ACETYL-L-CARNITINE & R-ALPHA LIPOIC ACID

Reduce the Bio-Markers of Aging!

Two dietary supplements powerful in their own right, when taken together the results are off the charts. Acetyl L-carnitine and alpha-lipoic acid, found naturally in products such as red meat and milk, researchers found that the concentration of free radicals in mitochondria, energy-producing organelles (part of the mitochondria) in their cells, were lower than when used independently or not at all.

Reducing the oxidative stress associated with ageing and boosting energy production; the tests sparked life back into aging rats, and might do the same for aging baby boomers, according to the following studies. These two vitamin-like nutrients have so many benefits that are unknown to the general public; it is my hope that after reading these studies that this will no longer be the case.

I have heard it said time and time again that aging is an excuse for deterioration, forgetfulness, joint pains, out of breath, sleeping disorders even loss of hair. Are these symptoms a result of aging alone or are there other contributing factors, I believe the answer is in the later.

Much of the brain damage that occurs during usual aging is identical to the brain damage found in all common neurodegenerative diseases. So much so, that many scientists now believe they may be one and the same process. By age 35, the damage becomes measurable on biomarker scales, as loss of memory, loss of motor control and balance, and a slowing of voluntary movement. It becomes obvious in many people by the age 60 seriously affecting their ability to function in normal daily life.

Restoring the Aging Brain: UC Berkeley;
three articles in the February 19, 2002 issue of Proceedings of the National Academy of Sciences (PNAS), Bruce N. Ames, professor of molecular and cell biology at UC Berkeley, fed older rats’ two chemicals acetyl-L-carnitine and alpha-lipoic acid, and his colleagues reported surprising results. Not only did the older rats do better on memory tests, they had more pep, and the energy-producing organelles in their cells worked better. "With the two supplements together, these old rats got up and did the Macarena," said Ames, also a researcher at Children's Hospital Oakland Research Institute (CHORI). "The brain looks better, they are full of energy - everything we looked at looks more like a young animal.1

"The animals seem to have much more vigor and are much more active than animals not on this diet, signaling massive improvement to these animals' health and well-being," said former UC Berkeley post-doctoral fellow Tory M. Hagen, now an assistant professor at the Linus Pauling Institute at Oregon State University, Corvallis.  "And we also see a reversal in loss of memory.   That is a dual-track improvement that is significant and unique. This is really starting to explode and move out of the realm of basic research into people."

One of the three PNAS articles probes the reasons behind this rejuvenation, concluding that the two chemicals "tune up" the energy-producing organelles that power all cells, the mitochondria. Both chemicals are normally used in mitochondria.

Ames calls mitochondria the "weak link in aging." Evidence has been piling up, he said, that deterioration of mitochondria is an important cause of aging. A significant cause of this deterioration, he believes, is the accumulation of destructive free radicals by-products of normal metabolism - that disable enzymes and other chemicals.

The combination therapy targets mitochondria to get rid of destructive radicals and to boost the activity of a damaged enzyme, carnitine- acetyl-transferase, that plays a key role in burning fuel in mitochondria. The researchers hoped that the anti-oxidant alpha-lipoic acid would do the former, and that flooding the cell with acetyl-L-carnitine, one of two proteins that the enzyme acts on, would achieve the latter.

Experiments showed that this regimen worked. Associate researcher Jiankang Liu of CHORI, UC Berkeley postdoctoral fellow David W. Killilea and Ames demonstrated that the enzyme carnitine acetyltransferase is less active in old rats than in young rats, and that it binds less tightly to acetyl-L-carnitine in older rats.

Supplementation with acetyl-L-carnitine or a combination of acetyl-L-carnitine and alpha-lipoic acid restored the enzyme's activity nearly to that found in young rats and substantially restored binding to acetyl-L-carnitine.

"The acetyl-L-carnitine is protecting the protein and the higher levels are enabling the protein to work, while alpha-lipoic acid knocks down oxygen radicals," Ames said. "Each chemical solves a different problem - the two together are better than either one alone."

Ames and Hagen have long had an interest in mitochondria as they relate to aging, and they were intrigued by a 1999 Italian study that showed acetyl-L-carnitine, when fed to old rats, improved mitochondrial activity.

Recent follow-up study builds on and confirms the Berkeley study; May/2006,  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, 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 Nutrition2) (doi: 10.1016/j.clnu.2006.02.005), 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 (300 mg per kg body weight per day), alpha-lipoic acid (100 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 per cent, compared to placebo.

Supplementation with either compound independently only reduced the level of ROS by about nine per cent.

Similar benefits were observed for other markers of the ageing process including lipid peroxides and protein oxidation due to the combination supplement.

"Our study strongly suggests that supplementation of mitochondrial metabolites, carnitine and lipoic acid may prevent mitochondrial damage and restore mitochondrial function during ageing process," said the researchers.

"Alpha-lipoic acid protects mitochondria by removing free radicals and improves the recycling of other antioxidants. Carnitine is more potent in restoring mitochondrial energy production. Thus the combination is complementary," they concluded.

Brain damage, whether it manifests as Alzheimer’s, Parkinson’s, Lou Gerhig’s disease or in another form, depends to some extent on the genetic inheritance of the person, which makes some cell complexes in the brain more vulnerable than others. In the US alone, Alzheimer’s, the most common form of brain damage, afflicts more than four million diagnosed cases, and another estimated four million undiagnosed cases. Parkinson’s, the second most common brain disease, afflicts over one million people. Sadly with today’s aging population and lack of funding, more than half of all Americans and Canadians will spend their latter years in nursing homes being unfit to care for themselves. You can’t rely on the federal health system to protect you from this fate, if you want to keep your brain intact you have to learn to protect yourself.

Reduce free radical damage to the mitochondria is your first task in saving your brain power. Most damage takes place where the energy is produced, at the inner membrane of the mitochondria; this is where the body burns calories. Heat is produced when food is burned, producing energy. The kind of food you eat depends on what you burn. Fast food, sugary drinks and Bing eating produce poor fuel to get you through the day, run your car on Coke and see how far you get. Environmental toxins and the food quality you eat are contributing factors in premature aging. “You know the saying, you are what you eat, another way to look at it is; the amount of energy you get depends on what fuel was burned.

Additional Brain Research for Acetyl-L-Carnitine and Alpha Lipoic Acid;
2/18/2008- Researchers, led by Jiankang Liu from the Institute for Brain Aging and Dementia at the University of California (Irvine), report that the nutrients work together synergistically - a result not previously reported.3

A risk assessment from scientists at the Council for Responsible Nutrition (CRN), published in the journal Regulatory Toxicology and Pharmacology (doi: 10.1016/j.yrtph.2006.06.007) reported that an adult human observed safe limit (OSL) of 2000 mg for the nutrient.

The new study measured the activity of mitochondria in adipocytes in the presence of LA (lipoic acid) and/or ALC (acetyl-L carnitine) at a concentration of 0.1, 1 and 10 micromoles per litre for 24 hours. The mass of the mitochondria and their oxygen consumption were measured, in addition to several genetic markers.

Liu and co-workers report that the combination of LA and ALC increased the mass, oxygen consumption, mitochondrial DNA expression, and fatty acid oxidation in the fat cells.

"However, the treatments with LA or ALC alone at the same concentrations showed little effect on mitochondrial function and biogenesis," noted the researchers.

Dr. Liu noted: "Lipoic acid and acetyl-L-carnitine have become very hot after our reports on the complementary effects on improving memory and ambulatory activity in old rats," relating to studies published in the Proceedings of the National Academy of Science in 2002 (Vol. 99, Pages 1870-1875, 1876-1881, and 2356-61).

Diabetic Neuropath and Pain Reduction Study;

The vitamin-like substance acetyl-L-carnitine appears to help ease the pain caused by diabetic neuropathy, a common complication of diabetes that results in painful damage to nerves.

1/7/2005- Researchers from Italian L-carnitine manufacturer Sigma-Tau and Wayne State University in Detroit evaluated data from two randomized placebo-controlled trials carried out over a year on more than 1,200 diabetic patients in the US, Canada, and Europe. The studies included tests on both 500mg and 1,000 mg doses of acetyl-L-carnitine daily.

Writing in the January issue of Diabetes Care (28:89-94), the researchers report that pain, 'the most bothersome symptom' of the condition, was significantly improved in one study and in the combined cohort taking the 1,000 mg dose. Pain relief was greatest among those who had diabetes for the shortest time period, they noted, and these patients also showed improvements in nerve structure and perception of vibration.

Diabetes, a Rising Epidemic;

Diabetes and particularly type 2 diabetes is rising fast around the world as a result of the increasing tendency towards overweight. The number of people in the UK with diabetes has surged to 1.8 million from 400,000 in just eight years, according to recent figures, with most of these -1.5 million - suffering from type 2 diabetes. An estimated 19 million people are affected by diabetes in the EU, equal to four per cent of the total population. This figure is projected to increase to 26 million by 2030. In the US, there are over 20 million people with diabetes, equal to seven per cent of the population. The total costs are thought to be as much as $132 billion, with $92 billion being direct costs from medication, according to 2002 American Diabetes Association figures.

This “epidemic” is largely driven by a concomitant obesity epidemic, which is seen not only in affluent countries, but in industrializing countries as well, concomitant with the rapid change toward Western life-style patterns worldwide.

While longer studies are needed to examine the full effect of acetyl-L-carnitine on neuropathic pain, researchers suggest that it could also help delay progression of the condition or reduce its severity.

Conclusion;

It is abundantly clear that these two nutrients alleviate many health problems; it is necessary to point out that these tests used pure patented ingredients and the R-Alpha Lipoic Acid.
“Quality products give quality results.”

Remember if you use these supplements, you do so at your own choice and risk, as they have not been approved for brain protection by Health Canada or the US FDA. But they have approved countless drugs.

  1. http://www.berkeley.edu/news/media/releases/2002/02/19_diet.html
  2. http://www.nutraingredients.com/news/ng.asp?n=67762-l-carnitine-alpha-lipoic-acid-aging
  3. http://www.nutraingredients.com/news/ng.asp?n=83317-lipoic-acid-acetyl-l-carnitine-diabetes

 Other Published studies for Lipoic Acid & Acetyl L Carnitine:
-improved mental fatigue with those suffering chronic fatigue syndrome,
-helpful in patients with multiple sclerosis, reduces their fatigue,
-reduce alcohol-induced cellular damage to organs,
-helpful in geriatric patients with mild depression,
-more effective than tamoxifen, acute and early chronic Peyronie's disease,
-may help individuals with degenerative cerebellar ataxia,
-clinically useful preventing neuronal death after peripheral nerve trauma,
-helpful with Alzheimer's disease, by protecting amyloid-beta neurotoxicity,
-helpful for people with HIV/AIDS,
-reduces diabetes during pregnancy

Additional References for Antioxidant Defenses:

Alleva R et al. The protective role of ubiquinol-10 against formation of lipid hydroperoxides in human seminal fluid. 1997. Molec Aspects Med 18, Suppl: S221-228.

Dlugosz A et al. The chemoprotective effect of coenzyme Q on lipids in the paint and lacquer industry workers. 1998. Intl J Occup Med Env Health 11: 153-163.

Ernster L et al. Biochemical, physiological and medical aspects of ubiquinone function. 1995. Biochim Biophys Acta 1271: 195-204.

Forsmark-Andree P et al. Evidence for a protective effect of endogenous ubiquinol against oxidative damage to mitochondrial protein and DNA during lipid peroxidation. 1994. Molec Aspects Med 15, Suppl: S73-S81.

Forsmark-Andree P et al. Lipid peroxidation and changes in the ubiquinone content and the respiratory chain enzymes of submitochondrial particles. 1997. Free Radic Biol Med 22: 391-400.

Halliwell B et al. Free radicals in biology and medicine, 3rd edn. Oxford, 1999.

Harman D. Aging: A theory based on free radical and radiation chemistry. 1956. J Gerontol 12: 298-300.

Harman D. The biological clock: the mitochondria? 1972.
J Am Geriatr Soc 20: 145-147.

Harman D. Extending functional life span. 1998. Exp Gerontol 33: 95-112.

Humphries KM et al. Inhibition of NADH-linked mitochondrial respiration by 4-hydroxy-2-nonenal. 1998. Biochemistry 37: 552-557.

Kontush A et al. Antioxidative activity of ubiquinol-10 at physiologic concentrations in human low density lipoprotein. 1995. Biochem Biophys Acta 1258: 177-187.