Terman A, Brunk UT. Oxidative stress, accumulation of biological garbage, and aging. Antioxid Redox Signal ; Malinin NL, West XZ, Byzova TV. Hekimi S, Lapointe J, Wen Y. Trends Cell Biol ; Venkataraman K, Khurana S, Tai TC. Oxidative stress in aging Y matters of the heart and mind. Int J Mol Sci ; Malhotra JD, Miao H, Zhang K, et al.

Antioxidants reduce endoplasmic reticulum stress and improve protein secretion. PNAS ; Martin GM. Genetics and the pathobiology of ageing. Philos Trans R Soc Lond B Biol Sci ; Martin GM, Austad SN, Johnson TE. Genetic analysis of ageing: role of oxidative damage and environmental stresses.

Nat Genet ; Humphries KM, Szweda PA, Szweda LI. Aging: a shift from redox regulation to oxidative damage. Free Radic Res ; Islam MT. Anxioxidant activities of dithiol alpha-lipoic acid. Bangladesh J Med Sci ; Singh U, Jialal I.

Alpha-lipoic acid supplementation and diabetes. Nutr Rev ; Huang EA, Gitelman SE. The effect of alpha-lipoic acid on oxidative stress in adolescents with type 1 diabetes mellitus.

Pediatr Diabetes ; Evans JL, Heymann CJ, Goldfine ID, et al. Pharmacokinetics tolerability, and fructosamine-lowering effect of a novel, controlled release formulation of alpha-lipoic acid.

Endocr Pract ; Gulliams T. Time-Release Lipoic Acid: More Marketing than Data. Stevens Point, WI: Point Institute; pp Farr SA, Poon HF, Dogrukol-Ak D, et al.

The antioxidants alpha-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice. J Neurochem ; Lovell MA, Xie C, Xiong S, et al. J Alzheimers Dis ; Cummings BP, Stanhope KL, Graham JL, et al.

Dietary fructose accelerates the development of diabetes in UCD-T2DM rats: amelioration by the antioxidant, alpha-lipoic acid. Am J Physiol Regul Integr Comp Physiol ;RR Maczurek A, Hager K, Kenklies M, et al.

Adv Drug Deliv Rev ; Ziegler D, Schatz H, Conrad F, et al. Effects of treatment with the antioxidant alpha-lipoic acid on cardiac autonomic neuropathy in NIDDM patients. A 4-month randomized controlled multicenter trial DEKAN study. Deutsche Kardiale Autonome Neuropathie.

Diabetes Care ; Heitzer T, Finckh B, Albers S, et al. Beneficial effects of alpha-lipoic acid and ascorbic acid on endothelium-dependent, nitric oxide-mediated vasodilation in diabetic patients: relation to parameters of oxidative stress.

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Vision Weight Loss. L-Carnitine and Alpha Lipoic Acid Reduce Aging and Boost Energy. Some of the foods that contain a good amount of lipoic acid are red meat, organ meat, spinach, broccoli, tomatoes, beets, etc. Lipoic acid can also be used in supplements in some cases such as fat burning, improvement in metabolism, blood glucose control, collagen production , etc.

Anti-aging can quickly be accelerated by roaming around in the sun. It is the number one cause for creating permanent damage to the skin, leading to skin wrinkles, pigmentation, discoloration, and age spots.

It has been scientifically proved that moisturizers or serums containing alpha-lipoic acid can slow down aging by improving elasticity, reducing wrinkles, fine lines, and roughness in the skin.

It is also helpful in raising other antioxidants in the body, such as glutathione, that protects against skin damage. Studies have shown that consuming these antioxidants in the form of supplements or applied topically on the skin can be very useful for the health and quality of life.

Pro Tip: Whenever you apply any moisturizer, serum, or face oils, spend some time minutes to gently massage your face to activate microcirculation that helps the skin absorb those ingredients better and relaxes your face muscles.

Also, it gives it a nice calming effect. If you go to a dermatologist with any skin problems, they will always tell you to wear a sunscreen with at least an SPF of 30 in it.

Sun damage can happen even when there is no sun outside, cloudy or raining. Sunscreen is for every season, forecast and place, whether you are inside or outside your house. Lipoic acid is based on both water and fat-soluble, making it easier for our skin to absorb it quickly within the layers for better protection against the sun's harmful radiations.

Lipoic acid is considered to be a natural exfoliant and can help with the process of collagen breakdown. It helps with the minimization of the appearance of pores and clearing breakouts, scars and pigmentation. It reduces dullness and helps regulate the right amount of oil production, which helps with the skin's texture, leaving it soft, smooth, glowy and supple.

People with nearly all skin types and all skin concerns can use skincare products consisting of lipoic acid. Lipoic acid can be used to even out skin tone, brighten up the skin, improve skin texture, reduce signs of aging, and future damage to the skin.

Lipoic acid is even useful for people with sensitive skin dealing with acne, breakouts, pigmentation, scars, inflammation, etc. There are many other health benefits which can be experienced by using lipoic acid such as:. It is a disease related to metabolic issues that results in high blood sugar.

Diabetes can affect every organ of the body resulting in kidney failure, loss of vision and heart diseases. Studies have shown that lipoic acid can bring high blood sugar to lower blood sugar levels in both animals and humans.

Experts have found out that lipoic acid can help bring blood sugar to a lower level, eliminating the fat that gathers in muscle cells that target the insulin less effectively. Nerve damage can cause pain, abnormal sensations and numbness.

Oxidative stress causes diabetes, Lyme disease, shingles, thyroid disease, and kidney failure.

LA is absorbed rapidly from the gastrointestinal tract Hagen et al. Studies have shown that the gastrointestinal absorption of LA is highly variable and its efficiency appears to be reduced when ingested in the diet, suggesting that the absorption of LA competes with other nutrients Packer et al.

Gastrointestinal uptake of LA is fast and its presence in the plasma is followed by a fast clearance Shay et al.

The plasmatic half-life of LA is 30 min. Urinary excretion is maximal 3—6 h following LA administration. Moreover, only a small amount of the administered LA is excreted in the unaltered form Bustamante et al.

There are no recommendations for daily LA intake in humans. has been reported Packer et al. placebo Shay et al. In spite of that, the exact doses that could induce adverse human health effect are still to be set up.

Neurodegenerative diseases are a heterogeneous group of disorders described by progressive and selective neuronal death with degeneration of specific brain regions Arivazhagan and Panneerselvam, ; Lin and Beal, ; Savitha and Panneerselvam, , often associated with abnormal deposits of proteins in neurons or extracellularly Chen et al.

Neurodegeneration is characterized by its insidious and chronic progressive onset and aging has been considered the main risk factor Lin and Beal, ; Chen et al. During aging, deleterious changes accumulate, causing the gradual decline of the biochemical and physiological functions Arivazhagan and Panneerselvam, ; Kumaran et al.

Moreover, aging individuals are susceptible to degeneration of selective brain regions Aliev et al. Over the last decades, a wide range of studies have shown that progression of neurodegeneration is associated with increased DNA damage partly is attributed to an imbalance between antioxidant and prooxidant factors; Chen et al.

In addition, mitochondrial decline, leading to cognitive dysfunction Liu, ; Aliev et al. Oxidative stress and mitochondrial dysfunction are interrelated mechanisms that play a central role in aging brain Santos et al. Although the exact mechanisms underlying the effects of unbalanced redox signaling are not completely elucidated, studies suggest that it plays a role in the pathogenesis of neurodegenerative disorders Liu et al.

Brain aging has been related to structural alterations and inflammation, accompanied by cognitive and memory dysfunctions Bagh et al. With the aging of the world population and the increasing life expectancy, the risk of developing neurodegenerative diseases is higher than ever, as they are affecting millions of people each year in epidemic proportions Santos et al.

As a result, an inevitable socioeconomic burden on our health care systems will occur. Effective prophylactic and therapeutic treatments are urgent for this group of seemingly inexorable diseases.

In this review we will focus on discussing the ameliorating effects of LA on cognitive deficits observed in animal models of aging and neurodegenerative disorders.

Alzheimer's disease AD is the most common neurodegenerative disorder that causes dementia and affects middle to old-aged individuals Hager et al. AD is characterized by progressive loss of cognitive functions, including memory, language, and reasoning Di Domenico et al.

Studies have investigated the effects of LA in experimental AD models Jesudason et al. For instance, Quinn et al. LA treatment was shown to reduce hippocampal-dependent memory deficits, significantly improving learning and memory in the Morris water maze in comparison to Tg mice that did not receive LA.

However, no significant differences in β-amyloid levels were found between Tg mice that received LA in comparison to the ones that did not receive LA, indicating that chronic LA supplementation in the diet can ameliorate hippocampal memory impairments in Tg mice without any effect on β-amyloid levels or plaque deposition.

Another study assessed the effects of LA in senescence-accelerated mouse prone 8 SAMP8 mice, associated to learning and memory impairments, and showed that LA can improve memory, in different paradigms Farr et al. In object recognition, results indicated that mice that received LA presented a higher memory index than vehicle-treated mice.

On the other hand, Siedlak et al. The authors concluded that, although oxidative stress has been proposed to mediate amyloid pathology and cognitive decline in aging, long-term LA administered within tolerable nutritional levels, presented limited benefit.

Parkinson's disease PD is the second most frequent neurodegenerative disorder in aging individuals and features motor symptoms related to dopaminergic neuronal loss in the substantia nigra , which results in decreased striatal dopaminergic terminals Beal, ; De Araujo et al.

Studies have shown that, in addition to rescuing cognitive deficits, LA is also able to ameliorate motor impairment related to PD.

The effects of LA were examined in a rat model of PD induced by rotenone. was evaluated after the administration of rotenone in the open-field and square bridge tests. The authors reported that LA improved rotenone-induced behavioral deficits.

In the open-field test, LA significantly increased the ambulation frequency, increased the number of stops, elevated the activity index and lessened the inactive sittings, but did not increase the rearing frequency in comparison to the group that received rotenone.

In the Square bridge test, treatment with LA protected the rats from falling as compared to rotenone group Zaitone et al. The effects of LA in lipolysaccharide LPS -induced inflammatory PD model were also evaluated Li et al. No significant recovery was observed in dyskinesia in PD mice that received LA.

However, a significant amelioration was observed in the adhesive removal test, in which LA treatment significantly decreased the reaction time in comparison to the LPS group. Huntington's disease HD is a chronic neurodegenerative disease and a hereditary autosomal-dominant disorder of the central nervous system caused by a single genetic mutation Ross et al.

This disorder is classically characterized by motor symptoms and cognitive and behavioral features Ross et al. A HD model that has been easily replicated in animals is based on the treatment with 3-nitropropionic acid 3-NP , which promotes development of mitochondrial dysfunctions leading to bioenergetic failure energy impairment, oxidative stress, and excitotoxicity.

A study by Mehrotra et al. Administration of LA improved spatial memory acquisition and retrieval assessed using the Morris water maze. Analysis of time taken and distance traveled to find the platform in the target quadrant revealed that LA supplementation for 21 days to 3-NP—treated animals resulted in a lower latency and the distance traveled was also reduced.

In addition, the average number of platform crossings in the probe trial was increased in 3-NP treated animals that received LA. Thus, the authors demonstrated that LA supplementation improved spatial memory by ameliorating the iron- and copper-induced oxidative injury observed in age-related disorders.

In the Y-maze test, animals display a preference to explore the novel arm of the maze, making fewer entrances in the previously explored arm, due to spontaneous alternation.

The authors showed that 3-NP—treated animals traveled a significantly lower distance, assessed by the number of entries in the novel arm, and that supplementation with LA reversed these deficits. Consistent evidence indicate that memory is affected by aging in rodents as well as in humans.

A study by Liu et al. Results showed that LA supplementation alone or combined with another mitochondrial metabolite, acetyl-l-carnitine, improved both spatial and temporal memory.

In month old SAMP-8 mice, chronic LA administration improved cognition in both the T-maze footshock avoidance paradigm and the lever press appetitive task without inducing non-specific locomotor effects Farr et al. LA has also been reported to improve behavior of aged mice in an open-field memory test Stoll et al.

LA also and ameliorated acquisition and retrieval in a dose-dependent manner, in old female NMRI mice, in the active avoidance learning test Stoll et al. Cui et al. Another study reported the neuroprotective effects of LA in neurotoxicity model induced by AlCl 3 administration to mice Mahboob et al.

LA enhanced fear memory and social novelty preference in comparison to the AlCl 3 -treated group. In summary, current evidence indicates that LA is able to improve memory, reversing impairments associated to a variety of experimental models of neurodegenerative disorders, and exposure to neurotoxicants, as well as normal aging.

Table 1 summarizes in vivo studies investigating the neuroprotective effects of LA on behavioral parameters. Furthermore, LA was also shown to act as a memory-improving molecule in different learning and memory paradigms, including aversive, spatial, and recognition memory.

Table 1. Summary of studies testing the effects of LA on behavioral parameters in animal models. LA has been tested in humans, in studies by Hager and coworkers Hager et al. The authors examined the effect of LA for 24 and 48 months and observed that the treatment lead to a stabilization of cognitive function, verified by unchangeable records in two neuropsychological tests, mini-mental state examination MMSE and the AD assessment score, cognitive subscale ADAScog.

In vivo as well as in vitro studies have been performed in order to characterize cellular and molecular effects of LA underlying its memory-ameliorating activities Table 2.

The effects of LA on oxidative markers in various brain regions have been discussed in different studies in animals models of aging and neurodegenerative diseases Cui et al.

LA administration decreases lipid peroxidation evaluated by MDA Arivazhagan and Panneerselvam, ; Arivazhagan et al. Moreover, administration of LA reversed the augmentation of protein carbonyls levels in a radiation-induced cognitive dysfunction model Manda et al.

Table 2. Summary of in vivo studies testing cellular and molecular effects of LA. A study by Zaitone et al. In reserpine-treated rats, LA enhanced the amount of GSH, while diminishing GSSG levels in the striatum. Moreover, LA decreased NO concentrations in striatum and pre-frontal cortex, without significantly affecting S-nitrosothiol levels.

LA also increased enzymatic activities of GPx and GST in the striatum Bilska et al. Reserpine significantly decreased enzymatic activity of L-γ-glutamyl transpeptidase γ-GT , while pretreatment with LA was able to restore it. The effects of LA on oxidative stress in rotenone parkinsonian rat brains were investigated, showing that LA can reduce lipid peroxidation and protein carbonylation Zaitone et al.

LA also lowered the levels of MDA and nitrite in the 6-OHDA-induced rat model of hemi-parkinsonism Jalali-Nadoushan and Roghani, Karunakaran et al. R-LA induced significant reductions in markers of oxidative modifications in transgenic AD mice model, significantly decreasing HO-1 and protein-bound HNE levels Siedlak et al.

Inman et al. The results showed that after 4 and 11 months of dietary LA, respectively, LA treatment increased antioxidant genes and protein expression, protected retinal ganglion cell RGC , and improved retrograde transport.

Dietary therapy also reduced lipid peroxidation, protein nitrosylation, and DNA oxidation in a retina model of glaucoma. Accumulation of metal ions also has been associated with increased oxidative stress related with aging and neurodegenerative disorders.

Suh et al. However, Liu et al. There are multiple cell death mechanisms implicated in neurodegeneration. Apoptosis is a highly controlled cellular process that can be activated by two pathways: extrinsic, which is a receptor-mediated pathway, and intrinsic, which is mediated by signals from the mitochondria.

Both pathways culminate at cleavage-dependent activation of aspartate-specific effector caspases caspases-3, 6, and 7. Manda et al. They observed that pre-treatment with LA prevented radiation-induced decreases of total, nonprotein and protein-bound sulfhydryl T-SH, NP-SH, and PB-SH levels in the cerebellum.

Moreover, LA treatment also improved the cytoarchitecture of cerebellum, increasing the number of intact Purkinje cells and granular cells when compared to untreated irradiated mice.

Mehrotra et al. The results showed that LA decreased malondialdehyde, protein carbonyls, reactive oxygen species and nitrite levels, and increased Mn-superoxide dismutase and CAT activity. LA improved activity of enzymes from the mitochondrial respiratory chain, altered cytochrome levels, increased histochemical staining of complex-II and IV, increased in-gel activity of complex-I to V, and increased mRNA expression of respiratory chain complexes.

Stoll et al. The results showed that LA improved age-related NMDA receptor deficits B max. No changes were observed regarding muscarinic, benzodiazepine, and α 2 -adrenergic receptor deficiencies.

Thus, the authors concluded that LA-induced memory improving effects may be related to partial reparation of NMDA receptor deficits that accompany aging.

A loss of dopaminergic neurons is particularly relevant to PD, in which genetic and environmental factors are involved Di Domenico et al.

Jalali-Nadoushana and Roghania using a rat model of hemi-parkinsonism 6-OHDA found that LA prevented neuronal loss on the left side of the substantia nigra pars compacta SNpc Jalali-Nadoushan and Roghani, In a study using the LPS-induced inflammatory PD model, Li et al.

Zaitone et al. Li et al. Moreover, the authors showed that LA inhibited the stimulation of nuclear factor-κB NF-κB and expression of pro-inflammatory molecules in M1 microglia. The results showed that LA significantly decreased rotenone-induced mtDNA damage.

Liu et al. Dietary administration of LA significantly reduced oxidized RNA levels and reversed mitochondrial structural deterioration induced by aging in the hippocampus.

Dwivedi et al. The results indicated that arsenic and dichlorvos induced oxidative stress and cholinergic dysfunction in brain, which was significantly protected by the supplementation with LA. Seidman et al. Their results showed that mtDNA deletions associated with aging were reduced by LA and this effect appeared to be related to the mitochondrial capacity to protect and repair mtDNA against age-induced injury.

Palaniappan and Dai investigated the effect of LA administration to aged rats and verified a reduction of mitochondrial lipid peroxidation, 8-oxo-dG and oxidized glutathione GSSG and increased GSH, ATP, and electron transport chain ETC complex activities in the brain. The SAMP8 mouse strain is an experimental model that displays increased oxidative stress accompanied by memory decline associated to a rapid aging process.

In order to determine the mechanisms underlying LA-induced reversion of memory deficits exhibited by SAMP8 mice, Poon et al.

The levels of three proteins neurofilament triplet L protein, a-enolase, and ubiquitous mitochondrial creatine kinase were significantly increased, while protein carbonylation was reduced in lactate dehydrogenase B, dihydropyrimidinase-like protein 2, and a-enolase in aged SAMP8 mice that received LA, suggesting that, in addition to improving learning and memory, LA also can restore specific proteins in aged SAMP8 mouse brain.

Evidence indicates that deregulation in neurotransmitter systems, including decreased levels of neurotransmitters, decline in the number of receptors, and lower responsiveness to neurotransmitters can be key features of neurological disorders Payton et al.

Arivazhagan and Panneerselvam investigated the effect of LA on levels of neurotransmitters dopamine, serotonin, and norepinephrine , and showed that LA treatment can improve neurotransmitter function in models of neurodegenerative diseases.

Jesudason et al. The results showed that AD mice treated with LA exhibited enhanced levels of serotonin, dopamine, and norepinephrine, and the concentration of metabolites 5-hydroxyindole acetic acid 5-HIAA and homovanillic acid HVA gradually returned to normal.

Ahmed explored the effect of LA on brain acetylcholinesterase AChE activity. The authors demonstrated that LA can ameliorate neurological injury related to Aβ and Al excess, by significantly restoring AChE activity. In addition, the authors showed that the treatment with LA restored the parameters of total homocysteine tHcy , insulin, insulin like growth factor-1 IGF-1 , interlukin-1β IL-1β and tumor necrosis factor-α TNF-α.

Mahboob et al. LA treatment increased the expression of muscarinic receptor genes M1, M2 and choline acetyltransferase ChaT relative to AlCl 3 -treated group. There are many studies examining the neuroprotective actions of LA using in vitro models of neurodegeneration Tirosh et al.

For example, Ono et al. The results showed that both LA and DHLA inhibited fAβ formation from amyloid β, as well as their expansion, and undermined preformed fAβs in a dose dependent manner. Lovell et al. In β-amyloid-intoxicated C6 glioma cells, LA increased cell viability and MnSOD expression.

The increased GSSH and decreased GSH mitochondrial levels induced by Aβ were reversed by treatment with LA Xing et al. The study by Deuther-Conrad et al. de Arriba et al. Tirosh et al. Kamarudin et al. Suppression of NF-κβ p65 translocation and production of proinflammatory cytokines IL-6 and TNF-α followed inhibition of cleaved caspase Yamada et al.

They showed that all types of LAs were effective in preventing cell death. R-LA and S-LA also enhanced expression of genes related to anti-oxidative response such as heme oxygenase-1 HO-1 and phase II detoxification enzymes such as NAD P H:Quinone Oxidoreductase 1 NQO1.

Other studies evaluated the effect of LA on in vitro model of PD. Moreover, Zhang et al. LA has been proposed to exert a modulatory control on the cellular redox status.

Due to its ability to be interconverted in one of its two forms—i. LA has been described to regenerate other antioxidants, such as vitamin C and E, to increase GSH levels, and to provide modulation of proteins and transcription factors Packer et al.

Extracellular redox state is also regulated by LA, once its reduced form, DHLA, can interact with cystine, reducing it to cysteine, thereby stimulating its uptake by the cell, which in turn stimulates GSH synthesis Han et al.

For instance, Jiang et al. Prevention of sevoflurane-induced apoptosis by LA was accomplished through recovery of Akt and GSK3-β phosphorylation levels in the hippocampus Ma et al.

Sancheti et al. Compelling evidence indicates that LA displays memory-ameliorating properties in a variety of experimental models of neurodegenerative diseases, as well as in memory decline associated with aging in rodents.

Studies aiming to assess the neuroprotective effects of LA on behavioral outcomes showed that LA can reduce memory deficits in different behavioral paradigms on AD Quinn et al.

In humans, two studies in AD patients have supported the positive cognitive effects of LA Hager et al. Many studies reported beneficial effects of LA in the rat brain or neuronal cell cultures, using different molecular markers of oxidative stress, such as reduction in the levels of lipid peroxides and protein carbonyls, recycling endogenous antioxidants such as vitamin C and E, increasing glutathione levels Packer et al.

LA was also shown to display anti-inflammatory properties Deuther-Conrad et al. In vivo and in vitro studies showed that LA ameliorated neurodegeneration in the hippocampus, decreasing neuronal apoptosis and caspase-3 protein levels, supporting a neuroprotective role mediated by the mitochondrial cell death pathway.

It has unusually broad-ranging actions against both water-soluble and fat-soluble free radicals, both inside cells and in the supportive tissues outside. R-Lipoic acid, known as or RLA, binds up free radicals in fatty or protein-rich tissues.

Navigating cellular membranes throughout the body also means that lipoic acid can cross the blood-brain barrier. Glutathione is essential for healthy eyes, skin, kidneys, liver and more.

R-Lipoic acid restores glutathione, as well as vitamins C and E, and CoQ10, reducing vulnerability to chronic degenerative disease, and making it one of the most powerful defensive antioxidants against aging. R-Lipoic acid is a key nutrient for safeguarding mitochondria from damage. As they generate energy, mitochondria naturally produce oxidative by-products.

Without adequate antioxidants to clear these, mitochondria lack protection and decay faster with age, leading to more rapid cellular decline.

In addition, RLA is a specific protector for nerves and nerve-related tissues, helping reduce diabetic nerve damage, protecting the brain, retina, and offering anti-aging benefits. It is used in Europe for glucose regulation, nerve conditions, liver protection, and insulin resistance.

Although lipoic acid is available through the diet in red and organ meats, and vegetables like spinach, broccoli, potatoes, tomatoes, carrots, and beets, in food it is bound to the amino acid lysine, and digestive enzymes cannot break the lysine bond.

So it is not very bioavailable, meaning it cannot circulate freely and do its job. The R-Lipoic acid variant RLA is the natural, bio-identical form and the only type of lipoic acid that exists in nature.

Kavin Panneerselvam from the Kasturba Medical College in Mangalore, and Sundaram Kumaran from the University of Madras in India, gave L-carnitine and alpha-lipoic acid separately or together to young, middle aged, and older rats. When the compounds, found naturally in products such as red meat and milk, were used together the researchers found that the concentration of free radicals in mitochondria, energy-producing organelles in their cells, were lower than when used independently or not at all.

The new research, published on-line in the journal Clinical Nutrition, divided 60 male albino Wistar rats into 10 groups, depending on age young, middle-aged, or old and supplementation with placebo saline solution , L-carnitine only mg per kg body weight per day , alpha-lipoic acid mg per kg body weight per day , or both.

After 60 days of supplementation, the researchers found that the level of reactive oxygen species ROS generation in the older rats was significantly higher than in younger and middle-aged rats.

Supplementation with the L-carnitine, alpha-lipoic acid combination reduced the level of ROS by 28 percent, compared to placebo. Supplementation with either compound independently reduced the level of ROS by about 9 percent. Similar benefits were observed for other markers of the ageing process including lipid peroxides and protein oxidation due to the combination supplement.

Carnitine is more potent in restoring mitochondrial energy production. This supports previous work by researchers at the University of California, Berkeley, and the Children's Hospital Oakland Research Institute led by Professor Bruce Ames.

The University of California patented use of the combination of acetyl-l-carnitine and alpha-lipoic acid to rejuvenate cells. Ames, through the Bruce and Giovanna Ames Foundation, and Hagen founded a company in called Juvenon to license the patent from the university.

Panneerselvam, K. and S.