# Lipid peroxidation

Category: Metabolism

Also known as: MDA, malondialdehyde, 4-HNE

Lipid peroxidation is the oxidative breakdown of lipids, primarily targeting polyunsaturated fatty acids (PUFAs) due to their multiple unstable double bonds. Peat described it as a process where free radicals extract electrons from lipids, generating a cascade of toxic…

12 passages · 3 authors · 1988–2023 · Most-cited: [Ray Peat](https://bioenergeticoracle.com/md/voices/ray-peat/index.md)

Canonical page: https://bioenergeticoracle.com/concepts/lipid-peroxidation

## Synthesis

**Lipid peroxidation** is the *oxidative breakdown of lipids*, primarily targeting **polyunsaturated fatty acids (PUFAs)** due to their multiple unstable double bonds. [Source 3, 4] Peat described it as a process where free radicals extract electrons from lipids, generating a cascade of toxic byproducts including **malondialdehyde (MDA)**, **acrolein**, and **4-hydroxynonenal (4-HNE)**. [Source 3, 6] While enzymatic peroxide formation occurs in controlled pathways, the term lipid peroxidation typically denotes the spontaneous, uncontrolled chain reaction that propagates through cell structures, destroying the unstable PUFAs and leaving behind a residue of saturated fats. [Source 5, 11] This chain reaction continues until something intervenes to break it, with the smaller oxidized fragments often being the most toxic and capable of spreading the oxidation further. [Source 8, 9]

The toxicity of lipid peroxidation products is mechanistically precise and devastating. **Acrolein**, released during PUFA degradation, directly inhibits mitochondrial function by poisoning *cytochrome oxidase*, the crucial respiratory enzyme, resulting in a decreased ability to produce energy. [Source 6] It also inhibits the cellular regulation of the excitatory amino acid glutamate, contributing to prolonged nerve excitation. [Source 6] **Malondialdehyde** is a known human carcinogen that acts like a glue, wrecking cellular architecture, while the aldehydes produced by fat breakdown react with cell proteins, making them antigenic and triggering autoimmune responses. [Source 1, 9] Peat argued that lipid peroxidation products are *chaotropic*, meaning they lower the rigidity of cellular regions by damaging the underlying protein skeleton, and that the resulting "membrane fluidity" often corresponds to the chaos of a damaged cell protein structure rather than a healthy state. [Source 10]

Peat identified several catalysts that accelerate lipid peroxidation, with **iron** playing a central role. When metals like iron, aluminum, or lead accumulate in cells, they accelerate peroxidation in proportion to the unsaturation of the cell's lipids. [Source 1] The stress-induced enzyme *heme oxygenase* releases free iron from heme groups, and the resulting free bilirubin is associated with lipid peroxidation and DNA damage. [Source 1] **Estrogen** synergizes with this process by increasing hypoxia inducible factor (HIF), which promotes iron absorption and activates aromatase, creating a vicious cycle. [Source 1] **Nitric oxide**, whose synthesis estrogen promotes in the brain, is a free radical that directly activates peroxidation. [Source 5] Cortisol also contributes, as its destabilizing effects lead to increased lipid peroxidation, which in turn decreases protective steroid synthesis. [Source 12]

The pathological consequences of lipid peroxidation are most evident in the brain and vascular system. High levels of acrolein and other PUFA degradation products are found in the brain in **Alzheimer's disease**, and the "prion" diseases like CJD and mad cow disease produce their damage by activating lipases that release PUFAs and generate lipid peroxides. [Source 6] In **multiple sclerosis**, lipid peroxidation is very high, with elevated isoprostanes and prostaglandins in brain tissue, and the intolerance for heat in MS patients may relate to the release of free fatty acids that fuel further peroxidation. [Source 5] The process also depletes brain DHA, and Chris Masterjohn noted that some neurological problems may stem from this depletion caused by peroxidation. [Source 7] In atherosclerosis, the plaques contain very little unsaturated fat precisely because it has been peroxidized so rapidly. [Source 5] An oil researcher consuming an Eskimo-style diet saw his blood lipid peroxides, measured as MDA, reach a level 50 times higher than normal, and his sperm count dropped to zero. [Source 2]

The body possesses some defenses against this process, but they reveal the inherent toxicity of the substrates. Georgi Dinkov explained that the enzyme **catalase** is specifically activated to detoxify the aldehydes produced during PUFA metabolism, and it does not get activated when saturated fat is consumed. [Source 3] However, chronically elevated catalase is itself correlated with cancer. [Source 3] Peat observed that traditional Eskimos, despite high PUFA intake, may have been protected by consuming whole animals including the thyroid gland and brain, which provided **thyroid hormone**, **cholesterol**, and the protective steroids **pregnenolone**, **progesterone**, and **DHEA** that broadly protect against peroxidative damage. [Source 2] Saturated fats like coconut oil do not produce these aldehydes and are metabolized differently, similar to glucose, entering mitochondria directly without generating the toxic byproducts. [Source 3, 10] Peat's personal experience with coconut oil produced an immediate increase in metabolic rate, suggesting his metabolism had been chronically inhibited by something easily alleviated by diluting the toxic unsaturated fats. [Source 10]

## People also ask

### Why are polyunsaturated fats more prone to lipid peroxidation than saturated fats?

Peat described that polyunsaturated fatty acids contain multiple unstable double bonds, which makes them highly susceptible to free radicals extracting electrons and initiating a spontaneous, uncontrolled chain reaction of oxidative breakdown.

### How does lipid peroxidation damage mitochondria?

The entry explains that acrolein, a toxic byproduct released during PUFA degradation, directly poisons cytochrome oxidase, the crucial respiratory enzyme, thereby inhibiting mitochondrial function and decreasing energy production.

### What protective effect did Peat attribute to coconut oil?

Peat argued that saturated fats like coconut oil are metabolized differently from PUFAs, entering mitochondria directly without generating toxic aldehyde byproducts, and his personal experience showed it immediately increased his metabolic rate.

## Related concepts

- [Unsaturated oils](https://bioenergeticoracle.com/md/concepts/unsaturated-oils/index.md)
- [Adrenaline](https://bioenergeticoracle.com/md/concepts/adrenaline/index.md)
- [Age Pigment (Lipofuscin)](https://bioenergeticoracle.com/md/concepts/age-pigment-lipofuscin/index.md)
- [Albumin](https://bioenergeticoracle.com/md/concepts/albumin/index.md)
- [Alzheimer's and Dementia](https://bioenergeticoracle.com/md/concepts/alzheimer-s-and-dementia/index.md)
- [Amyloid](https://bioenergeticoracle.com/md/concepts/amyloid/index.md)

## Cited passages

Passage numbers match the `[Source N]` markers in the synthesis above.

### Source 1 — Estrogen, iron, degenerative aging, and progesterone

Ray Peat · Newsletter · 2021

> Some of the products of lipid peroxidation, interacting with iron and other cell materials, become the very complexly structured age pigment, lipofuscin. Among the substances in these dark granules are some heme molecules, protected against elimination, which can catalyze the conversion of oxygen to water, without producing usable energy; the pigment becomes a drain on fuel and oxygen, creating a constant reductive, oxygen deficient, stress. This tendency to reduce oxygen contributes to the formation of vicious circles, inducing hypoxia inducible factor, HIF, which is a crucial factor in promoting iron absorption, and which activates many potentially dangerous enzymes, including heme oxygenase, HO, which turns heme groups into free iron, carbon monoxide, and bilirubin. HIF also activates aromatase, increasing estrogen (Samarajeewa, et al., 2013). About 60% of newborn babies are jaundiced for a few days, showing that the stress of being born has activated their HO, turning heme into its toxic components. The presence of free bilirubin is known to be associated with lipid peroxidation and DNA damage (Basu, et al. 2014). Better prenatal conditions would probably reduce the incidence of neonatal jaundice and stress, and this might involve avoidance of highly unsaturated fats and large iron supplements, and avoiding stressful medical procedures. Stresses that increase exposure to excess iron and PUFA can shorten the life span of red blood cells, adding to the burden of heme and lipid peroxides. The well known association of the autoimmune diseases with excessive estrogen probably involves the increases of hypoxia, HIF, HO, iron, and PUFA under the influence of estrogen. Aldehydes produced by the breakdown of fats react with cell proteins, making them antigenic, while episodes of hypoxia and hypoglycemia make the immune system more reactive.
>
> All microorganisms require iron to grow, so limiting the availability of iron will limit their ability to be infective. Our respiratory and digestive membranes secrete two proteins, lactoferrin and transferrin, which have a very high affinity for iron atoms, as well as other germicidal properties, and provide a first defense against infection.

### Source 2 — Oils in Context

Ray Peat · Article · 2006 · https://raypeat.com/articles/nutrition/oils-in-context.shtml

> # Oils in Context
>
> An oil researcher [0] spent 100 days eating what he considered to be the "Eskimo diet," seal blubber and mackerel paste. He observed that his blood lipid peroxides (measured as malondialdehyde, MDA) reached a level 50 times higher than normal, and although MDA is teratogenic, he said he wasn't worried about fathering deformed children, because his sperm count had gone to zero. Evidently, he didn't have a very thorough understanding of the Eskimo way of life. In most traditional cultures, the whole animal is used for food, including the brain and the endocrine glands. Since unsaturated fats inhibit thyroid function, and since Eskimos usually have a high caloric intake but are not typically obese, it seems that their metabolic rate is being promoted by something in their diet, which might also be responsible for protecting them from the effects experienced by the oil researcher. (According to G. W. Crile, the basal metabolic rate of Eskimos was 125% of that of people in the United States.) People who eat fish heads (or other animal heads) generally consume the thyroid gland, as well as the brain. The brain is the body's richest source of cholesterol, which, with adequate thyroid hormone and vitamin A, is converted into the steroid hormones pregnenolone, progesterone, and DHEA, in proportion to the quantity circulating in blood in low-density lipoproteins. The brain is also the richest source of these very water-insoluble (hydrophobic) steroid hormones; it has a concentration about 20 times higher than the serum, for example. The active thyroid hormone is also concentrated many-fold in the brain. DHEA (dehydroepiandrosterone) is known to be low in people who are susceptible to heart disease [1] or cancer, and all three of these steroids have a broad spectrum of protective actions. Thyroid hormone, vitamin A, and cholesterol, which are used to produce the protective steroids, have been found to have a similarly broad range of protective effects, even when used singly. For example, according to MacCallum,
>
> [references]
>
> A high level of serum cholesterol is practically diagnostic of hypothyroidism, and can be seen as an adaptive attempt to maintain adequate production of the protective steroids.

### Source 3 — A Bioenergetic View of Dementia [Generative Energy #20]

Danny Roddy · Interview · Feb 3, 2016 · https://www.youtube.com/watch?v=8lDx8Y93iwk

> **Georgi Dinkov:** Well, I mean, lipid peroxidation, in simplest terms, is just the oxidative breakdown of lipids, whatever lipids you happen to ingest. And basically, in this process, there's a lot of free radicals that have been generated and they sort of extract or steal electrons from the lipids in the cell. Officially, basically, the theory says they steal electrons from the cell membranes. And whenever you have these electrons being withdrawn, this results in cell damage. Most often, it affects the polyunsaturated fatty acids because they contain multiple double bonds, right? So they're not fully saturated with hydrogen atoms. Whenever you ingest these polyunsaturated fatty acids, in the process of them being converted into acyl-CoA, which is the initial entry step into the Krebs cycle, they generate a lot of bad byproducts. And one of them is malonylaldehyde, which is the one I mentioned. Saturated fatty acids, they don't produce these aldehydes. Basically, the saturated acids are metabolized differently, similar to glucose. they can get transported directly into the mitochondria, and they're much more easily converted into acyl-CoA. I don't know how I can explain it more easily without going into the details of the Krebs cycle and beta-oxidation, which will get very technical. But in order for you to properly detox, there's a special enzyme which humans have. It's called catalase, and it's one of the main enzymes that allows us to withstand the effects of polyunsaturated fatty acids. This immediately tells you. And the enzyme catalase is active primarily when you ingest some kind of a poison, especially the PUFAs. So if you don't eat PUFA, the levels of catalase are lower and basically it has been shown that overactive catalase enzyme, even though it's good for you, it's known that it detoxifies these aldehydes, elevated levels of catalase chronically are correlated with cancer. Catalase doesn't get activated when you eat saturated fat.

### Source 4 — A Bioenergetic View of Dementia [Generative Energy #20]

Danny Roddy · Interview · Feb 3, 2016 · https://www.youtube.com/watch?v=8lDx8Y93iwk

> **Danny Roddy:** And did you want to talk about lipid peroxidation just in general? Ray mentions it a ton, but you have to do a little legwork to figure out just for a layman what that process is. It's normal in a certain extent for cell division and growth, but then in aging, it becomes out of control. And did you want to talk about the process to where lipid peroxidation kind of goes off the rails and becomes too much?

### Source 5 — Multiple sclerosis, protein, fats, and progesterone

Ray Peat · Article · 2009 · https://raypeat.com/articles/articles/ms.shtml

> The rumen of cows, sheep, and goats contains bacteria that convert the polyunsaturated fats into more saturated fats.
>
> Unsaturated fats inhibit the enzymes that digest protein, and MS patients have been reported to have poor digestion of meat (Gupta, et al., 1977).
>
> The polyunsaturated fats are in themselves toxic to mitochondria, and suppress glucose oxidation, and inhibit the thyroid function, with the same suppressive effect on the ability to oxidize glucose, but they are also turned, enzymically, into the prostaglandins, and non-enzymically, by spontaneous lipid peroxidation, into the toxic isoprostanes.
>
> The isoprostanes, and some of the prostaglandins, are elevated in the brain and other tissues of people with MS.
>
> Lipid peroxidation is very high in multiple sclerosis.
>
> Nitric oxide (whose synthesis is promoted by estrogen in most parts of the brain) is a free radical that activates peroxidation.
>
> Lipid peroxidation selectively destroys, naturally, the unstable polyunsaturated fats.
>
> In atherosclerosis, the blood vessel plaques contain very little unsaturated fat.
>
> This is because they are peroxidized so rapidly, but their high ratio of saturated to unsaturated fats has been used to argue that the polyunsaturated oils are "heart protective."
>
> Similar arguments are often made in MS, though some studies don't support the idea that there is a lack of any of the unsaturated fats.
>
> Since lipid peroxidation is very high, it would be reasonable to assume that there was an abundance of polyunsaturated fats being peroxidized through reactions with catalysts such as iron (S.M. LeVine, 1997) and nitric oxide and peroxynitrile. I believe that an important aspect of the intolerance for heat so often reported in people with MS could be the tendency of relative hyperthermia to release increased amounts of free fatty acids into the blood stream. Women, because of estrogen's effects, usually have much higher levels of free fatty acids in the blood than men do. Estrogen increases the release of free fatty acids from stored fat, and the unsaturated fats synergize with both estrogen and prolactin, increasing their effects. Temperature regulation apparently involves some nerve cells that sense temperature very accurately, and change their activity accordingly. Water has a remarkably high heat capacity, meaning that it takes a relatively large amount of heat to change its temperature.

### Source 6 — The Great Fish Oil Experiment

Ray Peat · Article · 2008 · https://raypeat.com/articles/articles/fishoil.shtml

> Apparently, anything that depletes the cell's energy, lowering ATP, allows an excess of calcium to enter cells, contributing to their death (Ray, et al., 1994).
>
> Increasing intracellular calcium activates phospholipases, releasing more polyunsaturated fats (Sweetman, et al., 1995)
>
> The acrolein which is released during lipid peroxidation inhibits mitochondrial function by poisoning the crucial respiratory enzyme, cytochrome oxidase, resulting in a decreased ability to produce energy (Picklo and Montine, 2001). (In the retina, the PUFA contribute to light-induced damage of the energy producing ability of the cells [King, 2004], by damaging the same crucial enzyme.)
>
> Besides inhibiting the ability of nerve cells to produce energy from the oxidation of glucose, acrolein inhibits the ability of cells to regulate the excitatory amino acid glutamate (Lovell, et al., 2000), contributing to the excitatory process.
>
> High levels of acrolein (and other products of PUFA degradation) are found in the brain in Alzheimer's disease (Lovell, et al., 2001).
>
> The "prion" diseases, CJD and TSE/BSE (mad cow disease) have many features in common with Alzheimer's disease, and several studies have shown that the "prion" protein produces its damage by activating the lipases that release polyunsaturated fatty acids and produce lipid peroxides (Bate, et al., 2004, Stewart, et al., 2001).
>
> Acrolein reacts with DNA, causing "genetic" damage, and also reacts with the lysine in proteins, for example contributing to the toxicity of oxidized low density lipoproteins (LDL), the proteins that carry cholesterol and that became famous because of their involvement in the development of atherosclerosis that was supposedly caused by eating saturated fats.
>
> My newsletter on mad cow disease discussed the evidence incriminating the use of fish meal in animal feed, as a cause of the degenerative brain diseases, and earlier newsletters (glycemia, and glycation) discussed the reasons for thinking that inappropriate glycation of lysine groups in proteins, as a result of a lack of protective carbon dioxide/carbamino groups, produces the amyloid (or "prion") proteins that characterize the dementias.

### Source 7 — #96: Authoritarianism | Vaccine Sophistry | Coronavirus | Essential Fatty Acids? | Ray Peat with Chris Masterjohn

Danny Roddy · Interview · Jan 22, 2023 · https://open.spotify.com/episode/428YOkwFkNdiy6rxtsuR4b

> **Danny Roddy:** Yeah, fair enough. I've always thought this was like an academic argument. You know, I it's like I mean, if you eat an egg or you eat oysters, you're going to get some level of these. And so I really always left that stuff up to Ray. I never got too deeply into it. I remember you sent me Precious Yet Perilous like 10 years ago. And you're like, Danny, you really should read this.
>
> **Chris Masterjohn:** I do think it has practical aspects because there are conditions where you could have depletion of DHA for other reasons. And as an example... You were talking about lipid peroxidation. So one of the things that lipid peroxidation does is create a lot of harmful stuff. But another thing it does is deplete those fatty acids in the brain. So I do think it's plausible that there are people who have neurological problems because of the lipid peroxidation in the brain. and that part of the results, part of the causation is a depletion of brain DHA. And I also think that just in general, people are relatively suboptimal in DHA in the modern context because the omega-6 to omega-3 ratios are so thrown off. So I think people that don't eat any seafood and whose only eggs are commercial eggs, and who are otherwise eating a ton of vegetable oils. $10

### Source 8 — Ray Peat Email Advice Depository — Post 923

Ray Peat · Email · Dec 11, 2022

> **Question:** If oxidized ldl is already oxidized, does it continue to cause lipid peroxidation in our blood vessels and cause inflammation and oxidative stress? Or is oxidized LDL only partially oxidized, and being so, it would continue to have a pathological effect?
>
> **Ray Peat:** Yes, the oxidized fragments keep spreading the oxidation, with the smaller products often being the most toxic.

### Source 9 — The ThermoDiet Podcast Episode 114 - Georgi Dinkov

Georgi Dinkov · Interview · Nov 27, 2022 · https://www.youtube.com/watch?v=Twpszx115qQ

> **Tyler Woodward:** In that regard, so do you think it's most of the lipid peroxidation, which is like when the free radicals hit everything in the cell, bouncing around and cause lipid peroxidation, the base of those double bonds to break apart, which results in the formation of like MDA, myelodaldehyde, the... Basically, it's like glue that just wrecks the cell. Do you think it's worse? Is that mostly from lipid peroxidation from the iron? What's not reacting in the cell? Or is it from the oxidizing of the PUFAs in the cell? Or is it both?
>
> **Georgi Dinkov:** Well, no, the oxidation of the PUFO in the cell, I mean, basically, whether it's a PUFO or saturated fat, it's effective in the same. The beta-oxidation is this repeated cyclical process that cuts off like two molecules every single time until the whole chain is exhausted, right? And then it gets converted into acetyl-CoA and gets fed into the Krebs cycle. So that process is fine. However, just the presence of the PUFO, because there's molecular oxygen and hydroxyl radicals floating... you know, around, they're always subject to basically portion of them reacting with that hydroxyl radical or the superoxide anion and forming a fatty acid radical, right? And those fatty acid radicals are extremely toxic. They're known to be mutagenic and carcinogenic, right? But on the other hand, the evidence for that is already conclusive. I think the NIH listed it back in 2010. It put it on its list of known human carcinogens. They have possible, probable, and known. Malonylaldehyde moved very quickly, I think, between 2001 when it was on the list of possible ones. At this point, it's now on the list of known. uh but pretty much all the all the other aldehydes uh and the ones that they scare us the most unfortunately turns out to be the least problematic which is acetaldehyde which is the first step in the metabolism of alcohol um and basically they say oh alcohol the danger associated with is because of acetaldehyde uh just like malone the aldehyde we think it's you know but somehow the media attention is all acetaldehyde and not a malone the aldehyde which which we actually produce in a much higher amounts on a daily basis from our food right Unless you're alcoholic, acetaldehyde is a lot less problematic for you than malonylaldehyde is, and various other aldehydes. So basically, the full number of PUFO peroxidation byproducts is unknown, but basically, they're all, without exception, toxic aldehydes or alcohols. with a very unstable structure.

### Source 10 — From PMS to Menopause: Female Hormones in Context

Ray Peat · Book · 1997

> **Ray Peat:** In red blood cells, which have sometimes been wrongly described as "hemoglobin enclosed in a cell membrane," it has been known for a long time that lipid peroxidation of unsaturated fats weakens the cellular structure, causing the cells to be destroyed prematurely. Lipid peroxidation products are known to be "chaotropic," lowering the rigidity of regions of cells considered to be membranes. But the red blood cell is actually more like a sponge in structure, consisting of a "skeleton" of proteins, which (if not damaged by oxidation) can hold its shape, even when the hemoglobin has been removed. Oxidants damage the protein structure, and it is this structural damage which in turn increases the "fluidity" of the associated fats. So, it is probably true that in many cases the liquid unsaturated oils do increase "membrane fluidity," but it is now clear that in at least some of those cases the "fluidity" corresponds to the chaos of a damaged cell protein structure. (N. V. Gorbunov, "Effect of structural modification of membrane proteins on lipid-protein interactions in the human erythrocyte membrane," Bull. Exp. Biol. & Med 116(11), 1364-67. 1993). Although I had stopped using the unsaturated seed oils years ago, and supposed that I wasn't heavily saturated with toxic unsaturated fat, when I first used coconut oil I saw an immediate response, that convinced me my metabolism was chronically inhibited by something that was easily alleviated by "dilution" or molecular competition. I had put a tablespoonful of coconut oil on some rice I had for supper, and half an hour later while I was reading, I noticed I was breathing more deeply than normal. I saw that my skin was pink, and I found that my pulse was faster than normal--about 98, I think. After an hour or two, my pulse and breathing returned to normal.

### Source 11 — #96: Authoritarianism | Vaccine Sophistry | Coronavirus | Essential Fatty Acids? | Ray Peat with Chris Masterjohn

Danny Roddy · Interview · Jan 22, 2023 · https://open.spotify.com/episode/428YOkwFkNdiy6rxtsuR4b

> **Chris Masterjohn:** I don't know that I caught that. Wouldn't nobody agree that there is some minimal amount of peroxidation that you want under what circumstance?
>
> **Danny Roddy:** Okay, so lipid peroxidation, that's a bad thing, right? It harms mitochondria. It's damaging to self.
>
> **Chris Masterjohn:** I think that technically you have... peroxides formed enzymatically in the enzymatic reactions that you would separate from uncontrolled lipid peroxidation. Usually when someone refers to lipid peroxidation, they're talking about random spontaneous lipid peroxidation in the cell membrane that has the possibility of a lipid peroxidation chain reaction, which would destroy the cell membrane. And they're not talking about... literally what might literally be peroxides formed enzymatically in a pathway when they say that it's sort of like the way when people talk about ketones they're not talking about fructose even though fructose is a ketone and they are talking about um beta hydroxybutyrate even though beta hydroxybutyrate is not a ketone alcohol
>
> **Danny Roddy:** Okay, so I guess I was talking with him and I was like, Ray, isn't the fact that they're harmful, like they're a precursor to this harmful event, like wouldn't that mean that it was just not really like a necessary thing in a cell? Again, I know I'm looking at this very simplistically, but he was like, yeah, that's why I think they're not essential because they're the precursors to lipid proxidation. Or a cell can't be so susceptible to lipid proxidation when DHA isn't around.

### Source 12 — Natural Immunity and Viral Infections

Ray Peat · Newsletter · Aug 1988

> The consequent increase of lipid peroxidation will decrease steroid synthesis. Stress also leads to the production of intracellular toxins, including ammonia and carbon monoxide, which tend to perpetuate the blocked state.
>
> Just as with the anesthetic substances which modify the physical state of the cell, retarding viral replication, the oxidative protective system has several points at which intervention is possible to support detoxification, and to promote protein turnover.
>
> ## Injecting Enzymes
>
> Although natural promotion of the enzymes which degrade proteins and nucleic acids will help to shift the equilibrium away from virus production, recent research shows that it can be therapeutic to inject enzymes (nucleases, both DNAase and RNAase) which degrade viral nucleic acids. Using labelled enzymes, it has been demonstrated that virus and enzyme can enter the cytoplasm in the same vesicle. In herpetic keratitis, the enzyme is used as drops and also injected under the conjunctiva, and in infectious mononucleosis and viral encephalitis it is injected intramuscularly. In treating a viral paralysis of bees, the enzyme is administered as an aerosol. It was found that treatment increased the viability and productivity of outwardly healthy bees, apparently by curing a latent viral infection.
>
> While W. F. Koch was interested in the body's own oxidative free radical system of destroying toxins and pathogens, he studied several natural quinones found in medicinal plants. Recent work has found that phototoxins extracted from plants can kill mouse-cytomegalovirus without damaging the mouse cells. These researchers selected chemicals which do not disrupt genetic material, recognizing the probability of serious side effects.
>
> Although injected enzymes and plant toxins are safer than some current chemotherapies, the basic approach to controlling viral diseases should be to support natural immunity, by maintaining energy production at a high level, by unblocking and stabilizing the detoxifying enzymes, including mono-oxygenases, proteolytic enzymes, SOD, and nucleases, and by avoiding prolonged catabolic states. Many natural substances are available which promote these ends, without risk.

_Generated 2026-07-20 from the Bioenergetic Oracle corpus._