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Article ; Online: Non-genetic influences on lipoprotein(a) concentrations.

Enkhmaa, Byambaa / Berglund, Lars

2022 Volume 349, Page(s) 53–62

Abstract: An elevated level of lipoprotein(a) [Lp(a)] is a genetically regulated, independent, causal risk factor for cardiovascular disease. However, the extensive variability in Lp(a) levels between individuals and population groups cannot be fully explained by ... ...

Abstract	An elevated level of lipoprotein(a) [Lp(a)] is a genetically regulated, independent, causal risk factor for cardiovascular disease. However, the extensive variability in Lp(a) levels between individuals and population groups cannot be fully explained by genetic factors, emphasizing a potential role for non-genetic factors. In this review, we provide an overview of current evidence on non-genetic factors influencing Lp(a) levels with a particular focus on diet, physical activity, hormones and certain pathological conditions. Findings from randomized controlled clinical trials show that diets lower in saturated fats modestly influence Lp(a) levels and often in the opposing direction to LDL cholesterol. Results from studies on physical activity/exercise have been inconsistent, ranging from no to minimal or moderate change in Lp(a) levels, potentially modulated by age and the type, intensity, and duration of exercise modality. Hormone replacement therapy (HRT) in postmenopausal women lowers Lp(a) levels with oral being more effective than transdermal estradiol; the type of HRT, dose of estrogen and addition of progestogen do not modify the Lp(a)-lowering effect of HRT. Kidney diseases result in marked elevations in Lp(a) levels, albeit dependent on disease stages, dialysis modalities and apolipoprotein(a) phenotypes. In contrast, Lp(a) levels are reduced in liver diseases in parallel with the disease progression, although population studies have yielded conflicting results on the associations between Lp(a) levels and non-alcoholic fatty liver disease. Overall, current evidence supports a role for diet, hormones and related conditions, and liver and kidney diseases in modifying Lp(a) levels.
MeSH term(s)	Cardiovascular Diseases/blood ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/therapy ; Cholesterol, LDL ; Estradiol ; Estrogen Replacement Therapy ; Estrogens ; Exercise ; Female ; Humans ; Lipoprotein(a)/adverse effects ; Lipoprotein(a)/blood ; Lipoprotein(a)/genetics ; Risk Factors
Chemical Substances	Cholesterol, LDL ; Estrogens ; Lipoprotein(a) ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2022-05-21
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2022.04.006
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Article ; Online: Lp(a) and SARS-CoV-2: A conspiracy of two mysteries.

Enkhmaa, Byambaa / Berglund, Lars

Journal of internal medicine

2021 Volume 291, Issue 1, Page(s) 8–10

MeSH term(s)	COVID-19/blood ; Cardiovascular Diseases ; Humans ; Lipoprotein(a)/blood ; SARS-CoV-2 ; Thromboembolism
Chemical Substances	Lipoprotein(a)
Language	English
Publishing date	2021-10-29
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural
ZDB-ID	96274-0
ISSN	1365-2796 ; 0954-6820
ISSN (online)	1365-2796
ISSN	0954-6820
DOI	10.1111/joim.13356
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Article ; Online: Lipoprotein(a) and diet-a challenge for a role of saturated fat in cardiovascular disease risk reduction?

Law, Hayley G / Meyers, Frederick J / Berglund, Lars / Enkhmaa, Byambaa

The American journal of clinical nutrition

2023 Volume 118, Issue 1, Page(s) 23–26

Abstract: In this perspective, we discuss new evidence relating to current dietary recommendations to reduce SFA intake to modulate an individual's global risk of CVD. Although it is well established that lowering dietary SFA intake has a beneficial effect on LDL ... ...

Abstract	In this perspective, we discuss new evidence relating to current dietary recommendations to reduce SFA intake to modulate an individual's global risk of CVD. Although it is well established that lowering dietary SFA intake has a beneficial effect on LDL cholesterol concentrations, findings increasingly indicate an opposite effect on lipoprotein(a) [Lp(a)] concentrations. In recent years, many studies have firmly established a role for an elevated Lp(a) concentration as a genetically regulated, causal, and prevalent risk factor for CVD. However, there is less awareness of the effect of dietary SFA intake on Lp(a) concentrations. This study discusses this issue and highlights the contrasting effect of reducing dietary SFA intake on LDL cholesterol and Lp(a), 2 highly atherogenic lipoproteins. This calls attention to the need for precision nutrition approaches that move beyond a "one-size-fits-all" approach. To illustrate the contrast, we describe the dynamic contributions of Lp(a) and LDL cholesterol concentrations to CVD risk during interventions with a low-SFA diet, with the hope that this will stimulate further studies and discussions regarding dietary management of CVD risk.
MeSH term(s)	Humans ; Dietary Fats/pharmacology ; Cholesterol, LDL ; Lipoprotein(a) ; Cardiovascular Diseases/prevention & control ; Fatty Acids ; Diet ; Risk Reduction Behavior
Chemical Substances	Dietary Fats ; Cholesterol, LDL ; Lipoprotein(a) ; Fatty Acids
Language	English
Publishing date	2023-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	280048-2
ISSN	1938-3207 ; 0002-9165
ISSN (online)	1938-3207
ISSN	0002-9165
DOI	10.1016/j.ajcnut.2023.05.017
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Article ; Online: COVID-19 and public health efforts in Mongolia

Tumenbayar Bayasgalan / Erdembileg Anuurad / Enkhmaa Byambaa

Journal of Clinical and Translational Science, Vol

A lesson maybe learned?

2021 Volume 5

Keywords	Coronavirus ; novel virus ; new infection ; spread control measurements ; Asia ; Medicine ; R
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Cambridge University Press
Document type	Article ; Online
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Article ; Online: Statins and Lp(a): The plot thickens.

Enkhmaa, Byambaa / Berglund, Lars

Atherosclerosis

2019 Volume 289, Page(s) 173–175

MeSH term(s)	Apoprotein(a) ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Lipoprotein(a) ; Molecular Weight ; Phenotype
Chemical Substances	Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Lipoprotein(a) ; Apoprotein(a) (EC 3.4.21.-)
Language	English
Publishing date	2019-08-06
Publishing country	Ireland
Document type	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	80061-2
ISSN	1879-1484 ; 0021-9150
ISSN (online)	1879-1484
ISSN	0021-9150
DOI	10.1016/j.atherosclerosis.2019.07.021
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Article ; Online: Cardiovascular Disease Mortality in Mississippi, 2000-2018.

Mendy, Vincent L / Rowell-Cunsolo, Tawandra / Bellerose, Meghan / Vargas, Rodolfo / Enkhmaa, Byambaa / Zhang, Lei

Preventing chronic disease

2022 Volume 19, Page(s) E09

Abstract: Introduction: Cardiovascular disease (CVD) is the leading of cause of death in Mississippi. We explored trends in CVD death rates among adults in Mississippi aged 35 years or older to assess changes from 2000 through 2018.: Methods: We extracted data ...

Abstract	Introduction: Cardiovascular disease (CVD) is the leading of cause of death in Mississippi. We explored trends in CVD death rates among adults in Mississippi aged 35 years or older to assess changes from 2000 through 2018. Methods: We extracted data from Mississippi Vital Statistics from 2000 through 2018. We used underlying cause-of-death codes from the International Classification of Diseases, Tenth Revision (ICD-10) to identify CVD deaths; we included all cases with codes I00-I09, I11, I13, I20-I51, I60-I69, and I70. We calculated age-adjusted CVD death rates for the overall population by age, race, sex, and race-by-sex groups. Results: Overall, the age-adjusted CVD death rate declined from 832.3 deaths per 100,000 population in 2000 to 550.5 deaths per 100,000 in 2018, a relative decline of 33.9% and an average annual decline of -2.3% (95% CI, -2.7% to -1.8%). Age-adjusted CVD death rates declined from 2000 through 2018 for all groups, but the magnitude of decline varied by subgroup (men, -2.0%; women, -2.6%; non-Hispanic Black, -2.4%; non-Hispanic White, -2.2%; non-Hispanic Black women, -3.0%; non-Hispanic White women, -2.5%; non-Hispanic Black men -2.1%; non-Hispanic White men -2.0%). Age-specific analysis indicated a significant average annual increase of 1.7% (95% CI, 0.6%-2.9%) from 2011 through 2018 for the group aged 55 to 64 years. Conclusion: From 2000 through 2018, age-adjusted CVD death rates in Mississippi declined for all age/race/sex groups. However, the magnitude of decline varied by subgroup. Targeted interventions for CVD risk reduction are needed for adults aged 55 to 64 years in Mississippi, the only age group in which we observed a significant annual increase in CVD death rates.
MeSH term(s)	Adult ; Blacks ; Cardiovascular Diseases ; Ethnicity ; Female ; Humans ; International Classification of Diseases ; Male ; Mississippi/epidemiology
Language	English
Publishing date	2022-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2135684-1
ISSN	1545-1151 ; 1545-1151
ISSN (online)	1545-1151
ISSN	1545-1151
DOI	10.5888/pcd19.210385
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Reducing saturated fat intake lowers LDL-C but increases Lp(a) levels in African Americans: the GET-READI feeding trial.

Law, Hayley G / Khan, Muhammad A / Zhang, Wei / Bang, Heejung / Rood, Jennifer / Most, Marlene / Lefevre, Michael / Berglund, Lars / Enkhmaa, Byambaa

Journal of lipid research

2023 Volume 64, Issue 9, Page(s) 100420

Abstract: Reducing dietary saturated fatty acids (SFA) intake results in a clinically significant lowering of low-density lipoprotein cholesterol (LDL-C) across ethnicities. In contrast, dietary SFA's role in modulating emerging cardiovascular risk factors in ... ...

Abstract	Reducing dietary saturated fatty acids (SFA) intake results in a clinically significant lowering of low-density lipoprotein cholesterol (LDL-C) across ethnicities. In contrast, dietary SFA's role in modulating emerging cardiovascular risk factors in different ethnicities remains poorly understood. Elevated levels of lipoprotein(a) [Lp(a)], an independent cardiovascular risk factor, disproportionally affect individuals of African descent. Here, we assessed the responses in Lp(a) levels to dietary SFA reduction in 166 African Americans enrolled in GET-READI (The Gene-Environment Trial on Response in African Americans to Dietary Intervention), a randomized controlled feeding trial. Participants were fed two diets in random order for 5 weeks each: 1) an average American diet (AAD) (37% total fat: 16% SFA), and 2) a diet similar to the Dietary Approaches to Stop Hypertension (DASH) diet (25% total fat: 6% SFA). The participants' mean age was 35 years, 70% were women, the mean BMI was 28 kg/m
MeSH term(s)	Adult ; Female ; Humans ; Male ; Black or African American ; Cholesterol, LDL/blood ; Diet ; Dietary Fats/administration & dosage ; Lipoprotein(a)/blood
Chemical Substances	Cholesterol, LDL ; Dietary Fats ; Lipoprotein(a)
Language	English
Publishing date	2023-07-22
Publishing country	United States
Document type	Randomized Controlled Trial ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1016/j.jlr.2023.100420
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Article ; Online: Diet and Lp(a): Does Dietary Change Modify Residual Cardiovascular Risk Conferred by Lp(a)?

Enkhmaa, Byambaa / Petersen, Kristina S / Kris-Etherton, Penny M / Berglund, Lars

Nutrients

2020 Volume 12, Issue 7

Abstract: Lipoprotein(a) [Lp(a)] is an independent, causal, genetically determined risk factor for cardiovascular disease (CVD). We provide an overview of current knowledge on Lp(a) and CVD risk, and the effect of pharmacological agents on Lp(a). Since evidence is ...

Abstract	Lipoprotein(a) [Lp(a)] is an independent, causal, genetically determined risk factor for cardiovascular disease (CVD). We provide an overview of current knowledge on Lp(a) and CVD risk, and the effect of pharmacological agents on Lp(a). Since evidence is accumulating that diet modulates Lp(a), the focus of this paper is on the effect of dietary intervention on Lp(a). We identified seven trials with 15 comparisons of the effect of saturated fat (SFA) replacement on Lp(a). While replacement of SFA with carbohydrate, monounsaturated fat (MUFA), or polyunsaturated fat (PUFA) consistently lowered low-density lipoprotein cholesterol (LDL-C), heterogeneity in the Lp(a) response was observed. In two trials, Lp(a) increased with carbohydrate replacement; one trial showed no effect and another showed Lp(a) lowering. MUFA replacement increased Lp(a) in three trials; three trials showed no effect and one showed lowering. PUFA or PUFA + MUFA inconsistently affected Lp(a) in four trials. Seven trials of diets with differing macronutrient compositions showed similar divergence in the effect on LDL-C and Lp(a). The identified clinical trials show diet modestly affects Lp(a) and often in the opposing direction to LDL-C. Further research is needed to understand how diet affects Lp(a) and its properties, and the lack of concordance between diet-induced LDL-C and Lp(a) changes.
MeSH term(s)	Adult ; Aged ; Carbohydrates ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/therapy ; Cholesterol, LDL/blood ; Cholesterol, LDL/metabolism ; Diet/methods ; Dietary Fats/administration & dosage ; Fatty Acids/administration & dosage ; Female ; Heart Disease Risk Factors ; Humans ; Hypolipidemic Agents/therapeutic use ; Lipoprotein(a)/blood ; Lipoprotein(a)/metabolism ; Male ; Middle Aged
Chemical Substances	Carbohydrates ; Cholesterol, LDL ; Dietary Fats ; Fatty Acids ; Hypolipidemic Agents ; Lipoprotein(a)
Language	English
Publishing date	2020-07-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12072024
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Article ; Online: Temporal Trends in Hypertension Death Rate in Mississippi, 2000-2018.

Mendy, Vincent L / Rowell-Cunsolo, Tawandra / Bellerose, Meghan / Vargas, Rodolfo / Zhang, Lei / Enkhmaa, Byambaa

American journal of hypertension

2021 Volume 34, Issue 9, Page(s) 956–962

Abstract: Background: In Mississippi, hypertension as a leading cause of death moved from 15th in 2000 to 11th in 2018, but research on temporal trends is limited. We examined temporal trends in hypertension-related mortality among Mississippi adults by age, sex, ...

Abstract	Background: In Mississippi, hypertension as a leading cause of death moved from 15th in 2000 to 11th in 2018, but research on temporal trends is limited. We examined temporal trends in hypertension-related mortality among Mississippi adults by age, sex, and race. Methods: We extracted data on the number of deaths due to hypertension among adults aged 45 or older annually from 2000 to 2018 from Mississippi Vital Statistics. We used underlying cause-of-death codes from the International Classification of Diseases, Tenth Revision to identify hypertension deaths. We calculated the annual percentage change (trend segment) and average annual percentage change (AAPC) in age-adjusted hypertension death rates from 2000 to 2018 and examined differences in the AAPC by age, sex, and race. Results: From 2000 through 2018, the age-adjusted hypertension death rate increased annually by 3.0% (AAPC 3.0%, 95% confidence interval, 1.9%-4.0%) with 3 distinct time periods. There was an average annual increase in age-adjusted hypertension death rates for all subgroups, i.e., men, women, Blacks, Whites, White females, Black males, and White males. The highest magnitude of increase was among those aged 45-64 years (AAPC 6.0%), men (AAPC 4.5%), Whites (AAPC 3.5%), and White men (AAPC 6.2%) compared with other age groups, women, Blacks, and Black men, respectively. Conclusions: For nearly 2 decades, there was an increase in age-adjusted hypertension death rates among Mississippi adults aged 45 years or older. Blood pressure lowering interventions that target hypertensive adults are needed.
MeSH term(s)	African Americans/statistics & numerical data ; Age Distribution ; Female ; Humans ; Hypertension/ethnology ; Hypertension/mortality ; Male ; Middle Aged ; Mississippi/epidemiology ; Race Factors ; Sex Distribution ; United States ; Whites/statistics & numerical data
Language	English
Publishing date	2021-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639383-4
ISSN	1941-7225 ; 1879-1905 ; 0895-7061
ISSN (online)	1941-7225 ; 1879-1905
ISSN	0895-7061
DOI	10.1093/ajh/hpab068
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Article ; Online: Lp(a)-Associated Oxidized Phospholipids in Healthy Black and White Participants in Relation to apo(a) Size, Age, and Family Structure.

Berglund, Lars / Kim, Kyoungmi / Zhang, Wei / Prakash, Nishant / Truax, Kevin / Anuurad, Erdembileg / Enkhmaa, Byambaa

Journal of the American Heart Association

2021 Volume 10, Issue 17, Page(s) e020158

Abstract: Background Lp(a) (lipoprotein(a)) is the major lipoprotein carrier of oxidized phospholipids (OxPL) and this function mediates Lp(a) atherogenicity. However, the relationship between OxPL, Lp(a), and genetic and biological characteristics remains poorly ... ...

Abstract	Background Lp(a) (lipoprotein(a)) is the major lipoprotein carrier of oxidized phospholipids (OxPL) and this function mediates Lp(a) atherogenicity. However, the relationship between OxPL, Lp(a), and genetic and biological characteristics remains poorly understood. We assessed the relationship between Lp(a)-bound OxPL, apolipoprotein(a) (apo(a)) size, age, and family structure in 2 racial groups. Methods and Results Healthy Black and White families were recruited from the general population (age: 6-74 years, n=267). OxPL and Lp(a) levels were assayed enzymatically; apo(a) isoform,
MeSH term(s)	Adolescent ; Adult ; Aged ; Apoprotein(a)/genetics ; Blacks/genetics ; Child ; Humans ; Lipoprotein(a)/genetics ; Middle Aged ; Oxidation-Reduction ; Phospholipids ; Whites/genetics ; Young Adult
Chemical Substances	Lipoprotein(a) ; Phospholipids ; Apoprotein(a) (EC 3.4.21.-)
Language	English
Publishing date	2021-08-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.120.020158
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