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{{High density lipoprotein}}
{{High density lipoprotein}}
{{CMG}}; {{AE}} {{AN}}; {{RT}}
{{CMG}}; {{AE}} {{AN}}; {{RT}}
==Overview==
High density lipoprotein (HDL) is considered "good cholesterol" as its levels are inversely proportional to CAD.  It is regarded as a positive cardiac [[risk factor]] if the levels are below 35 mg/dL or total cholesterol to HDL ratio in > 5.0 (in men) or total cholesterol to HDL ratio in > 4.5 (in women).  When the levels are above 60 mg/dL it is considered a negative cardiac risk factor.


==Causes==
==Causes==
* HDL cholesterol is a positive [[cardiac risk factor]] if
===Causes of Low HDL===
*:* HDL < 35 mg/dL
*:* Total cholesterol to HDL ratio in > 5.0 (in men)
*:* Total cholesterol to HDL ratio in > 4.5 (in women)
* Negative cardiac risk factor if HDL > 60 mg/dL
 
===Causes of Decreased HDL===
* Apolipoprotein deficiency: [[Hypoalphalipoproteinemia]] can be of three types.  
* Apolipoprotein deficiency: [[Hypoalphalipoproteinemia]] can be of three types.  
# Impaired synthesis of apo A-I: [[apo A-I deficiency]], apo A-I/C-III deficiency, apo A-I structural variants
# Impaired synthesis of apo A-I: [[Apo A-I deficiency]], Apo A-I/C-III deficiency, Apo A-I structural variants
# Increased catabolism: [[familial HDL deficiency]] or [[Tangier disease]]
# Increased catabolism: [[Familial HDL deficiency]] or [[Tangier disease]]
# Enzymatic changes: genetic, reduced activity of [[lipoprotein lipase]], elevated liver triglyceride lipase activity, [[Lecithin cholesterol acyltransferase deficiency|LCAT (lecithin cholesterol acyltransferase) deficiency]]
# Enzymatic changes: genetic, reduced activity of [[lipoprotein lipase]], elevated liver triglyceride lipase activity, [[Lecithin cholesterol acyltransferase deficiency|LCAT (lecithin cholesterol acyltransferase) deficiency]]
* [[Insulin resistance]]<ref name="pmid23565456">{{cite journal |author=Sanyal D, Ghosh S, Mukherjee P, Mukherjee S, Chowdhury S |title=Dyslipidemia, metabolic syndrome, and liver enzymes in impaired glucose tolerance and new onset untreated, type 2 diabetes Indian subjects |journal=Indian J Endocrinol Metab |volume=16 |issue=Suppl 2 |pages=S434–5 |year=2012 |month=December |pmid=23565456 |pmc=3603104 |doi=10.4103/2230-8210.104121 |url=}}</ref>
* [[Insulin resistance]]<ref name="pmid23546765">{{cite journal |author=Filippatos TD, Rizos EC, Tsimihodimos V, Gazi IF, Tselepis AD, Elisaf MS |title=Small High-Density Lipoprotein (HDL) Subclasses are Increased with Decreased Activity of HDL-Associated Phospholipase A2 in Subjects with Prediabetes |journal=[[Lipids]] |volume= |issue= |pages= |year=2013 |month=April |pmid=23546765 |doi=10.1007/s11745-013-3787-1 |url=}}</ref><ref name="pmid23565456">{{cite journal |author=Sanyal D, Ghosh S, Mukherjee P, Mukherjee S, Chowdhury S |title=Dyslipidemia, metabolic syndrome, and liver enzymes in impaired glucose tolerance and new onset untreated, type 2 diabetes Indian subjects |journal=Indian J Endocrinol Metab |volume=16 |issue=Suppl 2 |pages=S434–5 |year=2012 |month=December |pmid=23565456 |pmc=3603104 |doi=10.4103/2230-8210.104121 |url=}}</ref>
* [[Diabetes mellitus]]<ref name="pmid23565456">{{cite journal |author=Sanyal D, Ghosh S, Mukherjee P, Mukherjee S, Chowdhury S |title=Dyslipidemia, metabolic syndrome, and liver enzymes in impaired glucose tolerance and new onset untreated, type 2 diabetes Indian subjects |journal=Indian J Endocrinol Metab |volume=16 |issue=Suppl 2 |pages=S434–5 |year=2012 |month=December |pmid=23565456 |pmc=3603104 |doi=10.4103/2230-8210.104121 |url=}}</ref>
* [[Diabetes mellitus]]<ref name="pmid23565456">{{cite journal |author=Sanyal D, Ghosh S, Mukherjee P, Mukherjee S, Chowdhury S |title=Dyslipidemia, metabolic syndrome, and liver enzymes in impaired glucose tolerance and new onset untreated, type 2 diabetes Indian subjects |journal=Indian J Endocrinol Metab |volume=16 |issue=Suppl 2 |pages=S434–5 |year=2012 |month=December |pmid=23565456 |pmc=3603104 |doi=10.4103/2230-8210.104121 |url=}}</ref>
* [[Metabolic syndrome]]<ref name="pmid23564803">{{cite journal |author=Elme A, Utriainen M, Kellokumpu-Lehtinen P, ''et al.'' |title=Obesity and physical inactivity are related to impaired physical health of breast cancer survivors |journal=Anticancer Res. |volume=33 |issue=4 |pages=1595–602 |year=2013 |month=April |pmid=23564803 |doi= |url=}}</ref>
* [[Metabolic syndrome]]<ref name="pmid23404653">{{cite journal |author=Dullaart RP, de Boer JF, Annema W, Tietge UJ |title=The inverse relation of HDL anti-oxidative functionality with serum amyloid a is lost in metabolic syndrome subjects |journal=[[Obesity (Silver Spring, Md.)]] |volume=21 |issue=2 |pages=361–6 |year=2013 |month=February |pmid=23404653 |doi=10.1002/oby.20058 |url=}}</ref><ref name="pmid23564803">{{cite journal |author=Elme A, Utriainen M, Kellokumpu-Lehtinen P, ''et al.'' |title=Obesity and physical inactivity are related to impaired physical health of breast cancer survivors |journal=Anticancer Res. |volume=33 |issue=4 |pages=1595–602 |year=2013 |month=April |pmid=23564803 |doi= |url=}}</ref>
* Drugs
* Drugs
# [[Beta-blocker]]s<ref name="pmid1353932">{{cite journal |author=Klein W |title=[Antihypertensive therapy and modification of metabolic risk factors (glucose and lipid metabolism)] |language=German |journal=Z Kardiol |volume=81 |issue=6 |pages=295–302 |year=1992 |month=June |pmid=1353932 |doi= |url=}}</ref>
# [[Beta-blocker]]s<ref name="pmid1353932">{{cite journal |author=Klein W |title=[Antihypertensive therapy and modification of metabolic risk factors (glucose and lipid metabolism)] |language=German |journal=Z Kardiol |volume=81 |issue=6 |pages=295–302 |year=1992 |month=June |pmid=1353932 |doi= |url=}}</ref>
Line 26: Line 23:
# [[Mifepristone]]<ref name="pmid22399518">{{cite journal |author=Page ST, Krauss RM, Gross C, ''et al.'' |title=Impact of mifepristone, a glucocorticoid/progesterone antagonist, on HDL cholesterol, HDL particle concentration, and HDL function |journal=J. Clin. Endocrinol. Metab. |volume=97 |issue=5 |pages=1598–605 |year=2012 |month=May |pmid=22399518 |doi=10.1210/jc.2011-2813 |url=}}</ref>
# [[Mifepristone]]<ref name="pmid22399518">{{cite journal |author=Page ST, Krauss RM, Gross C, ''et al.'' |title=Impact of mifepristone, a glucocorticoid/progesterone antagonist, on HDL cholesterol, HDL particle concentration, and HDL function |journal=J. Clin. Endocrinol. Metab. |volume=97 |issue=5 |pages=1598–605 |year=2012 |month=May |pmid=22399518 |doi=10.1210/jc.2011-2813 |url=}}</ref>
* Liver disease
* Liver disease
* [[Menopause]]<ref name="pmid23497470">{{cite journal |author=Jouyandeh Z, Nayebzadeh F, Qorbani M, Asadi M |title=Metabolic syndrome and menopause |journal=J Diabetes Metab Disord |volume=12 |issue=1 |pages=1 |year=2013 |pmid=23497470 |pmc=3598172 |doi=10.1186/2251-6581-12-1 |url=}}</ref><ref name="pmid23531683">{{cite journal |author=Worsley R, Robinson PJ, Bell RJ, Moufarege A, Davis SR |title=Endogenous estrogen and androgen levels are not independent predictors of lipid levels in postmenopausal women |journal=Menopause |volume= |issue= |pages= |year=2013 |month=March |pmid=23531683 |doi=10.1097/GME.0b013e318279bd4a |url=}}</ref>
* [[Menopause]]<ref name="pmid23531683">{{cite journal |author=Worsley R, Robinson PJ, Bell RJ, Moufarege A, Davis SR |title=Endogenous estrogen and androgen levels are not independent predictors of lipid levels in postmenopausal women |journal=Menopause |volume= |issue= |pages= |year=2013 |month=March |pmid=23531683 |doi=10.1097/GME.0b013e318279bd4a |url=}}</ref>
* [[Obesity]]:High BMI is strongly associated with low serum HDl levels<ref name="pmid23564803">{{cite journal |author=Elme A, Utriainen M, Kellokumpu-Lehtinen P, ''et al.'' |title=Obesity and physical inactivity are related to impaired physical health of breast cancer survivors |journal=Anticancer Res. |volume=33 |issue=4 |pages=1595–602 |year=2013 |month=April |pmid=23564803 |doi= |url=}}</ref>
* [[Obesity]]:High BMI is strongly associated with low serum HDl levels<ref name="pmid23564803">{{cite journal |author=Elme A, Utriainen M, Kellokumpu-Lehtinen P, ''et al.'' |title=Obesity and physical inactivity are related to impaired physical health of breast cancer survivors |journal=Anticancer Res. |volume=33 |issue=4 |pages=1595–602 |year=2013 |month=April |pmid=23564803 |doi= |url=}}</ref>
* Puberty in males
* Puberty in males
* [[Uremia]]<ref name="pmid23443874">{{cite journal |author=Khoueiry G, Abdallah M, Saiful F, ''et al.'' |title=High-density lipoprotein in uremic patients: metabolism, impairment, and therapy |journal=Int Urol Nephrol |volume= |issue= |pages= |year=2013 |month=February |pmid=23443874 |doi=10.1007/s11255-012-0366-y |url=}}</ref>
* [[Uremia]]<ref name="pmid23311247">{{cite journal |author=Cabarkapa V, Djerić M, Stosić Z, Sakac V, Zagorka LC, Vucković B |title=Evaluation of lipid parameters and bioindices in patients with different stages of chronic renal failure |journal=[[Vojnosanitetski Pregled. Military-medical and Pharmaceutical Review]] |volume=69 |issue=11 |pages=961–6 |year=2012 |month=November |pmid=23311247 |doi= |url=}}</ref> <ref name="pmid23443874">{{cite journal |author=Khoueiry G, Abdallah M, Saiful F, ''et al.'' |title=High-density lipoprotein in uremic patients: metabolism, impairment, and therapy |journal=Int Urol Nephrol |volume= |issue= |pages= |year=2013 |month=February |pmid=23443874 |doi=10.1007/s11255-012-0366-y |url=}}</ref>
* Familial combined hypolipidemia<ref name="pmid22659251">{{cite journal |author=Minicocci I, Montali A, Robciuc MR, ''et al.'' |title=Mutations in the ANGPTL3 gene and familial combined hypolipidemia: a clinical and biochemical characterization |journal=J. Clin. Endocrinol. Metab. |volume=97 |issue=7 |pages=E1266–75 |year=2012 |month=July |pmid=22659251 |doi=10.1210/jc.2012-1298 |url=}}</ref>
* Familial combined hypolipidemia<ref name="pmid22659251">{{cite journal |author=Minicocci I, Montali A, Robciuc MR, ''et al.'' |title=Mutations in the ANGPTL3 gene and familial combined hypolipidemia: a clinical and biochemical characterization |journal=J. Clin. Endocrinol. Metab. |volume=97 |issue=7 |pages=E1266–75 |year=2012 |month=July |pmid=22659251 |doi=10.1210/jc.2012-1298 |url=}}</ref>
* Elevated [[CETP]] ([[cholesteryl ester transfer protein]]) activity: Polymorphism of the gene TaqIB (CETP gene) is known to be associated with variations in the plasma concentrations of CETP. A gene variant called TaqIB1 is associated with a higher CETP concentration and lower HDL-C levels in the plasma. Two other mutations that result in similar findings are A373P and R451Q.<ref name="pmid22928361">{{cite journal |author=Pachocka LM, Włodarczyk M, Nowicka G, Kłosiewicz-Latoszek L, Wolańska D, Stolarska I |title=[CETP gene TaqIB polymorphism and plasma lipids in patients with overweight and obesity] |language=Polish |journal=Rocz Panstw Zakl Hig |volume=63 |issue=2 |pages=149–54 |year=2012 |pmid=22928361 |doi= |url=}}</ref><ref name="pmid23157875">{{cite journal |author=Rahimi Z, Nourozi-Rad R, Rahimi Z, Parsian A |title=Strong interaction between T allele of endothelial nitric oxide synthase with B1 allele of cholesteryl ester transfer protein TaqIB highly elevates the risk of coronary artery disease and type 2 diabetes mellitus |journal=Hum. Genomics |volume=6 |issue= |pages=20 |year=2012 |pmid=23157875 |pmc=3500247 |doi=10.1186/1479-7364-6-20 |url=}}</ref><ref name="pmid23129316">{{cite journal |author=Li YY, Wu XY, Xu J, Qian Y, Zhou CW, Wang B |title=Apo A5 -1131T/C, FgB -455G/A, -148C/T, and CETP TaqIB gene polymorphisms and coronary artery disease in the Chinese population: a meta-analysis of 15,055 subjects |journal=Mol. Biol. Rep. |volume=40 |issue=2 |pages=1997–2014 |year=2013 |month=February |pmid=23129316 |doi=10.1007/s11033-012-2257-9 |url=}}</ref><ref name="pmid22854712">{{cite journal |author=Rejeb J, Omezzine A, Boumaiza I, ''et al.'' |title=Four polymorphisms of cholesteryl ester transfer protein gene and coronary stenosis in a Tunisian population |journal=J Cardiovasc Med (Hagerstown) |volume=13 |issue=9 |pages=546–53 |year=2012 |month=September |pmid=22854712 |doi=10.2459/JCM.0b013e3283569b24 |url=}}</ref>
* Elevated [[CETP]] ([[cholesteryl ester transfer protein]]) activity: Polymorphism of the gene TaqIB (CETP gene) is known to be associated with variations in the plasma concentrations of CETP. A gene variant called TaqIB1 is associated with a higher CETP concentration and lower HDL-C levels in the plasma. Two other mutations that result in similar findings are A373P and R451Q.<ref name="pmid22928361">{{cite journal |author=Pachocka LM, Włodarczyk M, Nowicka G, Kłosiewicz-Latoszek L, Wolańska D, Stolarska I |title=[CETP gene TaqIB polymorphism and plasma lipids in patients with overweight and obesity] |language=Polish |journal=Rocz Panstw Zakl Hig |volume=63 |issue=2 |pages=149–54 |year=2012 |pmid=22928361 |doi= |url=}}</ref><ref name="pmid23157875">{{cite journal |author=Rahimi Z, Nourozi-Rad R, Rahimi Z, Parsian A |title=Strong interaction between T allele of endothelial nitric oxide synthase with B1 allele of cholesteryl ester transfer protein TaqIB highly elevates the risk of coronary artery disease and type 2 diabetes mellitus |journal=Hum. Genomics |volume=6 |issue= |pages=20 |year=2012 |pmid=23157875 |pmc=3500247 |doi=10.1186/1479-7364-6-20 |url=}}</ref><ref name="pmid23129316">{{cite journal |author=Li YY, Wu XY, Xu J, Qian Y, Zhou CW, Wang B |title=Apo A5 -1131T/C, FgB -455G/A, -148C/T, and CETP TaqIB gene polymorphisms and coronary artery disease in the Chinese population: a meta-analysis of 15,055 subjects |journal=Mol. Biol. Rep. |volume=40 |issue=2 |pages=1997–2014 |year=2013 |month=February |pmid=23129316 |doi=10.1007/s11033-012-2257-9 |url=}}</ref><ref name="pmid22854712">{{cite journal |author=Rejeb J, Omezzine A, Boumaiza I, ''et al.'' |title=Four polymorphisms of cholesteryl ester transfer protein gene and coronary stenosis in a Tunisian population |journal=J Cardiovasc Med (Hagerstown) |volume=13 |issue=9 |pages=546–53 |year=2012 |month=September |pmid=22854712 |doi=10.2459/JCM.0b013e3283569b24 |url=}}</ref>
Line 36: Line 33:
* High carbohydrate diet
* High carbohydrate diet


===Causes of Increased HDL===
===Causes of High HDL===
* Drugs
* Drugs
# [[Desogestrel and Ethinyl Estradiol]]
# [[Niacin]]
# [[Niacin]]
# [[Fibrate]]s
# [[Fibrate]]s
# [[Statin]]s
# [[Statin]]s
* [[Chronic alcoholism]]: Alcohol consumption raises HDL cholesterol levels by possibly increasing the transport rate of [[apolipoprotein]]s A-I and A-II.  [[Alcohol]] consumption of 30-40 g/day (1-3 drinks/day) or more has been shown to increase HDL-C levels. <ref name="pmid2862791">{{cite journal |author=Dai WS, LaPorte RE, Hom DL, ''et al.'' |title=Alcohol consumption and high density lipoprotein cholesterol concentration among alcoholics |journal=Am. J. Epidemiol. |volume=122 |issue=4 |pages=620–7 |year=1985 |month=October |pmid=2862791 |doi= |url=}}</ref>
* [[Chronic alcoholism]]: Alcohol consumption raises HDL cholesterol levels by possibly increasing the transport rate of [[apolipoprotein]]s A-I and A-II.  [[Alcohol]] consumption of 30-40 g/day (1-3 drinks/day) or more has been shown to increase HDL-C levels.<ref name="pmid18702334">{{cite journal |author=Krawiec A, Cylwik B, Chrostek L, Supronowicz Z, Szmitkowski M |title=[The effect of chronic alcohol abuse on the lipids, lipoproteins and apolipoproteins concentrations in the sera] |language=Polish |journal=[[Polski Merkuriusz Lekarski : Organ Polskiego Towarzystwa Lekarskiego]] |volume=24 |issue=144 |pages=521–5 |year=2008 |month=June |pmid=18702334 |doi= |url=}}</ref><ref name="pmid2862791">{{cite journal |author=Dai WS, LaPorte RE, Hom DL, ''et al.'' |title=Alcohol consumption and high density lipoprotein cholesterol concentration among alcoholics |journal=Am. J. Epidemiol. |volume=122 |issue=4 |pages=620–7 |year=1985 |month=October |pmid=2862791 |doi= |url=}}</ref>
* Extensive aerobic exercise
* Extensive aerobic exercise
* [[Alcoholic liver disease]]
* [[Alcoholic liver disease]]
Line 48: Line 46:
* Oral [[estrogen]] replacement therapy
* Oral [[estrogen]] replacement therapy
* [[CETP]] deficiency (single [[gene]] defects in 16q21)<ref name="pmid23189141">{{cite journal |author=Chantepie S, Bochem AE, Chapman MJ, Hovingh GK, Kontush A |title=High-density lipoprotein (HDL) particle subpopulations in heterozygous cholesteryl ester transfer protein (CETP) deficiency: maintenance of antioxidative activity |journal=PLoS ONE |volume=7 |issue=11 |pages=e49336 |year=2012 |pmid=23189141 |pmc=3506611 |doi=10.1371/journal.pone.0049336 |url=}}</ref><ref name="pmid22339301">{{cite journal |author=Niesor EJ, von der Mark E, Calabresi L, ''et al.'' |title=Lipid and apoprotein composition of HDL in partial or complete CETP deficiency |journal=Curr Vasc Pharmacol |volume=10 |issue=4 |pages=422–31 |year=2012 |month=July |pmid=22339301 |doi= |url=}}</ref>
* [[CETP]] deficiency (single [[gene]] defects in 16q21)<ref name="pmid23189141">{{cite journal |author=Chantepie S, Bochem AE, Chapman MJ, Hovingh GK, Kontush A |title=High-density lipoprotein (HDL) particle subpopulations in heterozygous cholesteryl ester transfer protein (CETP) deficiency: maintenance of antioxidative activity |journal=PLoS ONE |volume=7 |issue=11 |pages=e49336 |year=2012 |pmid=23189141 |pmc=3506611 |doi=10.1371/journal.pone.0049336 |url=}}</ref><ref name="pmid22339301">{{cite journal |author=Niesor EJ, von der Mark E, Calabresi L, ''et al.'' |title=Lipid and apoprotein composition of HDL in partial or complete CETP deficiency |journal=Curr Vasc Pharmacol |volume=10 |issue=4 |pages=422–31 |year=2012 |month=July |pmid=22339301 |doi= |url=}}</ref>
* early stage [[primary biliary cirrhosis]] <ref name="pmid1568727">{{cite journal |author=Crippin JS, Lindor KD, Jorgensen R, ''et al.'' |title=Hypercholesterolemia and atherosclerosis in primary biliary cirrhosis: what is the risk? |journal=Hepatology |volume=15 |issue=5 |pages=858–62 |year=1992 |month=May |pmid=1568727 |doi= |url=}}</ref><ref name="pmid4054519">{{cite journal |author=Jahn CE, Schaefer EJ, Taam LA, ''et al.'' |title=Lipoprotein abnormalities in primary biliary cirrhosis. Association with hepatic lipase inhibition as well as altered cholesterol esterification |journal=Gastroenterology |volume=89 |issue=6 |pages=1266–78 |year=1985 |month=December |pmid=4054519 |doi= |url=}}</ref>
* Early stage [[primary biliary cirrhosis]] <ref name="pmid1568727">{{cite journal |author=Crippin JS, Lindor KD, Jorgensen R, ''et al.'' |title=Hypercholesterolemia and atherosclerosis in primary biliary cirrhosis: what is the risk? |journal=Hepatology |volume=15 |issue=5 |pages=858–62 |year=1992 |month=May |pmid=1568727 |doi= |url=}}</ref><ref name="pmid4054519">{{cite journal |author=Jahn CE, Schaefer EJ, Taam LA, ''et al.'' |title=Lipoprotein abnormalities in primary biliary cirrhosis. Association with hepatic lipase inhibition as well as altered cholesterol esterification |journal=Gastroenterology |volume=89 |issue=6 |pages=1266–78 |year=1985 |month=December |pmid=4054519 |doi= |url=}}</ref>


==References==
==References==

Latest revision as of 15:14, 28 January 2015

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]; Raviteja Guddeti, M.B.B.S. [3]

Overview

High density lipoprotein (HDL) is considered "good cholesterol" as its levels are inversely proportional to CAD. It is regarded as a positive cardiac risk factor if the levels are below 35 mg/dL or total cholesterol to HDL ratio in > 5.0 (in men) or total cholesterol to HDL ratio in > 4.5 (in women). When the levels are above 60 mg/dL it is considered a negative cardiac risk factor.

Causes

Causes of Low HDL

  1. Impaired synthesis of apo A-I: Apo A-I deficiency, Apo A-I/C-III deficiency, Apo A-I structural variants
  2. Increased catabolism: Familial HDL deficiency or Tangier disease
  3. Enzymatic changes: genetic, reduced activity of lipoprotein lipase, elevated liver triglyceride lipase activity, LCAT (lecithin cholesterol acyltransferase) deficiency
  1. Beta-blockers[5]
  2. Benzodiazepines
  3. Anabolic steroids
  4. Diuretics
  5. Progestins
  6. Mifepristone[6]
  • Liver disease
  • Menopause[7]
  • Obesity:High BMI is strongly associated with low serum HDl levels[4]
  • Puberty in males
  • Uremia[8] [9]
  • Familial combined hypolipidemia[10]
  • Elevated CETP (cholesteryl ester transfer protein) activity: Polymorphism of the gene TaqIB (CETP gene) is known to be associated with variations in the plasma concentrations of CETP. A gene variant called TaqIB1 is associated with a higher CETP concentration and lower HDL-C levels in the plasma. Two other mutations that result in similar findings are A373P and R451Q.[11][12][13][14]
  • Smoking
  • Lack of physical exercise[4]
  • High carbohydrate diet

Causes of High HDL

  • Drugs
  1. Desogestrel and Ethinyl Estradiol
  2. Niacin
  3. Fibrates
  4. Statins

References

  1. Filippatos TD, Rizos EC, Tsimihodimos V, Gazi IF, Tselepis AD, Elisaf MS (2013). "Small High-Density Lipoprotein (HDL) Subclasses are Increased with Decreased Activity of HDL-Associated Phospholipase A2 in Subjects with Prediabetes". Lipids. doi:10.1007/s11745-013-3787-1. PMID 23546765. Unknown parameter |month= ignored (help)
  2. 2.0 2.1 Sanyal D, Ghosh S, Mukherjee P, Mukherjee S, Chowdhury S (2012). "Dyslipidemia, metabolic syndrome, and liver enzymes in impaired glucose tolerance and new onset untreated, type 2 diabetes Indian subjects". Indian J Endocrinol Metab. 16 (Suppl 2): S434–5. doi:10.4103/2230-8210.104121. PMC 3603104. PMID 23565456. Unknown parameter |month= ignored (help)
  3. Dullaart RP, de Boer JF, Annema W, Tietge UJ (2013). "The inverse relation of HDL anti-oxidative functionality with serum amyloid a is lost in metabolic syndrome subjects". Obesity (Silver Spring, Md.). 21 (2): 361–6. doi:10.1002/oby.20058. PMID 23404653. Unknown parameter |month= ignored (help)
  4. 4.0 4.1 4.2 Elme A, Utriainen M, Kellokumpu-Lehtinen P; et al. (2013). "Obesity and physical inactivity are related to impaired physical health of breast cancer survivors". Anticancer Res. 33 (4): 1595–602. PMID 23564803. Unknown parameter |month= ignored (help)
  5. Klein W (1992). "[Antihypertensive therapy and modification of metabolic risk factors (glucose and lipid metabolism)]". Z Kardiol (in German). 81 (6): 295–302. PMID 1353932. Unknown parameter |month= ignored (help)
  6. Page ST, Krauss RM, Gross C; et al. (2012). "Impact of mifepristone, a glucocorticoid/progesterone antagonist, on HDL cholesterol, HDL particle concentration, and HDL function". J. Clin. Endocrinol. Metab. 97 (5): 1598–605. doi:10.1210/jc.2011-2813. PMID 22399518. Unknown parameter |month= ignored (help)
  7. Worsley R, Robinson PJ, Bell RJ, Moufarege A, Davis SR (2013). "Endogenous estrogen and androgen levels are not independent predictors of lipid levels in postmenopausal women". Menopause. doi:10.1097/GME.0b013e318279bd4a. PMID 23531683. Unknown parameter |month= ignored (help)
  8. Cabarkapa V, Djerić M, Stosić Z, Sakac V, Zagorka LC, Vucković B (2012). "Evaluation of lipid parameters and bioindices in patients with different stages of chronic renal failure". Vojnosanitetski Pregled. Military-medical and Pharmaceutical Review. 69 (11): 961–6. PMID 23311247. Unknown parameter |month= ignored (help)
  9. Khoueiry G, Abdallah M, Saiful F; et al. (2013). "High-density lipoprotein in uremic patients: metabolism, impairment, and therapy". Int Urol Nephrol. doi:10.1007/s11255-012-0366-y. PMID 23443874. Unknown parameter |month= ignored (help)
  10. Minicocci I, Montali A, Robciuc MR; et al. (2012). "Mutations in the ANGPTL3 gene and familial combined hypolipidemia: a clinical and biochemical characterization". J. Clin. Endocrinol. Metab. 97 (7): E1266–75. doi:10.1210/jc.2012-1298. PMID 22659251. Unknown parameter |month= ignored (help)
  11. Pachocka LM, Włodarczyk M, Nowicka G, Kłosiewicz-Latoszek L, Wolańska D, Stolarska I (2012). "[CETP gene TaqIB polymorphism and plasma lipids in patients with overweight and obesity]". Rocz Panstw Zakl Hig (in Polish). 63 (2): 149–54. PMID 22928361.
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