Long-term cognition and longevity via minimizing oxidative stress

Oxidative stress is an imbalance between free radicals and antioxidants in your body. Free radicals are oxygen-containing molecules with an uneven number of electrons. The uneven number allows them to easily react with other molecules. Free radicals can cause large chain chemical reactions in your body because they react so easily with other molecules. These reactions are called oxidation. They can be beneficial or harmful.
The balance between ROS and antioxidants is optimal, as both extremes, oxidative and antioxidative stress, are damaging. Therefore, there is a need for accurate determination of individual’s oxidative stress levels before prescribing the supplement antioxidants.
healthy diet is the most effective way to get the antioxidants your body needs. Fruits, vegetables, grains, eggs and nuts are all useful sources of antioxidants. Despite the marketing hype, antioxidants found in so-called superfoods are no more effective than those in regular fruit and veg, so you’re better off saving your money.
But it’s a different story when it comes to antioxidant supplements. Research has found antioxidant supplements may cause more harm than good. A 2012 meta analysis of over 70 trials found antioxidant supplements are ineffective or even detrimental to health. The reasons are unclear, but the added nutritional benefits from consuming antioxidants in a healthy diet is likely to contribute to this. Also, the high concentrations of antioxidants associated with supplement use can lead to problems.

Oxidative stress can increase as one ages.

Oxidative stress can trigger a number of human diseases.

Aging is the most obvious risk factor for AD. Free radicals are involved. The probability of this involvement is supported by the fact that neurons are extremely sensitive to attacks by destructive free radicals. Furthermore, lesions are present in the brains of AD patients that are typically associated with attacks by free radicals (eg, damage to DNA, protein oxidation, lipid peroxidation, and advanced glycosylation end products).
Cumulative oxidative stress, disrupted mitochondrial respiration, and mitochondrial damage are related with various neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, and others.
 Oxidative stress causes damage to cell function with aging and is involved in a number of age-related disorders including atherosclerosis, arthritis, and neurodegenerative disorders. In the neurodegenerative diseases, oxidative stress has been implicated in amyotrophic lateral sclerosis, Parkinson disease, Huntington disease, and Alzheimer disease (AD). 
Cellular changes show that oxidative stress is an event that precedes the appearance of the hallmark pathologies of the disease, neurofibrillary tangles, and senile plaques.
Growing evidence has demonstrated that oxidative stress is an important factor contributing to the initiation and progression of AD. 

Oxidative stress hurts telomere length.

Oxidative stress can cause thymic atrophy.

Mitochondrial, or any oxidative stress may cause cognitive decline.

To minimize oxidative stress

Alcohol promotes the generation of reactive oxygen specise (ROS) and/or interferes with the body’s normal defense mechanisms against these compounds through numerous processes, particularly in the liver. For example, alcohol breakdown in the liver results in the formation of molecules whose further metabolism in the cell leads to ROS production. Alcohol also stimulates the activity of enzymes called cytochrome P450s, which contribute to ROS production. Further, alcohol can alter the levels of certain metals in the body, thereby facilitating ROS production. Finally, alcohol reduces the levels of agents that can eliminate ROS (i.e., antioxidants). The resulting state of the cell, known as oxidative stress, can lead to cell injury. ROS production and oxidative stress in liver cells play a central role in the development of alcoholic liver disease.
Alcohol-induced oxidative stress is linked to the metabolism of ethanol involving both microsomal and mitochondrial systems. Ethanol metabolism is directly involved in the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). These form an environment favourable to oxidative stress.
Oxidative stress and DNA damage occur in the developing hippocampus and cerebellum as a result of alcohol administration.
Alpha-lipoic acid decreases DNA damage and oxidative stress induced by alcohol in the developing hippocampus and cerebellum of rat. Here are food sources.

Overall, current evidence suggests that antioxidant supplementation can lower oxidative biomarkers in subjects with increased oxidative stress levels, but not in healthy individuals with “normal” oxidative stress levels.

Note that Acai berries are no better than applesauce.

Fat accumulation (obesity) is correlated with systemic oxidative stress in humans and mice.
Obesity is characterized by chronic low grade inflammation with permanently increased oxidative stress. Over-expression of oxidative stress damages cellular structures together with under-production of anti-oxidant mechanisms, leading to the development of obesity-related complications. 
Excessive caloric intake acutely causes oxidative stress, GLUT4 carbonylation, and insulin resistance in healthy men.
Alternate day calorie restriction improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma.

The circadian clock controls the transcription of genes involved in cellular antioxidative defense.
A dysfunctional circadian oscillation is seen in night workers who have higher levels of oxidative stress damage and lower levels of antioxidant defenses.

The antioxidant properties of cocoa may be responsible for many pharmacological effects, including the inhibition of lipid peroxidation and the protection of LDL-cholesterol against oxidation, and increase resistance to oxidative stress.

Increasing age, tobacco, heme iron intake from meat and fish and transferrin saturation were independently and positively associated lipoperoxidation , while non-heme iron was negatively associated. Vegetables, vitamin C intake and serum ferritin were positively associated with antioxidant capacity, whereas saturated fatty acids and meat intake were negatively associated.

Excessive dietary fructose results in an elevation of uric acid which results in mitochondrial oxidative stress.
Chronic consumption of fructose results in markedly higher baseline levels of mitochondrial reactive oxygen species. 
Fructose fed rats showed  low-grade metabolic inflammation. Inflammation was associated with oxidative damage to hepatic lipids in young and adult rats.
A short-term fructose-rich diet induced mitochondrial dysfunction and oxidative stress, associated with an increased concentration of inflammatory markers in rats.
A high-fat/high-fructose rat diet resulted in increased oxidative stress both in the brain mitochondria and in the frontal cortex and decreased expression of the Nrf2 gene.
Excessive consumption of fructose causes cardiometabolic dysfunctions through oxidative stress and inflammation.
A study of 20 physically trained males showed that the addition of fructose to a pre-exercise glucose supplement triggers oxidative stress.
Long-term apple juice consumption decreases memory function in rats, possibly through an increase in oxidative stress in the brain, in turn induced by fructose overloading. Fruit juice of any sort is a potent source of fructose. Moderate fruit consumption is OK, though, due to the fiber.
Maternal high-fructose consumption provokes placental oxidative stress resulting in asymmetrical fetal growth restriction in rats.
Table sugar (sucrose) is 1/2 fructose. Reduced glutathione levels characterize the hepatic oxidative stress due to sucrose ingestion in rats.
The role of oxidative stress (OS), during early metabolic syndrome (MetS), on amyloidogenic processes in a MetS rat model induced by sucrose. MetS caused OS damage as indicated by serum and hypothalamus lipid peroxidation and elevated serum catalase activity.
A single dose of oral sucrose significantly increased ATP use and oxidative stress in premature neonates.
Increased total DNA damage and oxidative stress in brain are associated with decreased longevity in high sucrose diet fed to obese rats.
Fructose (from sugar and corn syrup) worsens glycation, oxidative stress, mitochondrial dysfunction, insulin resistance, and chronic inflammation.
A substantial increase was observed in triglycerides, total, LDL and VLDL cholesterols while decrease was observed in HDL cholesterols as sugar content of diet increases. Whereas significant decrease was observed in glutathione-s-transferase, superoxide dismutase, catalase and reduced glutathione levels, substantial increase was observed in malondialdehyde, an index of lipid peroxidation.
Mitochondria from sucrose-fed rats generated hydrogen peroxide (strong oxidant) at a higher rate than the control mitochondria. The increased rate of H2O2 generation in sucrose-fed mitochondria corresponded to decreased levels of reduced glutathione and vitamin E.
A high-sucrose diet increases reactive oxygen species generation, and proton leak in liver mitochondria.

Excessive iron supplementation with vitamin C exacerbates oxidative stress in the gastrointestinal tract leading to ulceration in healthy individuals, exacerbation of chronic gastrointestinal inflammatory diseases and can lead to cancer.
When present in excess within cells and tissues, iron disrupts redox homeostasis and catalyzes the propagation of reactive oxygen species (ROS), leading to oxidative stress.
Excess iron is especially damaging when there is already oxidative stress.
An excess of iron can find it’s way to the brain, causing oxidative stress, the damage to neurons.

Advanced Glycation End Products

Methylglyoxal, a major component of advanced glycation end products (AGES), increase oxidative stress in rats.
Accumulation of AGEs has been found in healthy aging persons, and this accumulation is higher during high glucose concentrations (high blood sugar).
dry heat cooking (toast, roasted almonds and other nuts)
baked or fried (but not boiled) potatoes
Cocaine promotes oxidative stress and microglial-macrophage activation in rat cerebellum.
fried food
dry cereal
bread crusts
High fat diet (fast food)-induced mitochondrial DNA damage correlates with mitochondrial dysfunction and increased oxidative stress in skeletal muscle and liver.

BBQ chicken & bacon (high fat)
any animal-derived foods
high blood sugar
Long-term fructose consumption accelerates glycation and several age-related variables in male rats.
Fructose ingestion enhances atherosclerosis and deposition of advanced glycated end-products in cholesterol-fed rabbits.

sunflower sprouts
A low-starch plant-based diet.
Cloves, allspice and cinnamon are the leading spices that offer significant protection against the formation of advanced glycation end-products (AGE). Oregano, rosemary, sage, thyme marjoram, tarragon, rosemary and turmeric, also showed an ability to inhibit glycation.

Dietary intake of arsenic (rice if often a culprit) increases oxidative stress.

Eat beet leaves

Eat blueberries: Blueberries may work via stilbenes.

Broccoli spouts shown by twelve healthy subjects (6 males and 6 females) who consumed fresh broccoli sprouts (100 g/day).

Calorie restriction

A robust, functional circadian rhythm.

Consume cocoa – best ultra dark, or just use cocoa powder.

Fish oil and multivitamin supplementation reduces oxidative stress but not inflammation in healthy older adults.



Curcumin, a yellow coloring agent extracted from turmeric, shows strong anti-oxidative and anti-inflammatory activities when used as a remedy for the prevention and treatment of chronic diseases.
Curcumin vs. oxidative stress in mouse mitochondria.
Curcumin alleviates oxidative stress via heat shock proteins in heat-stressed quails.
Turmeric and curcumin appear to be beneficial in preventing diabetes-induced oxidative stress in rats despite unaltered hyperglycemic status.
Curcumin vs. oxidative stress due to iron overload.
curcumin vs. oxidative stress → less chronic inflammation.
curry (culinary intake) may not be sufficient

Consume adequate calcium.

Vitamin E (do not supplement).


Rigorous and prolonged exercise results in an oxidative stress level that is detrimental to human health. This is especially true for untrained exercisers.
Exercise prevents oxidative damage by reducing oxidative stress in those with high blood pressure.
Exercise increases the production of antioxidant enzymes, not only in the muscle that’s active during exercise but other organs around the body. This protection against oxidative damage may be less so for seniors.

Exercise and regular physical activity counteract the deleterious effects of aging, not only by combating sarcopenia, obesity, and mitochondrial dysfunction, the major triggers of oxidative stress and inflammation in aging, but also by exerting additional antioxidant and anti-inflammatory actions as illustrated in Figure 2.

Figure 2
Modulation of oxidative stress and inflammation in aging by exercise.

Glutathione is a major antioxidant that can help prevent oxidative stress through the removal of reactive oxygen species (ROS). Exogenous administration of glutathione is able to protect cells against oxidative stress-induced mitochondria-mediated apoptosis. Glycine and N-acetylcysteine (GlyNAC) supplementation in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, genotoxicity, muscle strength, and cognition. Sulforaphane can also boost glutathione. The best source of sulforaphane is broccoli sprouts.
Adequate sleep and sulforaphane→ increased glutathione → less oxidative stress.
Exercise with boost glutathione level.
Curcumin may boost glutathione level.

Gotu kola (Centella asiatica) protects against D-galactose induced behavioral, oxidative damage and mitochondrial dysfunction in mice.

A Mediterranean Diet. A plant-based diet supplies antioxidants that, unlike pills, work! Epidemiological studies have established a positive correlation between the intake of fruits and vegetables and prevention of diseases thought to be caused by oxidative damage. A quality plant-based diet features polyphenols, Polyphenols overtake dietary vitamin C and vitamin E for disease prevention. Flavonoids are also polyphenols.
Polyphenols are best preserved by steaming or microwaving colorful veggies.
Polyphenols mop up damaging free radicals (better than pills).
Polyphenols mop up damaging free radicals (better than pills)
Polyphenols act via activation of the Nrf2 transcription factor. Lots of phytochemicals do this.
Eat spinach and other dark leafy greens.
Eat sprouted beans, seeds, and grains, especially after temperature stress.
By virtue of its lipophilic nature and low molecular weight, sulforaphane displays significantly higher bioavailability than the polyphenol-based dietary supplements that also activate Nrf2. Nrf2 activation induces cytoprotective genes such as those playing key roles in cellular defense mechanisms including redox status and detoxification.
Eat lentils. Eat vitexin – found in fenugreek and mung beans.

Use melatonin if one is middle aged or older. Older folks have significantly less melatonin secretion in the evening. Melatonin is also produced during the day as a result of infrared light exposure.

Oats via avenanthramides and phenolic acids.

Pyrroloquinoline quinone (PQQ) is potentially effective for preventing neurodegeneration caused by oxidative stress. Here are high-PQQ foods.

Rosemary for less oxidative stress from a high-fat diet.

Regular consumption of strawberries may enhance body defences against oxidative challenges.



By Otto

I am a health enthusiast, engineer, and maker.

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