The Chemical Reactions Occurring In Our Body During Digestion

An exploration of what we don’t really ruminate on

Dr Joel Yong, PhD
Feb 22 · 6 min read
Photo by Bill Oxford on Unsplash

tend to think of our digestive system at a very simple level. We eat food, our stomach acids break it down, our intestines absorb it, and whatever that isn’t absorbed is excreted into the toilet bowl.

Unfortunately, life isn’t that simple. There are many more chemical reactions that are ongoing within the body — to an extent that we may not even be aware of them!

Lipid Peroxidation

One of these key reactions that occurs to the food that we eat is lipid peroxidation. This reaction occurs when an unsaturated fatty acid reacts with a pro-oxidant species to form an unstable lipid peroxide, and this lipid peroxide can decompose further into toxic by-products.

As it is said in this research article,

The stomach acts as a bioreactor and is an excellent medium for enhancing lipid peroxidation, generation of free radicals, secondary lipid peroxidation products and co-oxidation of vitamins.

The stomach environment does not only break down complex food particles — it also promotes lipid peroxidation.

But what can these lipid peroxide products do?

The same article also mentions that:

Red-meat lipid peroxidation in the stomach results in postprandial oxidative stress (POS) which is characterized by the generation of a variety of reactive cytotoxic aldehydes including malondialdehyde (MDA). MDA is absorbed in the blood system reacts with cell proteins to form adducts resulting in advanced lipid peroxidation end products (ALEs), producing dysfunctional proteins and cellular responses. The pathological consequences of ALEs tissue damage include inflammation and increased risk for many chronic diseases that are associated with a Western-type diet.

We’d therefore be looking at an issue of oxidative stress in the case of red meat lipid peroxidation. Reactive chemicals such as MDA are produced, and MDA can react with cell proteins to cause them to lose their function, which also ends up impairing a healthy cellular response. As a result, if we are consuming too many foods that promote lipid peroxidation, the pro-inflammatory transcription pathways (such as the nuclear factor kappa B, or NF-κB pathway) that signal a higher risk of chronic diseases are upregulated.

The use of unsaturated fats for frying foods at high temperatures can also contribute to lipid peroxidation prior to the ingestion of the fried foods. Hence, fried foods also do pose a risk for lipid peroxidation.

Oxidative Stress

And when we’ve got too much of these lipid peroxide products swimming about in our body, it gets into a stage of oxidative stress.

Our body is in a balance between pro-oxidation and anti-oxidation. The idea of oxidation involves the transfer of electrons from one species to another.

If Species A is able to extract electrons from Species B, then Species A is considered to be a pro-oxidant, and Species B gets oxidised. If Species C can donate electrons to the oxidised Species B and help it to maintain stability, then Species C is considered to be an antioxidant. The main pro-oxidants in the body are termed as reactive oxygen species (ROS).

However, if the oxidised Species B/C are chemically unstable and have to extract electrons from somewhere else to maintain their stability, then we’d be seeing a sequential chain reaction of oxidation and electron transfers that can cause a ripple effect of chemical instability in our bodies.

The cells in our body, for instance, produce glutathione as an antioxidant counterbalance to any pro-oxidation species to keep it in check.

The nuclear factor-erythroid 2 p45-related factor 2 (or nuclear respiratory factor 2, nrf2) transcriptional pathway in the body is one of the major regulators of antioxidant production. It is said to be “the primary transcription factor protecting cells from oxidative stress by regulating cytoprotective genes, including the antioxidant glutathione (GSH) pathway.”

However, the rate of GSH production is not going to automatically increase to counteract the effects of a chronically subpar diet. That fried chicken may look mouthwateringly delectable, but eating too much of it consistently can shift the pro-oxidant/antioxidant balance towards favouring the chain reaction occurring more frequently.

Chemical oxidation is selfish and indiscriminate — if Species A needs electrons, it will just attack anything anywhere with the least resistance to giving up electrons.

As GSH functions as a very willing electron donor, we’d be better off stimulating our cells to produce more of it via the nrf2 pathway, and that is because of the idea of GSH regeneration and cycling.

Two molecules of GSH can accept electrons and be oxidised into a single molecule of oxidised glutathione (which we term as GSSG). GSSG can be reduced back into GSH within the cell via the activity of the glutathione reductase (GR) enzyme. Hence, these 2 molecules of GSH can be constantly cycled back and forth between their reduced GSH and their oxidised GSSG states, and deal with the transfer of hundreds of electrons.

This continuous GSH cycling allows for the neutralisation of many ROS molecules over the cell’s lifespan. In comparison, dietary antioxidants such as Vitamin C (ascorbic acid) can only deal with the transfer of 2 electrons (where it gets oxidised into dehydroascorbic acid)… unless there is adequate GSH to deal with the regeneration of Vitamin C back into its reduced ascorbic acid form. However, while GSH can reduce dehydroascorbic acid, ascorbic acid cannot reduce GSSG, because their redox potentials are different. Hence, we cannot rely on Vitamin C to regenerate GSH, but alpha lipoic acid can do so.

When is this oxidative stress a problem?

We tend to think that the consumption of certain foods leads to a higher risk of developing cancer.

However, the sequence of events aren’t really that clear. Some foods do contain higher levels of polycyclic aromatic hydrocarbons (PAHs), such that:

Processed food (through smoking) and cooked food (charcoal cooked) also contribute substantially to the intake of PAHs. The type of cooking, cooking temperature, time, amounts of fat, and oil influence the formation of PAHs.

The simplest PAH in existence is benzopyrene, which on its own is not really a problem. Unfortunately, the liver’s enzymes will biochemically process benzopyrene into a highly reactive epoxide, which then allows it to do its damage by reacting with cellular DNA and forcing mutations that can ultimately result in the development of cancer, which is more likely to happen if there was insufficient glutathione to neutralise the epoxides before they reacted with cell DNA.

Awareness is key

We do need to understand that there will be various other reactions happening when our food is being digested, and that these are just part of the numerous reactions that happen uncontrolled.

This is one reason why some drugs and omega-3 supplements are manufactured with enteric coatings that do not decompose in the stomach environment, but will decompose in the intestines to allow for the absorption of the product in an un-peroxidised form — we don’t really want the unsaturated omega-3 fatty acids to fully undergo lipid peroxidation in the stomach now, do we?

But who would have thought that we could get such a sequence of events just by eating all that unhealthy food consistently over a long period of time?

Joel Yong, PhD, is a biochemical engineer/scientist, an educator and a writer. He has authored 5 ebooks (available on in Kindle format) and co-authored 6 journal articles in internationally peer-reviewed scientific journals. His main focus is on finding out the fundamentals of biochemical mechanisms in the body that the doctors don’t educate the lay people about, and will then proceed to deconstruct them for your understanding — as an educator should.

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