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Oxidative stress and genetics
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Section 1: Intro
Chapter 30, Oxidative stress, substances and genetics. This is a specific training for the Toxo Sensor genetic test. This test looks at three different categories. The first is oxidative stress. You might have heard of this word before. It is all mediated by free radicals, which are toxic chemicals that are produced by our metabolism and by conversion of oxygen. For one thing, this can damage the tissues and cause ageing, one of the critical factors for ageing of skin and everything. It can also cause cancer.
Section 2: Free radicals
If we look at free radicals in cells, there is one very good example. Around 5 % of oxygen that we use to convert energy is converted into a very potent free radical called superoxide. This happens outside the cells, in the cells cytoplasm, inside of the cell. The cell also has something like power houses that convert energy and are called mitochondria. You also get superoxide produced in mitochondria. However, nature found out that there is something happening in there and it is dangerous for cells health. It gave us different genes that produce enzymes. There is the SOD1 gene that converts superoxide to a different substance, hydrogen peroxide inside the cytoplasm. The SOD3 gene does the same thing. It produces it outside the cell and SOD2 does it inside the mitochondria. Hydrogen peroxide is also a free radical. However, it is then processed into other free radicals. Then, eventually it is neutralized. This is a very critical protection that we have through these genetic variations.
The problem is that quite a lot of people have a genetic variation in the SOD2 gene. This means that inside the mitochondria, neutralization of superoxide is not going to happen. If we look at the science here, which is actually cut out from the report, we see the SOD2 gene, the superoxide dismutase 2 in the mitochondria. This here is like the catalogue number of the genetic variation. As you know, we have three genotypes; C/C on both of the genes, T/T on both genes or one gene has a C and the other one has a T in this genetic variation. This is how common it is in the population. 20 % have C/C, 53 % have T/T and so on. This is the result of this particular person. If you do not know much about this, I would recommend the training for the simple disease risk statistics that will explain it all to you. For the C/C genotype, 20 % have a good protection against free radicals. 53 % have only one active gene, so there is limited protection. For the T/T genotype, there are two defective genes. This is the science behind it.
This is the first aspect, the superoxide dismutase. Then, there are some other genes that neutralize other free radicals. There is the GPX1 gene. It is a selenoprotein. It means that this protein is produced but it needs selenium to become active. So, the GPX1 gene has instructions of how to build a small machine, an enzyme. This latter requires selenium to be integrated. Then, it can recognize free radicals and neutralize them. This is the general principle. So, what we find is if people have a selenium deficiency, they do not take in enough selenium, not enough of these proteins are activated and they have a low activity and a low protection from these free radicals.
Science has also shown that if you then increase selenium by eating food that contains a lot of selenium or by supplements, you can increase the activity. This is the case of normal people who have too little selenium. Now, there is a genetic variation in the GPX1 gene that changes the blueprint of the protein. What happens is that this protein is still produced but it is slightly modified. Even when it integrates selenium, it can neutralize free radicals, however, its binding or function is less effective, let us say for example, 50 % less effective. This means that even when you have normal levels of selenium, you get low levels of activity. Science has shown that if you increase selenium much higher, you get more activity and you can kind of rescue the protection against free radicals. If you have a genetic variation, this is possible through having higher levels of selenium. This here is the GPX1 gene, glutathione peroxidase. This is the genetic variation code again. This is what the gene does. You see 67 % have good protection. In 26 %, one of the gene is modified and in 7 % both genes have this genetic variation, meaning lower protection. This here again is the science. As you can see, there is a lot of science going on here. It is something science has known for many years.
Section 3: Coenzyme Q10
Now we move to the next factor for oxidative stress. You might have realized that beauty creams and beauty products often contain coenzyme Q10 because this latter can be modified and activated in our body and then we get a very good protection against free radicals, which, as I said, are one integral part of ageing. It is meant to reduce ageing. Some take coenzyme Q10, though it is expensive, as a supplement and an addition.
When coenzyme Q10 reaches our body, it has no effect. It first needs to be activated by an enzyme. Again, an enzyme is like scissors that cut open coenzyme Q10 and then convert it to ubiquinal. Ubiquinal is the active form and has a strong antioxidant effect. It can grab onto free radicals and neutralize them. It is indeed a good protection against free radicals. This here is the gene.
This is what it does. 66 % have a normal conversion activity. 30 % have a reduced activity. Only one of the two genes does work. So, you expect about half of the activity. 4 % of the population have a T/T genotype and they do not benefit from it at all because the coenzyme Q10 cannot be converted into ubiquinal and even though people take this expensive supplement they cannot convert it into the protective effect that they hope to get from it. So, what is happening in these people is you get the genetic variation that the coenzyme q10 cannot be converted and free radicals are not neutralized. So, one thing you can do is actually instead of taking coenzyme Q10 when this gene has this genetic variation, you can take the active ubiquinal. It does not have to be converted anymore. That can then neutralize free radicals.
Alternatively, there are other free radicals inhibitors like vitamin E, vitamin C, alpha lipoic acid that have a similar role and can also neutralize free radicals. This here is cut out from the oxidative stress part of the Toxo Sensor. First, you get a summary. You have a slightly elevated level of oxidative stress. Here you see your oxidative stress in cells can be normal. It can be very high depending on how many of the protective genes have detrimental genetic variations. This person can activate coenzyme Q10 to ubiquinal. So, here we are in the possible part. It could not also be possible. coenzyme Q10 is a recommended antioxidant. Otherwise, you would only be left with vitamin C, E, A or ubiquinal. Coenzyme Q10 here is absolutely functional.
Also, the daily requirement of selenium is increased because we need it more to activate the GPX1 gene which I have explained to you. The recommended dose of antioxidants is slightly higher than normal. So, this is the kind of information you get in the report. Then, if you have an increased antioxidant risk, you get prevention advice. It is in a very simple language so you can read through it once to find out what kind of recommendations we give.
One is antioxidant-rich diet. You could either do it by modifying your diet in which the Nutrition Sensor will help you to change your diet to get more free radicals inhibitors. In addition, it is possible to take supplements that contain these antioxidants. We have one product, which is the NutrimeNutrition, where we actually dose each of these antioxidants based on your genetics so that to make sure you get the right antioxidants in the right dosage. Some key antioxidants are vitamin C, E, β-carotene, and alpha lipoic acid. Then, there is either coenzyme Q10 or ubiquinal. As you remember, it is either one or the other.
Then, there is selenium which depends on how much it is required. Actually, there is one interesting point. Some people who say: why do you do a genetic test, how much selenium do you need and why do you do a blood test? The problem is irrespective of the blood test, you would say the selenium level in blood should be a certain amount because you say this is the healthier area. So, you would try to adapt everyone to be in the right area. Then, you would say this is now in the right amount but from science we have seen that some people require a much higher amount because of the low GPX1 activity.
So, if you just normalize it in the normal area, you would actually not reach the right amount that you should get for this person. So, the blood test would again try to put everyone in the same basket, claiming that everyone needs the same amount of selenium in the blood but we have seen that this is not necessarily correct. Then, you could use two cups of coffee per day. Coffee has a lot of antioxidants. Science has shown that women who drink two or more cups of coffee and have a certain genetic variation do benefit from a delayed occurrence of breast cancer. This is 7 years later on average. Some women do really benefit from drinking coffee while others do not.
Section 4: Substances affecting the body Q10
This was antioxidants or oxidative stress. The next thing is the substances that affect our body in different ways. For example, there is alcohol dependence. There are people who have a genetic tendency to be more alcohol dependent while others have a protection from it. Here is the result. This again is how you see them in the report. Your risk of alcohol dependence might be normal or might be increased. If it is increased, you should be aware of the increased risk and should reduce alcohol and maybe avoid it all together to reduce the risk of developing this dependence.
Then, there is the question of how quickly caffeine is broken down. You know that some people say they can drink coffee before they go to bed others cannot sleep anymore if they drink coffee in the afternoon. So, here we see how fast coffee or caffeine is broken down. Then, there is the use of cannabis has been shown to increase the risk of schizophrenia if the use was before the age of 16 and a certain genetic variation was present. Some teenagers who consume cannabis and have a certain genetic variation and by combining these two in adolescence increases the risk of schizophrenia later in life by 11 fold. It is a significant risk. Most people were already past this age, in this case it might not be interesting but it might be understandable if schizophrenia is present and that this might have played a role.
Then, the effect of coffee on breast cancer can either delay the onset or it cannot have any effect on the onset. Then, it can be positive or negative to drink coffee. These are the two genes that are relevant, the COMT gene and the CYP1A2 gene. If you do not know what all of this means, please do watch the simple disease risk statistics which explains the whole concept very well. If you look at the COMT gene, this is cut out from the report, this is how you can see it in the report. This explains what it does. For the A/A genotype, it says no effect on increased risk of alcoholism. For the A/G genotype, 55 % of the general population have it. For the increased risk of schizophrenia when cannabis is consumed before the age of 16, it is 2.5 times higher risk but a normal risk of alcoholism. For the T/G genotype, it is 10.9 fold higher risk. This is the science behind it in case you want to check up what we claim here.
This is the end of chapter 30, Oxidative stress, substances and genetics as a specific training for the Toxo Sensor.