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  1. #1
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Cool ++Enhancing Mitochondrial Function: AOR's MITO CHARGER sponsored by Cognitive Nutr.++



    http://www.cognitivenutrition.com/en/
    http://www.bodybuilding.com/store/uniq/uniq.htm




    Big thanks to Steve from Cognitive Nutrition for sponsoring this log with Mito Charger from Advanced Orthomolecular Research. I also purchased some Cognitive Nutrition PEA 750mg to give some brief feedback on.

    I also use numerous other AOR products including Ortho Core as my multi source, Ortho Mind for cognitive health, Advanced Whey, Greens n' Berries, Ortho Glucose II, Ortho Liver II, Advanced Biotics, Vitamin D3 Liquid and more... AOR has done a tremendous job on many of their newest formulations in the past year or two. As much as I have liked them in the past, they continue to strive to new heights.

    This might be a hard product to 'Feel' or notice within weeks, but done right, long term I do believe these nutrients can assist in preventing disease and enhancing performance by improving the health of the cell. You should feel and notice a difference with time as improved mito functioning works its powers. I think anyone can appreciate the ingredients and dosings provided here and see the quality product for what it is. I would quickly take this product over 90% of anything out there if I were to pick from all the products to use in the supplement world. I hope to take 3-6 caps early on most days over the next month in this log, but this is def. a staple as I purchased another 6 bottles for myself and family. My dad and mom are in their 70's and doing just fine with my advice so far.

    This log will likely be as much about providing info as it is simply providing workout/training feeback to any of the interested bb.com members. I hope to begin using my indoor bike training for cardio as I have a new love for endurance competition which will compete with my love for bodybuilding/strength training. I was hoping to do a very short bulk/strength gain in the next two months, but because I can't wait to begin using a bike trainer now, it may be very limited this year. Oh well, at least I will be healthy and get in great shape and stay fairly lean.


    MITO CHARGER from AOR:



    Serving Size: 6 Capsules
    R(+)- Lipoic Acid 150 mg
    Co-Enzyme Q10 100 mg
    Rhodiola Rosea (min. 3% rosavins, 1% salidroside) 150 mg
    Benfotiamine 150 mg
    Oxaloacetic acid (Benagene) 100 mg
    D-Uridine 50 mg
    Gynostemma Pentaphyllum Extract 100 mg
    Acetyl-L-Carnitine (ALCAR) 1500 mg


    This is one of the products I have had on my most wanted list for close to a year now. If you learn more about disease, aging and performance enhancement, you'll soon discover that there is no way either can be addressed optimally without first providing healthy mitochondria.


    Here is a little starting info From Wiki:

    Mitochondria are sometimes described as "cellular power plants" because they generate most of the cell's supply of adenosine triphosphate (ATP), used as a source of the chemical energy. In addition to supplying cellular energy, mitochondria are involved in a range of other processes, such as signaling, cellular differentiation, cell death, as well as the control of the cell cycle and cell growth. Mitochondria have been implicated in several human diseases, including mitochondrial disorders and cardiac dysfunction, and may play a role in the aging process.


    Here is AOR's writeup for their product ProChondria which is exactly the same as Mito Charger except Mito has ALCAR instead of the carnitine precursor GBB. ALCAR is preferable imo.
    http://www.aorpro.ca/assets/PDF/PRO%...rochondria.pdf


    Product Purpose:
    Maintains mitochondrial health
    + Mitochondrial Dysfunction
    + Enhances mitochondrial activity on six different levels
    + Ultimate Free Radical quencher
    + Important for virtually all diseases




    The Importance of the Mitochondria
    The cell is the basis of all life, and the mitochondrion is the power plant that keeps the cell
    operating. A simple but effective metaphor for what is one of the most significant and complex biochemical relationships known to science. Without mitochondria, cells simply do not produce the energy needed for the human body to function or even survive. It comes as little surprise, that any state of mitochondrial dysfunction can be associated with a host of metabolic conditions, including metabolic syndrome, aging, obesity, kidney, liver and neurological diseases.


    Mitochondria and ATP
    Mitochondria are bacteria-sized organelles, and thousands are located inside the membrane of each cell. The primary function of the mitochondria is to convert organic materials (originating mainly from the food we eat) into energy in the form of ATP (adenosine triphosphate - the immediate fuel of life). The rate at which the mitochondria perform this function is called the Basal Metabolic Rate (BMR), and an increased BMR leads to increased insulin sensitivity, which in turn leads to the greatest safeguard against a host of metabolic disorders, including the increasingly present Metabolic Syndrome.


    The Vicious Cycle
    Ironically, the mitochondria's ability to produce ATP also results in the simultaneous production of other, unproductive metabolic by-products, particularly ROS (reactive oxygen species) free radicals.


    The Mitochondrial Theory of Aging
    The aforementioned 'vicious cycle' has become known as the Mitochondrial Theory of Aging. An inefficient mitochondrion generates more free radicals than an efficient one. This is because, as we age, more fuel (in the form of glucose, amino acids and fatty acids) is required for each mitochondrion to produce the same amount of ATP, resulting in an increased ratio of ROS-to-ATP production. To complicate matters further, mitochondrial DNA (mtDNA) differs from the DNA of the nucleus and other organelles in that mtDNA has no enzymatic defense against oxidative stressors, self-generated or not. In-vivo studies have provided evidence for the Mitochondrial Theory of Aging so conclusive that one leading researcher summarized it this way: "It is generally accepted that oxidative mitochondrial decay is a major contributor to aging."


    Maintaining The Power Plant - With Cocktails
    As we have seen, the relative clarity of the mitochondria's role within human biochemistry is coupled with an inherent vulnerability that must be addressed if any attempt is to be made with regard to enhancing mitochondrial health. The process of addressing the elusive prerequisites to mitochondrial health is so intricate that professional medical societies have been established exclusively for its study. These include the Mitochondrial Research Society (Buffalo, N.Y.), the Mitochondrial Physiology Network (Innsbruck, Austria), and the United Mitochondrial Disease Foundation (Pittsburgh, PA), among others. Their efforts have helped to create a plethora of complex nutraceutical formulations designed to enhance mitochondrial function and health from every conceivable perspective.


    I also hope to post more on the Mitochondrial Theory of aging, Mitochondria Diseases and the interesting nutrient research done by the likes of Dr. Bruce Ames and others.

    For a more in-depth reading from AOR on Mitochondria and anti-aging, check out their Advances Magazine Vol3 Issue3:
    http://www.aor.ca/assets/Research/pd...0Plant%203.pdf


    Last edited by Peter LeDrew; 10-30-2009 at 01:28 PM.
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  2. #2
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Began ++Charging++ my Mitochondria today Oct. 30/09

    I took my first doses today. 3 caps upon waking and I will take another 2-3 caps soon before I workout. Still undecided what training I am doing. Just purchased this!



    I am def. thinking of trying this out right away and making that my leg/cardio training.


    ALCAR is best dosed early in the day because of its effects on dopamine stimulation so I advise people when using Mito Charger to dose it predominately earlier in the day. A full 6 caps is def. not needed, depending on age, health, weight, etc... even 2-3 caps would provide benefits esp. when you look into the synergy of Mito Charger ingredients.


    btw for pre-workout boost considering trying out Greens N Berries from AOR with your current fav. pre-workout. I made my own formula which I may post here along the way which has this. GnB's contains many Nitrate rich veggies which enhance Nitric oxide release and may boost stamina. Then you have all the other phytochemicals found in the included greens and veggies which provide numerous health benefits. The doses are awesome in this product, the selection of ingredients is great and it actually tastes very nice esp. when you add it to other flavored ingredients. I even put this in my protein powders for a more complete MRP like shake.
    Last edited by Peter LeDrew; 10-30-2009 at 01:29 PM.
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  3. #3
    Registered User bloodsimple1234's Avatar
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    Thumbs up

    very nice Peter! had my eye on this one myself!


    also have my eye on ortho mind as well.Never had that one!

    big fan of orthocore and the whole AOR line!




    anyway,subd!
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  4. #4
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Originally Posted by bloodsimple1234 View Post
    very nice Peter! had my eye on this one myself!


    also have my eye on ortho mind as well.Never had that one!

    big fan of orthocore and the whole AOR line!




    anyway,subd!
    Thanks Pete!

    I have been using AOR for a long time and both Ortho Mind and Ortho Core are staples. Lots of good stuff in Ortho Mind.
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  5. #5
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Non-genetic Strategies to Ameliorate Mitochondrial Dysfunction

    More from AOR


    Strategy. Theoretical Basis. Example

    1: Enzyme Bypass. Provide energy beyond the site of the enzyme defect. Succinate, Co-Enzyme Q10

    2. Anti-oxidants. Reduce free radical damage to cell structures. Vitamin E, C, Lipoic acid.

    3. Alternative energy. Use an anaerobic system not requiring mitochondria. Creatine Monohydrate exogenous ATP.

    4. Reduce lactate. Reduce acidosis, more energy into the mitochondria. Dichloroacetate, thiamine.

    5. Strength exercise. Improve strength, reduce number of mutant mtDNA Weights, isometrics.

    6. Endurance exercise. Improve endurance, reduce cardiovascular risks Jogging, cycling, walking.

    7.Nucleotide precursors. Prevent depletion of nucleotide pool (for DNA synthesis). Triacetyluridine, d-ribose, d-uridine

    8. Vasodilation. Prevent vascular spasm in MELAS stroke. L-arginine, gynostemma entaphyllum



    How It All Works

    Enzyme Bypass:
    The theory here is to circumvent a defect along the mitochondrial Electron Transport Chain which produces ATP. This chain is initiated when electrons are transferred to a lipid-soluble carrier called a ubiquinone, which in turn crosses the cellular membrane.
    The supplemental form of ubiquinone is Co-Enzyme Q10 (Co-Q10), and studies have shown that it can expedite the Complex II phase of the Electron Transport Chain by up to 200%.


    Anti-oxidants:
    The universal anti-oxidant/free radical dichotomy certainly has mitochondrial applications as well, but the vulnerability of mtDNA alters the circumstances. Conventional anti-oxidants such as vitamins C and E are certainly useful, but the ideal mitochondrial anti-oxidant appears to be a-lipoic acid, or simply lipoic acid (preferably composed of the R(+)- enantiomer ). Lipoic acid is metabolized to its active form, diHydrolipoic acid (DHLA) inside the mitochondrion itself by the enzyme known as pyruvate dehydrogenase complex (PDH). This process, (and equally importantly, the dynamics of this process) produces intense biological activity, including the regeneration and recycling of vitamins C and E and enhanced insulin sensitivity.


    Alternative Energy:
    This tactic involves the maximal utilization of a source of ATP that does not require any mitochondrial participation, thus augmenting overall ATP production without burdening dysfunctional or aging mitochondria. Both creatine monohydrate and the herb rhodiola rosea have demonstrated a capacity to increase ATP production, although the latter appears to do so by actually rejuvenating the mitchondria's capacity to synthesize ATP.


    Reducing Lactate:
    The strategy here is to stimulate the enzyme pyruvate dehydrogenase - which is responsible for directing pyruvate into the mitochondria and away from lactate production. This can be done with the drug dichloroacetate as well as with vitamin B1 supplementation. The latter option has been made even more appealing by the development of benfotiamine, a form of thiamin that is nearly 5 times more bio-available than conventional thiamin.


    Nucleotide Precursors:
    Nucleotides are the structural units of DNA and RNA - including mtDNA and mtRNA. As mitochondrial dysfunction is closely associated with the depletion of nucleotides, maintaining a healthy nucleotide pool is paramount. Triacetyluridine, a chemoprotective drug that is a precursor of uridine (an RNA nucleotide), is believed to be capable of this. Naturally-derived uridine supplements have been studied for their ability to improve mitochondrial function in patients with HIV.


    Vasodilation:
    Vasodilation (the widening of the blood vessels due to relaxation of smooth muscle in the vessel wall) is linked to the mitochondria via the production of nitric oxide. The mitochondria are primary targets of nitric oxide, and even small amounts can regulate ATP synthesis. MELAS (or mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) is a mitochondrial disorder caused by mutations in the mtDNA of endothelial cells that lead to their dysfunction. Supplementation with L-arginine, a nitric oxide donor, has been shown to ameliorate the symptoms of MELAS. Other nitric oxide
    enhancers include citrulline malate and the highly efficient gynostemma pentaphyllum.


    With this in mind, AOR formulated Mito Charger.





    References:
    Liu, J. et al (2002) Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites. Ann NY Acad Sci 959: 133-66.

    Tarnopolsky MA, et al. Nutritional and exercise-based therapies in the treatment of mitochondrial disease. Curr Opin Clin Nutr Metab Care. 2002. Nov;5(6):619-29.

    Mazzio EA, Soliman KF. Effects of enhancing mitochondrial oxidative phosphorylation with reducing equivalents and ubiquinone on 1-methyl-4-phenylpyridinium toxicity and complex I-IV damage in neuroblastoma cells. Biochem Pharmacol. 2004. Mar 15;67(6):1167-84.

    Abidov M, et al. Effect of extracts from Rhodiola rosea and Rhodiola crenulata (Crassulaceae) roots on ATP content in mitochondria of skeletal muscles. Bull Exp Biol Med. 2003 Dec;136(6):585-7.

    Banasch M, et al. Uridine supplementation enhances hepatic mitochondrial function in thymidine-analogue treated HIV-infected patients. AIDS. 2006 Jul 13;20(11):1554-6.
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  6. #6
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Popped 2 caps of Cognitive Nutrition PEA 750mg while watching Donnie Darko!!!

    Happy Halloween!!!


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  7. #7
    onigami!@#!$@ mer-der-ah's Avatar
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    Originally Posted by Peter LeDrew View Post
    Just purchased this!


    excellent purchase my friend, i have one too from tacx. best investment ever. just make sure you have a spare rear wheel with hub/cassette to match your bike's gear config as your tire will wear out a bit from using the cycle trainer OR there's special training wheels you can get and shouldn't smell like burning rubber either :P
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  8. #8
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Originally Posted by mer-der-ah View Post
    excellent purchase my friend, i have one too from tacx. best investment ever. just make sure you have a spare rear wheel with hub/cassette to match your bike's gear config as your tire will wear out a bit from using the cycle trainer OR there's special training wheels you can get and shouldn't smell like burning rubber either :P
    I was going to get tacx, but these were the ones available locally and I like supporting the local business... they sponsor and run most of the races which keeps everyone training and motivated... I would never have given up cycling 14yrs ago had there been more races back then.

    I got a spare tire for indoor training only. Getting a workout in tomorrow morning now. Enjoyed a quiet evening with my GF.
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  9. #9
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Maybe 1 Day?

    This has to be the ultimate challenge. I am a million miles away from doing an Ironman, but I will never rule it out. At this time in my life I am not ready and not committed to such an ordeal. I look to enjoy racing much smaller events for now.

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  10. #10
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Hitting my indoor trainer soon.

    I decided I will begin keeping track of my experience with Mito Charger a little better with some variables that might be affected by the ingredients in MC. ie. Energy, mood, mental acuity, motivation, stress, endurance, strength, libido, sleep and Body composition/appearance. If anyone else has any suggestions let me know.
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  11. #11
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    Team Molecular Nutrition Peter LeDrew's Avatar
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    Originally Posted by SwolenONE View Post
    sweet formula, subbed
    I agree 110% which is why I now have 7 bottles!


    I am also now using my own pre-workout mix which is made up of numerous ingredients/products that I have all used before. I can post it up if anyone is interested. It def. leaves few stones left uncovered in a natural performance enhancement product. I'm thinking it would cost a good $200+ to buy if it was sold anywhere.
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  13. #13
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    Cool

    I Might look to do an ironman one day once I get into my upper 30's or early 40's.


    looking good Peter.
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  14. #14
    misc me when I'm gone antbanks's Avatar
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    Originally Posted by Peter LeDrew View Post
    I agree 110% which is why I now have 7 bottles!


    I am also now using my own pre-workout mix which is made up of numerous ingredients/products that I have all used before. I can post it up if anyone is interested. It def. leaves few stones left uncovered in a natural performance enhancement product. I'm thinking it would cost a good $200+ to buy if it was sold anywhere.
    interested! interesting log as well
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  15. #15
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    Originally Posted by antbanks View Post
    interested! interesting log as well
    Thanks. I will try and get up everything that I put in it... Got it wrote down somewhere!?!

    I'm drinking some now with my last C-Bol before I hit chest.

    I have been on my trainer a few times already now. I am loving it! So convenient to just be able to jump on it when I get the time. I am thinking this will be perfect during lunch breaks from work. My legs have def. been feeling it today as they are heavy and a little sore. I have just been getting used to it with some intervals, but nothing 2 crazy yet. I'll stat getting up my workouts soon regarding this.

    Short on time now, I gotta hit the gym now.
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  16. #16
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    good stuff, i'll be watching this thread.

    just got 2 more bottles of ortho-core, never tried any of AOR's other supps though. i think i'm gonna buy ortho-mind and the greens/berries one. possibly this one too.
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  17. #17
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    Originally Posted by acarey617 View Post
    good stuff, i'll be watching this thread.

    just got 2 more bottles of ortho-core, never tried any of AOR's other supps though. i think i'm gonna buy ortho-mind and the greens/berries one. possibly this one too.
    Thanks. You will not regret using Ortho Core or any other AOR product. I am an obsessed perfectionist when it comes to supplementation and AOR is hands down my favorite overall company. They are very meticulous when it comes to formulation and one of the best in providing science-backed formulas. You also rarely see a prop. blend AOR product. I really try to support any company that aims to do things right for the consumer and have a deep understanding for the science. It's scary how many popular companies and products in this industry are run by those with little understanding of the science. Usually they simply use big prop. blends with popular or hyped ingredients.

    Greens n berries is perhaps my newest fav product alongside Mito Charger. It tastes pretty good considering what is in there and I find it blends very well with most protein flavors esp. vanilla and strawberry. I'll try and discuss other AOR products in this log when I get the time.
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    Originally Posted by Peter LeDrew View Post
    Thanks. You will not regret using Ortho Core or any other AOR product. I am an obsessed perfectionist when it comes to supplementation and AOR is hands down my favorite overall company. They are very meticulous when it comes to formulation and one of the best in providing science-backed formulas. You also rarely see a prop. blend AOR product. I really try to support any company that aims to do things right for the consumer and have a deep understanding for the science. It's scary how many popular companies and products in this industry are run by those with little understanding of the science. Usually they simply use big prop. blends with popular or hyped ingredients.

    Greens n berries is perhaps my newest fav product alongside Mito Charger. It tastes pretty good considering what is in there and I find it blends very well with most protein flavors esp. vanilla and strawberry. I'll try and discuss other AOR products in this log when I get the time.
    one of the better posts in a long time.Agreed 100%
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  19. #19
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    Cool The amazing Dr. Bruce Ames!

    Much of the reason for me taking products like AOR's Ortho Core and Mito Charger are based on the research of scientists like Dr. Bruce Ames. I have discussed his research here for many years now, but if you haven't heard about him you can listen to him directly right here: http://video.google.com/videoplay?do...5376505271736#


    He discusses Mitochondrial decay, inadequate micronutrient intake and his new Triage Theory. Some very interesting topics and nutrient discussion in relation to aging... I highly suggest taking the time to listen in. Personally I think he presents some of the strongest arguements to support supplementation of products like Mito Charger and a properly formulated multi-nutrient formulation such as Ortho Core or Multi Basics from AOR.

    Some main points in the video:

    Mitochondrial decay, (a decrease in membrane potential, respiratory control ratio, cardiolipin, and cellular oxygen consumption, and an increase in oxidant by-products) appears to be a major contributor to aging and associated degenerative diseases. Oxidative damage to DNA, RNA, proteins, and lipids in mitochondrial membranes is a major consequence of this decay, resulting in functional decline of mitochondria, cells, and organs.


    Feeding the mitochondrial metabolites acetyl carnitine and lipoic acid to old rats rejuvenates the mitochondria and improves brain and other function. The degenerative diseases accompanying aging, such as immune dysfunction, cancer, cognitive decline, and stroke, might be delayed by an inexpensive intervention.


    About 40 essential micronutrients are required for metabolism and include minerals, vitamins, amino acids and fatty acids. Micronutrient inadequacy (<EAR, i.e. >2 standard deviations below the RDA) is unusually widespread in the U.S. population (especially in the poor, children, adolescents, the obese, and the elderly) because of high consumption of calorie-rich micronutrient-poor unbalanced diets.


    Most of the world's population, particularly the poor, has inadequate intake of one or more micronutrients. Societal concern is low because no overt pathology has been associated with these levels of deficiency, e.g. 56% of the U.S. have intakes below the EAR for Mg and almost all African-Americans for vitamin D.


    My triage theory explains why the pathology is insidious. When a micronutrient is inadequate, nature selects for a rebalancing of metabolism, that ensures survival of the organism at the expense of metabolism whose lack has only longer term consequences. I propose that during evolution micronutrient shortages were very common, e.g. the 15 essential minerals, which are not distributed evenly on the earth. The consequences of this homeostatic response are, for example, DNA damage (future cancer), adaptive immune dysfunction (future severe infection), and mitochondrial decay (future cognitive dysfunction and accelerated aging). Much evidence supports this idea that micronutrient shortages accelerate aging.
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    Thank you for your efforts Dr. Ames!

    http://www.bruceames.org/

    http://en.wikipedia.org/wiki/Bruce_Ames


    Bruce Ames (born December 16, 1928) is a professor of Biochemistry and Molecular Biology at the University of California, Berkeley, and a senior scientist at Children's Hospital Oakland Research Institute (CHORI). He is the inventor of the Ames test, a system for easily and cheaply testing the mutagenicity of compounds.

    His research focuses on cancer and aging and he has authored over 500 scientific publications. He is among the few hundred most-cited scientists in all fields.

    Ames' current research includes identifying agents that delay the mitochondrial decay of aging, understanding the role of mitochondrial decay in aging, particularly in the brain, optimizing micronutrient intakes in the population to prevent disease, malnutrition, and obesity. He is also interested in mutagens as they relate to cancer prevention and aging.


    Yeah, he is in his 80's and still doing research!!!

    http://www.bruceames.org/bna2009.php

    Zhang H, Liu J, Ao N, Yao D, Yan B, Jia H, Jia L, Ames BN, Liu J. (2006) R-alpha-Lipoic acid and acetyl-L-carnitine, and their synergistic combination prevent mitochondrial dysfunction and oxidative damage in a rotenone-treated human neuroblastoma cellular model of Parkinsons disease (mitochondrial membrane potential/mitochondrial complex I/(-synuclein/ubiquitin/protein oxidation/oxidative DNA damage).

    These days, he seems to be very active getting the word out on his Triage theory.
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    Red face You're a Dean? Play on words.

    AOR's Mito Charger! Potent dosings of many proven ingredients including ALCAR and R-LA, but have you heard of Uridine?

    Serving Size: 6 Capsules
    R(+)- Lipoic Acid 150 mg
    Co-Enzyme Q10 100 mg
    Rhodiola Rosea (min. 3% rosavins, 1% salidroside) 150 mg
    Benfotiamine 150 mg
    Oxaloacetic acid (Benagene) 100 mg
    D-Uridine 50 mg
    Gynostemma Pentaphyllum Extract 100 mg
    Acetyl-L-Carnitine (ALCAR) 1500 mg


    How about some Uridine for your brain?


    FASEB J. 2008 Nov;22(11):3938-46. Epub 2008 Jul 7.

    Dietary uridine enhances the improvement in learning and memory produced by administering DHA to gerbils.
    Holguin S, Martinez J, Chow C, Wurtman R.

    Massachusetts Institute of Technology, 43 Vassar St., 46-5023, Cambridge, MA 02139, USA.

    This study examined the effects on cognitive behaviors of giving normal adult gerbils three compounds, normally in the circulation, which interact to increase brain phosphatides, synaptic proteins, dendritic spines, and neurotransmitter release. Animals received supplemental uridine (as its monophosphate, UMP; 0.5%) and choline (0.1%) via the diet, and docosahexaenoic acid (DHA; 300 mg/kg/day) by gavage, for 4 wk, and then throughout the subsequent period of behavioral training and testing. As shown previously, giving all three compounds caused highly significant (P<0.001) increases in total brain phospholipids and in each major phosphatide; giving DHA or UMP (plus choline) produced smaller increases in some of the phosphatides. DHA plus choline improved performance on the four-arm radial maze, T-maze, and Y-maze tests; coadministering UMP further enhanced these increases. (Uridine probably acts by generating both CTP, which can be limiting in phosphatide synthesis, and UTP, which activates P2Y receptors coupled to neurite outgrowth and protein synthesis. All three compounds also act by enhancing the substrate-saturation of phosphatide-synthesizing enzymes.) These findings demonstrate that a treatment that increases synaptic membrane content can enhance cognitive functions in normal animals.


    http://www.ncbi.nlm.nih.gov/pmc/arti...4/?tool=pubmed



    J Nutr Health Aging. 2009 Mar;13(3):189-97.

    Synapse formation is enhanced by oral administration of uridine and DHA, the circulating precursors of brain phosphatides.
    Wurtman RJ, Cansev M, Ulus IH.

    Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. dick@mit.edu

    OBJECTIVE: The loss of cortical and hippocampal synapses is a universal hallmark of Alzheimer's disease, and probably underlies its effects on cognition. Synapses are formed from the interaction of neurites projecting from "presynaptic" neurons with dendritic spines projecting from "postsynaptic" neurons. Both of these structures are vulnerable to the toxic effects of nearby amyloid plaques, and their loss contributes to the decreased number of synapses that characterize the disease. A treatment that increased the formation of neurites and dendritic spines might reverse this loss, thereby increasing the number of synapses and slowing the decline in cognition. DESIGN SETTING, PARTICIPANTS, INTERVENTION, MEASUREMENTS AND RESULTS: We observe that giving normal rodents uridine and the omega-3 fatty acid docosahexaenoic acid (DHA) orally can enhance dendritic spine levels (3), and cognitive functions (32). Moreover this treatment also increases levels of biochemical markers for neurites (i.e., neurofilament-M and neurofilament-70) (2) in vivo, and uridine alone increases both these markers and the outgrowth of visible neurites by cultured PC-12 cells (9). A phase 2 clinical trial, performed in Europe, is described briefly. DISCUSSION AND CONCLUSION: Uridine and DHA are circulating precursors for the phosphatides in synaptic membranes, and act in part by increasing the substrate-saturation of enzymes that synthesize phosphatidylcholine from CTP (formed from the uridine, via UTP) and from diacylglycerol species that contain DHA: the enzymes have poor affinities for these substrates, and thus are unsaturated with them, and only partially active, under basal conditions. The enhancement by uridine of neurite outgrowth is also mediated in part by UTP serving as a ligand for neuronal P2Y receptors. Moreover administration of uridine with DHA activates many brain genes, among them the gene for the m-1 metabotropic glutamate receptor [Cansev, et al, submitted]. This activation, in turn, increases brain levels of that gene's protein product and of such other synaptic proteins as PSD-95, synapsin-1, syntaxin-3 and F-actin, but not levels of non-synaptic brain proteins like beta-tubulin. Hence it is possible that giving uridine plus DHA triggers a neuronal program that, by accelerating phosphatide and synaptic protein synthesis, controls synaptogenesis. If administering this mix of phosphatide precursors also increases synaptic elements in brains of patients with Alzheimer 's disease, as it does in normal rodents, then this treatment may ameliorate some of the manifestations of the disease.



    Alzheimers Dement. 2008 Jan;4(1 Suppl 1):S153-68. Epub 2007 Dec 21.

    Oral administration of circulating precursors for membrane phosphatides can promote the synthesis of new brain synapses.
    Cansev M, Wurtman RJ, Sakamoto T, Ulus IH.

    Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.

    Although cognitive performance in humans and experimental animals can be improved by administering omega-3 fatty acid docosahexaenoic acid (DHA), the neurochemical mechanisms underlying this effect remain uncertain. In general, nutrients or drugs that modify brain function or behavior do so by affecting synaptic transmission, usually by changing the quantities of particular neurotransmitters present within synaptic clefts or by acting directly on neurotransmitter receptors or signal-transduction molecules. We find that DHA also affects synaptic transmission in mammalian brain. Brain cells of gerbils or rats receiving this fatty acid manifest increased levels of phosphatides and of specific presynaptic or postsynaptic proteins. They also exhibit increased numbers of dendritic spines on postsynaptic neurons. These actions are markedly enhanced in animals that have also received the other two circulating precursors for phosphatidylcholine, uridine (which gives rise to brain uridine diphosphate and cytidine triphosphate) and choline (which gives rise to phosphocholine). The actions of DHA aere reproduced by eicosapentaenoic acid, another omega-3 compound, but not by omega-6 fatty acid arachidonic acid. Administration of circulating phosphatide precursors can also increase neurotransmitter release (acetylcholine, dopamine) and affect animal behavior. Conceivably, this treatment might have use in patients with the synaptic loss that characterizes Alzheimer's disease or other neurodegenerative diseases or occurs after stroke or brain injury.


    I use a quality EPA/DHA rich fish oil, get my uridine from Mito Charger as well as using choline supplements like CDP-Choline which I get from AOR's Ortho Mind.
    Last edited by Peter LeDrew; 11-08-2009 at 10:29 AM.
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    Smile Ortho Core

    I hope to eventually bring in some discussion on AOR's premium multi Ortho Core. Why I believe it is a multi to choose over others, what makes it better and how to dose it best.
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    Overwhelming Evidence?

    J Neurol Sci. 2009 Aug 15;283(1-2):199-206. Epub 2009 Apr 1.

    The effect of acetyl-L-carnitine and R-alpha-lipoic acid treatment in ApoE4 mouse as a model of human Alzheimer's disease.
    Shenk JC, Liu J, Fischbach K, Xu K, Puchowicz M, Obrenovich ME, Gasimov E, Alvarez LM, Ames BN, Lamanna JC, Aliev G.

    Department of Biology and Electron Microscopy Research Center, University of Texas at San Antonio, San Antonio, TX 78249, USA.

    We measured age-dependent effects of human ApoE4 on cerebral blood flow (CBF) using ApoE4 transgenic mice compared to age-matched wild-type (WT) mice by use of [(14)C] iodoantipyrene autoradiography. ApoE4 associated factors reduce CBF gradually to create brain hypoperfusion when compared to WT, and the differences in CBF are greatest as animals age from 6-weeks to 12-months. Transmission electron microscopy with colloidal gold immunocytochemistry showed structural damage in young and aged microvessel endothelium of ApoE4 animals extended to the cytoplasm of perivascular cells, perivascular nerve terminals and hippocampal neurons and glial cells. These abnormalities coexist with mitochondrial structural alteration and mitochondrial DNA overproliferation and/or deletion in all brain cellular compartments. Spatial memory and temporal memory tests showed a trend in improving cognitive function in ApoE4 mice fed selective mitochondrial antioxidants acetyl-l-carnitine and R-alpha-lipoic acid. Our findings indicate that ApoE4 genotype-induced mitochondrial changes and associated structural damage may explain age-dependent pathology seen in AD, indicating potential for novel treatment strategies in the near future.


    Neurochem Res. 2009 Apr;34(4):755-63. Epub 2008 Oct 10.

    Mitochondrial decay in the brains of old rats: ameliorating effect of alpha-lipoic acid and acetyl-L-carnitine.
    Long J, Gao F, Tong L, Cotman CW, Ames BN, Liu J.

    Institute for Brain Aging and Dementia, University of California, Irvine, CA 92697-4540, USA.

    To investigate the mitochondrial decay and oxidative damage resulting from aging, the activities/kinetics of the mitochondrial complexes were examined in the brains of young and old rats as well as in old rats fed R-alpha-lipoic acid plus acetyl-L-carnitine (LA/ALC). The brain mitochondria of old rats, compared with young rats, had significantly decreased endogenous antioxidants and superoxide dismutase activity; more oxidative damage to lipids and proteins; and decreased activities of complex I, IV and V. Complex I showed a decrease in binding affinity (increase in K(m)) for substrates. Feeding LA/ALC to old rats partially restored age-associated mitochondrial dysfunction to the levels of the young rats. These results indicate that oxidative mitochondrial decay plays an important role in brain aging and that a combination of nutrients targeting mitochondria, such as LA/ALC, could ameliorate mitochondrial decay through preventing mitochondrial oxidative damage.


    Neurochem Res. 2009 Apr;34(4):755-63. Epub 2008 Oct 10.

    Mitochondrial decay in the brains of old rats: ameliorating effect of alpha-lipoic acid and acetyl-L-carnitine.
    Long J, Gao F, Tong L, Cotman CW, Ames BN, Liu J.

    Institute for Brain Aging and Dementia, University of California, Irvine, CA 92697-4540, USA.

    To investigate the mitochondrial decay and oxidative damage resulting from aging, the activities/kinetics of the mitochondrial complexes were examined in the brains of young and old rats as well as in old rats fed R-alpha-lipoic acid plus acetyl-L-carnitine (LA/ALC). The brain mitochondria of old rats, compared with young rats, had significantly decreased endogenous antioxidants and superoxide dismutase activity; more oxidative damage to lipids and proteins; and decreased activities of complex I, IV and V. Complex I showed a decrease in binding affinity (increase in K(m)) for substrates. Feeding LA/ALC to old rats partially restored age-associated mitochondrial dysfunction to the levels of the young rats. These results indicate that oxidative mitochondrial decay plays an important role in brain aging and that a combination of nutrients targeting mitochondria, such as LA/ALC, could ameliorate mitochondrial decay through preventing mitochondrial oxidative damage.


    FASEB J. 2007 Nov;21(13):3756-62. Epub 2007 Jul 10.

    Acetyl-L-carnitine and alpha-lipoic acid supplementation of aged beagle dogs improves learning in two landmark discrimination tests.
    Milgram NW, Araujo JA, Hagen TM, Treadwell BV, Ames BN.

    University of Toronto, Division of Life Sciences, Scarborough, Ontario, Canada. milgram@psych.utoronto.ca

    Beagle dogs between 7.6 and 8.8 years of age administered a twice daily supplement of alpha-lipoic acid (LA) and acetyl-L-carnitine (ALC) over approximately 2 months made significantly fewer errors in reaching the learning criterion on two landmark discrimination tasks compared to controls administered a methylcellulose placebo. Testing started after a 5 day wash-in. The dogs were also tested on a variable delay version of a previously acquired spatial memory task; results were not significant. The improved performance on the landmark task of dogs supplemented with LA + ALC provides evidence of the effectiveness of this supplement in improving discrimination and allocentric spatial learning. We suggest that long-term maintenance on LA and ALC may be effective in attenuating age-associated cognitive decline by slowing the rate of mitochondrial decay and cellular aging.


    Ann N Y Acad Sci. 2004 Nov;1033:108-16.

    Delaying the mitochondrial decay of aging with acetylcarnitine.
    Ames BN, Liu J.

    Nutritional Genomics Center, Children's Hospital Oakland Research Institute, Oakland, CA 94609, USA. bames@chori.org

    Oxidative mitochondrial decay is a major contributor to aging. Some of this decay can be reversed in old rats by feeding them normal mitochondrial metabolites, acetylcarnitine (ALC) and lipoic acid (LA), at high levels. Feeding the substrate ALC with LA, a mitochondrial antioxidant, restores the velocity of the reaction (K(m)) for ALC transferase and mitochondrial function. The principle appears to be that, with age, increased oxidative damage to protein causes a deformation of structure of key enzymes with a consequent lessening of affinity (K(m)) for the enzyme substrate. The effect of age on the enzyme-binding affinity can be mimicked by reacting it with malondialdehyde (a lipid peroxidation product that increases with age). In old rats (vs. young rats), mitochondrial membrane potential, cardiolipin level, respiratory control ratio, and cellular O(2) uptake are lower; oxidants/O(2), neuron RNA oxidation, and mutagenic aldehydes from lipid peroxidation are higher. Ambulatory activity and cognition decline with age. Feeding old rats ALC with LA for a few weeks restores mitochondrial function; lowers oxidants, neuron RNA oxidation, and mutagenic aldehydes; and increases rat ambulatory activity and cognition (as assayed with the Skinner box and Morris water maze). A recent meta-analysis of 21 double-blind clinical trials of ALC in the treatment of mild cognitive impairment and mild Alzheimer's disease showed significant efficacy vs. placebo. A meta-analysis of 4 clinical trials of LA for treatment of neuropathic deficits in diabetes showed significant efficacy vs. placebo.


    Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):1870-5.

    Feeding acetyl-L-carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress.
    Hagen TM, Liu J, Lykkesfeldt J, Wehr CM, Ingersoll RT, Vinarsky V, Bartholomew JC, Ames BN.

    Department of Biochemistry and Biophysics, Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.

    Erratum in:

    Proc Natl Acad Sci U S A 2002 May 14;99(10):7184.

    Mitochondrial-supported bioenergetics decline and oxidative stress increases during aging. To address whether the dietary addition of acetyl-l-carnitine [ALCAR, 1.5% (wt/vol) in the drinking water] and/or (R)-alpha-lipoic acid [LA, 0.5% (wt/wt) in the chow] improved these endpoints, young (2-4 mo) and old (24-28 mo) F344 rats were supplemented for up to 1 mo before death and hepatocyte isolation. ALCAR+LA partially reversed the age-related decline in average mitochondrial membrane potential and significantly increased (P = 0.02) hepatocellular O(2) consumption, indicating that mitochondrial-supported cellular metabolism was markedly improved by this feeding regimen. ALCAR+LA also increased ambulatory activity in both young and old rats; moreover, the improvement was significantly greater (P = 0.03) in old versus young animals and also greater when compared with old rats fed ALCAR or LA alone. To determine whether ALCAR+LA also affected indices of oxidative stress, ascorbic acid and markers of lipid peroxidation (malondialdehyde) were monitored. The hepatocellular ascorbate level markedly declined with age (P = 0.003) but was restored to the level seen in young rats when ALCAR+LA was given. The level of malondialdehyde, which was significantly higher (P = 0.0001) in old versus young rats, also declined after ALCAR+LA supplementation and was not significantly different from that of young unsupplemented rats. Feeding ALCAR in combination with LA increased metabolism and lowered oxidative stress more than either compound alone.


    Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):1876-81.

    Age-associated mitochondrial oxidative decay: improvement of carnitine acetyltransferase substrate-binding affinity and activity in brain by feeding old rats acetyl-L- carnitine and/or R-alpha -lipoic acid.
    Liu J, Killilea DW, Ames BN.

    Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720, USA.

    Erratum in:

    Proc Natl Acad Sci U S A 2002 May 14;99(10):7184.

    We test whether the dysfunction with age of carnitine acetyltransferase (CAT), a key mitochondrial enzyme for fuel utilization, is due to decreased binding affinity for substrate and whether this substrate, fed to old rats, restores CAT activity. The kinetics of CAT were analyzed by using the brains of young and old rats and of old rats supplemented for 7 weeks with the CAT substrate acetyl-l-carnitine (ALCAR) and/or the mitochondrial antioxidant precursor R-alpha-lipoic acid (LA). Old rats, compared with young rats, showed a decrease in CAT activity and in CAT-binding affinity for both substrates, ALCAR and CoA. Feeding ALCAR or ALCAR plus LA to old rats significantly restored CAT-binding affinity for ALCAR and CoA, and CAT activity. To explore the underlying mechanism, lipid peroxidation and total iron and copper levels were assayed; all increased in old rats. Feeding old rats LA or LA plus ALCAR inhibited lipid peroxidation but did not decrease iron and copper levels. Ex vivo oxidation of young-rat brain with Fe(II) caused loss of CAT activity and binding affinity. In vitro oxidation of purified CAT with Fe(II) inactivated the enzyme but did not alter binding affinity. However, in vitro treatment of CAT with the lipid peroxidation products malondialdehyde or 4-hydroxy-nonenal caused a decrease in CAT-binding affinity and activity, thus mimicking age-related change. Preincubation of CAT with ALCAR or CoA prevented malondialdehyde-induced dysfunction. Thus, feeding old rats high levels of key mitochondrial metabolites can ameliorate oxidative damage, enzyme activity, substrate-binding affinity, and mitochondrial dysfunction.
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    Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):2356-61.

    Memory loss in old rats is associated with brain mitochondrial decay and RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha -lipoic acid.
    Liu J, Head E, Gharib AM, Yuan W, Ingersoll RT, Hagen TM, Cotman CW, Ames BN.

    Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720, USA.

    Erratum in:

    Proc Natl Acad Sci U S A 2002 May 14;99(10):7184-5.

    Accumulation of oxidative damage to mitochondria, protein, and nucleic acid in the brain may lead to neuronal and cognitive dysfunction. The effects on cognitive function, brain mitochondrial structure, and biomarkers of oxidative damage were studied after feeding old rats two mitochondrial metabolites, acetyl-l-carnitine (ALCAR) [0.5% or 0.2% (wt/vol) in drinking water], and/or R-alpha-lipoic acid (LA) [0.2% or 0.1% (wt/wt) in diet]. Spatial memory was assessed by using the Morris water maze; temporal memory was tested by using the peak procedure (a time-discrimination procedure). Dietary supplementation with ALCAR and/or LA improved memory, the combination being the most effective for two different tests of spatial memory (P < 0.05; P < 0.01) and for temporal memory (P < 0.05). Immunohistochemical analysis showed that oxidative damage to nucleic acids (8-hydroxyguanosine and 8-hydroxy-2'-deoxyguanosine) increased with age in the hippocampus, a region important for memory. Oxidative damage to nucleic acids occurred predominantly in RNA. Dietary administration of ALCAR and/or LA significantly reduced the extent of oxidized RNA, the combination being the most effective. Electron microscopic studies in the hippocampus showed that ALCAR and/or LA reversed age-associated mitochondrial structural decay. These results suggest that feeding ALCAR and LA to old rats improves performance on memory tasks by lowering oxidative damage and improving mitochondrial function.


    Ann N Y Acad Sci. 2002 Apr;959:133-66.

    Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites.
    Liu J, Atamna H, Kuratsune H, Ames BN.

    Division of Biochemistry and Molecular Biology, University of California, Berkeley, California 94720, USA.

    Mitochondria decay with age due to the oxidation of lipids, proteins, RNA, and DNA. Some of this decay can be reversed in aged animals by feeding them the mitochondrial metabolites acetylcarnitine and lipoic acid. In this review, we summarize our recent studies on the effects of these mitochondrial metabolites and mitochondrial antioxidants (alpha-phenyl-N-t-butyl nitrone and N-t-butyl hydroxylamine) on the age-associated mitochondrial decay of the brain of old rats, neuronal cells, and human diploid fibroblast cells. In feeding studies in old rats, these mitochondrial metabolites and antioxidants improve the age-associated decline of ambulatory activity and memory, partially restore mitochondrial structure and function, inhibit the age-associated increase of oxidative damage to lipids, proteins, and nucleic acids, elevate the levels of antioxidants, and restore the activity and substrate binding affinity of a key mitochondrial enzyme, carnitine acetyltransferase. These mitochondrial metabolites and antioxidants protect neuronal cells from neurotoxin- and oxidant-induced toxicity and oxidative damage; delay the normal senescence of human diploid fibroblast cells, and inhibit oxidant-induced acceleration of senescence. These results suggest a plausible mechanism: with age, increased oxidative damage to proteins and lipid membranes, particularly in mitochondria, causes a deformation of structure of enzymes, with a consequent decrease of enzyme activity as well as substrate binding affinity for their substrates; an increased level of substrate restores the velocity of the reaction and restores mitochondrial function, thus delaying mitochondrial decay and aging. This loss of activity due to coenzyme or substrate binding appears to be true for a number of other enzymes as well, including mitochondrial complex III and IV.


    Ann N Y Acad Sci. 2002 Apr;959:491-507.

    Mitochondrial decay in the aging rat heart: evidence for improvement by dietary supplementation with acetyl-L-carnitine and/or lipoic acid.
    Hagen TM, Moreau R, Suh JH, Visioli F.

    Department of Biochemistry and Biophysics, Linus Pauling Institute, Oregon State University, Corvallis, Oregon 97331, USA. tory.hagen@orst.edu

    Mitochondrial decay has been postulated to be a significant underlying part of the aging process. Decline in mitochondrial function may lead to cellular energy deficits, especially in times of greater energy demand, and compromise vital ATP-dependent cellular operations, including detoxification, repair systems, DNA replication, and osmotic balance. Mitochondrial decay may also lead to enhanced oxidant production and thus render the cell more prone to oxidative insult. In particular, the heart may be especially susceptible to mitochondrial dysfunction due to myocardial dependency on beta-oxidation of fatty acids for energy and the postmitotic nature of cardiac myocytes, which would allow for greater accumulation of mitochondrial mutations and deletions. Thus, maintenance of mitochondrial function may be important to maintain overall myocardial function. Herein, we review the major age-related changes that occur to mitochondria in the aging heart and the evidence that two such supplements, acetyl-l-carnitine (ALCAR) and (R)-alpha-lipoic acid, may improve myocardial bioenergetics and lower the increased oxidative stress associated with aging. We and others have shown that feeding old rats ALCAR reverses the age-related decline in carnitine levels and improves mitochondrial beta-oxidation in a number of tissues studied. However, ALCAR supplementation does not appear to reverse the age-related decline in cardiac antioxidant status and thus may not substantially alter indices of oxidative stress. Lipoic acid, a potent thiol antioxidant and mitochondrial metabolite, appears to increase low molecular weight antioxidant status and thereby decreases age-associated oxidative insult. Thus, ALCAR along with lipoic acid may be effective supplemental regimens to maintain myocardial function.
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    Registered User bloodsimple1234's Avatar
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    Thumbs up

    Peter,I really appreicate the extra time you take to post the research!
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    Originally Posted by bloodsimple1234 View Post
    Peter,I really appreicate the extra time you take to post the research!
    At least someone does!!! lol, yeah time consuming, but I enjoy getting the beneficial info out for some reason... I really enjoy supporting great companies and products so we can continue to see better and better products in the future. I could just say Mito Charger is a fantastic product and AOR is a super company, but backing it up with some science and info really brings the message clear.

    I`ve been reading this research for a long time so when a formula like this comes along, it is obvious to me the product is heavily based on science and a log worthy product. I have been educating and explaining this kind of thing to my family for quite some time as well so with aging parents, it really is important that I get things right. My dad is 70 and very healthy, while mom is late 60`s and equally healthy. Both have recently begun Mito Charger, but have been using many health-related products such as Ortho Core for many years on my suggestion. I`m always on the look out for the best and continually AOR`s formulas stand out as easy first choices.

    btw, once again, big thanks to Steve of Cognitive Nutrition for supplying me the product and making this log happen!

    Where are you Steve?
    Last edited by Peter LeDrew; 11-08-2009 at 02:04 PM.
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    I'll try and post up some early thoughts on my experiences so far. Like I stated previously, I have been dosing 6 caps most days, but long term I would be satisfied with even 2-3.

    Energy has been great and one weird notable effect has actually been Deja Vu. Weird, maybe I can predict the future now, but last night it was surreal. It seemed like I was reading threads and posts here that I have seen before... really vivid and strange. I don't know what is to blame or if it has anything to do with MC, perhaps I need to spend less time on bb.com! Maybe I am slowing down aging so much I am going back in time and know what happened in the future? Not srs of course.
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  28. #28
    Team Molecular Nutrition Peter LeDrew's Avatar
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    Had an awesome 40min workout on the bike trainer. Drenched in sweat even while working out in a freezing cold basement. I'll hopefully get some time to workout chest/back tomorrow and post up my experiences so far.
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    great info, keep the updates coming! i just ordered some of this myself. looking forward to intesne deja vu in the near future haha.

    i also bought both my parents a bunch of orth-core, they aren't as into health products as i am, and i can't stand to see them take centrum multivitamins .

    looking at the research behind AOR's products makes me feel good about buying them, puts nearly all sports supp co's to shame.
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  30. #30
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    Originally Posted by acarey617 View Post
    great info, keep the updates coming! i just ordered some of this myself. looking forward to intesne deja vu in the near future haha.

    i also bought both my parents a bunch of orth-core, they aren't as into health products as i am, and i can't stand to see them take centrum multivitamins .

    looking at the research behind AOR's products makes me feel good about buying them, puts nearly all sports supp co's to shame.
    Thanks!

    You're def. caring to provide your parents the best in multi-vitamin insurance. Smart choice and I am sure it will pay off for them... you are right btw about putting most companies to shame... I don't even think most people know the half of it... bb'ing companies have generally been improving, but still they have a lot of catching up to do as many informed consumers such as health professionals, etc... still think this industry is a joke.
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