Hydrogen Peroxide: Apparently Good for you?

They might just be trying to sell their product.
They may be selling, though they appear to know what they are talking about. I bought their toothpaste.
Mouthwash, The Silent Killer
Feb 20, 2024
Are you one of the millions who incorporate mouthwash into your daily oral care routine, believing that it’s essential for maintaining a healthy mouth?

What if I told you that this seemingly harmless habit could be doing more harm than good?

Research has shown that the regular use of antibacterial mouthwash can have detrimental effects on your oral and overall health. Not only does it disrupt your oral microbiome, literally causing bad breath and cavities, but its effects are even more far-reaching.

One study found that just seven days of using mouthwash led to a significant reduction in oral nitrite production by 90% and plasma nitrite levels by 25%. These reductions were associated with elevated blood pressure, highlighting the potential cardiovascular risks associated with mouthwash use.

Today we'll explore the disruptive impact of mouthwash on the oral microbiome, its role in inhibiting nitric oxide production, the hidden risks associated with its usage, and what to use instead to ensure a healthy mouth.

Mouthwash and the Oral Microbiome
Why is mouthwash so harmful?

The answer lies in its indiscriminate destruction of the oral microbiome—the diverse community of bacteria that inhabit our mouths and play a crucial role in maintaining our oral and overall health.

Contrary to popular belief, not all bacteria are bad; in fact, many are beneficial and help protect against harmful pathogens.

Commercial mouthwashes containing alcohol and other harsh chemicals not only kill harmful bacteria but also wipe out the beneficial bacteria that contribute to a healthy oral microbiome. This disruption can leave your mouth defenseless against cavities, gum disease, and bad breath.

Moreover, mouthwash interferes with the production of nitric oxide, a compound essential for various bodily functions, including cardiovascular health and even sexual health. Without the right balance of bacteria in the mouth, nitric oxide production may be impaired, potentially leading to issues such as high blood pressure and poor blood vessel function.

Research suggests that disruptions in the oral microbiome are also linked to conditions such as Alzheimer's disease and cardiovascular disease.

Maintaining a balanced oral microbiome is not just about fresh breath and healthy teeth; it's about supporting your body's natural functions. Disrupting this delicate balance with harsh mouthwash can have cascading effects, impacting not only your oral health but also your gut microbiome and, consequently, your overall wellbeing.

Do We Need Mouthwash?
From childhood, we've been instilled with the notion that keeping our mouths pristine and "germ-free" is paramount to good health. The mere mention of germs and bacteria often invokes images of sickness, and the looming threat of epidemics.

However, what if I told you that only 1% of bacteria are associated with disease, while the remaining 99% are benign and, in fact, beneficial to our well-being?

Surprisingly, there's a silver lining in the realm of oral health: plaque can actually be good for your teeth! A healthy oral microbiome possesses the remarkable ability to generate protective plaque, leaving your teeth feeling smooth, appearing shiny, and exuding cleanliness.

But where does this thriving oral microbiome originate? It's rooted in the good bacteria naturally present in your mouth.

Where did the idea of mouthwash even come from?

Surprisingly, the first mouthwash was created in 1879 and was formulated as a surgical antiseptic. In spite of its known antimicrobial properties it was thought of as a product in search of a use and promoted as a deterrent for halitosis and a floor cleaner.

Which sounds about right because that’s exactly what it does - it wipes your microbiome CLEAN of ALL bacteria - the good and the bad.

Laden with alcohol and harsh chemicals, these products indiscriminately eradicate not only harmful bacteria but also the beneficial ones. As a result, your mouth is left defenseless, susceptible to the onslaught of cavities, gum disease, and persistent bad breath.

Harmful Ingredients in Commercial Mouthwash
Commercial mouthwashes often contain a cocktail of synthetic chemicals, some of which can pose significant risks to your health. Here are a few key ingredients to be wary of:

Alcohol: Linked to liver failure, gastrointestinal issues, and even potential blindness or death.
Chlorine dioxide: Associated with severe vomiting, diarrhea, and liver failure.
Chlorhexidine: Known side effects include tooth and tongue staining, mouth sores, increased tartar, and tongue swelling.
Cocamidopropyl betaine: Can cause skin discomfort and eye irritation.
Parabens: Linked to cancer and allergic reactions, manifesting as itching, bumps, or burning of the skin.
These are just a few examples of the harmful ingredients commonly found in commercial mouthwash formulations. By opting for natural alternatives, you can protect your oral and overall health from unnecessary risks.

The Detrimental Effects of Alcohol and Non-Alcohol Mouthwash
By now you can see how alcohol-based mouthwashes have many negative effects on your health, but they aren't the only culprits when it comes to oral health hazards. Even non-alcohol varieties can wreak havoc on your oral and systemic well-being.

Here are some detrimental effects to consider:

Disruption of the Oral Microbiome

Any type of mouthwash, whether alcohol-free or containing alcohol, may indiscriminately kill off a high number of bacteria in your mouth. While some bacteria in your mouth can contribute to cavities and bad breath, others are vital components of your oral microbiome. This microbial community helps break down food and maintains healthy teeth and gums.

Regularly eliminating all bacteria in your mouth can disrupt this delicate balance, potentially leading to oral health issues.

Teeth Staining

The most common side effect of using mouthwash, according to a 2019 review, is teeth staining. Mouthwashes containing an ingredient called chlorhexidine (CHX), available only by prescription, are more likely to cause temporary teeth staining after use.

Additionally, mouthwashes that contain bright dyes are more likely to cause staining than dye-free alternatives, not to mention the potential toxicity of the chemicals that make up those dyes!

Increased Cancer Risk

Some mouthwashes may contain synthetic ingredients that have been linked to an increased risk of certain cancers. A 2016 study concluded that people who regularly use mouthwash may have a slightly elevated risk of head and neck cancers compared to those who never used mouthwash.

Most mouthwashes contain alcohol, a known cause of head and neck cancer (oral cavity, pharynx, larynx), likely through the carcinogenic activity of acetaldehyde, formed in the oral cavity from alcohol.

Further research is needed to understand the true extent of this risk and which ingredients may contribute to it.

Promoting Oral Health Naturally
As we have discussed, mouthwash, in addition to the risks associated with regular use, is not even effective at preventing or fixing the very thing people use it for - bad breath, and prevention of cavities and gum disease.

It’s time to ditch the toxic mouthwash and replace it with an oral care routine that helps your mouth to thrive - preventing cavities, gum disease and bad breath - naturally.

You might be wondering where you start, and we always recommend detoxing your mouth and re-establishing a healthy microbiome. The first step is with our Dental Detox Kit which is meticulously crafted to keep your oral microbiome balanced and thriving. The kit is a 60-day supply that contains our Dirty Mouth Toothpowder, Gum Drops, Bamboo Charcoal Floss Picks, Bamboo Toothbrush and Copper Tongue Scraper.

The Dirty Mouth Toothpowder is made with 3 detoxifying and remineralizing clays, nano-hydroxyapatite (the same mineral your teeth are made of), and baking soda to promote mouth alkalinity. This replaces your "toxi-paste" toothpaste.

Our Gum Drops are made with 11 essential oils to create a healthy balance of good bacteria inside your mouth, getting rid of toxins and impurities found on the surface of your teeth and gums.

Complete your routine with our Bamboo Charcoal Dental Picks and Copper Tongue Scraper, and you’ll be left with a detoxified mouth, strong teeth, and fresh breath!

With the Dental Detox Kit, you’ll revel in the assurance that you're not just nurturing your mouth, but also supporting optimal nitric oxide production.

Take Action for Your Oral Health
Mouthwash may seem like a harmless addition to your oral care routine, but its potential risks extend far beyond the confines of your mouth. From disrupting essential bacterial communities to compromising nitric oxide production, the consequences of regular mouthwash use are cause for concern.

It's time to take proactive steps towards healthier oral care practices. By prioritizing natural oral care alternatives, you not only safeguard your oral health but also contribute to your overall well-being. Embracing products free from toxic chemicals can nurture your mouth's delicate ecosystem and promote a balanced oral microbiome.

Remember, your oral health is not just about a bright smile—it's a cornerstone of vitality and longevity. By supporting your body's innate processes, such as nitric oxide production, you empower yourself to live a healthier, more vibrant life.

So, before you reach for that bottle of mouthwash, consider the broader implications for your health. Your body—and your smile—will thank you.



REFERENCES















Mouthwash use and cancer of the head and neck: a pooled analysis from the International Head and Neck Cancer Epidemiology Consortium (INHANCE) - PMC
 
They may be selling, though they appear to know what they are talking about. I bought their toothpaste.
I’ve been thinking about it all day and now I’m really sceptical about anything I put in my mouth to clean it, even coconut oil, it too has antibacterial properties.

How have you found their toothpaste?
 
Been using (comercial )toothpaste with sodium bicarbonate doing well fwiiw , one trick that helps with oral health is avoiding doing washes , immediately after meals , which has altered ph after meals ( link , this may help , Dr. Nick Z. with some hints )
 
I’ve been thinking about it all day and now I’m really sceptical about anything I put in my mouth to clean it, even coconut oil, it too has antibacterial properties.

How have you found their toothpaste?
I bought their toothpaste for nanoxim hydroxyapatite, which I mentioned here. They were the only 1 that had clean ingredients with nanoxim hydroxyapatite. I haven't really noticed a difference in the short time that I've been using it, though the main reason I got it is to prevent cavities and strengthen enamel.
 
I bought their toothpaste for nanoxim hydroxyapatite, which I mentioned here. They were the only 1 that had clean ingredients with nanoxim hydroxyapatite. I haven't really noticed a difference in the short time that I've been using it, though the main reason I got it is to prevent cavities and strengthen enamel.
I recall your thread on this, got me thinking about making my own toothpaste, then life got in the way, but now I’ve ordered some of what you’re using and will try it out too. I have sensitive gums since I was a teen and wisdom teeth came through impacting all of my teeth.
Thanks for this, spurring me on, and all the other info you’ve posted.

As far as HP is concerned, I’m going to try it as a ingestible to see if I can improve some health issues I haven’t been able to get on top of for a long time, mainly lack of energy and lethargy and some recurring candida problems. I ordered a 35% solution and will follow the protocol mentioned earlier in this thread.
 
Xylitol gum is suggested after meals because it stimulates the release of saliva without feeding bacteria. This means you can essentially rinse your mouth with saliva, leaving it with a good pH so remineralization can continue undisturbed. I find it is more helpful when the bad bacteria are more or less in control, but doesn't serve as much a purpose when the bad bacteria are not likely to quickly colonize. Still, rinsing with saliva is better for remineralization than rinsing with anything else most likely.
 
Well thank you Gaby for your wealth of knowledge, I will stop immediately. It’s something I’ve only started doing in the past week so hopefully I haven’t caused too much damage 🙏
Primal Life provided this do it yourself mouthwash recipe.
Commercial mouthwash products try to position themselves as beneficial anti-cavity solutions, but the truth is that they’re actually bad for your mouth! The harsh ingredients found in regular mouthwash formulas destroy all bacteria in your mouth- even the good bacteria that you need to fight toxins.

You can save yourself from unnecessary dental trauma by making your own mouthwash instead. You only need essential oils, filtered water, and baking soda to make a powerful DIY mouthwash.

Essential oils like tea tree and peppermint naturally fight bacterial infections and kill oral pathogens while nurturing tissue regeneration. As a result, essential oils offer a safe, natural, and powerful way to counteract gingivitis, reduce inflammation, and prevent the conditions that plaque and tartar love.

Blend the following ingredients to make your own remineralizing mouthwash:

2 drops tea tree essential oil
2 drops peppermint essential oil
½ cup of filtered water
pinch of Himalayan sea salt
2 tsp baking soda

**If using salt, heat water and dissolve the salt, let cool. Add baking soda and essential oils.

Just swish and spit twice a day to combat unwanted plaque and keep your smile looking as happy as you feel. You can even put some in a to-go spray bottle and "freshen on the go"!
I think this means the PerioBrite mouthwash I use sometimes is ok.
 
(Joe) What kind of treatments would be effective against such a critter?

A: Vit C and oxygen.

I wonder if this combination would create H2O2 in the body?


H2O2 is good against viruses and other pathogens:


Polyphenols from coffee and green tea can also create H2O2:

 
What session is that from? Thanks for the information.

Session 23 April 2022:

(Gaby) In a prior session, they were saying it was not mostly the US experiments that were a threat to humanity, but instead a space virus. So, if that's the case, in theory if there's a 4th density STS virus coming up, will it be a DNA or an RNA virus?

A: RNA.

Q: (Gaby) And what kind of disease will it produce?

A: Most likely to be similar to primitive smallpox.

Q: (Pierre) Primitive smallpox is nasty. It's a descendant of the Black Death.

(L) I think we decided that primitive smallpox was the Black Death.

(Gaby) Smallpox is a DNA virus. So if this is an RNA virus, it could be nastier I suppose.

(Pierre) With 79% death rate, it's nasty.

(Joe) What kind of treatments would be effective against such a critter?

A: Vit C and oxygen.
 
There seems to be a simple way (if you have necessary equipment) to create H2O2 in the body:

Thus the H2O2 concentration in brains of rats exposed to room air is calculated to be about 7.7 pM, rises 60% when O2 tension is increased to 100% O2, and increases 300% at 3 ATA 100% O2, where symptoms of central nervous system toxicity first become apparent. These studies support the concept that H2O2 is an important mediator of O2-induced injury to the central nervous system.

 
There seems to be a positive relation between H2O2 and iodine:

Lactoperoxidase (1.11.1.7, LPO) is a mammalian heme peroxidase observed in most mammals except some rodents. It is secreted from mammary, salivary, and other mucosal glands including the lungs, bronchi, and nasal passages.1 LPO is a member of the innate immune system and acts as a natural defense against bacterial and viral agents.2 It utilizes hydrogen peroxide (H2O2) to convert thiocyanate (SCN−) and iodide (I−) ions into the harsh antimicrobial compounds, hypothiocyanite (OSCN−)3, 4 and hypoiodite (IO−).5, 6

One would think the strong oxidizing agent H2O2 itself should be capable of destroying most invasive microbes, but nature has provided a strong defense against H2O2 destruction by the dismutase activity of the highly active enzyme catalase, found in almost all cellular life. The noxious ions OSCN− and OI− are therefore required to circumvent H2O2 inactivation and are produced as the first line of mammalian defense against airborne microbes including viral agents.

It is clear from present observations that in the presence of H2O2, iodide is converted into hypoiodite and the protective effects of the oxidized iodide have already been enumerated.34 It was reported that hypoiodite ions very rapid oxidize thiol groups, irreversibly oxidize both NAD(P)H and β-nicotinamide mononucleotide, react directly with thioether groups to produce sulfoxides and stimulate the oxidation of the primary amine moieties.34-37 These quick, irreversible effects of hypoiodite and hypothiocyanite results in elimination of many microbial pathogens.20, 38-40

The present studies clearly show that LPO with H2O2 converts iodide into hypoiodite. We emphasize here that the production of strong oxidants by the lactoperoxidase system (LPO + H2O2 + SCN−/I−) plays a powerful role in the innate immune defense against pathogenic bacteria, fungi, viruses, and parasites. This means that LPO is an indispensable enzyme in the fight against microbial infections and the iodine supplementation is a practical means of supporting this protection.


 
Lactoperoxidase (LPO) is an enzyme found in several exocrine secretions including the airway surface liquid producing antimicrobial substances from mainly halide and pseudohalide substrates. Although the innate immune function of LPO has been documented against several microbes, a detailed characterization of its mechanism of action against influenza viruses is still missing. Our aim was to study the antiviral effect and substrate specificity of LPO to inactivate influenza viruses using a cell-free experimental system. Inactivation of different influenza virus strains was measured in vitro system containing LPO, its substrates, thiocyanate (SCN⁻) or iodide (I⁻), and the hydrogen peroxide (H2O2)-producing system, glucose and glucose oxidase (GO). Physiologically relevant concentrations of the components of the LPO/H2O2/(SCN⁻/I⁻) antimicrobial system were exposed to twelve different strains of influenza A and B viruses in vitro and viral inactivation was assessed by determining plaque-forming units of non-inactivated viruses using Madin-Darby canine kidney cells (MDCK) cells. Our data show that LPO is capable of inactivating all influenza virus strains tested: H1N1, H1N2 and H3N2 influenza A viruses (IAV) and influenza B viruses (IBV) of both, Yamagata and Victoria lineages. The extent of viral inactivation, however, varied among the strains and was in part dependent on the LPO substrate. Inactivation of H1N1 and H1N2 viruses by LPO showed no substrate preference, whereas H3N2 influenza strains were inactivated significantly more efficiently when iodide, not thiocyanate, was the LPO substrate. Although LPO-mediated inactivation of the influenza B strains tested was strain-dependent, it showed slight preference towards thiocyanate as the substrate. The results presented here show that the LPO/H2O2/(SCN⁻/I⁻) cell-free, in vitro experimental system is a functional tool to study the specificity, efficiency and the molecular mechanism of action of influenza inactivation by LPO. These studies tested the hypothesis that influenza strains are all susceptible to the LPO-based antiviral system but exhibit differences in their substrate specificities. We propose that a LPO-based antiviral system is an important contributor to anti-influenza virus defense of the airways.


This is good news, but when you look how much of hypoiodite is produced in the human body you can see that there is a wide variation:


Obviously, increasing the production or decreasing the destruction of H2O2 should increase the production of hypoiodite.
 
Catalase enzyme prevents excessive accumulation of the strongly oxidizing agent H2O2 which otherwise can do damage to the cells. Because of this preventive effect of catalase, important cellular processes which generate H2O2 as a by-product can proceed safely. Biochemical analysis of catalase has shown that it binds endogenously to 24,25(OH)2D3 [26]. In our results, the catalase enzyme activity was significantly reduced in the presence of [1,25(OH)2D3], while the cultures treated with hydrogen peroxide alone showed a marked increased level of catalase enzyme in the cell pellet. This finding again showed the antioxidant nature of Vitamin D3 metabolite which is protecting neuronal cells from the harmful effect of H2O2. In the absence of Vitamin D3 treatments to the neuronal cells, H2O2 caused a significant upregulations of catalase enzyme in order to neutralize its damaging effect to the neurons.


In the current work, we report that an endogenous binding protein for 24,25(OH)2D3 is catalase, based on sequence analysis of the isolated protein. Additional studies indicated that 25(OH)D3 was an effective competitor for binding, whereas 1,25(OH)2D3 only poorly displaced [3H]24,25(OH)2D3. The data suggest that signal transduction may occur through modulation of hydrogen peroxide production.


In intestine, 24,25(OH)2D3, which is made under conditions of calcium-, phosphate-, and 1,25(OH)2D3 sufficiency, inhibits the stimulatory actions of 1,25(OH)2D3 on phosphate and calcium absorption. In the current work, we provide evidence that 24,25(OH)2D3-mediated signal transduction occurs mechanistically through increased H2O2 production which involves binding of 24,25(OH)2D3 to catalase and resultant decreases in enzyme activity. Physiological levels of H2O2 mimicked the action of 24,25(OH)2D3 on inhibiting 1,25(OH)2D3-stimulated phosphate uptake in isolated enterocytes. Moreover, the molecular basis of such inhibition was suggested by the presence of two thioredoxin domains in the 1,25D3-MARRS protein/ERp57: Exposure of cells to either 24,25(OH)2D3 or H2O2 gradually reduced 1,25(OH)2D3 binding to 1,25D3-MARRS protein, between 10 and 20 min of incubation, but not to VDR. Feeding studies with diets enriched in the antioxidants vitamins C and E showed that net phosphate absorption in vivo nearly doubled relative to chicks on control diet. Antioxidant diets also resulted in increased [3H]1,25(OH)2D3 binding to both 1,25D3-MARRS and VDR, suggesting benefits to both transcription- and membrane-initiated signaling pathways. Intriguingly, phosphorous content of bones from birds on antioxidant diets was reduced, suggesting increased osteoclast activity. Because mature osteoclasts lack VDR, we analyzed a clonal osteoclast cell line by RT-PCR and found it contained the 1,25D3-MARRS mRNA. The combined data provide mechanistic details for the 1,25(OH)2D3/24,25(OH)2D3 endocrine system, and point to a role for the 1,25D3-MARRS protein as a redox-sensitive mediator of osteoclast activity and potential therapeutic target.


The steroid hormone 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] rapidly stimulates the uptake of phosphate in isolated chick intestinal cells, while the steroid 24,25-dihydroxyvitamin D3 [24,25(OH)2D3] inhibits the rapid stimulation by 1,25(OH)2D3. Earlier work in this laboratory has indicated that a cellular binding protein for 24,25(OH)2D3 is the enzyme catalase. Since binding resulted in decreased catalase activity and increased H2O2 production, studies were undertaken to determine if pro-oxidant conditions mimicked the inhibitory actions of 24,25(OH)2D3, and anti-oxidant conditions prevented the inhibitory actions of 24,25(OH)2D3. An antibody against the 24,25(OH)2D3 binding protein was found to neutralize the inhibitory effect of the steroid on 1,25(OH)2D3-mediated 32P uptake. Incubation of cells in the presence of 50 nM catalase was also found to alleviate inhibition. In another series of experiments, isolated intestinal epithelial cells were incubated as controls or with 1,25(OH)2D3, each in the presence of the catalase inhibitor 3-amino-1,2,4-triazole, or with 1,25(OH)2D3 alone. Cells exposed to hormone alone again showed an increased accumulation of 32P, while cells treated with catalase inhibitor and hormone had uptake levels that were indistinguishable from controls. We tested whether inactivation of protein kinase C (PKC), the signaling pathway for 32P uptake, occurred. Incubation of cells with phorbol-13-myristate (PMA) increased 32P uptake, while cells pretreated with 50 µM H2O2 prior to PMA did not exhibit increased uptake. Likewise, PMA significantly increased PKC activity while cells exposed to H2O2 prior to PMA did not. It is concluded that catalase has a central role in mediating rapid responses to steroid hormones.


It seems that vitamin D can help us to decrease catalase and increase H2O2.
 
I wrote before about how cholecalciferol is not very good at raising calcitriol, but in this case we don't want to raise calcitriol but 24,25(OH)2D3, and for that the cholecalciferol is a great solution. So it all depends on what you want to raise.

Hormonal regulation of calcium (Ca) absorption was investigated in a cholecalciferol (vitamin D(3))-supplemented group (hVitD) vs. a control group (cVitD) of growing Great Danes (100 vs. 12.5 micro g vitamin D(3)/kg diet). Although Ca intakes did not differ, fractional Ca absorption was significantly lower in the hVitD group than in the cVitD group. There were no differences in plasma concentrations of Ca, inorganic phosphate, parathyroid hormone, growth hormone or insulin-like growth factor I between groups. Plasma 25-hydroxycholecalciferol [25(OH)D(3)] concentrations were maintained in the hVitD dogs at the same levels as in the cVitD dogs due to increased turnover of 25(OH)D(3) into 24,25-dihydroxycholecalciferol [24,25(OH)(2)D(3)] and 1,25-dihydroxycholecalciferol [1,25(OH)(2)D(3)]. In hVitD dogs, the greater plasma 24,25(OH)(2)D(3) concentration and the enhanced metabolic clearance rate (MCR) of 1,25(OH)(2)D(3) indicated upregulated 24-hydroxylase activity. The increased MCR of 1,25(OH)(2)D(3) decreased plasma 1,25(OH)(2)D(3) concentrations. In hVitD dogs, the greater production rate of 1,25(OH)(2)D(3) was consistent with the 12.9-fold greater renal 1alpha-hydroxylase gene expression compared with cVitD dogs and compensated to a certain extent for the accelerated MCR of 1,25(OH)(2)D(3). The moderately decreased plasma 1,25(OH)(2)D(3) concentration can only partially explain the decreased Ca absorption in the hVitD dogs. Intestinal vitamin D receptor concentrations did not differ between groups and did not account for the decreased Ca absorption. We suggest that 24,25(OH)(2)D(3) may downregulate Ca absorption.


 
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