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Lipoprotein (a) [Lp(a)] is strongly linked to atherosclerotic cardiovascular disease (ASCVD). It is made up of an apolipoprotein(a) or apo(a)-specific protein coupled to a low-density lipoprotein (LDL) core.
It is an independent risk factor for ASCVD, which includes coronary artery disease, heart attacks, and strokes. There are considerable differences in Lp(a) levels between various ethnic groups, which raises concerns about the possible influence of ethnicity on cardiovascular risk.
What do we know about Lp(a) and ethnicity?
This summer, a study from the UK Biobank examined both white and black individuals.
The frequency distribution of Lp(a) concentration can be seen in the left figures, A and B. The X axis in both of these illustrations is the same; it displays the rise in Lp(a) concentration.
100 milligrams per deciliter (mg/dl) equates to 215 nanomole per liter(nmol/l).
The following conclusions can be drawn:
You can observe that Lp(a) is considerably more likely to be elevated among black persons.
We observe a wider distribution than in the case of white persons.
Instead of a more gradual gradient, you see a very sudden drop off in white persons.
The percentage of those with blood levels above 240 nanomole per liter is 3.8% in white people and 6.9% in black people.
You can see that at every cutoff point, the black population will have a higher frequency than the white population.
Risk of cardiovascular events (charts C and D). The line illustrates how the hazard ratio increases along with an increase in Lp(a) concentration. What’s intriguing is this:
The graphs don’t really differ that much. The unpredictability is what makes things really diverse.
The gray region represents the 95% confidence interval.
If you focus on white people, and in this image, we’re comparing the hazard ratio for a specific Lp(a) to the reference Lp(a) (the reference is the population median).
The population’s median concentration is 20 millimole per liter, or 11 milligrams per deciliter.
You can see that it reaches a maximum hazard ratio of 2.7 in the white population, but with a severely constrained 95% confidence interval.
The hazard ratio rises to between 2.6 and 2.7 among the black population. Therefore, the direction is unchanged; nevertheless, notice the magnitude of the 95% confidence interval.
What’s noteworthy here is that the variability is so high, which may explain why you can be deceived when examining 10 individuals.
Understanding the Diversity in Lipoprotein (a) Levels
Current research is examining the genetic basis of Lp(a) levels, which may be altered by both genetic and environmental variables.
Studies have found significant variances in Lp(a) levels between people from various ethnic origins, pointing to a possible hereditary component to these variations.
In a sizable multi-ethnic cohort, one study that was published in the “European Heart Journal” in 2017 looked at Lp(a) levels in relation to various nationalities.
Over 60,000 people with a variety of racial and ethnic backgrounds, including populations from Europe, Africa, South Asia, and East Asia, had their data analyzed by the researchers.
The findings revealed significant differences in Lp(a) levels between various ethnic groupings, with those of African and South Asian ancestry exhibiting the highest levels and those of European and East Asian ancestry exhibiting the lowest levels.
In 2019, another study that was included in the “Journal of Lipid Research” examined Lp(a) levels in people of Hispanic descent. The researchers discovered that Hispanics with different ancestries also exhibited different Lp(a) levels.
Additionally, compared to people of European or African heritage, people of Native American descent tended to have greater Lp(a) levels among the Hispanic population.
These findings show that ethnicity can greatly affect Lp(a) levels, underscoring the need for additional research to identify the underlying genetic and environmental causes of these variances.
Genetic Determinants of Lipoprotein (a) Diversity
The LPA gene, which produces apolipoprotein(a), is principally responsible for the genetic basis of Lp(a) levels. Single nucleotide polymorphisms (SNPs) and copy number variations (CNVs) in the LPA gene have been connected to variations in Lp(a) levels in various groups.
A genome-wide association study (GWAS) was carried out in a 2017 study that was published in “Nature Genetics” to find genetic variations linked to Lp(a) levels.
Over 100,000 people with a variety of racial and ethnic backgrounds, including populations from Europe, Africa, and South Asia, had their data analyzed by the researchers.
They discovered a number of genetic variations in the LPA gene that were highly related to Lp(a) levels and contributed significantly to the observed ethnic disparities.
Additionally, it was shown in this study that some genetic variations were more common in particular ethnic groups, which may have contributed to the observed differences in Lp(a) levels.
People of European heritage, on the other hand, had a higher frequency of variations connected to reduced Lp(a) levels, whereas people of African descent had a higher frequency of variants linked to elevated Lp(a) levels.
Environmental and Lifestyle Factors
The variation in Lp(a) levels among ethnicities may also be influenced by environmental and lifestyle variables in addition to genetic causes. Lifestyle factors such as diet, exercise, and others can affect lipid profiles, including lipoprotein (a) levels.
A 2020 study that appeared in the “Journal of the American Heart Association” examined how food affected Lp(a) levels among various ethnic groups in the US.
A diverse group of more than 2,000 people’s food habits and Lp(a) levels were examined by the researchers.
They discovered that all ethnic groups were related to reduced Lp(a) levels while following a Mediterranean-style diet that is high in fruits, vegetables, whole grains, and healthy fats.
The variations in Lp(a) levels seen among various ethnic groups can also be attributed to socioeconomic circumstances, healthcare accessibility, and other environmental variables.
Implications for Cardiovascular Risk
The variation in Lp(a) levels among racial and ethnic groups has significant implications for managing and assessing cardiovascular risk.
For the purpose of delivering individualized and focused cardiovascular therapy, an awareness of these ethnic disparities is essential because raised lipoprotein (a) levels have been associated with a higher risk of ASCVD.
When interpreting the results of the Lp(a) test and determining a person’s cardiovascular risk, healthcare professionals should take these variances into account.
In order to successfully reduce their risk of developing ASCVD, people from ethnic groups with historically higher Lp(a) levels may benefit from more regular monitoring and proactive risk management techniques.
Conclusion
The variation in lipoprotein(a) among ethnic groups is an intriguing issue for cardiovascular medicine study. Significant differences in Lp(a) levels have been found between various ethnic groups in studies, and these differences appear to be affected by a mix of genetic and environmental variables.
These variances are mostly caused by genetic variations within the LPA gene, although environmental and lifestyle variables also play a part.
Understanding how ethnicity affects lipoprotein (a) levels has significant implications for managing and assessing cardiovascular risk.
The creation of more individualized cardiovascular care will benefit from greater knowledge of the underlying causes of these variances, which will ultimately result in better prevention and treatment plans for those who are at risk of ASCVD.
