Progesterone Is Bad If You Have Flu / Progesterone Is Good If You Have Flu

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Progesterone-Based Therapy Protects Against Influenza by Promoting Lung Repair and Recovery in Females

Over 100 million women use progesterone therapies worldwide. Despite having immunomodulatory and repair properties, their effects on the outcome of viral diseases outside of the reproductive tract have not been evaluated. Administration of exogenous progesterone (at concentrations that mimic the luteal phase) to progesterone-depleted adult female mice conferred protection from both lethal and sublethal influenza A virus (IAV) infection. Progesterone treatment altered the inflammatory environment of the lungs, but had no effects on viral load. Progesterone treatment promoted faster recovery by increasing TGF-β, IL-6, IL-22, numbers of regulatory Th17 cells expressing CD39, and cellular proliferation, reducing protein leakage into the airway, improving pulmonary function, and upregulating the epidermal growth factor amphiregulin (AREG) in the lungs. Administration of rAREG to progesterone-depleted females promoted pulmonary repair and improved the outcome of IAV infection. Progesterone-treatment of AREG-deficient females could not restore protection, indicating that progesterone-mediated induction of AREG caused repair in the lungs and accelerated recovery from IAV infection. Repair and production of AREG by damaged respiratory epithelial cell cultures in vitro was increased by progesterone. Our results illustrate that progesterone is a critical host factor mediating production of AREG by epithelial cells and pulmonary tissue repair following infection, which has important implications for women’s health.


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Problem

Influenza infection severity may be mediated by estradiol and/or progesterone.

Method of Study
An exploratory study was designed to evaluate 17‐β‐estradiol and progesterone on influenza infection and examine immune‐mediated response in a mouse model. Inoculation with placebo or mouse‐adapted H1N1 influenza virus occurred. Treatment groups included 17‐β‐estradiol, progesterone, ovariectomy, and pregnancy. Mice were assessed for morbidity and mortality. Toll‐like receptor gene studies and airspace cell differentials were performed.

Results
Onset of morbidity was earlier and morbidity duration greater for progesterone. Absence of morbidity/mortality and overall survival was greater for 17‐β‐estradiol. Airspace cell differentials suggest improved immune cell recruitment for 17‐β‐estradiol. Pregnant mouse data demonstrate significant mortality during the period of increased progesterone. Select immune cell markers demonstrate patterns of regulation that may promote proper immune response to influenza infection for 17‐β‐estradiol.

Conclusion
Estradiol may play a protective and progesterone a detrimental role in the pathophysiology of influenza infection.
 

Tenacity

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Be careful. When some studies say "progesterone" in their abstract or title they're often referring to one of the synthetic progestins.
 
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jb116

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It's good:
Progesterone-Based Therapy Protects Against Influenza by Promoting Lung Repair and Recovery in Females

Over 100 million women use progesterone therapies worldwide. Despite having immunomodulatory and repair properties, their effects on the outcome of viral diseases outside of the reproductive tract have not been evaluated. Administration of exogenous progesterone (at concentrations that mimic the luteal phase) to progesterone-depleted adult female mice conferred protection from both lethal and sublethal influenza A virus (IAV) infection. Progesterone treatment altered the inflammatory environment of the lungs, but had no effects on viral load. Progesterone treatment promoted faster recovery by increasing TGF-β, IL-6, IL-22, numbers of regulatory Th17 cells expressing CD39, and cellular proliferation, reducing protein leakage into the airway, improving pulmonary function, and upregulating the epidermal growth factor amphiregulin (AREG) in the lungs. Administration of rAREG to progesterone-depleted females promoted pulmonary repair and improved the outcome of IAV infection. Progesterone-treatment of AREG-deficient females could not restore protection, indicating that progesterone-mediated induction of AREG caused repair in the lungs and accelerated recovery from IAV infection. Repair and production of AREG by damaged respiratory epithelial cell cultures in vitro was increased by progesterone. Our results illustrate that progesterone is a critical host factor mediating production of AREG by epithelial cells and pulmonary tissue repair following infection, which has important implications for women’s health.


It's bad:
Error - Cookies Turned Off

Problem

Influenza infection severity may be mediated by estradiol and/or progesterone.

Method of Study
An exploratory study was designed to evaluate 17‐β‐estradiol and progesterone on influenza infection and examine immune‐mediated response in a mouse model. Inoculation with placebo or mouse‐adapted H1N1 influenza virus occurred. Treatment groups included 17‐β‐estradiol, progesterone, ovariectomy, and pregnancy. Mice were assessed for morbidity and mortality. Toll‐like receptor gene studies and airspace cell differentials were performed.

Results
Onset of morbidity was earlier and morbidity duration greater for progesterone. Absence of morbidity/mortality and overall survival was greater for 17‐β‐estradiol. Airspace cell differentials suggest improved immune cell recruitment for 17‐β‐estradiol. Pregnant mouse data demonstrate significant mortality during the period of increased progesterone. Select immune cell markers demonstrate patterns of regulation that may promote proper immune response to influenza infection for 17‐β‐estradiol.

Conclusion
Estradiol may play a protective and progesterone a detrimental role in the pathophysiology of influenza infection.

Dear Hamster,

These charlatans used progestin in their little deceptive experiment. These compounds, although considered progesterone, are not like progesterone other than the fact they bind to proteins like the real stuff. This however makes them even more dangerous than estrogen as it will inhibit true progesterone's actions.
 
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ecstatichamster
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Dear Hamster,

These charlatans used progestin in their little deceptive experiment. These compounds, although considered progesterone, are not like progesterone other than the fact they bind to proteins like the real stuff. This however makes them even more dangerous than estrogen as it will inhibit true progesterone's actions.

they did? Thank you
 
J

jb116

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they did? Thank you
Yes, in fact they start off with the word progesterone but in the full literature that's their driving argument as a reference to the progestins that are so immensely dispensed in the industry and how "useful" they are - since progesterone is, in truth, so useful. As they go along, you start seeing that its progestins they are actually using. And all their references of previous studies to confirm their own experiment is with the use of ---- progestins :)
 

schultz

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Jul 29, 2014
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2,653
I think they used actual progesterone. There is nothing to indicate they didn't, although in the discussion portion of the study they do start talking about progestins in a generalized way, which makes them look a bit incompetent. My criticism would be the way the progesterone was administered, which was via a pellet. Given how Ray has talked about how difficult it is to keep progesterone dissolved in solvent, I am not sure how well a pellet of progesterone would work or if it would crystallize at the site of insertion. (Pellet ingredients are: cholesterol, cellulose, lactose, phosphates and stearates). All of mice were OVX.

It's not clear to me that any of the mice died in the E2, P, OVX study group, unless I am missing something? If this is the case, then what they are looking for is morbidity and inflammatory markers. The E2 group had significantly higher IL-6 and TNF whereas the P group had significantly higher IL-10 inhibits and TLR-9.

Il-10 is generally considered anti-inflammatory and protects against LPS.

Anyway, that's my assessment. I'd love to hear another persons take on it though. I am probably bias.
 
J

jb116

Guest
I think they used actual progesterone. There is nothing to indicate they didn't, although in the discussion portion of the study they do start talking about progestins in a generalized way, which makes them look a bit incompetent. My criticism would be the way the progesterone was administered, which was via a pellet. Given how Ray has talked about how difficult it is to keep progesterone dissolved in solvent, I am not sure how well a pellet of progesterone would work or if it would crystallize at the site of insertion. (Pellet ingredients are: cholesterol, cellulose, lactose, phosphates and stearates). All of mice were OVX.

It's not clear to me that any of the mice died in the E2, P, OVX study group, unless I am missing something? If this is the case, then what they are looking for is morbidity and inflammatory markers. The E2 group had significantly higher IL-6 and TNF whereas the P group had significantly higher IL-10 inhibits and TLR-9.

Il-10 is generally considered anti-inflammatory and protects against LPS.

Anyway, that's my assessment. I'd love to hear another persons take on it though. I am probably bias.
The incompetence is the focal point. That right there becomes a conundrum. They mention, "The global use of progestin compounds, the prevalence of pregnancy and the composite results from these studies support the importance of further investigation to understand the underlying mechanism(s) responsible for the above findings."
That's all well and good, but in order to uphold that directive, you'd have to account for all variables. Just as one would account for variables within a single experiment, one finds themselves with a much bigger task at keeping to consistency in order to establish some scientific truth while referencing other supporting studies. So you either have "further investigation" which entails using the same materials and conditions as the ones used in your references or you concede to the fact you've changed the variables. The inconsistency to me suggests either intentional slight-of-hand or they simply botched the scientific process along the way, even if it means the stage at which you report the procedure, methods, and material. All in all, it loses credence.

Almost forgot to add: the proof that they were progestins is this: "...This study was designed to specifically evaluate the contributions of estradiol and progesterone on influenza infection by a hormonal add-back approach..."

***If you haven't guessed it, "add-back therapy" in this industry is either Aygestin or Prempro.
Aygestin is a progestin. Prempro is a combo of estrogen and progestin.

In addition to that, because several other studies exist showing this immune effect specifically citing "progestin" safe to say this study is simply useless to consider and overall a pile of crap.
 
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