The utilization of natural antioxidants to reduce oxidative stress is a promising therapeutic approach to prevent diseases by reducing ROS. Flavonoids, phenolic compounds, antioxidant vitamins like vitamin C, and amino acids such as N-acetyl cysteine are commonly used as a single unit or mixed to provide beneficial effects. These improvements can be traced to mitochondrial function, antibacterial effects to heavy metal elimination and detoxification.
Detox as weight gain solution?
Commonly, detox diets or supplementations are thought to serve as a weight loss solution. Nevertheless, a detox regime comprises laxatives, vitamins, minerals, bioactive compounds called “cleansing foods,” starvation fasts, high fiber smoothies or juices, and even a sauna to eliminate the toxins from the body. A typical detox or cleanse is not precisely targeted to weight loss. The vitamin content may help metabolic pathways and reduce inflammation but not be considered weight loss mechanisms.
The correct assessment of body composition can be attainable through bioelectrical impedance analysis (BIA). This assessment can provide a better understanding of intracellular water content and body compartments.
The word “toxin” is loosely used and could refer to environmental pollutants such as synthetic chemicals, heavy metals, processed foods, or even harsh cleaning products. However, detox programs never claim to eliminate a particular contaminant. They have been commercially focused de stop a wide range of toxins.
So how does detox work? Most detox uses a mix of antioxidant vitamins, phenolic and bioactive compounds that target different metabolic pathways and up-regulate antioxidant enzyme production and function or binding to harmful substances and excreting them through the gastrointestinal tract. Here is a list of the multiple active compounds used as a detox and their process.
Vitamins A ((retinol, retinoic acid), vitamin C (L-ascorbic acid, ascorbic acid, ascorbate), vitamin E (α-tocopherol), β-carotene are commonly used as antioxidants. An antioxidant is defined as any substance able to eliminate ROS and derivatives (RNS, or reactive sulfur species, RSS), directly or indirectly, acting as an antioxidant defense regulator, or reactive species production inhibition.
An acute deficiency of vitamin C is associated with an increased metabolic consumption due to critical illness-induced oxidative stress. Indeed, conditions such as trauma, ischemia/reperfusion injury, and sepsis can trigger oxidative stress, and vitamin C could become insufficient to cover the excessive production of reactive oxygen species (ROS).
As part of the injury-induced inflammatory response, the release of proinflammatory cytokines by Nf-Kb, and ROS’s overproduction leading to uncoupling of mitochondrial phosphorylation, activation of nicotinamide adenine dinucleotide phosphate oxidase, lipoxygenase, cyclooxygenase and inducible nitric oxidase (iNOS), and oxidation of catecholamines. Lastly, if Vitamin C cannot provide enough antioxidant support to counteract the ROS, this will lead to cellular injury, endothelial dysfunction, and progressive organ failure.
Pleiotropic Effects of Vitamin C
|Direct radical scavenger||Superoxide
|Reduction of ROS-production||Inhibition of activation of NADPH oxidase
Inhibition of activation of xanthine oxidase
Reduction of leakage of electrons from the E- transport chain
Inhibition of iNOS
|Regeneration of antioxidants||a-tocopherol, protecting against lipid peroxidation
|Anti-inflammatory||Inhibition of NF-kB, reducing pro-inflammatory mediators|
|Immune support||Improvement of chemotaxis
Stimulation of interferon production
Enhancement of neutrophilic bacterial killing
Support of lymphocyte proliferation
Modulating regulatory T-cells
Inhibiting bacterial replication
Production of host defense peptides
|Recycling BH4, a cofactor of tyrosine hydroxylase
|Increase of catecholamine sensitivity||Binding adrenergic receptors|
|Tightening of endothelial barrier||Improves function of tight junctions|
|Improving microcirculatory potency||Inhibition of TNF-a|
N-acetyl-cysteine is the natural derivate of the amino acid L-cysteine. Since 1960, NAc has been used as a mucolytic, and later it was applied to the treatment of acetaminophen poisoning.
- Mucolytic action: NAC can break disulfide bridges of glycoproteins of mucus. This results in reduced viscosity.
- Acetaminophen poisoning: NAC can replenish hepatic glutathione (GSH).
NAC’s antioxidant activity can be related to these mechanisms:
- Direct scavenger of specific ROS and oxidative species.
- Cys precursor, which is a building block of glutathione synthesis promoting the synthesis and function of several antioxidant enzymes
- A breaking effect on disulfides and the ability to restore thiol pools, which regulate the redox state.
The utilization of multiple vitamins or amino acids, such as Vitamin C and NAC as antioxidants has been widely used and studied with positive results. The clinical applications of these compounds are the result of their mayor interaction with antioxidant enzymes or electron donation potential, which ultimately reduce oxidative stress. It is outstanding to use these compounds to target toxicity, scavenge free radicals and enhance glutathione function to counteract acute conditions. – Ana Paola R. Arciniega. Master in Clinical Nutrition.
Spoelstra-de Man, Angélique M E et al. “Vitamin C: should we supplement?.” Current opinion in critical care vol. 24,4 (2018): 248-255. doi:10.1097/MCC.0000000000000510
Aldini, Giancarlo, et al. “N-Acetylcysteine as an antioxidant and disulphide breaking agent: the reasons why.” Free radical research 52.7 (2018): 751-762.
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Dr. Alex Jimenez DC, MSACP, CCST, IFMCP*, CIFM*, CTG*
Licensed in Texas & New Mexico