Do you have the right genes for ozone therapy?

by | May 4, 2017 | 5 comments

If you have suffered from a condition like Lyme disease or chronic fatigue and have tried many interventions without the expected success, you might have come across the idea that your genes are to blame.
 
Many people these days think that our genes determine the success of a therapy and that in order to find that right one, one has to act in accordance with one’s DNA.
 
For a successful ozone therapy the right genes are supposedly intact SOD variants.
 
Some people assume that ozone therapy creates oxidative stress and that without proper genetic defenses, we could cause damage: burn our cells or induce debilitating Herxheimer reactions with too much of a good thing.
 
Is there something to it?
 
Let’s take a look.

SOD – What does it mean and what does it do? 

First, let’s get some of the abbreviations out of the way:

SOD stands for superoxide dismutase.

It is an enzyme which scavenges the free oxygen radical superoxide O2-. Without SOD, superoxide O2- would cause some serious damage to cells.

Consequently, it is assumed that an impaired SOD gene would lead to a lack of SOD enzymes and so to too many superoxide radicals and hence cause too much oxidation. An overactive SOD gene could lead to an overabundance of SOD enzymes and hence to less superoxide radicals and in turn to a better protection against oxidant radicals.

There are three different types of SOD enzymes: SOD1, SOD2, and SOD3.

 

SOD enzymes

Some colorful drawings to keep you from falling asleep: SOD1 is also called CuZnSOD, because it contains copper and zinc. It is mostly found inside cells. SOD2 is also called MnSOD, because it contains manganese, it is mostly found in the mitochondria. SOD3 is also called ECSOD because it is found in extracellular fluid. It also contains zinc and copper. Source: Wikipedia.

SNP stands for single nucleotide polymorphism and is a fancy name for a variant of a gene. SOD genes also have different variants, or different SNP.
 
There are many different SNPs. In order to keep track of them, one has assigned an ID number to each SNP. The SNP ID numbers start with “rs”. Assigning numbers to each SNP makes it easy to search for them in a data base.
 

What does it mean to be homozygous or heterozygous for an SOD gene?

Now, let’s say you have received your genetic test results and next to one of the SOD variants you see two big pluses on a red background. It can look quite alarming, like this one:
 
 
This example shows that the person, is homozygous for three different variants of the SOD2 gene: rs2758331, rs2855262, rs4880.
 
Homozygous means in this case that the person has received the same variant of the gene from both parents. Heterozygous would be if she had received a different variant from her mother and a different from her father.
 
In any case, the red color and the two pluses seem to insinuate that there is some emergency situation present.
 
Is this really the case?
 

Your test shows alleles not mutations

One of the first things to know is your consumer DNA test shows alleles not mutations of genes.
 
What is the difference?
 
Alleles are common variants of genes. Like blue or green eyes, they do not code for diseases. Having blue or brown eyes is not something that impacts your health. It is just a benign variation of a trait.
 
Mutation means a permanent change of your DNA which causes a disease. It is something bad. Like for example G6PD deficiency: this results in a condition which does not allow you to consume certain beans or receive certain medications since it could result in uncontrolled bleeding. If you have this mutation, your body is unable to produce the G6PD enzyme and you need to be careful what you consume.
 
So even if you are homozygous negative or positive for a certain SNP of an allele it does not mean that the given gene variant is suppressed to the point of causing an actual disease. It can even mean that it is overexpressed, since as this blogger points out:
 

“SOD1 polymorphisms, like many enzyme polymorphisms, can be either and [sic] up-regulation or a down-regulation of enzyme activity.”

https://www.geneticlifehacks.com/sod1-gene-polymorphisms/

So being homozygous positive for a certain SOD variant could mean that you are actually overexpressing that variant! And that instead of believing that you are burning up with oxygen you might be actually overprotected from oxidative stress.
 
Darn it, that kind of messes up the “Let’s interpret our snipses” fun a little bit, I find.
 
Yes, there is a link to SOD gene variants and conditions like ALS, but those are mutations not alleles. Consumer DNA test don’t test for them.
 

The most important SOD2 variant

Let’s go back to the example.

Let’s pick what is often cited as the most important SOD2 SNP: rs4880.

 

SOD2 SNP

 

Looking at the test above, all it tells us, is that the person has received the same variant from her mom as from her dad. For now, it is just raw data.

What we would like to know though, what consequence does this have for the ability to handle oxidative stress, correct?

In order to find out, we have to do what all the interpreters of those type of genetic tests do: consult www.snpedia.com. The site collects all the research on all the SNPs and makes it easy to look them up.

After typing in rs4880 this is what we get:

 

rs4880 SOD2 SNP

Here comes the shocker (or not if we remember what we found out above): that we do not know for sure whether having the rs4880 variant of the SOD2 gene means that you are producing more or less of this enzyme. Since there is a “conflict” in research. The science is not clear.

So following the logic of believers in SOD SNP, being homozygous for rs4880 could mean you are either overprotected against the damages of superoxide radicals or that you are underprotected and especially vulnerable.

The page then goes on to list a bunch of research papers on that variant with links to many diseases. Some of them quite scary sounding like heart disease and cancer.

Pay attention to one crucial word though: association. The listed research papers are all associations. Those are not cause and effect relationships. Meaning: science doesn’t really know what real life meaning those SNPs have for you or if any at all.

No actual double blind randomized studies have been performed to find out what rs4880 causes or not. What this “research” is based on is statistical acrobatics on a bunch of data, trying to find meaning in numbers. Evaluating risk, not real diseases.

So taking supplements to help with those type of genetic “defects” is equivalent to have one’s breasts amputated due to similarly imperfect research: it is an overreaction based on shoddy science.

 

Would you like to pick my brain about SOD and ozone? Book a Skype session with me! It'll be fun.

Ok, I’m German, so no guarantees about the fun part. But you could enjoy it anyway 🤓.

Book Me!

 

Should you do ozone therapy with SOD SNPs present?

Ok, good. So now we know that having certain SOD SNP doesn’t really mean anything under normal circumstances.
 
But when doing ozone therapy, one is introducing major amounts of oxidative free radicals, so it is assumed. For sure the SOD SNPs play a role with the most reactive of all oxygen species, ozone?
 
Well, let’s see what we got.
 
1. First off: Ozone does not create any significant amounts of superoxide molecules. Apparently, this is not how ozone works. It works by creating a temporary increase in H2O2, a bunch of ozonides or lipid oxidation products (LOPs) which then results in a cascade of increased antioxidant activity.
 
Superoxide dismutase though is only and exclusively responsible for the breakdown of superoxide molecules. No other oxidation by-products. It splits superoxide into H2O2 and O2. This is the chemical equation:

equation superoxide to h2o2

Hence the lack of SOD which only neutralizes the superoxide radical is of no consequence for those who do ozone therapy.

2. Ozone is known to significantly increase SOD production.

Here a copy of the beginning of a 9 pages chapter from the book “Ozone Therapy. Oxidative Conditioning, Basis for its Clinical Effectiveness” dealing ONLY with how ozone therapy increases SOD activity.

Ozone Therapy. Oxidative Conditioning, Basis for its Clinical Effectiveness

It turns out, if you have low SOD levels, ozone therapy is likely the best thing you can do to increase them.

 

Ozone Therapy. Oxidative Conditioning, Basis for its Clinical Effectiveness

You like ozone therapy and get off on arcane statistical analyses? Then this is the book for you: it has everything to make the heart of a science geek jump with joy. Word puzzles made out of perplexing abbreviations, obscure biochemical, and medical terminology. Extra bonus for the linguistical fiend: it is written by Cuban non-native English speakers. The bottom line of all the linguistic tongue-twisters: ozone therapy is good and it increases SOD activity.

 
3. Observation does not match theory. There are many people who have various SOD SNPs constellations and yet do very well on ozone therapy.
 
Which shows that your SOD SNPs are not a good predictor for how you will react to ozone.
 
Join the Facebook group “Ozone to Health” to meet people with various SOD SNP who greatly benefit from O3.
 

Other reasons why you should pay no attention to your SOD SNPs

The common gene tests only look at SOD2 and SOD3 SNP. The two most important ones seem to be SOD1 And SOD2. All three genes work independently. One cannot conclude from the status of SOD2 to the status of SOD1. So the interpretation of your SOD activity based on SOD2 or SOD3 alone is questionable.
 
Not all oxidative stress is created equal. There is oxidative stress stemming from ozone therapy which is good. It primes your body through oxidative preconditioning and the hormesis effect. It creates good free oxygen radicals which support cell signalling and all other major body functions.
 
Then there is oxidative stress from environmental factors, radiation, lack of oxygen, or other shock situations. This is bad. It damages your cells.
 
Another sources of bad oxidative stress are toxic metals.
 
– Practitioners who test their patients’ SOD SNP do so primarily when patients do poorly on ozone therapy. It is part of “trouble shooting” and finding the right approach for a patient. Unfortunately, this distorts the statistical picture. Since, in order to find out if it is indeed the SNP which is responsible for a bad reaction to ozone, one would have to also look at the genes of patients who did great with ozone. This is how you exclude the role a certain factor plays in the outcome of a therapy or not.
 
Yet in clinical settings, this is hardly ever done.
 
Additional tests are mostly performed to find answers to a problem. If there is no problem because the patient does great on ozone and improves, there is no need to run an additional genetic test.
 
So practitioners might very well have patients who greatly benefit from ozone therapy and have all sorts of “bad” SOD SNP, but would never know since they don’t look for it.
 
– When it comes to genes, things are complex and many factors are still unknown. An underactive SNP or an overactive one could be overcompensated by transcriptional control, epigenetic regulation and post-transcriptional modifications. So if according to your SNP your production of SOD could be impaired, other factors might come into play which will result in normal SOD levels, in spite of the “damaged” SNP. Read here.
 
– SNP research deals in risks not really cause and effect of the SNPs. It is statistical numbers juggling. No real clinical observations or double blind controlled studies are being performed to assess the real life importance of SNP.

 

– The science behind DNA interpretations is still very much in its infancy, rife with errors and inconsistencies. Here an example:

Nowhere are the problems with statistics more blatant than in studies of genetic influences on disease. In 2007, for instance, researchers combing the medical literature found numerous studies linking a total of 85 genetic variants in 70 different genes to acute coronary syndrome, a cluster of heart problems. When the researchers compared genetic tests of 811 patients that had the syndrome with a group of 650 (matched for sex and age) that didn’t, only one of the suspect gene variants turned up substantially more often in those with the syndrome — a number to be expected by chance.

“Our null results provide no support for the hypothesis that any of the 85 genetic variants tested is a susceptibility factor” for the syndrome, the researchers reported in the Journal of the American Medical Association.”

 

Which are the right genes for ozone therapy?

If you belong to the species of homo sapiens, chances are good you have the right genes in order to do ozone therapy. As a matter of fact, if you are any type of mammal, you will likely benefit from ozone therapy.

 

Family of homo sapiens with dog

Do you resemble any of the creatures in this photo? If so, then ozone therapy could benefit you.

With one (theoretical) exception: it is assumed by many ozone experts that people with the G6PD deficiency should not do ozone therapy since the G6P enzyme is critical for how ozone therapy works. I quote this is a theoretical exception since I don’t know of any cases of people with this condition who had an adverse reaction to ozone therapy. As a matter of fact, Prof. Bocci cites a case in his book “Ozone, a New Medical Drug” of a woman with G6PD deficiency who benefited from ozone. Yet, at the same time he cautions against the use of ozone therapy with the G6PD condition.

If you satisfy the above mentioned criteria (positive for homo sapiens) and yet still do poorly on ozone therapy, the likely culprit are toxic metals, not genes. Contrary to the belief of many ozone practitioners, ozone will not chelate mercury and other metals.

Another culprit can be candida and yeast. Ozone can both help with yeast infections (the underlying cause of which is mostly mercury poisoning) but it can also make it worse. How is that? Under the right circumstances ozone can push your body into ketosis, and especially candida is able to not only survive on ketones but even go systemic.

More on that here.

 

Bottom line

If at any point in the past few years you have followed news relating to health and medicine, you certainly have come across the increased criticism today’s scientists face: the fact that many medical dogmas are based on fraudulent studies. Many of those are epidemiological studies which are essentially numbers and raw data having been moved around by statisticians to find meaning where there was none. Observational studies are famously unable to find a cause and effect. Yet, both are often used as basis for wide ranging governmental health policies with often disastrous effects.
 
Genetic tests and their interpretations are epidemiological studies on steroids: it is a pure numbers manipulation game.
 
It is a self-feeding monster: the more popular those test become, the more data there is available. There more data there is, the more numbers there are to play around with, and to assign significance to things which have none.
 
I will leave you with this quote which succinctly sums up the problem:
 
“Many consumers who are determined to learn what their DNA holds are looking for some measurement of risk — diseases that they’re genetically predisposed to develop, or weaknesses that might inform proactive lifestyle changes. But assessing that risk completely would essentially require the interpretation of a language of which our current understanding is very incomplete. While services want people to able to understand their genetic data, the reality is that science still understands very little of the language of the human genome.”
 
 
Comments: You would like to tell me that I am full of it and have no clue what I am talking about? But hopefully in a nice way? Have your way! Or you would like to tell me how much you enjoyed reading my article? I would love that! Scroll further down to find the comments section. 

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Information provided is for informational purposes only and is not a substitute for professional medical advice. No health claims for these products have been evaluated by the United States Food and Drug Administration (FDA), nor has the FDA nor any other medical authority approved these products to diagnose, cure, or prevent disease. Since every person is unique, we highly recommend you to consult with your licensed health care practitioner about the use of ozone products in your particular situation. Neither The Power of Ozone nor the manufacturers of these items are responsible for the misuse of this equipment. It is highly advised to receive professional council from a licensed doctor before using Ozone Therapy on yourself.

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