Updated on April 13, 2023
Although oxidative stress might not be the most dangerous form of cellular damage, individuals should still take measures to protect themselves. And while oxidative stress has long been recognized as a part of many pathologies, newer perspectives have begun to see the utility of nutritional supplements for oxidative stress as a means of symptom management.
Damage caused by oxidative stress is implicated in a broad array of adverse health conditions. For individuals with conditions exacerbated by oxidative stress, gaining control of oxidative stress through a therapeutic oxidative stress supplement could be the key to experiencing better symptom management while avoiding further damage.
At the same time, healthy individuals can benefit from reducing their level of oxidative stress as a result of its subclinical negative impact on the body. While healthy maintenance control is not yet in the mainstream medical consensus, there is reason to believe that lowering oxidative stress via glutathione supplementation could help individuals optimize their health and well-being. Understanding why glutathione supplementation might be beneficial requires diving into the biological details of oxidative stress and exploring how the body reacts when its abilities to compensate for this stress are exceeded.
Oxidative stress is the process by which reactive oxygen species (ROS) produced by normal metabolic processes undergo chemical reactions with proteins, DNA, or lipids, which in turn inhibits the cell from making use of those molecules normally. The high-level impact of ROS reactions with physiological molecules includes tissue damage and dysfunction, potentially contributing to a wide variety of health complications.
Although the physiological basis for why this is the case is far from simple, medical science has begun to understand the most common risk vectors for oxidative stress.
Most individuals are exposed to oxidative stress on a regular basis without any noticeable adverse health impacts occurring. Nonetheless, the risks of oxidative stress are enduring, and individuals can benefit from taking preventative action to protect themselves. Ultraviolet radiation, which causes oxidative stress at high levels in the event of a sunburn, is the most common source of oxidative stress. Cigarette smoke and alcohol consumption are important contributors to oxidative stress, because both contain primary ROS in the mixtures themselves and also secondary ROS, which is generated by the body breaking down the toxic chemicals in the mixtures.
However, individuals who avoid getting sunburns and abstain from smoking and drinking alcohol can still experience oxidative stress because normal aerobic metabolism is the primary source of oxidative stress. This means that individuals simply cannot rely solely on good health habits to protect them nor can they assume their levels of oxidative stress are low.
Additionally, for individuals who have health issues linked to oxidative stress, such as autism, the body’s ability to cope with the baseline level of metabolically-induced oxidative stress is totally insufficient. Thus, autistic individuals can experience an abundance of oxidative stress-related symptoms, like executive dysfunction and irritability, as well as gastrointestinal issues like diarrhea. Meanwhile, individuals with neurological conditions might see further neurodegeneration and subsequent loss of function as oxidative stress rises.
In the course of metabolism, the body breaks down energy sources, then uses a series of chemical reactions to synthesize the metabolized molecules that cells use for energy or other essential functions. Some of these metabolic chemical reactions leave behind unwanted waste products in the form of ROS. Thus, higher metabolic activity generates more oxidative stress.
In healthy individuals, the oxidative stress created by metabolism is tightly controlled by the body, and minimal damage results. In fact, many endogenous molecules are made in the body specifically for the purpose of lowering oxidative stress and repairing the damage it causes. These molecules are critical because if ROS are left unchecked, then they can readily cause damage to DNA.
This means that each ROS in circulation carries with it a very small possibility of causing serious illness. When antioxidant molecules and DNA damage repair molecules are depleted or their synthesis is inhibited by malnutrition or an underlying medical condition, the reactive oxygen species balloon in number, and cells suffer.
When cells experience very high levels of ROS, their self-destruct mechanisms are triggered to prevent the ailing cell from causing damage to its neighbors through its malfunctions. For cells like neurons, the consequences of self-destruction can wreak havoc on one’s quality of life. Neuronal death is implicated in several adverse neurological health conditions. For other cells, self-destruction is detrimental to the functioning of the tissue in which the cell resides. In liver tissue, dying cells leave the individual with a reduced ability to clean their blood of toxins, causing other downstream problems.
However, cellular damage can occur without causing the death of the cell. In the case of non-fatal cellular damage, ROS often react with enzymes, reducing their ability to catalyze chemical reactions that the cell needs to survive. This can have serious consequences. Because the mitochondria are the organelle in which oxidative stress is the most likely to occur, it is the mitochondria that bear the brunt of enzymatic malfunction caused by ROS.
Because the mitochondria are responsible for producing the chemical energy the cell needs to perform its job, oxidative stress that damages enzymes can reduce the efficiency of the entire cell. Liver cells, for example, might experience a decrease in their rate of blood purification, whereas neurons might find it more difficult to activate themselves and relay electrochemical messages to other neurons. Each of these outcomes results in poorer health.
Additionally, oxidative stress causes inflammation when uncontrolled. In the neurological context, neuroinflammation is thought to be linked to cognitive dysfunction and deficiencies of the working memory. More broadly, inflammation tends to reduce the effectiveness of whatever tissue in which it occurs regardless of the initial cause. This means that oxidative stress could hypothetically reduce the efficiency of any tissue in the body which can experience inflammation; it also means that disorders that are aggravated by inflammation might benefit from supplements for oxidative stress.
Given that oxidative stress is deleterious to cells, most people are eager to reduce the amount of it their cells experience. However, using the metric that less oxidative stress is better can lead to undesirable results; surprisingly, total prevention of oxidative stress incidents might not be desirable.
In animal models, for example, low levels of oxidative stress were found to improve lifespan. And research also shows that eliminating oxidative stress entirely via excessive amounts of antioxidants ended up decreasing the animals’ lifespans. The explanation for this effect is relatively straightforward: much like the way muscle fibers cannot grow larger and stronger without first experiencing some tearing damage, small amounts of oxidative stress are necessary to keep various systems smoothly functioning.
More concretely, researchers know that certain white blood cells use cached free radicals as part of the lethal cocktail they deliver to bacterial pathogens. Without any oxidative stress whatsoever, these immune cells couldn’t do their job and the immune system as a whole would be weakened. There is evidence that other cells can make use of oxidative stress in similarly beneficial capacities. Notwithstanding this positive aspect, there is no evidence that high levels of oxidative stress are beneficial, so there is still a strong scientific basis for reducing oxidative stress, including through an oxidative stress nutritional supplement.
But how should individuals go about managing oxidative stress in a way that doesn’t leave them deficient in the baseline level of ROS they need? Although science currently lacks a definitive answer to this question, there is reason to believe there is a way forward nonetheless. Indeed, if an individual could provide their cells with the antioxidant molecules their cells can use only as needed, then there is a much smaller likelihood of completely depleting the necessary ROS.
This means the ideal antioxidant molecule would be something the cells already use in that capacity. With this aspect in mind, the antioxidant glutathione might be the best of the available nutritional supplements for oxidative stress for individuals who don’t want to risk weakening their systems.
Glutathione is an appealing choice for individuals seeking to reduce their level of oxidative stress safely because cells already use glutathione prolifically. Animals, plants, fungi, and many bacteria synthesize glutathione from several essential amino acids and use it to defend themselves against oxidative stress by exploiting its ROS-receptive chemical structure.
Because most life forms synthesize glutathione for themselves, it is often consumed in food, although it is not a nutrient. Stomach acid typically breaks down orally consumed glutathione into its constituent parts, which are later re-assembled by cells for the purposes of regulating oxidative stress. When cells detect high levels of oxidative stress, they direct glutathione molecules to the problem area. Once there, glutathione reacts with the ROS, safely removing them from circulation and preventing them from damaging cellular machinery.*
Afterward, the cells direct the newly oxidized glutathione molecule elsewhere to be recycled safely. Excess quantities of glutathione are safely stored in several different cellular holding vaults, which keeps them from causing excessive reduction of oxidative stress.
Although cells rely on glutathione as their first line of defense against oxidative stress, in conditions of very high oxidative stress, glutathione supplies can run low and damage can result. This means that providing one’s cells with an extra supply of glutathione via supplementation could mean the difference between experiencing oxidative stress damage and remaining healthy.*
Increasing the proportion of glutathione’s chemical precursors in the diet doesn’t solve the problem, because synthesizing glutathione from its precursors takes precious time, which can allow oxidative stress to cause damage before the newly produced glutathione can be brought to bear. Additionally, people are unlikely to anticipate when their body’s glutathione supply is running low; glutathione levels are known to decrease with age and low levels are associated with a number of serious health conditions.
Significantly, an insufficient glutathione supply has no early symptoms, although individuals might begin experiencing symptoms of inflammation stemming from the damage caused by oxidative stress. Maintaining a larger supply of glutathione preventatively through an oxidative stress supplement is thus a good strategy for individuals who want to avoid gaps in their protection.*
Glutathione supplements currently on the market are readily used by cells to improve their ability to combat oxidative stress.* Using sophisticated delivery systems, these supplements are guaranteed to reach where the body can use them, unlike with glutathione in food form.*
This could have significant benefits for individuals; for example, research has shown that oral glutathione supplements can increase cellular glutathione concentrations by as much as 260 percent in immune cells.* Glutathione as an oxidative stress supplement is also highly tolerable, and in clinical settings, most individuals find the side effects of glutathione supplements to be transient and mild. Of those who do report side effects, headache and minor nausea are the most common complaints.
Although the clinical impact of glutathione supplementation is still under investigation, preliminary participant accounts indicate it could reduce the intensity of oxidative stress-related symptoms, which means that supplementation could be broadly applicable for a range of neurological and gastrointestinal conditions. For individuals beginning to experience cognitive deficits, evidence suggests that a high-quality glutathione supplement might help manage their oxidative stress levels sufficiently for an improved level of cognition.*
Future research will shed greater light on the details of how glutathione supplementation should be used clinically. In the meantime, individuals who suffer from oxidative stress-associated conditions can be confident in the safety of glutathione as an emerging oxidative stress supplement that has the potential to significantly improve quality of life.*
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