Lifelong discrimination linked to high blood pressure in black people

AHA news: lifelong discrimination linked to high blood pressure in black people

Enduring a lifetime of discrimination may increase the risk of high blood pressure in Black people but not in Hispanic, Chinese or white people, a new study suggests.

Previous research has linked lifelong discrimination to the development of high blood pressure, also known as hypertension, in Black people. This new study, however, is among the first to look at multiple types of discrimination in a large multi-ethnic group over a period of time.

The study included 3,297 Black, Hispanic, Chinese and white adults from 45 to 84 years old. They did not have high blood pressure at the start of the study. Participants were asked to report experiences of lifetime and everyday discrimination.

Lifetime discrimination measures included six items, such as being denied a promotion or having life made difficult by neighbors. Everyday discrimination, meanwhile, consisted of nine items, such as being treated with less respect than others or being harassed in day-to-day life.

After nearly two decades, almost half of participants developed high blood pressure. Black participants who reported lifetime discrimination had a 35% increased risk of hypertension, even after accounting for age, income, education, body mass index, physical activity and other factors. Everyday discrimination, however, did not appear to contribute to risk for hypertension.

“Discrimination impacts the health of Black Americans and it should be recognized as a major public health problem,” said Allana T. Forde, lead author of the study published last week in the Journal of the American Heart Association. In November, the American Heart Association issued a “call to action” advisory acknowledging structural racism as “a fundamental cause of poor health and disparities in cardiovascular disease.”

“Health professionals should look beyond traditional risk factors, such as diet and physical activity, and acknowledge discrimination as another risk factor,” said Forde, a researcher at the National Institutes of Health’s National Institute on Minority Health and Health Disparities.

Surprising for researchers, she said, was that lifetime discrimination did not reach the level of statistical significance for contributing to high blood pressure among Chinese and Hispanic participants, even after accounting for being born outside the United States.

Studies in other areas of the U.S. are needed to confirm the findings, researchers said, because the new study was limited to those living in five large cities and one county. In addition, the study only assessed discrimination experiences once at the start of the study, making it unclear what impact changes in discrimination exposure might have had on hypertension development during the follow-up period.

“There is always a concern that not enough subjects were included in the study to show differences in populations or that not all relevant variables were accounted for,” said Dr. Willie Lawrence, chief of cardiology at the Research Medical Center in Kansas City, Missouri. He was not involved in the study.

When measuring decades of discrimination that leads to hypertension, other social determinants of health also must be accounted for. These include health care access, transportation options and a person’s neighborhood.

“Whether communities have sidewalks and green spaces impacts health,” Lawrence said. “If we want to make people healthier, we have to not only eliminate disparities in health care delivery, but we must also seek equity in housing, neighborhoods and education.”

Overall, the study found Black people reported the highest levels of discrimination. About 65% reported lifetime discrimination compared to 42% of Hispanic people, 40% of white people and 23% of Chinese people. Black people most often attributed the unfair treatment to race, whereas white people by far attributed it to non-racial factors such as age, sex or religion. Hispanic and Chinese people were about evenly split between feeling the discrimination was motivated by race versus other factors.

For everyday discrimination, 52% of Black people, 32% of white people, 26% of Hispanic people and 20% of Chinese people reported high levels of exposure.

“Race is complicated in America. It is not genetic,” Lawrence said. “So, I’m not ready to believe that when people of other colors are treated the way Black Americans have been treated for decades that they won’t have higher rates of high blood pressure.”

Even so, he said, “it’s an important study that adds to our belief that social factors impact health.”

Certain, however, is that Black people have higher rates of high blood pressure than other racial and ethnic groups. According to AHA statistics, about 58% of Black adults in the U.S. have the condition, which increases the risk for heart attack and stroke.

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Blood pressure medications decrease death and severe disease in COVID-19 patients

At the start of the pandemic, there was concern that certain drugs for high blood pressure might be linked with worse outcomes for COVID-19 patients.

Because of how the drugs work, it was feared they would make it easier for the coronavirus to get inside the body’s cells. Nevertheless, many national medical societies advised patients to continue taking their medication.

With the potential for a second wave, it was essential to investigate whether patients could safely continue using these drugs. So, our team at the University of East Anglia set out to discover what effect they have on the progress of COVID-19.

Instead of putting patients at risk, we found that these medications actually lower the risk of death and severe disease in COVID-19 patients.

Bad outcomes cut by one-third

We pooled data from 19 relevant COVID-19 studies that included patients taking two particular types of blood pressure medication: angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs). This allowed us to look at the outcomes of more than 28,000 COVID-19 patients to assess the effects of these drugs.

ACEIs and ARBs work by acting on the renin-angiotensin-aldosterone system (RAAS), which is essential for regulating blood pressure and the balance of fluids and electrolytes. These drugs were also thought to potentially increase the expression of a protein found on the surface of cells called angiotensin-converting enzyme 2 (ACE2).

Apart from helping regulate blood pressure, the ACE2 protein is also what allows the coronavirus to enter the body’s cells. This is why there were concerns about patients using these drugs. If the medications increased the amount of ACE2 present on cells, it was suspected they would make it easier for the virus to infect them, worsening a patient’s condition.

But when we looked at the outcomes of patients taking ACEIs and ARBs compared with those not on these medications, this wasn’t the case.

We found no evidence that these medications might increase the severity of COVID-19 or the risk of death. On the contrary, among patients taking ACEIs and ARBs that had been prescribed to treat high blood pressure, there was actually a significantly lower risk of death, being admitted to intensive care or being put on ventilation. We observed a reduction of such events by one-third in this group.

It may be that these medications actually have a protective role—particularly in patients with high blood pressure.

What’s behind this effect?

It’s not clear why patients taking ACEIs and ARBs experienced less severe disease, but there are a couple of points to consider.

The first is that while theoretically these drugs were thought to increase ACE2 levels, there’s no convincing evidence that this actually happens. We don’t have any clinical data on the effects of these drugs on ACE2 expression in human tissue.

And even if these drugs do increase ACE2 levels in cells, not all of it is surface-bound. Additional ACE2 that appears elsewhere in the cell might not function as an entry point for SARS-CoV-2.

There’s also a second potentially relevant piece of information. Infection with SARS-CoV-2 may also lead to an overreaction of the RAAS pathway – which is what these blood pressure drugs target—and inflammation. This increased inflammatory process is thought to be the culprit for acute lung injury and can lead to worsening pneumonia and acute respiratory distress syndrome. Hence, it might be that taking medications that inhibit the RAAS system prevents such a sequence of events and improves clinical outcomes in COVID-19.

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