Tools
Low HDL Cholesterol
Introduction
High-density lipoprotein (HDL) cholesterol is a class of lipoproteins characterized by a dense protein structure and a diameter of approximately 8–12 nanometers.[1] HDL particles are composed of a hydrophobic core consisting largely of esters and triglycerides, surrounded by a layer of phospholipids, free cholesterol, and apolipoproteins. HDL levels are routinely measured via enzymatic assays, which quantify the cholesterol content of HDL particles after the precipitation or inhibition of other lipoprotein classes. Additionally, different methods have been used to subclassify HDL particle number: size and density via ultracentrifugal flotation rate and mass concentration of lipoprotein particles.[2] Further, HDL can be subcategorized by gel electrophoresis and by apolipoprotein composition.
HDL cholesterol has many antiatherogenic properties, including reverse cholesterol transport, a process that removes cholesterol from peripheral tissues and transports it to the liver for clearance by macrophages.[3] Moreover, HDL has many anti-inflammatory, antioxidative, and endothelial-protective functions.[3] Due to these characteristics, HDL particles play a role in reducing cardiovascular risk.
Etiology
Register For Free And Read The Full Article
Search engine and full access to all medical articles- 10 free questions in your specialty
- Free CME/CE Activities
- Free daily question in your email
- Save favorite articles to your dashboard
- Emails offering discounts
Learn more about a Subscription to StatPearls Point-of-Care
Etiology
Low HDL cholesterol levels can have a wide range of etiologies, including lifestyle factors, metabolic and endocrine disorders, genetic causes, medication-related effects, and diseases associated with chronic inflammation. One of the most common etiologies of low HDL cholesterol levels is lifestyle. Specifically, obesity, smoking, and physical inactivity contribute to low HDL levels.[4][5] Furthermore, research indicates that diets high in simple sugars and trans fats are inversely associated with HDL cholesterol levels. Considering diet, exercise, and other lifestyle factors is essential when a patient has low levels of HDL cholesterol.
Additionally, metabolic and endocrine disorders can lead to low levels of HDL cholesterol. Insulin resistance, as in type 2 diabetes mellitus, reduces HDL by promoting the overproduction of very-low-density lipoprotein in the liver.[6] Moreover, hypothyroidism and liver disease can lead to reduced HDL cholesterol levels due to altered apolipoprotein metabolism rates and decreased HDL cholesterol synthesis, respectively.[7][8] Thus, a thorough evaluation for metabolic syndrome and polyglandular autoimmune syndromes is paramount in determining the etiology of low HDL levels.
Genetic defects in cholesterol production can result in syndromes such as Fish Eye disease, familial hypoalphalipoproteinemia, familial HDL deficiency, and Tangier disease. A mutation in the apolipoprotein A-I gene causes familial hypoalphalipoproteinemia. Familial HDL deficiency shares genetic links with Tangier disease, an autosomal codominant condition characterized by the absence of HDL cholesterol in homozygous individuals.[9] The low HDL concentration leads to premature coronary artery disease and cholesteryl ester deposition in the reticuloendothelial system, causing organomegaly and xanthoma production.[10]
Lastly, a deficiency in lecithin cholesterol acyltransferase (LCAT) impairs HDL maturation, ultimately leading to low HDL cholesterol levels, as in Fish Eye disease.[11] Corneal opacities, nephropathy, and proteinuria characterize this disease. Typically, early-onset cardiovascular disease is not present with LCAT deficiency. Medications, specifically beta blockers and anabolic steroids, may also lead to a decrease in specific subtypes of HDL cholesterol.[12] Therefore, it is crucial for clinicians to properly review a patient's medication history when considering etiologies of low HDL cholesterol.
Epidemiology
Approximately 20% of the adult population has low HDL cholesterol, with a prevalence significantly higher in males (29% of men vs 9% of women).[CDC. Total and High-Density Lipoprotein Cholesterol in Adults: United States, 2015–2018. https://www.cdc.gov/nchs/products/databriefs/db363.htm] Additionally, low HDL cholesterol levels are more common in White and Asian adults.[CDC. Total and High-Density Lipoprotein Cholesterol in Adults: United States, 2015–2018. https://www.cdc.gov/nchs/products/databriefs/db363.htm] The case prevalence of hereditary low HDL cholesterol is not well established, but most genetic etiologies are rare.
Pathophysiology
The pathophysiology of low HDL cholesterol depends upon the etiology. For example, in patients with hypoalphalipoproteinemia, specific mutations result in distinct phenotypes. In children with identified mutations in apolipoprotein A-I (the principal component of HDL), levels are reduced by approximately 50% in the heterozygotes. Conversely, the homozygotes are deficient in plasma HDL, consistent with an autosomal dominant genetic pattern. Additionally, adenosine triphosphate-binding cassette transporter (ABC1) mutations are common in both familial HDL deficiency and Tangier disease.[12][13] These ABC1 mutations result in impaired cholesterol clearance by macrophages, predisposing patients to an increased risk of early atherosclerotic disease. These macrophages transform into foam cells, contributing to the development of early-onset coronary artery disease.
Familial combined hypolipidemia patients have mutations in ANGPTL3 (encoding the angiopoietin-like 3 protein). ANGPTL3 inhibits the action of lipoprotein lipase (LPL), leading to reduced cholesterol levels. Patients who are heterozygous or homozygous for these mutations have lower HDL cholesterol concentrations than noncarriers. Despite the low HDL level associated with these mutations, affected individuals have a lower cardiac risk because their low-density lipoproteins levels are also low. However, complete LPL deficiency, seen in homozygotes of lipoprotein lipase gene mutations, leads to severe hypertriglyceridemia and chylomicronemia.[14][15]
Additionally, low HDL cholesterol states can result from increased HDL catabolism or increased clearance. Specifically, elevated triglyceride-rich lipoproteins promote cholesteryl ester transfer protein (CETP) activity, which leads to a decrease in HDL through the transferrence of cholesteryl esters in exchange for triglycerides.[16] Conditions like insulin resistance accelerate the process of CETP transference.[16] Furthermore, inflammation and oxidative stress can enhance HDL catabolism through the hepatic scavenger receptor class B type 1, a receptor involved in the clearance of HDL.[17]
History and Physical
Most patients with low HDL do not exhibit symptoms or have physical findings. However, some of the syndromes mentioned above have clinical findings that offer clues to the diagnosis. For patients with insulin resistance, physical examination can reveal acanthosis nigricans, skin tags, and central obesity.[18] Diseases characterized by elevated low-density lipoproteins and triglycerides can manifest with xanthomas and xanthelasmas, which are yellow lipid deposits that accumulate in macrophages beneath the skin. Furthermore, Fish Eye disease is phenotypically characterized by severe corneal opacities. Patients with Tangier disease may exhibit hepatosplenomegaly, enlarged tonsils or lymph nodes, or arcus corneae (lipid deposits in the eye).[19]
Evaluation
Fasting lipid panels will reveal the levels of total cholesterol, low-density lipoproteins, HDL, and triglycerides. Additionally, nuclear magnetic resonance (NMR) can measure particle numbers. However, quantification via NMR is not standardized and is often difficult to interpret.[2][20] Additionally, certain diseases (eg, Fish Eye disease) are associated with proteinuria and nephropathy; assessing kidney function with a basic metabolic panel and urinalysis is reasonable if this disease is suspected. Furthermore, blood sugar quantification is reasonable if HDL abnormalities associated with metabolic syndrome are a consideration.
Treatment / Management
HDL levels are generally inversely proportional to cardiovascular disease risk. However, the clinical correlation between HDL cholesterol elevation and cardiac disease is incompletely understood. While results from several studies have shown that higher HDL levels are associated with a lower risk of cardiovascular disease, a 2009 meta-analysis failed to find this association after adjusting for changes in LDL cholesterol.[21] Furthermore, results from a 2022 cohort study demonstrated that very high HDL cholesterol levels are paradoxically associated with higher mortality in patients with coronary artery disease. Thus, the need to treat HDL levels is unclear and is not currently a standard of care in cholesterol management.[22]
Despite the lack of evidence for HDL-targeted medications, multiple pharmacological options are available that raise HDL levels and lower LDL and triglyceride levels. Among the medications that raise HDL cholesterol, niacin has the most significant effect, resulting in a 15% to 30% increase in serum HDL concentration.[23] Although niacin raises HDL in the absence of any other lipid abnormality, there is little evidence that the addition of niacin to statin therapy has any cardiovascular benefit.[23] In the AIM High trial, the addition of niacin to statins in patients with well-controlled LDL cholesterol showed no cardiovascular benefit despite a significant increase in HDL levels.(A1)
The infusion of apolipoprotein A-I (apoA-I) has been investigated for its potential cardiovascular benefits, as apoA-I levels are strongly associated with a reduced risk of cardiovascular disease in patients already on statin therapy.[24] A large study examined the effects of consecutive weekly infusions of apoA-I versus placebo after a recent myocardial infarction to determine the benefits of apoA-I infusion therapy.[25] Patients who received the apoA-I infusion had an increase in cholesterol efflux capacity. However, further research is needed to determine if this therapy will translate to a reduction in major adverse cardiovascular events.(A1)
Therefore, no specific treatment is recommended solely to increase HDL cholesterol levels as a means to reduce cardiovascular disease risk. In patients with increased cardiovascular risk and low HDL cholesterol, regular exercise, adequate fruit and vegetable intake, reaching target body weight, and smoking/substance use cessation improve HDL cholesterol and decrease cardiovascular disease risk.[26][27][28] Thus, clinicians should focus on counseling patients with low HDL on the importance of lifestyle modification.(A1)
Differential Diagnosis
The differential diagnosis of low HDL cholesterol can include lifestyle factors such as poor diet or lack of exercise. Additionally, diabetes mellitus type 2 and hypothyroidism can be associated with low HDL levels. Rare causes, such as genetic disorders, can manifest with physical examination findings, such as subcutaneous lipid deposits in Tangier disease or Fish Eye disease. Certain medications can also induce low HDL levels, eg, both antihypertensive medications and diuretics can cause a decrease in HDL cholesterol and an increase in triglycerides, which is proportional to the dose. Beta-blockers cause a decrease in HDL secondary to increased triglycerides, although cardioselective beta-blockers have a smaller effect; alpha-blockers decrease triglycerides and increase HDL levels.[29][30]
Prognosis
According to the Framingham Heart Study, the risk of myocardial infarction increases by approximately 25% for every 5 mg/dL decrease in HDL cholesterol serum level below median values.[31] Furthermore, a low HDL cholesterol level is an independent risk factor for myocardial infarction in patients with established cardiovascular disease. Moreover, the SMART (Secondary Manifestations of Arterial Disease) study demonstrated that elevated HDL cholesterol is protective against future cardiac events in patients on statin therapy. Thus, patients have a better cardiovascular prognosis when HDL cholesterol levels are higher.[32]
Complications
Complications of low HDL cholesterol include an increased risk of atherosclerotic cardiovascular disease, impaired glucose metabolism and insulin resistance, increased inflammation/oxidative stress, and higher risk of cognitive decline due to vascular and neuroinflammatory effects.[33][34][35]
Deterrence and Patient Education
A healthy diet and regular exercise can treat low HDL cholesterol levels. Educating patients about healthy dietary choices, such as the Mediterranean diet, which reduces cardiovascular and overall mortality is essential. Further counseling on weight loss and exercise is also necessary. Foods high in saturated fats tend to increase LDL and HDL cholesterol while decreasing the triglyceride-rich lipoproteins. Furthermore, monounsaturated fats reduce insulin resistance and may indirectly increase HDL cholesterol levels. Continued yearly visits with the patient's primary care clinician remain the most effective way to screen for and improve low HDL cholesterol levels.
Enhancing Healthcare Team Outcomes
Addressing low HDL cholesterol and other lipid abnormalities requires an interdisciplinary care team. Other members of the healthcare team can assist the clinician in counseling the patient on diet, exercise, and weight loss.[36] Referrals to weight loss programs, nutrition consultations, physical therapy for functionally limiting orthopedic concerns, pharmacy services, and social work can improve patient outcomes.
The average primary care clinician's median visit length is only 10 minutes, which often limits discussions on the root cause of low HDL levels.[37] Many members of the health care team can assist in counseling patients and supporting them over multiple visits to optimize lifestyle modifications. Moreover, licensed therapists can assist with behavioral modification strategies, including smoking and alcohol cessation, and improved eating habits. Dieticians are also beneficial for individual consultations and for teaching patient classes about healthier cooking habits.
References
Ding Y, Wang Y, Opoku-Damoah Y, Wang C, Shen L, Yin L, Zhou J. Dual-functional bio-derived nanoparticulates for apoptotic antitumor therapy. Biomaterials. 2015 Dec:72():90-103. doi: 10.1016/j.biomaterials.2015.08.051. Epub 2015 Aug 31 [PubMed PMID: 26344366]
Rosenson RS, Brewer HB Jr, Ansell B, Barter P, Chapman MJ, Heinecke JW, Kontush A, Tall AR, Webb NR. Translation of high-density lipoprotein function into clinical practice: current prospects and future challenges. Circulation. 2013 Sep 10:128(11):1256-67. doi: 10.1161/CIRCULATIONAHA.113.000962. Epub [PubMed PMID: 24019446]
Level 3 (low-level) evidenceFeingold KR, Ahmed SF, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, de Herder WW, Dhatariya K, Dungan K, Hofland J, Kalra S, Kaltsas G, Kapoor N, Koch C, Kopp P, Korbonits M, Kovacs CS, Kuohung W, Laferrère B, Levy M, McGee EA, McLachlan R, Muzumdar R, Purnell J, Rey R, Sahay R, Shah AS, Singer F, Sperling MA, Stratakis CA, Trence DL, Wilson DP, Feingold KR, Grunfeld C. Effect of Inflammation and Infection on Lipids and Lipoproteins. Endotext. 2000:(): [PubMed PMID: 26561701]
Gaggini M, Saponaro C, Gastaldelli A. Not all fats are created equal: adipose vs. ectopic fat, implication in cardiometabolic diseases. Hormone molecular biology and clinical investigation. 2015 Apr:22(1):7-18. doi: 10.1515/hmbci-2015-0006. Epub [PubMed PMID: 25816312]
Ma B, Chen Y, Wang X, Zhang R, Niu S, Ni L, Di X, Han Q, Liu C. Cigarette smoke exposure impairs lipid metabolism by decreasing low-density lipoprotein receptor expression in hepatocytes. Lipids in health and disease. 2020 May 8:19(1):88. doi: 10.1186/s12944-020-01276-w. Epub 2020 May 8 [PubMed PMID: 32384892]
Taskinen MR. Diabetic dyslipidaemia: from basic research to clinical practice. Diabetologia. 2003 Jun:46(6):733-49 [PubMed PMID: 12774165]
Duntas LH. Thyroid disease and lipids. Thyroid : official journal of the American Thyroid Association. 2002 Apr:12(4):287-93 [PubMed PMID: 12034052]
Lewis GF, Rader DJ. New insights into the regulation of HDL metabolism and reverse cholesterol transport. Circulation research. 2005 Jun 24:96(12):1221-32 [PubMed PMID: 15976321]
Moudian I, Bakkach J, Zian Z, Ghailani Nourouti N, Barakat A, Bennani Mechita M. Genetic Underpinnings of Mitochondrial Cardiomyopathy: A Scoping 2010-2024 Update. DNA and cell biology. 2025 Jul 2:():. doi: 10.1089/dna.2025.0089. Epub 2025 Jul 2 [PubMed PMID: 40600299]
Level 2 (mid-level) evidenceKoseki M, Yamashita S, Ogura M, Ishigaki Y, Ono K, Tsukamoto K, Hori M, Matsuki K, Yokoyama S, Harada-Shiba M. Current Diagnosis and Management of Tangier Disease. Journal of atherosclerosis and thrombosis. 2021 Aug 1:28(8):802-810. doi: 10.5551/jat.RV17053. Epub 2021 May 14 [PubMed PMID: 33994407]
Pavanello C, Calabresi L. Genetic, biochemical, and clinical features of LCAT deficiency: update for 2020. Current opinion in lipidology. 2020 Aug:31(4):232-237. doi: 10.1097/MOL.0000000000000697. Epub [PubMed PMID: 32618730]
Level 3 (low-level) evidenceBrooks-Wilson A, Marcil M, Clee SM, Zhang LH, Roomp K, van Dam M, Yu L, Brewer C, Collins JA, Molhuizen HO, Loubser O, Ouelette BF, Fichter K, Ashbourne-Excoffon KJ, Sensen CW, Scherer S, Mott S, Denis M, Martindale D, Frohlich J, Morgan K, Koop B, Pimstone S, Kastelein JJ, Genest J Jr, Hayden MR. Mutations in ABC1 in Tangier disease and familial high-density lipoprotein deficiency. Nature genetics. 1999 Aug:22(4):336-45 [PubMed PMID: 10431236]
Rust S, Rosier M, Funke H, Real J, Amoura Z, Piette JC, Deleuze JF, Brewer HB, Duverger N, Denèfle P, Assmann G. Tangier disease is caused by mutations in the gene encoding ATP-binding cassette transporter 1. Nature genetics. 1999 Aug:22(4):352-5 [PubMed PMID: 10431238]
Musunuru K, Pirruccello JP, Do R, Peloso GM, Guiducci C, Sougnez C, Garimella KV, Fisher S, Abreu J, Barry AJ, Fennell T, Banks E, Ambrogio L, Cibulskis K, Kernytsky A, Gonzalez E, Rudzicz N, Engert JC, DePristo MA, Daly MJ, Cohen JC, Hobbs HH, Altshuler D, Schonfeld G, Gabriel SB, Yue P, Kathiresan S. Exome sequencing, ANGPTL3 mutations, and familial combined hypolipidemia. The New England journal of medicine. 2010 Dec 2:363(23):2220-7. doi: 10.1056/NEJMoa1002926. Epub 2010 Oct 13 [PubMed PMID: 20942659]
Genest JJ Jr, Martin-Munley SS, McNamara JR, Ordovas JM, Jenner J, Myers RH, Silberman SR, Wilson PW, Salem DN, Schaefer EJ. Familial lipoprotein disorders in patients with premature coronary artery disease. Circulation. 1992 Jun:85(6):2025-33 [PubMed PMID: 1534286]
Tall AR. Plasma cholesteryl ester transfer protein. Journal of lipid research. 1993 Aug:34(8):1255-74 [PubMed PMID: 8409761]
Acton S, Rigotti A, Landschulz KT, Xu S, Hobbs HH, Krieger M. Identification of scavenger receptor SR-BI as a high density lipoprotein receptor. Science (New York, N.Y.). 1996 Jan 26:271(5248):518-20 [PubMed PMID: 8560269]
Rafique S, Dihowm H, Parveen S, Jakoby M. Insulin-Induced Acanthosis Nigricans. Cureus. 2025 May:17(5):e83424. doi: 10.7759/cureus.83424. Epub 2025 May 3 [PubMed PMID: 40458329]
Winder AF, Alexander R, Garner A, Johnston D, Vallance D, McCreanor G, Frohlich J. The pathology of cornea in Tangier disease (familial high density lipoprotein deficiency). Journal of clinical pathology. 1996 May:49(5):407-10 [PubMed PMID: 8707957]
Vaisar T, Heinecke J. Quantification of high-density lipoprotein particle number by proton nuclear magnetic resonance: don't believe the numbers. Current opinion in lipidology. 2024 Oct 1:35(5):228-233. doi: 10.1097/MOL.0000000000000948. Epub 2024 Aug 19 [PubMed PMID: 39162237]
Level 3 (low-level) evidenceGhali WA, Rodondi N. HDL cholesterol and cardiovascular risk. BMJ (Clinical research ed.). 2009 Feb 16:338():a3065. doi: 10.1136/bmj.a3065. Epub 2009 Feb 16 [PubMed PMID: 19221138]
Liu C, Dhindsa D, Almuwaqqat Z, Ko YA, Mehta A, Alkhoder AA, Alras Z, Desai SR, Patel KJ, Hooda A, Wehbe M, Sperling LS, Sun YV, Quyyumi AA. Association Between High-Density Lipoprotein Cholesterol Levels and Adverse Cardiovascular Outcomes in High-risk Populations. JAMA cardiology. 2022 Jul 1:7(7):672-680. doi: 10.1001/jamacardio.2022.0912. Epub [PubMed PMID: 35583863]
AIM-HIGH Investigators, Boden WE, Probstfield JL, Anderson T, Chaitman BR, Desvignes-Nickens P, Koprowicz K, McBride R, Teo K, Weintraub W. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. The New England journal of medicine. 2011 Dec 15:365(24):2255-67. doi: 10.1056/NEJMoa1107579. Epub 2011 Nov 15 [PubMed PMID: 22085343]
Level 1 (high-level) evidenceBoekholdt SM, Arsenault BJ, Hovingh GK, Mora S, Pedersen TR, Larosa JC, Welch KM, Amarenco P, Demicco DA, Tonkin AM, Sullivan DR, Kirby A, Colhoun HM, Hitman GA, Betteridge DJ, Durrington PN, Clearfield MB, Downs JR, Gotto AM Jr, Ridker PM, Kastelein JJ. Levels and changes of HDL cholesterol and apolipoprotein A-I in relation to risk of cardiovascular events among statin-treated patients: a meta-analysis. Circulation. 2013 Oct 1:128(14):1504-12. doi: 10.1161/CIRCULATIONAHA.113.002670. Epub 2013 Aug 21 [PubMed PMID: 23965489]
Level 1 (high-level) evidenceMichael Gibson C, Korjian S, Tricoci P, Daaboul Y, Yee M, Jain P, Alexander JH, Steg PG, Lincoff AM, Kastelein JJ, Mehran R, D'Andrea DM, Deckelbaum LI, Merkely B, Zarebinski M, Ophuis TO, Harrington RA. Safety and Tolerability of CSL112, a Reconstituted, Infusible, Plasma-Derived Apolipoprotein A-I, After Acute Myocardial Infarction: The AEGIS-I Trial (ApoA-I Event Reducing in Ischemic Syndromes I). Circulation. 2016 Dec 13:134(24):1918-1930 [PubMed PMID: 27881559]
Moffatt RJ. Effects of cessation of smoking on serum lipids and high density lipoprotein-cholesterol. Atherosclerosis. 1988 Nov:74(1-2):85-9 [PubMed PMID: 3214483]
Wood PD, Stefanick ML, Dreon DM, Frey-Hewitt B, Garay SC, Williams PT, Superko HR, Fortmann SP, Albers JJ, Vranizan KM. Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. The New England journal of medicine. 1988 Nov 3:319(18):1173-9 [PubMed PMID: 3173455]
Level 1 (high-level) evidenceWood PD, Stefanick ML, Williams PT, Haskell WL. The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. The New England journal of medicine. 1991 Aug 15:325(7):461-6 [PubMed PMID: 1852180]
Level 1 (high-level) evidenceKasiske BL, Ma JZ, Kalil RS, Louis TA. Effects of antihypertensive therapy on serum lipids. Annals of internal medicine. 1995 Jan 15:122(2):133-41 [PubMed PMID: 7992988]
Level 1 (high-level) evidenceWolinsky H. The effects of beta-adrenergic blocking agents on blood lipid levels. Clinical cardiology. 1987 Oct:10(10):561-6 [PubMed PMID: 2889552]
Castelli WP. Cardiovascular disease and multifactorial risk: challenge of the 1980s. American heart journal. 1983 Nov:106(5 Pt 2):1191-200 [PubMed PMID: 6637784]
van de Woestijne AP, van der Graaf Y, Liem AH, Cramer MJ, Westerink J, Visseren FL, SMART Study Group. Low high-density lipoprotein cholesterol is not a risk factor for recurrent vascular events in patients with vascular disease on intensive lipid-lowering medication. Journal of the American College of Cardiology. 2013 Nov 12:62(20):1834-41. doi: 10.1016/j.jacc.2013.04.101. Epub 2013 Aug 21 [PubMed PMID: 23948286]
Drew BG, Duffy SJ, Formosa MF, Natoli AK, Henstridge DC, Penfold SA, Thomas WG, Mukhamedova N, de Courten B, Forbes JM, Yap FY, Kaye DM, van Hall G, Febbraio MA, Kemp BE, Sviridov D, Steinberg GR, Kingwell BA. High-density lipoprotein modulates glucose metabolism in patients with type 2 diabetes mellitus. Circulation. 2009 Apr 21:119(15):2103-11. doi: 10.1161/CIRCULATIONAHA.108.843219. Epub 2009 Apr 6 [PubMed PMID: 19349317]
Kao YC, Ho PC, Tu YK, Jou IM, Tsai KJ. Lipids and Alzheimer's Disease. International journal of molecular sciences. 2020 Feb 22:21(4):. doi: 10.3390/ijms21041505. Epub 2020 Feb 22 [PubMed PMID: 32098382]
Tabet F, Rye KA. High-density lipoproteins, inflammation and oxidative stress. Clinical science (London, England : 1979). 2009 Jan:116(2):87-98. doi: 10.1042/CS20080106. Epub [PubMed PMID: 19076062]
Valero-Elizondo J, Aneni EC, Osondu CU, Grandhi GR, Virani SS, Nasir K. Gaps in provider lifestyle counseling and its adherence among obese adults with prediabetes and diabetes in the United States. Preventive medicine. 2019 Dec:129():105815. doi: 10.1016/j.ypmed.2019.105815. Epub 2019 Aug 24 [PubMed PMID: 31454663]
Tai-Seale M, McGuire TG, Zhang W. Time allocation in primary care office visits. Health services research. 2007 Oct:42(5):1871-94 [PubMed PMID: 17850524]