Did you know?
Mitochondrial dysfunction is an underlying foundational element of most diseases.
As explained by Alex Vasquez, M.D., Ph.D., author of about 100 papers and 15 scientific books, in addition to producing most of your body’s energy in the form of ATP, your mitochondria also participate in many other processes, such as cellular signaling.
According to Vasquez, the data is “impressively clear” that those with type 2 diabetes, metabolic syndrome, and high blood pressure have dysfunctional mitochondria.
Your mitochondria also play an important role in inflammation and control apoptosis (cell death). These two roles make your mitochondria a player in diseases such as cancer, for example, as damaged cells fail to receive the message to self-destruct, and therefore continue their malignant growth.
Vasquez — who is an expert on inflammation — divides inflammation into three different forms, which exist on a continuum and overlap each other:
1. Metabolic inflammation (conditions such as hypertension and diabetes)
2. Allergic inflammation
3. Autoimmune inflammation
Chronic, low-level inflammation, which tends to underlie most chronic health conditions, he describes as “metabolic disturbance with cellular injury.” While mitochondrial dysfunction is involved in virtually ALL disease, the following bears mentioning, as they’re among the most common:
-Cancer
-Heart disease
-Seizure Disorders
-Asthma and allergies
-Autoimmune diseases
-Obesity
-Alzheimer’s
-Parkinson’s
-Depression
-Chronic fatigue syndrome
-Fibromyalgia
-Autism
-Type 2 diabetes
-Metabolic syndrome
-Hypertension
🦠 The role of mold on mitochondrial dysfunction and cytotoxicity
Mitochondria are the powerhouse of cells, which upon dysfunctions may lead to several diseases. Mycotoxins are the toxic secondary metabolites from fungi that are capable of causing diseases and death in humans and animals.
Findings suggest that mycotoxins such as citrinin, aflatoxin, and T‐2 toxin exert multi‐edged sword‐like effects in test systems causing mitochondrial dysfunction.
Mycotoxins can induce oxidative stress even at low concentration/dose that may be one of the major causes of mitochondrial dysfunction. On the other hand, activation of apoptotic caspases and other proteins by mycotoxins may lead to apoptotic cell death.
Thus, mycotoxins‐mediated mitochondrial dysfunction may be related to several chronic diseases which also makes these mycotoxins considerable as lead compounds for inducing toxic effects in cells.
What steps can you take to help restore mitochondrial function?
1. If you’re living in an environment with mold, get it cleaned up and get a high-quality air purifier.
2. Rebuild your gut lining, microbiome, cellular strength and restore oxygenation with BOO Fulvic Acid.
3. Detox. Before doing any kind of detox, you first need to rebuild so that the body is able to more adequately absorb nutrients and expel toxicity without herxing. Fulvic Acid not only works as a binder, chelator, and detoxifier, but it also improves nutrient absorption and remineralizes the body. If you have a history of mold exposure, toxic mold may be responsible for your stomach problems. That's because mycotoxins, the toxic byproduct of some molds, as well as the immune response to mycotoxins can cause damage to your intestinal lining and harm your gut microbiome, leading to leaky gut.
4. Switch to all-natural and non-toxic cleaning and personal care products. The environment plays a significant role in human health and disease. A systematic study conducted by The World Health Organization (WHO) estimated that 22% of global disease burden, including mental, behavioral, and neurological disorders, are due to preventable environmental factors. Environmental toxins are pervasive in all aspects of patient’s lives, including those found in the air, water, soil, food, and consumer products. Effects from exposures may be lifelong. Children experience a disproportionate share of the environmental disease burden.
Recent decades have seen a rapid increase in reported toxic effects of drugs and pollutants on mitochondria. Researchers have also documented many genetic differences leading to mitochondrial diseases, currently reported to affect ∼1 person in 4,300, creating a large number of potential gene-environment interactions in mitochondrial toxicity.
5. Try to only eat clean, pesticide-free, and non-GMO foods as much as possible. In a study published in the International Journal of Molecular Sciences, it was shown how pesticides induced morphological changes of mitochondria and dose-dependent apoptotic cell death. In short, pesticides can make a mess of mitochondrial function.
So how does glyphosate affect your mitochondria? Seneff speaks to this issue, noting that manganese appears to be involved. Glyphosate chelates manganese (plus many other minerals), which makes the plants deficient. In turn, the animals or humans who eat the plants do not get enough either. It’s worth explaining the chelation process a bit further. As Smith notes, glyphosate binds very strongly to micro minerals and doesn’t let them go. Fulvic acid can help to remineralize the body and mitigate the negative effects of glyphosate.
So even if there’s manganese in the plant you eat, your body cannot access and use it, because the glyphosate molecule holds it trapped within itself. Likewise, the plant is prevented from taking up the mineral, even if it’s in the soil. Your mitochondria require manganese to break down superoxide dismutase (SOD) and turn it into hydrogen peroxide, which is far less toxic, and eventually water. This is a very important process, as it protects your mitochondria from oxidative damage. Without manganese, this protection is lost.
6. Increase glutathione levels. Among the arsenal of antioxidants and detoxifying enzymes existing in mitochondria, mitochondrial glutathione (mGSH) emerges as the main line of defense for the maintenance of the appropriate mitochondrial redox environment to avoid or repair oxidative modifications leading to mitochondrial dysfunction and cell death. Fulvic Acid increases the activity of glutathione peroxidase.
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