estrogen therapy can lead to a significant reduction in triglycerides. Therefore, the form, route of administration, dose, and individual risk are important. [33]

Glucocorticosteroids can worsen lipid profiles not only directly, but also through increased glucose levels, increased appetite, weight gain, increased blood pressure, and the development of insulin resistance. This is especially true during long-term treatment of autoimmune, inflammatory, or oncological diseases. In such cases, the physician should evaluate the overall benefit-risk balance rather than discontinuing the drug on their own. [34]

Immunosuppressants and some antiviral drugs can alter lipid metabolism in patients after transplantation, with chronic viral infections, or with immune-inflammatory diseases. In these patients, dyslipidemia often has multiple causes: the disease itself, inflammation, medications, decreased kidney function, weight changes, and age. Therefore, correction requires coordination between a specialist and a physician managing cardiovascular risk. [35]

Group of drugs	Which indicator may worsen?	What is important to do
Glucocorticosteroids	Triglycerides, low-density lipoproteins	Assess dose, duration, glucose and weight
Estrogens orally	Triglycerides	Caution in pre-existing hypertriglyceridemia
Some beta blockers	Triglycerides, high-density lipoproteins	Evaluate alternatives for severe impairments
Some diuretics	Triglycerides and glucose	Check for metabolic side effects
Immunosuppressants and antiviral drugs	Mixed dyslipidemia	Interdisciplinary correction is needed

How a doctor looks for the cause of dyslipidemia

The first step is to confirm the disorder itself. Typically, they begin with a lipid profile: total cholesterol, high-density lipoproteins, triglycerides, calculated low-density lipoproteins, and non-high-density lipoprotein cholesterol. Endotext notes that in most cases, such a routine lipid profile is sufficient for an initial decision, but in complex situations, additional laboratory tests may be required. [36]

The second step is to determine whether there is a secondary cause. NICE recommends taking into account smoking, alcohol, blood pressure, body mass index, lipid profile, glycated hemoglobin, kidney function, transaminases, and thyroid-stimulating hormone levels for symptoms of hypo- or hyperthyroidism before starting statins and when assessing risk. This helps avoid missing a condition in which correcting the underlying cause could significantly improve lipids. [37]

The third step is to evaluate your family history. If relatives have had early heart attacks, strokes, very high cholesterol, pancreatitis associated with triglycerides, or have been taking lipid-lowering drugs since a young age, the likelihood of a hereditary cause is higher. Endotext emphasizes that in cases of severe disorders or onset at a young age, family history is especially important. [38]

The fourth step is to select additional tests if standard testing is insufficient. The 2026 guidelines recommend using lipoprotein A, apolipoprotein B, high-sensitivity C-reactive protein, triglycerides, and coronary calcium to refine risk assessment when this may influence treatment decisions. Apolipoprotein B is particularly useful in type 2 diabetes, high triglycerides, and cardiorenal-metabolic syndrome. [39]

The fifth step is to check whether the picture has changed after correcting the underlying cause. If hypothyroidism has been treated, glucose levels are under control, alcohol has been eliminated, weight is declining, the offending medication has been replaced, but lipids remain elevated, then severe primary or mixed dyslipidemia is likely. In this situation, treatment is focused not only on the underlying cause but also on reducing cardiovascular risk. [40]

The stage of searching for the cause	What do they check?	What can it show?
Lipid profile	Cholesterol, high-density lipoprotein, triglycerides, estimated low-density lipoprotein	Type of dyslipidemia
Metabolic screening	Glucose, glycated hemoglobin, weight, waist	Diabetes, insulin resistance, obesity
Endocrine testing	Thyroid-stimulating hormone, clinical signs of hormonal disorders	Hypothyroidism, Cushing's syndrome, menopausal factors
Organ check	Creatinine, glomerular filtration rate, urine, liver enzymes	Kidney and liver diseases
Hereditary risk analysis	Family history, lipoprotein A, genetic testing as indicated	Familial forms of dyslipidemia

When the cause is particularly dangerous

Familial hypercholesterolemia is considered the most dangerous cause of early atherosclerosis, as high levels of low-density lipoproteins begin in childhood. Endotext indicates that familial hypercholesterolemia is associated with the early development of atherosclerotic cardiovascular events, and homozygous forms can be accompanied by a very severe increase in low-density lipoproteins and external cholesterol deposits already in early life. [41]

The most dangerous cause of acute pancreatitis is very high hypertriglyceridemia. The American consensus defines severe elevation of triglycerides as 500 mg per deciliter and above, and values of 1000 mg per deciliter and above are associated with chylomicronemia; at levels above 1500 mg per deciliter, eruptive xanthomas, lipemia retinaculum, and pancreatitis may occur. [42]

Situations where several underlying causes overlap are especially dangerous. For example, a person with a hereditary predisposition to high triglycerides gains weight, develops type 2 diabetes, continues to drink alcohol, and begins taking a triglyceride-increasing medication. In such a situation, lipid levels can rise significantly more than a single factor, and treatment will require simultaneous correction of all underlying causes. [43]

High lipoprotein A is dangerous because it often goes undetected in a normal lipid profile. A person may have "tolerable" total cholesterol, but inherited high lipoprotein A increases the risk of atherosclerotic events. The 2026 guidelines indicate that lipoprotein A levels of 125 nanomoles per liter or higher, or 50 mg per deciliter or higher, are associated with an approximately 1.4-fold increased long-term risk of heart attack or stroke, and 250 nanomoles per liter is associated with at least a two-fold increased risk. [44]

Dyslipidemia associated with preexisting cardiovascular disease is also considered dangerous, as the underlying cause has already manifested as a complication. In this case, the conversation changes: it's necessary not only to determine the cause of the lipid imbalance but also to quickly reduce the risk of recurrent heart attack, stroke, or atherosclerosis progression. The 2026 guidelines reinstate specific target LDL levels based on risk, including lower targets for people with clinical atherosclerotic disease. [45]

Dangerous cause or situation	The main threat	Why you can't postpone
Familial hypercholesterolemia	Early atherosclerosis	High low-density lipoproteins are active from childhood
Triglycerides 1000 mg per deciliter or higher	Acute pancreatitis	Chylomicronemia is possible
High lipoprotein A	Heart attack and stroke at underestimated risk	The indicator is usually hereditary and stable.
Diabetes plus obesity	Mixed atherogenic dyslipidemia	The risk is higher than cholesterol alone indicates.
Dyslipidemia after heart attack or stroke	Recurrent vascular event	Secondary prevention is needed

FAQ

Can dyslipidemia be only hereditary?

Yes, but more often the picture is mixed: a hereditary predisposition is exacerbated by lifestyle, diabetes, hypothyroidism, kidney disease, pregnancy, or medications. Even with familial hypercholesterolemia, secondary factors can significantly worsen the lipid profile, so the doctor looks for not just one, but all possible causes. [46]

Why can high cholesterol appear suddenly?

A sudden deterioration in the lipid profile raises the possibility of a secondary cause: hypothyroidism, decompensated diabetes, nephrotic syndrome, dietary changes, weight gain, alcohol, pregnancy, or a new medication. Endotext specifically emphasizes that a secondary cause should be suspected if the lipid imbalance appears suddenly or worsens sharply. [47]

What tests help find the cause?

Typically, a complete lipid profile, glucose or glycated hemoglobin, renal function tests, urinalysis if protein is suspected, liver enzymes, thyroid-stimulating hormone if thyroid dysfunction is suspected, and an evaluation of medications and family history are needed. In complex cases, lipoprotein A, apolipoprotein B, and specialized evaluation of hereditary forms are added. [48]

Can hypothyroidism be the only cause of high cholesterol?

Yes, hypothyroidism can significantly increase low-density lipoprotein and total cholesterol, and after normalizing thyroid function, these levels can improve significantly. Therefore, the Endocrine Society recommends ruling out hypothyroidism before starting lipid-lowering treatment and rechecking lipids after hormone levels are normalized. [49]

Why are lipids dangerous in diabetes even if cholesterol is not very high?

In type 2 diabetes, the number of atherogenic particles and triglycerides often increases, and low-density lipoproteins can become smaller and denser. Therefore, total cholesterol or even standard low-density lipoproteins may underestimate risk, and in some cases, apolipoprotein B may be helpful. [50]

What medications most often worsen triglycerides?

Medications that can increase triglycerides include certain beta-blockers, diuretics, bile acid sequestrants, glucocorticosteroids, estrogens, human immunodeficiency virus protease inhibitors, tamoxifen, cyclophosphamide, and immunosuppressants. These medications should not be discontinued on your own, but if dyslipidemia is severe, discuss their potential role with your doctor. [51]

Can diet completely explain dyslipidemia?

Sometimes yes, especially if it's due to excess saturated fat, alcohol, sugar, sugary drinks, and rapid weight gain. But if low-density lipoproteins are very high, there's a family history of early heart attacks, xanthomas, or high lipoprotein A, diet alone can't explain the cause: a hereditary or mixed form must be sought. [52]

Key points from experts

Roger S. Blumenthal, MD, FAAC/AHA, chair of the 2026 Dyslipidemia Guidelines Task Force, and director of the Johns Hopkins Ciccarone Center for the Prevention of Cardiovascular Disease, said: “Prevention should start earlier: a healthy lifestyle remains the first step, but if lipid levels don’t reach the desired range, lipid-lowering medications should be considered sooner than they were 10 years ago.” [53]

Pamela B. Morris, MD, FAAC/AHA, vice chair of the 2026 Guidelines Task Force, and director of the Seinsheimer Cardiovascular Health Program at the Medical University of South Carolina, is an expert in personalized risk assessment: lipoprotein A, apolipoprotein B, high-sensitivity C-reactive protein, triglycerides, and coronary calcium help understand why risk may be higher than suggested by regular cholesterol alone. [54]

Connie B. Newman, MD, chair of the Endocrine Society's Lipid Management in Endocrine Diseases guideline, emphasizes the need to assess the lipid profile in adults with endocrine diseases, rule out hypothyroidism before initiating lipid-lowering treatment, and recheck lipids after thyroid hormone levels are normalized.[55]

Ira J. Goldberg, MD, co-chairs the Endocrine Society's Lipid Management in Endocrine Diseases guideline. His approach is particularly important for understanding diabetic and endocrine dyslipidemia: lipid abnormalities in diabetes, obesity, and hormonal disorders should be considered as part of overall cardiovascular risk, not as a separate metric in analysis. [56]

Kaye-Eileen Willard, MD, a member of the National Lipid Association and president of the National Lipid Association, commented on the 2026 guidelines and emphasized that the fight against cardiovascular events must begin before the first heart attack or stroke. This directly relates to the search for the causes of dyslipidemia, because early identification of hereditary and secondary factors changes the prognosis. [57]

Conclusion

The causes of dyslipidemia are rarely reduced to a single factor. In one patient, the leading role is played by familial hypercholesterolemia; in another, by diabetes mellitus and abdominal obesity; in a third, by hypothyroidism, nephrotic syndrome, or drug therapy; in a fourth, by high lipoprotein A, which is not detectable by normal total cholesterol. [58]

The most appropriate clinical approach is to first determine the type of lipid disorder, then rule out secondary causes, evaluate family history, measure additional risk markers if indicated, and only then choose the intensity of treatment. This approach protects against two mistakes: treating a "number" without understanding the cause and, conversely, attributing dangerous hereditary dyslipidemia solely to diet. [59]

The practical implications of searching for the cause are very specific: if the cause is reversible, its correction can dramatically improve lipids; if the cause is hereditary or the risk is already high, time must not be wasted and long-term prevention of heart attack, stroke and, in the case of very high triglycerides, acute pancreatitis must be implemented. [60]