ACE and ARB blood pressure meds (i.e losartan) and coronavirus concern

Harley

Member
I take losartan with Ramipril , in Italy it's called Giant .
So far so good
My girlfriend has liver problems and she takes Tenofovir
I noticed that all the medicine against Coroends with vir , so we joke that she is totally protected.
 
Following is an email from Chris Kresser regarding upregulation of ACE2 receptors from certain supplements. Based on what he's saying, anything that can increase expression of ACE2 receptors is theoretically at risk. All ACEIs and ARBs already do this, and, according to Chris, if we're taking high doses of Vitamins A&D, it compounds the problem even more. Naturally, am concerned for any of us using ARB or ACEI meds.

Hi, Everyone,

I wanted to share some important COVID-19-related updates with you, along with links to some articles I’ve found to be helpful.

Immune support
On the webinar I did last weekend, I offered several ideas for boosting immune function during the COVID-19 outbreak. Among them were propolis and high-dose vitamin A and D. I have since come across research suggesting that propolis and megadoses of A and D may not be a good idea because, at least in theory, they could increase the expression of angiotensin-converting enzyme (ACE2) receptors.

In many cases, botanicals, plant medicines, and nutrients like propolis and vitamins A and D have a modulatory effect—i.e., they upregulate or downregulate a function based on what is needed. That may be true here.

However, since coronavirus gets into our cells by hijacking ACE2 receptors, I think it’s probably wise to avoid anything that might upregulate those receptors. For this reason, I now suggest avoiding propolis and high doses of vitamins A and D during the COVID-19 pandemic. You can (and should) still eat adequate amounts of A and D in food, and can supplement with lower doses of vitamin D (e.g., 1,000 IU) if you live in a place where you’re getting minimal sun exposure, or your 25-D levels are below 40 mg/dL.

Younger people aren’t always safe from COVID-19
New data from the Centers for Disease Control and Prevention shows that nearly 40 percent of the COVID-19 patients in the United States that were sick enough to be hospitalized were aged 20 to 54. While the mortality rate in this group is still much lower than in patients aged 60 or higher, younger patients can experience serious complications including persistent lung damage. Many younger people I’ve spoken with seem to believe they aren’t at risk—this is, unfortunately, not the case.

The power of individual action in a viral pandemic
I still see and hear of (mostly younger) people who are ignoring the social distancing measures, congregating in larger groups, and taking a cavalier approach to COVID-19. This seems to stem from two misunderstandings: 1) younger people aren’t at risk, and 2) individual action won’t make much of a difference.

I addressed #1 in the last paragraph. As for #2, I refer you to an excellent graph and thought experiment by epidemiologist Britta Jewell. Assuming 30 percent growth of COVID-19 through the next month, she looked at the difference between one person taking aggressive social distancing action now versus seven days later, and found that a single person taking action now versus a week later would prevent 1,800 cases, 360 hospitalizations, 90 ICU visits, and 18 deaths. If you needed any extra motivation to practice effective social distancing and containment, this is it.

The paradox of preparation
Along the same lines, Jason Kottke wrote an excellent article explaining why, in a pandemic like COVID-19, appropriate actions to “flatten the curve” often seem like overkill both at the time they are taken, and in retrospect. He quotes physician Dr. James Hamblin:

“The thing is if shutdowns and social distancing work perfectly and are extremely effective it will seem in retrospect like they were totally unnecessary overreactions.”

and epidemiologist Mari Armstrong-Hough:

“You won’t ever know if what you did personally helped. That’s the nature of public health. When the best way to save lives is to prevent a disease rather than treat it, success often looks like an overreaction.”

Why meditation/mindfulness are so important during a crisis
As many of you know, I suffered from a severe chronic illness in my 20s and 30s. I learned many powerful lessons from that experience, but one of the most valuable was the importance of taking life one day at a time and not projecting my current reality too far into the future.

We’re all in that same boat today with COVID-19. Our lives have changed dramatically—and they may never be quite the same again. We’re plagued with uncertainties, and many of us are experiencing heightened fear and anxiety.

During times like this, a practice that can help keep our attention grounded in the present moment is vital. For me, meditation is that practice.

I know many people who want to try meditation, but are reluctant for various reasons. A couple years ago, I wrote an article called “The Top 5 Myths about Meditation” to address some of the hesitations that folks have. I also include a few suggestions for getting started with meditation at the end of the article, so check it out!

I hope you’re all staying healthy and taking care of yourselves and each other.

Warmly,
Chris
 
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Zooka15

Member
from what I keep seeing Losartan a ARB seems to be a treatment
 

Harley

Member
I am not an expert , I would just like to say that yesterday on tv a doctor said that we should ignore news about the dangers of bp medication in Corona virus.
I would also like to include this graph of corona deaths according to age in Italy:
 

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seppuku

Member
I'm mostly concerned about the vitamin d issue - there seems to be two completely opposing opinions on this, one that it helps protect, the other that it makes things worse. I always take d3 anyhow, but i bought my elderly parents some 5000iu pills last week, and now i'm wondering if i did the right thing
 
I'm mostly concerned about the vitamin d issue - there seems to be two completely opposing opinions on this, one that it helps protect, the other that it makes things worse. I always take d3 anyhow, but i bought my elderly parents some 5000iu pills last week, and now i'm wondering if i did the right thing
One thing to keep in mind is that people lacking vitamin D (greater in elderly and those with little or no sunlight exposure) have a weaker innate immune defense against SARS-CoV-2.
 
So, in laymen’s terms...ARBs and ACEi’s aren’t a concern?
 

readalot

New Member
https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=2ahUKEwj4soumx7noAhUllXIEHck4A-cQFjAAegQIAxAB&url=https%3A%2F%2Fwww.preprints.org%2Fmanuscript%2F202003.0191%2Fv1%2Fdownload&usg=AOvVaw3UdwZHpkfhHkpFokMMgflX

Recent preprint:

Discussion
In summary, through integrating public genomics, epigenomics and transcriptomics
data, we examined whether variation of the SARS-CoV2 receptor ACE2 gene
expression in different tissues across individuals can explain the differences in
infection susceptibility and outcome. Our findings are contrary to the expectation from
ACE2 being only a receptor for the virus, instead, its expression level is high in Asian
females and young people (Fig. 1 and Table 1), those who are known to be less
susceptible, and even less inflicted by severe or fatal outcome, while it is low in males,
further decrease with age and T2D, those who are most susceptible to bad outcome
(Fig. 1 and 3), suggesting at a population level a negative correlation between ACE2
expression and CovID19 severity and fatality.

At the molecular level, we found ACE2 anti-expressed genes in most tissues
and cells are highly enriched for virus infection pathways (Fig. 3a), estrogen strongly
and androgen moderately increase ACE2 expression in mouse and human tissues
(Fig. 2), whereas severe CoVID-19 induced IL-2 and IL7 repress ACE2 expression in
mouse T cells, and T2D reduced ACE2 expression and ACE2 expressing cells in
human tissues (Fig. 3). The effect of estrogen, androgen and cytokines are reflected
on clusters of estrogen and androgen receptors, STAT5, JUN, MYC and other TFs
binding at ACE2 regulatory regions, where hypertension QTLs and the great majority
of ACE2 eQTLs are also mapped to. Finally, as the eQTLs that show largest allele
frequency differences between ethnic groups are also the ones having close to full
penetrance in East Asians and also the strongest positive eQTLs on ACE2 expression
(Table 1), ACE2 expression differences among ethnic groups are indeed genetically
coded, which may also contribute to the differences in SARS-CoV2 infection outcome.
Our results established a counter argument against the speculation that high
ACE2 is a culprit in CoVID-19 outcome, and on the contrary supports a protective role
of high ACE2 expression against SARS-CoV2 fatality (Fig. 3h). The exceptionally
elevated basal level of ACE2 in Asian females (Fig. 1) and the strong positive ACE2
eQTLs in East Asians (Table 1) suggest that it could be the Asian females are more
protected against SARS-CoV and SARS-CoV2 severe symptoms rather than males
being more susceptible. Although we have analyzed thousands of samples, the sizes
of Asian samples and samples for some tissues are still small compared to others, it
remains to be seen whether larger samples will reveal similar patterns in the future
when more data become available.

The repression of ACE2 might be counteracted by higher basal ACE2 level,
which is inducible by higher sex hormone levels (that decrease with age) and
repressed by systemic inflammation (that increase with age and chronic diseases) (Fig.
2 and 3). For SARS-CoV2, the decrease of ACE2 might be further exacerbated by the
direct binding and consumption of ACE2 protein by the virus. Before the availability of
an effective vaccine to prevent SARS-CoV2 infection, a major task is to understand
the variations in severity and fatality of the infection in human populations, to which
ACE2 might be one of the contributors. Fortunately, the low ACE2 activity can be
rescued by dampening its negatively regulated downstream targets such as
angiotensin II or its receptors, such as by angiotensin II antagonist losartan 27.
 
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readalot

New Member
https://onlinelibrary.wiley.com/doi/epdf/10.1002/ddr.21656

As described above, ACE2 is the common binding site for both the SARS‐CoV of the 2002–2003 SARS epidemic and, most likely, also the SARS‐CoV‐2 strain underlying the current COVID‐19 epidemic. Hence, the suggestion to treat SARS patients with AT1R antagonists for increasing their ACE2 expression seems counter‐intuitive. However, several observations from studies on SARS‐CoV, which very likely are relevant also for SARS‐CoV‐2, seem to suggest otherwise. It has been demonstrated that the binding of the coronavirus spike protein to ACE2, its cellular binding site, leads to ACE2 downregulation, which in turn results in excessive production of angiotensin by the related enzyme ACE, while less ACE2 is capable of converting it to the vasodilator heptapeptide angiotensin 1–7. This in turn contributes to lung injury, as angiotensin‐stimulated AT1R results in increased pulmonary vascular permeability, thereby mediating increased lung pathology (Imai et al., 2005; Kuba et al., 2005). Therefore, higher ACE2 expression following chronically medicating SARS‐CoV‐2 infected patients with AT1R blockers, while seemingly paradoxical, may protect them against acute lung injury rather than putting them at higher risk to develop SARS. This may be accounted for by two complementary mechanisms: blocking the excessive angiotensin‐mediated AT1R activation caused by the viral infection, as well as upregulating ACE2, thereby reducing angiotensin production by ACE and increasing the production of the vasodilator angiotensin 1–7. These aspects on the role of dysregulated ACE2 in SARS‐CoV pathogenesis are reviewed in detail by de Wit et al., 2016. Incidentally, following the SARS‐CoV epidemic of 2002–2003, ACE2 inhibitors were suggested as SARS therapeutics (Huentelman et al., 2004; Turner et al., 2004); however, this proposal has not led to new drugs.
 
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