Chronic inflammation and cancer are health challenges that affect millions of individuals worldwide. Inflammation is your body’s natural response to injury or infection, characterized by redness, swelling and pain. However, when inflammation becomes persistent, it leads to tissue damage and contributes to the development of various diseases, including cancer.
Cancer itself is marked by the uncontrolled growth and spread of abnormal cells, which invade surrounding tissues and form harmful tumors. If left untreated, these conditions significantly impair quality of life and increase mortality rates. Mitochondria, often referred to as the powerhouses of the cell, play a key role in producing adenosine triphosphate (ATP), the energy currency essential for numerous cellular functions.
When mitochondrial function is compromised, ATP production decreases, leading to cellular energy deficits. This reduction in energy impairs the cell’s ability to regulate normal processes, fostering an environment ripe for chronic inflammation.
According to research published in Immunity,1 impaired mitochondrial function directly activates the NOD-like receptor protein 3 (NLRP3) inflammasome, a key component in the inflammatory response. This activation not only sustains inflammation but also creates conditions that promote cancer development by enabling cancer cells to thrive and evade your immune system.
Mitochondrial Function Is Intricately Involved in Inflammation and Cancer
The impact of mitochondrial dysfunction on inflammation and cancer is significant. Studies show that approximately 20% of all cancers are linked to chronic inflammation, highlighting the strong connection between these conditions.2 Additionally, individuals with mitochondrial disorders are at a higher risk of developing inflammatory diseases compared to the general population.3
• Millions of Americans are affected by mitochondrial dysfunction — In the U.S. alone, chronic inflammatory conditions affect close to 125 million adults,4 while cancer remains the second leading cause of death, accounting for more than 608,000 fatalities each year.5 Moreover, research indicates that mitochondrial dysfunction contributes to the resistance of cancer cells to conventional therapies, making treatment more challenging.6
• A call to action for better treatment for mitochondrial health — The statistics underscore the urgent need to address mitochondrial health as a strategy to combat both inflammation and cancer effectively.
Beyond their direct effects, chronic inflammation and cancer driven by mitochondrial dysfunction leads to a cascade of additional health problems. Persistent inflammation is associated with cardiovascular diseases, diabetes and neurodegenerative disorders, further compounding the burden on affected individuals.
• Cancer stems largely from mitochondrial dysfunction — Cancer progression often results in debilitating symptoms such as pain, fatigue and loss of organ function, which drastically reduces life expectancy and quality of life.
Understanding the role of mitochondrial dysfunction in driving inflammation and cancer not only illuminates therapeutic targets but also emphasizes the importance of maintaining mitochondrial health to prevent a wide array of serious health issues.
• Mitochondrial dysfunction is a key player in the development of NLRP3-related conditions — When mitochondria fail to produce adequate ATP, it sets off a cascade of cellular stress signals.
These signals activate the NLRP3 inflammasome, a protein complex that plays a significant role in the body’s inflammatory response.7 The activation of this inflammasome is linked to various diseases, including chronic inflammation and cancer, as it leads to uncontrolled cell death and tissue damage.
Study Reveals How Mitochondrial Dysfunction Fuels Inflammation and Cancer
A recent study investigated the intricate relationship between mitochondrial function and the activation of the NLRP3 inflammasome. The research focused on understanding how the inhibition of oxidative phosphorylation (OXPHOS), the process by which mitochondria produce ATP, affects cell death and inflammation.
The study employed various cell types, including myeloid cells, primary murine microglia, human monocyte-derived macrophages, HCT116 and HeLa cells, as well as conducted in vivo experiments using Xenopus laevis tadpoles.8
• The NLRP3 inflammasome negatively impacts mitochondrial health — The population studied encompassed a diverse range of cells to mimic different physiological conditions. The findings revealed that activators of NLRP3 significantly hinder mitochondrial ATP production, which in turn suppresses apoptosis, the process of programmed cell death.
This suppression allows damaged cells to survive longer than they should, contributing to inflammation and leading to cancer development. The study demonstrated that when OXPHOS is inhibited, mitochondrial cristae — the inner folds of mitochondria — undergo structural changes that trap cytochrome c, a molecule essential for apoptosis.9
• Other factors that diminish apoptosis — The research also showed that various NLRP3 activators, such as nigericin, imiquimod and extracellular ATP, inhibit apoptosis not by activating the inflammasome directly, but through their disruptive effects on mitochondrial function. These compounds cause the closure of crista junctions, preventing cytochrome c from being released into the cytoplasm, which is a necessary step for apoptosis to proceed.
• The impact of viral infections on mitochondrial function and apoptosis — It was observed that infections like SARS-CoV-2 could strongly suppress apoptosis by inhibiting the cleavage of caspase-3, an enzyme involved in the execution of apoptosis. This suppression not only hinders the removal of infected cells but also facilitates the activation of the NLRP3 inflammasome, thereby promoting an inflammatory response.10
Mitochondrial Dysfunction Is at the Root of Most Chronic Disease
Biologically, the mechanism at play involves the inhibition of mitochondrial ATP production by NLRP3 activators. When OXPHOS is blocked, mitochondria cannot produce sufficient ATP, leading to the rearrangement of cristae and retention of cytochrome c within the mitochondria. This retention prevents apoptosis, allowing damaged cells to survive and multiply unchecked.
• The process of NLRP3 signaling and activation — The suppression of ATP production provides a necessary signal for the activation of NLRP3. However, full activation of NLRP3 requires a second signal, highlighting the complexity of the inflammasome’s regulation.11
The study also compared the effects of different NLRP3 activators and OXPHOS inhibitors, revealing that while all these agents suppress apoptosis, only certain ones could activate NLRP3 without an additional signal.
• A way to control mitochondrial processes to facilitate healing — This comparison highlights the intricate relationship between mitochondrial function and inflammasome activation, suggesting that modulating mitochondrial processes could be an effective strategy for managing inflammation and reducing cancer risk.12
The research provides compelling evidence that mitochondrial dysfunction, specifically through the inhibition of OXPHOS, plays a pivotal role in suppressing apoptosis and activating the NLRP3 inflammasome.
This dual action not only fosters a proinflammatory environment but also allows for the survival of malignant cells, thereby linking reduced mitochondrial function to the progression of inflammation and cancer.13 As noted on Georgi Dinkov’s blog, the study demonstrates that mitochondrial dysfunction is a key player in both cancer and inflammation:14
“Yet another study, which demonstrates the inseparable link between metabolism and ‘structural’ problems such as cellular integrity and lifecycle (e.g. apoptosis), as well as mysterious processes of systemic inflammation, often occurring without any cause that medicine can identify.
Both of these processes are highly visible in cancer — i.e., lack of apoptosis in ‘cancer’ cells despite their wrecked genome and metabolic dysfunction, as well as their highly inflamed nature that ‘recruits’ nearby cells to the ‘cancer’ process through the cytokines the ‘cancer’ cells produce and releases in the blood.
In other words, all that takes for systemic inflammation and even cancer (i.e., lack of apoptosis in damaged cells) to form is reduced mitochondrial function, resulting in a prolonged drop of ATP levels.
Thus, chronic stress, inflammatory diet (PUFA anyone?), endocrine disruptors, and the ‘modern’ life characterized by never-ending soul-crushing routines are all direct causes of all our ailments as the one thing all those pathological processes have in common is their profoundly suppressive effects on mitochondria/OXPHOS.
Conversely, simply restoring/improving mitochondrial function may be enough to ameliorate/cure virtually all chronic diseases known to medicine.”
How to Address Mitochondrial Dysfunction and Reduce Inflammation
Your mitochondria power every cell in your body. When they don’t work properly, inflammation rises and damaged cells multiply instead of dying off naturally. Here’s how to support your mitochondrial function and restore cellular energy:
1. Eliminate processed foods and vegetable oils — The modern diet is rife with processed foods and vegetable oils rich in linoleic acid (LA) that damage your gut microbiome and promote harmful bacteria.
LA is a mitochondrial poison that compromises your cellular energy production. In addition to processed foods, avoid nuts and seeds as well to reduce LA intake. It’s also advisable to avoid dining out, since most restaurants use vegetable oils in their cooking, sauces and dressings.
Additionally, limit your consumption of chicken and pork, which are typically high in LA. Replace processed foods with whole, unprocessed foods and healthy fats such as grass fed butter, tallow and ghee. It’s wise to keep your LA intake below 5 grams from all sources. If you can get it below 2 grams, that’s even better. To help track your LA intake, enter all your daily meals into an online nutrition tracker.
2. Optimize carbohydrate intake — Carbohydrates play an important role in supporting mitochondrial function since glucose is the preferred fuel for energy production at the cellular level. Tailor your carbohydrate consumption to support cellular energy by aiming for at least 250 grams of targeted carbohydrates daily for most adults. Individuals with higher activity levels typically require more.
Introduce carbohydrates gradually to allow your gut to adapt, thereby minimizing digestive issues and endotoxin levels. Begin with white rice and whole fruits to nourish beneficial bacteria before considering vegetables, whole grains and starches. Avoiding high-fiber diets initially is important if your gut microbiome is compromised, as excessive fiber will increase endotoxin levels.
If your gut health is severely compromised, focus on easily digestible carbohydrates like dextrose water for the first week or two. Sip it slowly throughout the day to support gradual gut healing.
3. Reduce exposure to environmental toxins — Exposure to synthetic endocrine-disrupting chemicals (EDCs), estrogen and pervasive electromagnetic fields (EMFs) further impairs your cells’ ability to generate energy efficiently. This energy deficit makes it challenging to sustain the oxygen-free gut environment necessary for beneficial bacteria like Akkermansia to flourish.
Further, a lack of cellular energy creates an environment in your gut that favors endotoxin-producing bacteria, damaging mitochondria and creating a vicious cycle of worsening health. By tackling excess LA, estrogens (xenoestrogens found in everyday items like plastic), EDCs and EMFs, you restore your cellular energy and start down the path toward optimal mitochondrial function and health.
4. Get proper sun exposure and boost NAD+ levels — Take niacinamide (50 milligrams three times daily) to increase NAD+ production, which helps your mitochondria generate more energy. NAD+ enables proper cell death signaling and supports your immune system’s ability to identify and remove damaged cells.
Daily sun exposure is also important as it promotes cellular energy production by stimulating mitochondrial melatonin, offering powerful antioxidant protection. Start with brief morning exposures and gradually increase tolerance. It’s important to avoid direct sunlight during peak hours (from 10 a.m. to 4 p.m. in most U.S. regions) until you’ve eliminated vegetable oils from your diet for at least six months to reduce sunburn risk associated with stored linoleic acid.
Frequently Asked Questions About Mitochondrial Dysfunction and Inflammation
Q: What is the connection between mitochondrial dysfunction and chronic inflammation?
A: When mitochondria underproduce ATP, the body perceives this energy deficit as cellular stress. This stress triggers the NLRP3 inflammasome, a protein complex that amplifies inflammation. Over time, chronic inflammation damages tissues and can set the stage for serious conditions like cancer.
Q: How does mitochondrial dysfunction contribute to cancer development?
A: Damaged mitochondria hinder the cell’s ability to undergo apoptosis (programmed cell death). When apoptosis is suppressed, abnormal cells survive longer than they should, accumulating more mutations and fueling tumor growth. Additionally, chronic inflammation driven by impaired mitochondrial function creates an environment that supports cancer progression.
Q: Why is linoleic acid problematic for mitochondrial health?
A: LA, found in most vegetable oils and many processed foods, is considered a mitochondrial poison because it impairs cellular energy production. Consuming high amounts of LA results in both gut dysbiosis (an imbalance of gut bacteria) and heightened inflammation, further undermining mitochondrial function and overall health.
Q: Can improving carbohydrate intake help restore mitochondrial function?
A: Yes. Glucose is a key fuel for energy production (via oxidative phosphorylation) in the mitochondria. By incorporating adequate, easily digestible carbohydrates — such as white rice or whole fruits — you’ll be able to support cellular energy and encourage healthier gut bacteria. This approach is especially important if your gut microbiome is already compromised.
Q: What lifestyle strategies can support better mitochondrial function?
A: Key strategies include eliminating processed foods (especially those high in vegetable oils), optimizing carbohydrate intake, reducing exposure to toxins like endocrine disruptors and heavy electromagnetic fields, getting regular sun exposure, and boosting NAD+ levels (e.g., via niacinamide supplementation). These measures help reduce inflammation, restore proper cell death signaling, and protect against chronic diseases linked to mitochondrial dysfunction.
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