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Guillermou
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A very interesting report from Dr. Mercola. He asks ChatGPT about butyrate in colon cancer and its interaction with sulforaphane.

What exactly is butyrate?

• It is formed from the fermentation of:

• Soluble fiber (inulin, pectins)

• Resistant starch

• Some oligosaccharides

• It is produced by bacteria such as:

• Faecalibacterium prausnitzii

• Roseburia

• Eubacterium rectale

It is the main fuel for colonocytes (cells of the colon).

________________________________________

Protective effects against colon cancer

In the context of colorectal cancer (for example, as described in Colorectal Cancer), butyrate has several anticancer mechanisms:

1. It induces apoptosis in tumor cells

In cancer cells, metabolism is altered (Warburg effect).

Butyrate:

• Is not efficiently used as energy

• Accumulates in the nucleus

• Acts as a histone deacetylase inhibitor (HDAC)

• Activates tumor suppressor genes

• Induces apoptosis (programmed cell death)

Interesting fact:

In normal cells, it nourishes.

In tumor cells, it inhibits their growth.

This phenomenon is called the “butyrate paradox.”

________________________________________

2. Reduces inflammation

• Decreases NF-κB

• Reduces inflammatory cytokines

• Strengthens the intestinal barrier

Chronic inflammation is one of the major drivers of colorectal cancer.

________________________________________

3. Improves epithelial integrity

• Increases mucin production

• Strengthens tight junctions

• Reduces intestinal permeability

An intact barrier ↓ exposure to carcinogens.

________________________________________

4. Modulates the immune system

• Increases regulatory T cells

• Improves antitumor immune surveillance

________________________________________

What do the studies say?

In animal models:

• High-fiber diets → ↑ butyrate → ↓ tumors

In humans:

• Higher fiber intake → lower risk of colorectal cancer

• Cancer patients often have ↓ butyrate-producing bacteria

It is not a treatment, but it is an important metabolic protective factor.

________________________________________

How much butyrate is “protective”?

It is not easily measured in blood. The key points are:

• 25–35 g/day of total fiber

• Presence of resistant starch

• Microbiota capable of producing it

________________________________________

Butyrate in food vs. endogenous production

Butyrate:

• Is present in small amounts in butter and dairy products

• But its protective effect comes primarily from its production in the colon

________________________________________

In people with:

• SIBO (Small Intestinal Bacterial Overgrowth)

• Dysbiosis

• Low bacterial diversity

There may be:

• ↓ butyrate production

• ↑ inflammation

• ↑ long-term risk if it becomes chronic

However, fiber should be introduced gradually if symptoms are present.

But fiber intake should be gradual. ________________________________________

Clear Conclusion

Butyrate:

Nourishes colonocytes

Induces apoptosis in tumor cells

Reduces inflammation

Protects against colorectal cancer

Is one of the most important metabolites in prevention

________________________________________

Role of butyrate in precancerous colon lesions

When we talk about precancerous lesions in the colon, we are referring primarily to:

• Adenomas

• Adenomatous polyps

• Epithelial dysplasia

(stages prior to colorectal cancer)

Butyrate plays a particularly important role here.

________________________________________

What happens in a precancerous lesion

Before becoming cancerous:

• Cell proliferation increases

• Apoptosis decreases

• Epigenetic alterations appear

• Local inflammation is common

• Butyrate-producing bacteria decrease

It is an “intermediate” state, still reversible in many cases.

________________________________________

How Butyrate Acts in This Context

1. Epigenetic Regulation (very important)

Butyrate is a histone deacetylase (HDAC) inhibitor.

In precancerous lesions:

• Reactivates tumor suppressor genes

• Inhibits excessive proliferation

• Promotes normal cell differentiation

• Increases apoptosis of dysplastic cells

Its effect is clearer here than in advanced cancer.

________________________________________

2. Reduction of Local Inflammation

Precancerous lesions often coexist with:

• Chronic microinflammation

• Activation of NF-κB

• Increased oxidative stress

Butyrate:

• Reduces proinflammatory cytokines

• Improves the immune environment

• Decreases proliferative signals

Less inflammation = less stimulus for progression.

________________________________________

3. Reinforcing the intestinal barrier

In early lesions:

• Increased permeability is common

• More contact with luminal carcinogens

Butyrate:

• Strengthens tight junctions

• Increases mucin production

• Improves epithelial integrity

________________________________________

4. Evidence in Humans

In studies:

• Patients with adenomas have a lower abundance of butyrate-producing bacteria

• High-fiber diets reduce polyp recurrence

• Higher fecal butyrate levels are associated with a lower risk of progression

________________________________________

Key point: It depends on the metabolic context

The well-known concept of the “butyrate paradox”:

• In normal cells → it is fuel

• In dysplastic cells → it can act as an epigenetic regulator

• In advanced cancer → the effect is more variable

In precancerous lesions, it is usually more beneficial than in established tumors.

________________________________________

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