Lost Smell post-Covid

AndrewGesell

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Joined
Jan 13, 2021
Messages
74
Do you know anything that can help from that Facebook group? Thanks.

I hope it will come back for you. Sounds hard to live with. Mine isn't %0. I would say smell is %20. And taste is %60. I can't smell my partner on top of my sexual problems. It feels like a nightmare.
Well people are healing from that ***t all the time. Apparently I can heal back quickly too. If it really bugs you sure you'll find an answer. Gave you my best.
 

Cooper

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Oct 12, 2020
Messages
351
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EU
Well people are healing from that ***t all the time. Apparently I can heal back quickly too. If it really bugs you sure you'll find an answer. Gave you my best.
Ivermectin pills
Methylprednisolone
Amoxicillin

Just my quick research on a Facebook group revealed these ones. The first one seems safe. Thay guy went to a holistic doctor in California and they gave him that. He says that there are even articles about it.

I think sometimes in life, even if you feel like you are living in a nightmare and that things won't get better from that point, we should always hold on to our hope and imagine the bright days are on the way... I feel like universe is testing my patience.. Do you agree?

It seems being patient is key in a lot of situations. I have been dealing with Post Accutane for 7 years since i was a 16 year old boy. I had a rough life. Kind of a life that many people killed themselves because of it. I am healing now from it, i hope this smell will also heal with it.

Amen.
 

AndrewGesell

Member
Joined
Jan 13, 2021
Messages
74
Ivermectin pills
Methylprednisolone
Amoxicillin

Just my quick research on a Facebook group revealed these ones. The first one seems safe. Thay guy went to a holistic doctor in California and they gave him that. He says that there are even articles about it.

I think sometimes in life, even if you feel like you are living in a nightmare and that things won't get better from that point, we should always hold on to our hope and imagine the bright days are on the way... I feel like universe is testing my patience.. Do you agree?

It seems being patient is key in a lot of situations. I have been dealing with Post Accutane for 7 years since i was a 16 year old boy. I had a rough life. Kind of a life that many people killed themselves because of it. I am healing now from it, i hope this smell will also heal with it.

Amen.
Ivermectin is safe. I and my whole family had taken it.
 

md_a

Member
Joined
Aug 31, 2015
Messages
468
Bradykinin is also thought to be the cause of the dry cough, lack of smell and taste
.......

A loss of smell and/or taste has been reported by some patients with COVID‐19; and, a loss of smell has been reported in patients with HAE and in persons who take ACE inhibitors. There are anecdotes of individuals experiencing extreme thirst while having COVID‐19; and, elevated BK and ACE inhibitors are associated with increased thirst.
Based on our examination of basic and clinical studies, we hypothesize that dysregulated BK signaling is involved in COVID‐19 respiratory complications for the following reasons (also see Figure 1):
The severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2), which causes COVID‐19, is known to enter host cells in the respiratory system via the transmembrane protein, angiotensin converting enzyme 2 (ACE2)

SARS‐CoV infection depletes ACE2

ACE2 depletion increases levels of des‐Arg(9)‐bradykinin (DABK), which is a bioactive metabolite of BK that is associated with lung injury and inflammation

A possible role for BK in COVID‐19 respiratory distress is consistent with established evidence that, BK, histamine, and serotonin, have for long been known as key mediators of acute lung inflammation and respiratory distress

 

AndrewGesell

Member
Joined
Jan 13, 2021
Messages
74
Bradykinin is also thought to be the cause of the dry cough, lack of smell and taste
.......

A loss of smell and/or taste has been reported by some patients with COVID‐19; and, a loss of smell has been reported in patients with HAE and in persons who take ACE inhibitors. There are anecdotes of individuals experiencing extreme thirst while having COVID‐19; and, elevated BK and ACE inhibitors are associated with increased thirst.
Based on our examination of basic and clinical studies, we hypothesize that dysregulated BK signaling is involved in COVID‐19 respiratory complications for the following reasons (also see Figure 1):
The severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2), which causes COVID‐19, is known to enter host cells in the respiratory system via the transmembrane protein, angiotensin converting enzyme 2 (ACE2)

SARS‐CoV infection depletes ACE2

ACE2 depletion increases levels of des‐Arg(9)‐bradykinin (DABK), which is a bioactive metabolite of BK that is associated with lung injury and inflammation

A possible role for BK in COVID‐19 respiratory distress is consistent with established evidence that, BK, histamine, and serotonin, have for long been known as key mediators of acute lung inflammation and respiratory distress


I took cypro for the first times last week. It definitely affected me but felt no revitalization of smell.
 

md_a

Member
Joined
Aug 31, 2015
Messages
468
I took cypro for the first times last week. It definitely affected me but felt no revitalization of smell.
SARS‐CoV infection depletes ACE2
ACE2 depletion increases levels of bradykinin
Bradykinin is thought to be the cause of lack of smell and taste
 

md_a

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Joined
Aug 31, 2015
Messages
468

Angiotensin-converting enzyme (ACE) is a zinc-dependent peptidyldipeptide hydrolase found in blood and in the endothelium of many tissues

......​

A comprehensive insight into the role of zinc deficiency in the renin-angiotensin and kinin-kallikrein system dysfunctions in COVID-19 patients​

Abstract​

Hypozincemia is prevalent in severe acute respiratory syndrome coronavirus-2 (SARS-COV-2)-infected patients and has been considered as a risk factor in severe coronavirus disease-2019 (COVID-19). Whereas zinc might affect SARS-COV-2 replication and cell entry, the link between zinc deficiency and COVID-19 severity could also be attributed to the effects of COVID-19 on the body metabolism and immune response. Zinc deficiency is more prevalent in the elderly and patients with underlying chronic diseases, with established deleterious consequences such as the increased risk of respiratory infection. We reviewed the expected effects of zinc deficiency on COVID-19-related pathophysiological mechanisms focusing on both the renin–angiotensin and kinin-kallikrein systems. Mechanisms and effects were extrapolated from the available scientific literature. Zinc deficiency alters angiotensin-converting enzyme-2 (ACE2) function, leading to the accumulation of angiotensin II, des-Arg9-bradykinin and Lys-des-Arg9-bradykinin, which results in an exaggerated pro-inflammatory response, vasoconstriction and pro-thrombotic effects. Additionally, zinc deficiency blocks the activation of the plasma contact system, a protease cascade initiated by factor VII activation. Suggested mechanisms include the inhibition of Factor XII activation and limitation of high-molecular-weight kininogen, prekallikrein and Factor XII to bind to endothelial cells. The subsequent accumulation of Factor XII and deficiency in bradykinin are responsible for increased production of inflammatory mediators and marked hypercoagulability, as typically observed in COVID-19 patients. To conclude, zinc deficiency may affect both the renin–angiotensin and kinin-kallikrein systems, leading to the exaggerated inflammatory manifestations characteristic of severe COVID-19.

Conclusion​

Both the renin-angiotensin and kinin-kallikrein systems whose dysfunction accounts for a major mechanism in COVID-19 pathophysiology, are affected by zinc deficiency, thus possibly exaggerating COVID-19 manifestations. Zinc deficiency leads to ACE2 dysfunction, enhancing its enzymatic activity, which, although not proved yet, may be responsible for increased binding to SARS-coV-2. Zinc deficiency leads to ACE2 dysfunction, possibly enhancing COVID-19-associated ACE2 downregulation. ACE2 dysfunction affects both systems leading to the accumulation of angiotensin II, des-Arg9-bradykinin and Lys-des-Arg9-bradykinin, leading to enhanced pro-inflammatory response, vasoconstriction and prothrombotic effects. In addition, zinc deficiency affects cathepsin L functions resulting in the deficiency of bradykinins at the infection site and the decrease in their vasodilation activities. Finally, zinc deficiency inhibits the contact system activation by limiting FXII activation and inhibiting HMWK, prekallikrein and FXII binding to the endothelial cells, thus enhancing FXII accumulation and bradykinin deficiency. Taken together, these effects seem to contribute to increasing the production of inflammatory mediators and to altering the coagulation parameters in COVID-19 patients. However, whether zinc supplementation in COVID-19 patients may improve the outcome remains to be established.

 

Nemo

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Jul 8, 2019
Messages
2,163
Personally, I would try progesterone and pregnenolone right on top of the olfactory bulb. (Top of your nose, right between your eyes).

It's a neural structure and Covid has neurological effects and those hormones should help with clearance of toxins.

Alternatively, if it were me, I'd try ivermectin because we know the virus can infect the olfactory nerve that leads to the olfactory bulb and brain:


Buy a tube or two of ivermectin horse paste. It's cheap. You can get it at Amazon or at a tack and feed store or farm supply store.

It has a syringe inside about the size of a short pencil. The plunger is divided into five equal markings. One marking = roughly 0.45 mg of ivermectin per kg for a 120 pound/54 kg person. That's the dose recommended by Vladimir Zelenko, MD. Adjust according to your weight.

You squeeze out the dose of white paste. It looks kind of like toothpaste and that's about how much you use. You can put it in capsules or just eat it and get it down. You use one dose per day.

The treatment is five days of this, but most people get results in two days, even from pretty bad symptoms. It kicks spike protein off your ACE2 receptors plus works like glycine to do other good anti-inflammatory things.

Okay, I have to leave now to spread progesterone on my poor mother.
 
P

Peatness

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It would be very interesting to learn what percentage of covid patients with pre existing co morbidities were taking ARBs, ACE inhibitors, or thiazides diuretics which may cause zincuria and a decrease in tissue zinc concentration. Drug induced deficiencies are so common because doctors don’t warn patients about them.
 

Nemo

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Joined
Jul 8, 2019
Messages
2,163

Angiotensin-converting enzyme (ACE) is a zinc-dependent peptidyldipeptide hydrolase found in blood and in the endothelium of many tissues

......​

A comprehensive insight into the role of zinc deficiency in the renin-angiotensin and kinin-kallikrein system dysfunctions in COVID-19 patients​

Abstract​

Hypozincemia is prevalent in severe acute respiratory syndrome coronavirus-2 (SARS-COV-2)-infected patients and has been considered as a risk factor in severe coronavirus disease-2019 (COVID-19). Whereas zinc might affect SARS-COV-2 replication and cell entry, the link between zinc deficiency and COVID-19 severity could also be attributed to the effects of COVID-19 on the body metabolism and immune response. Zinc deficiency is more prevalent in the elderly and patients with underlying chronic diseases, with established deleterious consequences such as the increased risk of respiratory infection. We reviewed the expected effects of zinc deficiency on COVID-19-related pathophysiological mechanisms focusing on both the renin–angiotensin and kinin-kallikrein systems. Mechanisms and effects were extrapolated from the available scientific literature. Zinc deficiency alters angiotensin-converting enzyme-2 (ACE2) function, leading to the accumulation of angiotensin II, des-Arg9-bradykinin and Lys-des-Arg9-bradykinin, which results in an exaggerated pro-inflammatory response, vasoconstriction and pro-thrombotic effects. Additionally, zinc deficiency blocks the activation of the plasma contact system, a protease cascade initiated by factor VII activation. Suggested mechanisms include the inhibition of Factor XII activation and limitation of high-molecular-weight kininogen, prekallikrein and Factor XII to bind to endothelial cells. The subsequent accumulation of Factor XII and deficiency in bradykinin are responsible for increased production of inflammatory mediators and marked hypercoagulability, as typically observed in COVID-19 patients. To conclude, zinc deficiency may affect both the renin–angiotensin and kinin-kallikrein systems, leading to the exaggerated inflammatory manifestations characteristic of severe COVID-19.

Conclusion​

Both the renin-angiotensin and kinin-kallikrein systems whose dysfunction accounts for a major mechanism in COVID-19 pathophysiology, are affected by zinc deficiency, thus possibly exaggerating COVID-19 manifestations. Zinc deficiency leads to ACE2 dysfunction, enhancing its enzymatic activity, which, although not proved yet, may be responsible for increased binding to SARS-coV-2. Zinc deficiency leads to ACE2 dysfunction, possibly enhancing COVID-19-associated ACE2 downregulation. ACE2 dysfunction affects both systems leading to the accumulation of angiotensin II, des-Arg9-bradykinin and Lys-des-Arg9-bradykinin, leading to enhanced pro-inflammatory response, vasoconstriction and prothrombotic effects. In addition, zinc deficiency affects cathepsin L functions resulting in the deficiency of bradykinins at the infection site and the decrease in their vasodilation activities. Finally, zinc deficiency inhibits the contact system activation by limiting FXII activation and inhibiting HMWK, prekallikrein and FXII binding to the endothelial cells, thus enhancing FXII accumulation and bradykinin deficiency. Taken together, these effects seem to contribute to increasing the production of inflammatory mediators and to altering the coagulation parameters in COVID-19 patients. However, whether zinc supplementation in COVID-19 patients may improve the outcome remains to be established.


And here's Ray's validation about using zinc.
 

Motif

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Joined
Nov 24, 2017
Messages
2,757
My cousin had it almost a year ago and smell is not back to normal still.

maybe I should consider taking the vaccine though ?
 

Motif

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Nov 24, 2017
Messages
2,757
Btw. For ACE 2 I heard at the beginning of the pandemic that hesperidin is best for this.
 

Inaut

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Joined
Nov 29, 2017
Messages
3,620
Start sniffin oil (essential oils). You may need to retrain your olfactory in addition to repleting minerals and vitamins
 

AndrewGesell

Member
Joined
Jan 13, 2021
Messages
74

Angiotensin-converting enzyme (ACE) is a zinc-dependent peptidyldipeptide hydrolase found in blood and in the endothelium of many tissues

......​

A comprehensive insight into the role of zinc deficiency in the renin-angiotensin and kinin-kallikrein system dysfunctions in COVID-19 patients​

Abstract​

Hypozincemia is prevalent in severe acute respiratory syndrome coronavirus-2 (SARS-COV-2)-infected patients and has been considered as a risk factor in severe coronavirus disease-2019 (COVID-19). Whereas zinc might affect SARS-COV-2 replication and cell entry, the link between zinc deficiency and COVID-19 severity could also be attributed to the effects of COVID-19 on the body metabolism and immune response. Zinc deficiency is more prevalent in the elderly and patients with underlying chronic diseases, with established deleterious consequences such as the increased risk of respiratory infection. We reviewed the expected effects of zinc deficiency on COVID-19-related pathophysiological mechanisms focusing on both the renin–angiotensin and kinin-kallikrein systems. Mechanisms and effects were extrapolated from the available scientific literature. Zinc deficiency alters angiotensin-converting enzyme-2 (ACE2) function, leading to the accumulation of angiotensin II, des-Arg9-bradykinin and Lys-des-Arg9-bradykinin, which results in an exaggerated pro-inflammatory response, vasoconstriction and pro-thrombotic effects. Additionally, zinc deficiency blocks the activation of the plasma contact system, a protease cascade initiated by factor VII activation. Suggested mechanisms include the inhibition of Factor XII activation and limitation of high-molecular-weight kininogen, prekallikrein and Factor XII to bind to endothelial cells. The subsequent accumulation of Factor XII and deficiency in bradykinin are responsible for increased production of inflammatory mediators and marked hypercoagulability, as typically observed in COVID-19 patients. To conclude, zinc deficiency may affect both the renin–angiotensin and kinin-kallikrein systems, leading to the exaggerated inflammatory manifestations characteristic of severe COVID-19.

Conclusion​

Both the renin-angiotensin and kinin-kallikrein systems whose dysfunction accounts for a major mechanism in COVID-19 pathophysiology, are affected by zinc deficiency, thus possibly exaggerating COVID-19 manifestations. Zinc deficiency leads to ACE2 dysfunction, enhancing its enzymatic activity, which, although not proved yet, may be responsible for increased binding to SARS-coV-2. Zinc deficiency leads to ACE2 dysfunction, possibly enhancing COVID-19-associated ACE2 downregulation. ACE2 dysfunction affects both systems leading to the accumulation of angiotensin II, des-Arg9-bradykinin and Lys-des-Arg9-bradykinin, leading to enhanced pro-inflammatory response, vasoconstriction and prothrombotic effects. In addition, zinc deficiency affects cathepsin L functions resulting in the deficiency of bradykinins at the infection site and the decrease in their vasodilation activities. Finally, zinc deficiency inhibits the contact system activation by limiting FXII activation and inhibiting HMWK, prekallikrein and FXII binding to the endothelial cells, thus enhancing FXII accumulation and bradykinin deficiency. Taken together, these effects seem to contribute to increasing the production of inflammatory mediators and to altering the coagulation parameters in COVID-19 patients. However, whether zinc supplementation in COVID-19 patients may improve the outcome remains to be established.

Wow you answered my question before I could ask it. Thank you. dont lose my sense of smell nearly as much as I used to adding oysters in regularly. I can share this with others who face this.
 

Blue Water

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Joined
Apr 26, 2020
Messages
268
What was weird was that, I initially lost my taste, but my smell was affected still. When I would exercise and cause symptoms, I'd smell this metallic smell. I thought it was an odor from my sweat. I later learned it was actually just covid messing with my olfactory center, and exercise somehow brought on a worsening of my condition.
 
Joined
Nov 21, 2015
Messages
10,501
experiencing this now. Lost all sense of smell/taste a few days ago. 10% came back the next day. Then gone. I'm working on everything including zinc and oysters now.
 

AdoTintor

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Mar 6, 2020
Messages
405
@ecstatichamster perchance, in the noble pursuit of science, you could step through the protocols starting first with what you appear to be doing already i) RP methods to boost metabolism, then progressively moving up to ii) Grouf's natural protocol (OLE, NAC, Quercetin,...), leading to iii) H1/H2 and finally iv) IVM/HCQ. It would great to see at what point the spikes get knocked off, the earlier the better for safety. I recently got these nasal pump-sprays which may be of help administrating MB, OLE etc
 

RealNeat

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Jan 9, 2019
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HI
experiencing this now. Lost all sense of smell/taste a few days ago. 10% came back the next day. Then gone. I'm working on everything including zinc and oysters now.
You had your illness a while ago, but you are experiencing this now (August 2021?)
 

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