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A forum investigating the similarities between COVID-19 and fluoride poisoning, thyroid dysfunction and Gq/11 pathways.
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Forum Overview

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© 2020 PFPC - May 17, 2020
Last Entry Update: May 5, 2024

This forum investigates the pathophysiology of COVID-19 and compares findings to fluoride poisoning, pathways involving Gq/11 proteins, and the moderating/regulating effects of thyroid hormones.

We look at key events in cells, tissues, and the body's immune system, and list the literature documenting the similarities. It is an ongoing project - a collection of notes, for the time being.


While originally described as a disease causing acute-respiratory-distress-syndrome (ARDS), it is now believed that COVID-19 may involve multi-organ damage (Wang et al., 2020; Haeck et al., 2020; Atri et al., 2020; Qin et al., 2020). However, it is claimed that the pathways involving these varied conditions are not yet understood. There are over 2100 ongoing clinical trials underway, but to date none of these drugs have consistently proven effective (Liu et al., 2020). [UPDATE Sept. 2021: there are now over 8000 trials - Ed.]

In this forum, we hope to be able to show that pathways activated by aberrant Gq/11 signaling are at the core of both COVID-19 and fluoride poisoning and further, that these same pathways are regulated by thyroid hormones and TSH, the thyroid-stimulating hormone. Gq/11 are one of the four G protein families.

We have been able to trace almost all aspects of COVID-19 pathophysiology to pathways that are downstream of Gq/11 activation. As numerous agents already exist that target Gq/11 we hope that the information in this forum will contribute to finding effective therapeutic agents not just for COVID-19, but also for fluoride poisoning.

COVID-19 and Fluorosis

When we first researched COVID-19 and the pathways involved, we immediately noticed similarities to fluoride poisoning, or fluorosis.

For example, the pathways leading to lung conditions/damage observed in COVID-19 patients (Xiong et al., 2020) appear identical to those observed in workers exposed to fluorides (Wen et al., 2019).

Consider the following two statements:
"SARS-CoV-2 induced activation of apoptosis and P53 signalling pathway in lymphocytes may be the cause of patients' lymphopenia".
(Xiong et al., 2020)
"Long-term exposure to low level of fluoride induces apoptosis via p53 pathway in lymphocytes of aluminum smelter workers".
(Wen et al., 2019)

SEE: viewtopic.php?f=66&t=1881

This was clear first evidence that some aspects of COVID-19 and fluoride poisoning involved overlapping or similar pathways. Further evidence was found rather easily, once we started looking for it.

Both, COVID-19 and fluoride poisoning, exhibit elevated levels of inflammatory biomarkers and cytokines, including IL-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-α, and interleukin (IL)-2R (Atri et al., 2020; Qin et al., 2020; Varol et al., 2012; Lu et al., 2017; Sana et al., 2017; Afolabi et al., 2013).

Further, both increase NF-kappa B and cardiac troponins (Balsal, 2020; Oyagbemi et al., 2020; Wang et al., 2018; Sana et al., 2017).

IL-10 and TGF-b levels are also altered in both COVID-19 and fluoride poisoning (Wan et al., 2020; Xiong et al., 2020; Luo et al., 2017; Zhang et al., 2019).

There are other similarities.

As has been shown in animal studies of fluoride poisoning, liver damage is observed in some COVID-19 patients. Levels of ALT, AST, GGT are elevated in both conditions while albumin levels are reduced (Wang et al., 2020; Sun et al., 2020; Gu et al., 2020; Lu et al., 2017; Zhao et al., 2014; Kessabi et al., 1983; Xiong et al., 2007).

Blacks, who have a more sensitive thyroid status than whites, are at increased risk in both conditions (Millett et al., 2020; Akinkugbe et al., 2014).

Like in COVID-19, fluoride is more dangerous in patients suffering from glucose-6-phosphate dehydrogenase (G6PD) deficiency (Pornprasert et al., 2017; Kassi et al., 2020).

Numerous therapeutic agents proposed for treatment in COVID-19 have also been used to alleviate fluoride toxicity, such as resveratrol (Magrone at., 2020; Suzuki et al, 2018), melatonin (Martín Giménez et al., 2020; Zhao et al., 2017; Sana et al., 2017; Kumar et al., 2019), N-acetylcysteine (Assimakopoulos, 2020; Pawłowska-Góral et al., 2013), quercetin (Derosa et al., 2021; Nabavi et al., 2011), and Vitamin D (Martín Giménez et al., 2020; Kumar et al., 2012). Vitamin D deficiency is thought to be a risk factor in both conditions (Mitchell, 2020; Bondu et al., 2019).


We further focused our research on the G proteins Gq/11, as we have learned over the past 20 years that the majority of fluoride toxicity occurs via pathways regulated by the Gq/11 subfamily of G proteins. In biochemistry, fluoride is known as the "universal G protein activator", meaning it can act on all four G protein families. In the human body, the TSH receptor is the only known G-protein-coupled-receptor known to activate all four G protein families. Fluoride has been used as a TSH analogue in hundreds of studies.
We then investigated the role of thyroid hormones and thyroid status, comparing to diagnostic findings in COVID-19.

Each forum entry will list the correlations of COVID-19, fluoride poisoning, Gq/11 involvement, and thyroid hormones.

We will post as much of our research as we can - time permitting, in the hopes that it might be of benefit to all. Some of our friends in the scientific community are currently looking for therapeutic agents to combat COVID-19.

Perhaps this information might also alert others to the toxicity of fluoride, and help shed more light on the many adverse health effects caused by fluoride.

So far, not one study has yet investigated COVID-19 effects on the thyroid or tested for thyroid hormones and TSH levels in COVID-19 patients. [UPDATE Aug 20, 2020: The first study was e-published in July 2020, and more and more research is now being conducted. For the latest news, please see viewtopic.php?f=66&t=2040]

Topics in this forum:

Lung Damage: Apoptosis & p53 activation. viewtopic.php?f=66&t=1881
Cardiac Injury: Cardiac Troponins. viewtopic.php?f=66&t=1883
Renin-Angiotensin System (Ras)
Ras and ACE2
- ACE2/Mas
Angiotensin-II Type 1 Receptor - AT1R. viewtopic.php?f=66&t=4542
IL-2. viewtopic.php?f=66&t=1915
IL-6. viewtopic.php?f=66&t=1881
IL-8. viewtopic.php?f=66&t=1940
IL-10. viewtopic.php?f=66&t=1933
IL-17/TH17. viewtopic.php?f=66&t=2001
INF (Interferon). viewtopic.php?f=66&t=3665
NF-kappa B. viewtopic.php?f=66&t=1888
C-Reactive Protein (CRP). viewtopic.php?f=66&t=1886
Tumor Necrosis Factor (TNF-α). viewtopic.php?f=66&t=1895
TGF-b. viewtopic.php?f=66&t=1930
p21. viewtopic.php?f=66&t=1928
PAK1. viewtopic.php?f=66&t=1924
ERK/MAPK. viewtopic.php?f=66&t=1930
CD4. viewtopic.php?f=66&t=1941
CD8. viewtopic.php?f=66&t=1942
Creatine Kinase. viewtopic.php?f=66&t=1999
GGT. viewtopic.php?f=68&t=2000
DNMT3A. viewtopic.php?f=66&t=2480
Bradykinin. viewtopic.php?f=66&t=2571
RAGE. viewtopic.php?f=66&t=2751
Obesity. viewtopic.php?f=66&t=2757
NRF2. viewtopic.php?f=66&t=3039
IRE1. viewtopic.php?f=66&t=3116
VCAM-1. viewtopic.php?f=66&t=3522
PECAM-1. viewtopic.php?f=66&t=3521
SIRT1. viewtopic.php?f=66&t=3646
Virus Replication and Ca2+
LDH. viewtopic.php?f=66&t=3426
Thyroid Disease
Alzheimer's Disease. viewtopic.php?f=66&t=4210
- Resveratrol. viewtopic.php?f=66&t=1900
- FR900359.
- Melatonin. viewtopic.php?f=66&t=1920
- Vitamin D. viewtopic.php?f=66&t=1944
- Cathepsin L
- N-acetylcysteine. viewtopic.php?f=66&t=2006
- Dexamethasone. viewtopic.php?f=66&t=2196
- Quercetin. viewtopic.php?f=66&t=3007&p=3525#p3525
- Selenium. viewtopic.php?f=66&t=3116
- Fluvoxamine/fluoxetine. viewtopic.php?f=66&t=3810&p=4508#p4508
Age and the Immune System.
PFAS. viewtopic.php?f=66&t=2761
Blacks. viewtopic.php?f=66&t=1943
Glucose-6-phosphate dehydrogenase (G6PD) deficiency. viewtopic.php?f=66&t=1887
GABA. viewtopic.php?f=66&t=3605
Liver Function. viewtopic.php?f=66&t=1945
AST. viewtopic.php?f=66&t=1891
ALT. viewtopic.php?f=66&t=3575
LDH. viewtopic.php?f=66&t=1991
LPS - Endotoxin. viewtopic.php?f=66&t=5143
Kawasaki Disease
Histamine. viewtopic.php?f=66&t=3036&p=3586#p3586
Thrombosis. viewtopic.php?f=66&t=1884
Hyposmia. viewtopic.php?f=68&t=1958
Blood Pressure. viewtopic.php?f=68&t=1973
Myocarditis/Pericarditis. viewtopic.php?f=66&t=3483
Myelitis/MS/CNS. viewtopic.php?f=66&t=3566
Menstrual Changes. viewtopic.php?f=66&t=3642
Endothelin-1 (ET-1). viewtopic.php?f=66&t=4202
IgG4 RD. viewtopic.php?f=66&t=4933
Angiotensin-II Type 1 Receptor - AT1R. viewtopic.php?f=66&t=4542
The 3rd Loop
PINK1/Parkin Pathway. viewtopic.php?f=66&t=5756
- Diabetes. viewtopic.php?f=66&t=2048
- Heart Disease. viewtopic.php?f=66&t=2052
- Atherosclerosis. viewtopic.php?f=66&t=2050
- Kidney Injury. viewtopic.php?f=66&t=2058
- Metabolic Syndrome. viewtopic.php?f=66&t=3592

Numerous questions/discussion points:

1) Two conditions - COVID-19 and fluoride poisoning - apparently involve similar damage in various organs, as can be witnessed in many studies from around the world. In contrast to COVID-19, fluoride poisoning has been largely neglected and adverse health effects of fluoride are often downplayed by many Western public health agencies. Fluorosis is endemic in at least 25 countries across the globe, China and India being the worst affected (Pramanik, 2017). In India alone, 62 million people are affected, 6 million of whom are children under 14 years old (Srikanth, 2009). Even in Western countries, fluoride poisoning is ever-increasing. The majority of US teens now have dental fluorosis - a sign that fluoride intake was excessive during crucial times of development (Wiener et al., 2018).

2) The two conditions share identical pathways. If treatments work in the fight against COVID-19, is it possible that they might also be of benefit in fluoride poisoning? And vice versa? Could the vast amount of research on fluoride effects be of benefit in assessing COVID-19? Would/could treatment involve specific inhibitors of the Gq/11 family? Correction of thyroid status?

3) Are those living in endemic fluorosis or iodine-deficient areas at higher risk of COVID-19 infection? Increased organ damage? Does altitude play a role?

4) As the involvement of thyroid hormones can be documented - does thyroid status influence disease severity in COVID-19, as it does in fluoride poisoning? Serum ACE activities change in proportion to thyroid hormone levels. What effects does COVID-19 have on the thyroid and thyroid hormone metabolism?

PFPC Canada - May 17, 2020

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