Deen said...
Thank you for the insight, if we could figure out how to increase catalase and reduce the hydrogen peroxide then we have done it!!
Easier said than done so hopefully someone somewhere could figure out, perhaps a naturopath?
Ready for a bit of a biochemistry lesson? lol
It's not as simple as increasing catalase (CAT). CAT has a reduced form and an oxidized form. The reduced form can reduce hydrogen peroxide to water (H2O2 --> H2O + O2), and in doing so, CAT turns into the oxidized form. In order to be transformed back to its reduced state so that it can reduce more hydrogen peroxide, other reducing enzymes have to act upon it. This is called antioxidant regeneration.
And herein lies the problem with UC patients.
The genes that make those reducing enzymes that regenerate the enzymes that reduce hydrogen peroxide, are damaged. So hydrogen peroxide does not get broken down as much as it should. An excess builds in the cell, leaks out of the cell, and damages the colon wall.
I am applying this knowledge to CAT to help you understand a concept. In reality, even though it reduces hydrogen peroxide, the excess of hydrogen peroxide in UCers is not caused by a malfunction in CAT, because CAT levels don't really change in any given cell.
Glutathione (GSH), superoxide dism.utase (SOD), and glutathione S-transferase Pi (GSTP) also reduce hydrogen peroxide, and it is a lack of these that drive UC. For example, I have double mutations (each gene copy is damaged) in SOD2 and GSTP1. The other GSTP gene, called GSTP2, I have one good copy. This means my cells can barely reduce hydrogen peroxide to water, and my compromised reduction capacity has lead to UC.
CAT alone cannot deal with all the hydrogen peroxide in cells. The bulk of that work is done by GSH, SOD and GSTP. These either reduce hydrogen peroxide directly into water (H2O), or they regenerate anti-oxidants in the body from their oxidized forms to their reduced forms so that they can in turn reduce hydrogen peroxide. For example, GSH regenerates vitamin E from its oxidized state to its reduced state. Vitamin E is used by the body to protect itself from free radicals like singlet oxygen, hydroxyl anions, and superoxides. Without antioxidants, these free radical forms of oxygen react with our cells and wreak havoc. They can also damage DNA which makes people age faster. Hydrogen peroxide, while technically not a free radical, behaves as one at low concentrations, by damaging cells it comes into contact with, like the colon wall. Vitamin E does not reduce hydrogen peroxide specifically, but it's a good example of how redox dynamics work. If a person's body lacks reduction capacity, then vitamin E won't be turned over as much, so that person will have to take more vitamin E in their diet. People with great antioxidant regeneration (no genetic mutation) can regenerate vitamin E for a longer time before it has to be replaced.
Unfortunately, you can't consume GSH, SOD, and GSTP. It doesn't make its way from digestion to cells, it gets destroyed. You can get GSH IVs, but they clear the kidneys in less than 2 hours.
Most UCers who get their genetics done and run their genetic code through a detox genetics generator will probably discover they have SOD, GSTP and GSH mutations.
So you see, even if we could consume catalase (CAT) and somehow get it into our cells, it won't matter because the mechanisms for regenerating it are broken in UCers. It's like saying... all the plants in this house need watering (oxidized antioxidants), so let's go buy a bunch of plants that are already full of water (reduced antioxidants) and put them in the house (eat reduced antioxidants). You'll have more watered plants in the house, but it won't make the dry plants wet. For that you need a watering can (functional reducing enzymes).
To fix it, you have to be able to consume the specific antioxidant that is missing from the cells, IN ITS REDUCED FORM ONLY, and somehow get it into the cells. If you consume the oxidized form, it will make your UC worse because that oxidized form will have to be regenerated within the cells from regenerative resources that are already low in UCers. For example, if you consume oxidized vitamin E (which is usually expired vitamin E), the body will waste its reduction capacity to turn it into reduced vitamin E. Similarly, anything in our lifestyles, including stress, that increases oxidation, will challenge reduction capacity. This is why stress is such a big driver of UC... when you're stressed the body releases adrenaline, which instructs the body to speed up its metabolism, which creates more radical oxygen species and hydrogen peroxide as a byproduct, which requires more reduction capacity to deal with. In a healthy person, the body would create more reduction capacity to deal with the stress, to a point (most people have a breaking point with stress). In UCers, the breaking point is a much lower threshold.
Even if we don't know the magic anti-oxidant that UCers need yet, we at least know that UCers should never take oxidized forms of anything, and to avoid everything in life that increases oxidation. So just google "what causes oxidative stress". Any effort that the body has to put into reducing an antioxidant we take, will cause more hydrogen peroxide to build because reduction resources have been diverted away.
As far as I can tell, the antioxidants that actually combat hydrogen peroxide without compromising reduction capacity are: curcumin, sulforaphane, and butyrate. The first two can be taken orally. Butyrate is hard to get into the bowel, so it's better to eat foods that make colonic bacteria produce physiologic butyrate. But I don't think these methods are perfect. I am taking them now and I'm about
to enter remission, but when I'm stressed I still have bad bowel days. There is a novel antioxidant we need that I can't identify yet. I'm assuming Dr. Pravda will know. I'm currently studying university biochemistry and I'm hoping I will be able to do more in depth research as my expertise grows.
Some may wonder why this hydrogen peroxide problem only manifests in the colon in UCers. For one thing, excess hydrogen peroxide affects the entire body... people with UC are prone to excess inflammation systemically. However, it manifests in the colon the most, and especially the distal colon, because that is where the most oxidative stress in the body is taking place. The colon is full of toxic waste that cells don't want. Colonic epithelium cells turnover very quickly, so there is high metabolic activity in them. And there are constantly bacteria in the colon dying and breaking down, releasing their oxidized components. The colon is basically a reactive oxygen species (ROS) epicentre. So when you can't deal with ROS, you will have colon problems. I suspect that a lot of people at higher risk of colon cancer, but who don't have UC, also have compromised reduction capacity... but not as bad as UCers.
The good news is that UCers have perfectly normal immune systems. We don't have "auto-immune". What we have is malfunctioning redox systems in our cells. When the colon wall gets damaged by peroxide, it begins to leak gut bacteria past the mucosa, and then the immune system reacts with inflammation. That's why it LOOKS like an immune disease, but the immune problem is upstream. The root problem is the hydrogen peroxide causing the gut wall to become leaky in the first place.
Post Edited (VanJordan) : 3/12/2022 1:50:27 AM (GMT-7)