![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 16 of 16. This is the beginning of the thread.
Posted by raybakes on October 14, 2004, at 9:12:36
Hi everyone, went to an interesting conference at the weekend, ed mitchell, the astronaut was there, and skip atwater from the monroe institute was there talking about hemi sync.
I took a few supplements along as I didn't want to get brain fog and miss most of what they were saying - serrapeptase worked really well at keeping the blood going to my brain, but I was amazed at how well betaine worked at keeping me alert. Methylation was obviously helping with my brain energy, but why? I bought a biochemistry book in one of the breaks and it said that 70% of all methylation reactions in the body are used to form creatine - previously I've done really badly on creatine, but now I can take a small amount as long as I've taken plenty of folinic acid (not folate) sublingual B12, and betaine (and sometimes some methionine). Now if I take a little creatine, I stay alert. The book also mentioned that creatine can work to maintain correct acid/alkaline balance in cells too.
I've always wondered why methylation and SAMe are helpful in depression - is it because the brain is starving of energy? It's also interesting that creatine can reduce antibodies and raise glutathione, as glutathione needs a lot of energy to keep it activated.
http://hdlighthouse.org/see/diet/supplements/creatine/creatine14.htm
Ray
Posted by raybakes on October 14, 2004, at 9:30:47
In reply to brain fog and creatine/methylation, posted by raybakes on October 14, 2004, at 9:12:36
found creatine protects dopamine function and against dopamine toxicity (some articles say that dopamine is an oxidant).
http://journals.humanapress.com/ArticleDetail.pasp?issn=0895-8696&acode=JMN:21:3:191
Posted by jujube on October 14, 2004, at 10:25:04
In reply to brain fog and creatine/methylation, posted by raybakes on October 14, 2004, at 9:12:36
I've been reading that L-carnitine is another supplement that is important for healthy brain function. Apparently in one study involving people with Alzeimer's disease (don't know how big the study was), the progression of the disease was significantly reduced in those receiving 2 grams per day of acetyl-L-carnitine orally for a year. Although often called an amino acid because of its chemical makeup, L-carnitine is actually a vitamin-like nutrient related in structure to the B vitamins.
Tamara
> Hi everyone, went to an interesting conference at the weekend, ed mitchell, the astronaut was there, and skip atwater from the monroe institute was there talking about hemi sync.
>
> I took a few supplements along as I didn't want to get brain fog and miss most of what they were saying - serrapeptase worked really well at keeping the blood going to my brain, but I was amazed at how well betaine worked at keeping me alert. Methylation was obviously helping with my brain energy, but why? I bought a biochemistry book in one of the breaks and it said that 70% of all methylation reactions in the body are used to form creatine - previously I've done really badly on creatine, but now I can take a small amount as long as I've taken plenty of folinic acid (not folate) sublingual B12, and betaine (and sometimes some methionine). Now if I take a little creatine, I stay alert. The book also mentioned that creatine can work to maintain correct acid/alkaline balance in cells too.
>
> I've always wondered why methylation and SAMe are helpful in depression - is it because the brain is starving of energy? It's also interesting that creatine can reduce antibodies and raise glutathione, as glutathione needs a lot of energy to keep it activated.
>
> http://hdlighthouse.org/see/diet/supplements/creatine/creatine14.htm
>
> Ray
>
Posted by raybakes on October 14, 2004, at 11:01:05
In reply to Re: brain fog and creatine/methylation » raybakes, posted by jujube on October 14, 2004, at 10:25:04
> I've been reading that L-carnitine is another supplement that is important for healthy brain function. Apparently in one study involving people with Alzeimer's disease (don't know how big the study was), the progression of the disease was significantly reduced in those receiving 2 grams per day of acetyl-L-carnitine orally for a year. Although often called an amino acid because of its chemical makeup, L-carnitine is actually a vitamin-like nutrient related in structure to the B vitamins.
>
Hi Tamara, until yesterday I did really badly with acetyl l carnitine, but I found out it needed three molecules of SAMe to synthesize it - so i took it along with b12, folate and betaine, and it felt wonderful - I pushed it to see how much I could take, 1g was about right for me, 2g pulled me down a bit and sped up my bowels - maybe it increased acetylcholine and so peristalsis? With one gramme i felt an incredible glow up and down my spine!Ray
Posted by jujube on October 14, 2004, at 11:13:32
In reply to Re: brain fog and creatine/methylation » jujube, posted by raybakes on October 14, 2004, at 11:01:05
> > I've been reading that L-carnitine is another supplement that is important for healthy brain function. Apparently in one study involving people with Alzeimer's disease (don't know how big the study was), the progression of the disease was significantly reduced in those receiving 2 grams per day of acetyl-L-carnitine orally for a year. Although often called an amino acid because of its chemical makeup, L-carnitine is actually a vitamin-like nutrient related in structure to the B vitamins.
> >
>
> Hi Tamara, until yesterday I did really badly with acetyl l carnitine, but I found out it needed three molecules of SAMe to synthesize it - so i took it along with b12, folate and betaine, and it felt wonderful - I pushed it to see how much I could take, 1g was about right for me, 2g pulled me down a bit and sped up my bowels - maybe it increased acetylcholine and so peristalsis? With one gramme i felt an incredible glow up and down my spine!
>
> Ray
Ray,Hmmm - sounds like another supplement to add to my list to try I think. I have been trying to convince my aunt to get my uncle started on some natural supplements such as carnitine since he is in the early stages of alzeimers (plus he has high blood pressure and high cholestoral and is on medication for all as well as an AD). I think I will keep pushing. I have sent her a lot of info on a number of supplements that may be effective, so maybe she'll start looking at natural alternatives and adjuncts more seriously.
Another question: Have you tried Co-enzyme Q10 for energy, etc.? I am thinking of trying a product that combines the Q10 with flaxseed oil. I really need something for energy that doesn't cause anxiety. But, I also tend to have low blood pressure, so I don't want anything that could significantly lower my blood pressure. Thanks
Tamara
Posted by Larry Hoover on October 15, 2004, at 12:11:16
In reply to brain fog and creatine/methylation, posted by raybakes on October 14, 2004, at 9:12:36
> Hi everyone, went to an interesting conference at the weekend, ed mitchell, the astronaut was there, and skip atwater from the monroe institute was there talking about hemi sync.
>
> I took a few supplements along as I didn't want to get brain fog and miss most of what they were saying - serrapeptase worked really well at keeping the blood going to my brain, but I was amazed at how well betaine worked at keeping me alert. Methylation was obviously helping with my brain energy, but why? I bought a biochemistry book in one of the breaks and it said that 70% of all methylation reactions in the body are used to form creatine - previously I've done really badly on creatine, but now I can take a small amount as long as I've taken plenty of folinic acid (not folate) sublingual B12, and betaine (and sometimes some methionine). Now if I take a little creatine, I stay alert. The book also mentioned that creatine can work to maintain correct acid/alkaline balance in cells too.I'm glad you're helping to push my brain back into a good zone, Ray. Here are a few abstracts about creatine. I don't know if I own some, or not. But it's certainly going to be something I keep on my shelf.
Neurosci Res. 2002 Apr;42(4):279-85.
Effects of creatine on mental fatigue and cerebral hemoglobin oxygenation.
Watanabe A, Kato N, Kato T.
Department of Neuropsychiatry, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo, 113-8655, Tokyo, Japan.
While the role of creatine in preventing muscle (peripheral) fatigue for high performance athletes is well understood, its biochemical role in prevention of mental (central) fatigue is not. Creatine is abundant in muscles and the brain and after phosphorylation used as an energy source for adenosine triphosphate synthesis. Using double-blind placebo-controlled
paradigm, we demonstrated that dietary supplement of creatine (8 g/day for 5 days) reduces mental fatigue when subjects repeatedly perform a simple mathematical calculation. After taking the creatine supplement, task-evoked increase of cerebral oxygenated hemoglobin in the brains of subjects measured by near infrared spectroscopy was significantly reduced, which is
compatible with increased oxygen utilization in the brain.
Brain Res. 1999 Jan 16;816(1):124-30.Exogenous creatine delays anoxic depolarization and protects from hypoxic damage: dose-effect relationship.
Balestrino M, Rebaudo R, Lunardi G.
Department of Neurological Sciences, University of Genova, Via De Toni 5, 16132, Genoa, Italy.
Incubation of hippocampal slices with different concentrations of creatine (0.5, 1, 10, 25 mM) results in a dose-dependent increase in intracellular phosphocreatine (PCr). Electrophysiological evidence suggests that this effect can protect neurons from anoxic damage by delaying the depletion of ATP during oxygen deprivation. In this paper we show that incubation of
brain slices with varying doses of creatine increases intracellular phosphocreatine and delays anoxic depolarization (AD) in a dose-dependent way. Specifically, addition to the incubation medium of 1 mM creatine significantly increased AD latency during hypoxia and prevented irreversible neuronal damage. Adding 0.5 mM creatine had no significant effect. Higher concentrations of creatine (up to 25 mM) did not provide any better protection. Our data also suggest a linear correlation between intracellular PCr and AD latency. These data report neural protection by exogenous creatine at concentrations lower than those usually reported in the literature. Copyright 1999 Elsevier Science B.V.
Amino Acids. 2002;23(1-3):221-9.Role of creatine and phosphocreatine in neuronal protection from anoxic and ischemic damage.
Balestrino M, Lensman M, Parodi M, Perasso L, Rebaudo R, Melani R, Polenov S, Cupello A.
Department of Neurological and Vision Sciences, University of Genova, Italy.
Phosphocreatine can to some extent compensate for the lack of ATP synthesis that is caused in the brain by deprivation of oxygen or glucose. Treatment of in vitro rat hippocampal slices with creatine increases the neuronal store of phosphocreatine. In this way it increases the resistance of the tissue to anoxic or ischemic damage. In in vitro brain slices pretreatment with creatine delays anoxic depolarization (AD) and prevents the irreversible loss of evoked potentials that is caused by transient anoxia, although it seems so far not to be active against milder, not AD-mediated, damage. Although creatine crosses poorly the blood-brain barrier, its administration in vivo at high doses through the intracerebroventricular or the intraperitoneal way causes an increase of cerebral phosphocreatine that has been shown to be of therapeutic value in vitro. Accordingly, preliminary data show that creatine pretreatment decreases ischemic damage in vivo.
J Neurochem. 2001 Jan;76(2):425-34.On the mechanisms of neuroprotection by creatine and phosphocreatine.
Brustovetsky N, Brustovetsky T, Dubinsky JM.
Department of Neuroscience, University of Minnesota, Minneapolis 55455, USA.
Creatine and phosphocreatine were evaluated for their ability to prevent death of cultured striatal and hippocampal neurons exposed to either glutamate or 3-nitropropionic acid (3NP) and to inhibit the mitochondrial permeability transition in CNS mitochondria. Phosphocreatine (PCr), and to a lesser extent creatine (Cr), but not (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK801), dose-dependently ameliorated 3NP toxicity when applied simultaneously with the 3NP in Mg2+-free media. Pre-treatment of PCr for 2 or 5 days and Cr for 5 days protected against glutamate excitotoxicity equivalent to that achieved by MK801 post-treatment. The combination of PCr or Cr pre-treatment and MK801 post-treatment did not provide additional protection, indicating that both prevented the toxicity attributable to secondary glutamate release. To determine if Cr or PCr directly inhibited the permeability transition, mitochondrial swelling and depolarization were assayed in isolated, purified brain mitochondria. PCr reduced the amount of swelling induced by calcium by 20%. Cr decreased mitochondrial swelling when inhibitors of creatine kinase octamer-dimer transition were present. However, in brain mitochondria prepared from rats fed a diet supplemented with 2% creatine for 2 weeks, the extent of calcium-induced mitochondrial swelling was not altered. Thus, the neuroprotective properties of PCr and Cr may reflect enhancement of cytoplasmic high-energy phosphates but not permeability transition inhibition.
J Neurochem. 2000 May;74(5):1968-78.Protective effect of the energy precursor creatine against toxicity of glutamate and beta-amyloid in rat hippocampal neurons.
Brewer GJ, Wallimann TW.
Department of Medical Microbiology/Immunology, Southern Illinois University School of Medicine, Springfield, Illinois 62794-9626, USA. gbrewer@siumed.edu
The loss of ATP, which is needed for ionic homeostasis, is an early event in the neurotoxicity of glutamate and beta-amyloid (A(beta)). We hypothesize that cells supplemented with the precursor creatine make more phosphocreatine (PCr) and create larger energy reserves with consequent neuroprotection against stressors. In serum-free cultures, glutamate at 0.5-1 mM was toxic to embryonic hippocampal neurons. Creatine at >0.1 mM greatly reduced glutamate toxicity. Creatine (1 mM) could be added as late as 2 h after glutamate to achieve protection at 24 h. In association with neurotoxic protection by creatine during the first 4 h, PCr levels remained constant, and PCr/ATP ratios increased. Morphologically, creatine protected against glutamate-induced dendritic pruning. Toxicity in embryonic neurons exposed to A(beta) (25-35) for 48 h was partially prevented by creatine as well. During the first 6 h of treatment with A(beta) plus creatine, the molar ratio of PCr/ATP in neurons increased from 15 to 60. Neurons from adult rats were also partially protected from a 24-h exposure to A(beta)
(25-35) by creatine, but protection was reduced in neurons from old animals. These results suggest that fortified energy reserves are able to protect neurons against important cytotoxic agents. The oral availability of creatine may benefit patients with neurodegenerative diseases.
Brain Res. 2000 Mar 31;860(1-2):195-8.Neuroprotective effects of creatine administration against NMDA and malonate toxicity.
Malcon C, Kaddurah-Daouk R, Beal MF.
Neurochemistry Laboratory, Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
We examined whether creatine administration could exert neuroprotective effects against excitotoxicity mediated by N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid. Oral administration of 1% creatine significantly attenuated striatal excitotoxic lesions produced by NMDA, but had no effect on lesions produced by AMPA or kainic acid. Both creatine and nicotinamide can exert significant protective effects against malonate-induced striatal lesions. We, therefore, examined whether nicotinamide could exert additive neuroprotective effects with creatine against malonate-induced lesions. Nicotinamide with creatine produced significantly better neuroprotection than creatine alone against malonate-induced lesions. Creatine can, therefore, produce significant neuroprotective effects against NMDA mediated excitotoxic lesions in vivo and the combination of nicotinamide with creatine exerts additive neuroprotective effects.
Exp Gerontol. 2000 Dec;35(9-10):1165-83.Neuronal plasticity and stressor toxicity during aging.
Brewer GJ.
Department of Neurology, School of Medicine, Southern Illinois University, Springfield, IL, 62794-9626, USA. gbrewer@siumed.edu
Brain aging, Alzheimer disease and stroke share common elements of deficits in calcium regulation, declines in mitochondrial function, increases in generation of reactive oxygen species (ROS), accumulated damage from ROS and immune system dysfunction. The problem is to distinguish less significant side reactions, such as gray hair, from aspects of aging that contribute to disease. Toward establishing cause and effect relationships, a neuron cell culture system is described that allows comparisons with age under uniform environmental conditions. This neuron culture model indicates that susceptibility to death by apoptosis and consequences of the inflammatory response from beta-amyloid are age-related and an inherent characteristic of the neurons. Further mechanistic investigations are possible. New therapeutic approaches are suggested that combine inhibition of calcium overloads (calcium channel blockers), reduced ROS damage (melatonin, N-acetyl-cysteine), and bolstered mitochondrial function and energy generation (creatine). Together with newly demonstrated capabilities for adult and aged neuron regeneration and multiplication, i.e. plasticity, these approaches offer new hope toward reversing age-related decrements and damage from neurodegenerative disease.
> I've always wondered why methylation and SAMe are helpful in depression - is it because the brain is starving of energy? It's also interesting that creatine can reduce antibodies and raise glutathione, as glutathione needs a lot of energy to keep it activated.
Yes. But also, methylation is a required component of DNA transcription, something you need to do every single day. If the rate of protein synthesis falls, everything bogs down.
>
> http://hdlighthouse.org/see/diet/supplements/creatine/creatine14.htm
>
> Ray
>Lar
Posted by raybakes on October 15, 2004, at 12:17:54
In reply to Re: brain fog and creatine/methylation » raybakes, posted by jujube on October 14, 2004, at 11:13:32
> Hmmm - sounds like another supplement to add to my list to try I think. I have been trying to convince my aunt to get my uncle started on some natural supplements such as carnitine since he is in the early stages of alzeimers (plus he has high blood pressure and high cholestoral and is on medication for all as well as an AD). I think I will keep pushing. I have sent her a lot of info on a number of supplements that may be effective, so maybe she'll start looking at natural alternatives and adjuncts more seriously.Hi Tamara,
Have you heard about AD, high cholesterol and high blood pressure all being symptoms of syndrome X (basically insulin resistance)?
I found the acetyl carnitine good, but it takes a lot of work to make it work for me - if I don't take two or three other supplements with it, I feel a lot worse!
http://www.edelsoncenter.com/Alzheimers/alzheimers_disease_update.htm
"In multivariate analysis including apolipoprotein E4 phenotype, age, education, systolic blood pressure, total cholesterol concentration, fasting glucose concentration, and insulin concentration, apolipoprotein E4 phenotype, age, education, total cholesterol, and insulin were significantly associated with Alzheimer's disease"
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9366728&dopt=Abstract
>
> Another question: Have you tried Co-enzyme Q10 for energy, etc.? I am thinking of trying a product that combines the Q10 with flaxseed oil. I really need something for energy that doesn't cause anxiety. But, I also tend to have low blood pressure, so I don't want anything that could significantly lower my blood pressure.I have taken Co Q10 in the past and got on really well with it - found different brands had different effects - some did absolutely nothing for me! Read a warning recently that Co Q10 can be toxic in low oxygen environments. The warning was in product info for a Co Q10 analogue called 'idebenone', that claims to not suffer the low oxygen toxicty of Co Q10. Flax sounds OK too, should be good to protect the mitochondrial membrane - flax is rich in 'lignans' too, which have immune balancing properties. If your uncle is taking statin drugs for his cholesterol, he might want to take Co Q10 too, as Co Q10 is made from cholesterol, and Co Q10 can get dangerously low when taking them.
With your low blood pressure, do you think it's anything to do with adrenals - I've heard people with low adrenal function produce low levels of aldosterone, the steroid that helps reabsorb sodium and raises blood pressure.
Hope you can convince your uncle about alternative ideas!
Ray
Posted by jujube on October 15, 2004, at 12:29:20
In reply to Re: brain fog and creatine/methylation » jujube, posted by raybakes on October 15, 2004, at 12:17:54
Posted by raybakes on October 15, 2004, at 12:55:36
In reply to Re: brain fog and creatine/methylation » raybakes, posted by Larry Hoover on October 15, 2004, at 12:11:16
> I'm glad you're helping to push my brain back into a good zone, Ray. Here are a few abstracts about creatine. I don't know if I own some, or not. But it's certainly going to be something I keep on my shelf.Wow, thanks for all those abstracts Lar!
I've had creatine on my shelf for a year but always got a pounding headache when I took it. It was only when I found out that 70% of all methylation reactions are used to make creatine, that I tried it again. I needed to stock up on methyl donors before I took it (my favourite sublingual B12, folinic acid and betaine). When fully 'methylated' creatine feels brilliant for me! Interesting that creatine kinase is inhibited by mercury and other heavy metals.
Creatine in some abstracts, has been found to protect dopamine and tyrosine hyroxylase too.
Do you know if the sulphation of dopamine is important in dopamine transport/storage? Just seen a few references to free dopamine acting as an oxidant?
Thanks,
Ray
Posted by Larry Hoover on October 15, 2004, at 13:03:23
In reply to Re: brain fog and creatine/methylation » jujube, posted by raybakes on October 15, 2004, at 12:17:54
> > Another question: Have you tried Co-enzyme Q10 for energy, etc.? I am thinking of trying a product that combines the Q10 with flaxseed oil. I really need something for energy that doesn't cause anxiety. But, I also tend to have low blood pressure, so I don't want anything that could significantly lower my blood pressure.
>
> I have taken Co Q10 in the past and got on really well with it - found different brands had different effects - some did absolutely nothing for me! Read a warning recently that Co Q10 can be toxic in low oxygen environments. The warning was in product info for a Co Q10 analogue called 'idebenone', that claims to not suffer the low oxygen toxicty of Co Q10. Flax sounds OK too, should be good to protect the mitochondrial membrane - flax is rich in 'lignans' too, which have immune balancing properties. If your uncle is taking statin drugs for his cholesterol, he might want to take Co Q10 too, as Co Q10 is made from cholesterol, and Co Q10 can get dangerously low when taking them.It's a fairly recent finding that CoQ10 uptake is highly dependent on fat, as it is not very water soluble. Considering the high price of this supp (expected to fall next year, as new supplies come on line), you'll get substantially more bang for the buck if you take CoQ10 that is in a fat base, such as rice bran oil (LEF brand), or this example of flax oil. You're really not taking it for the oil content (that's a bonus, if they use an oil that's good for you), you're taking it that way because uptake can be nearly 10 times as much as dry powders of equivalent dose.
Lar
Posted by raybakes on October 15, 2004, at 13:08:02
In reply to Re: CoQ10 » raybakes, posted by Larry Hoover on October 15, 2004, at 13:03:23
>
> It's a fairly recent finding that CoQ10 uptake is highly dependent on fat,Thanks Lar - think that explains why some brands were a waste of time for me!
Ray
Posted by Larry Hoover on October 15, 2004, at 13:29:22
In reply to Re: brain fog and creatine/methylation » Larry Hoover, posted by raybakes on October 15, 2004, at 12:55:36
>
> > I'm glad you're helping to push my brain back into a good zone, Ray. Here are a few abstracts about creatine. I don't know if I own some, or not. But it's certainly going to be something I keep on my shelf.
>
> Wow, thanks for all those abstracts Lar!You're welcome. I was just unpacking a big box of stuff I ordered in, and there was a 1 kilo jar of creatine.
> I've had creatine on my shelf for a year but always got a pounding headache when I took it. It was only when I found out that 70% of all methylation reactions are used to make creatine, that I tried it again. I needed to stock up on methyl donors before I took it (my favourite sublingual B12, folinic acid and betaine). When fully 'methylated' creatine feels brilliant for me! Interesting that creatine kinase is inhibited by mercury and other heavy metals.
Point made. I have a profound response to betaine, but I'm not certain the effect is only mediated via methyl donation. Methinks there's more to betaine than that, overall. Didn't know about that effect of mercury. I think my amalgams have injured me, and that seems a reasonable metabolic pathway to consider trying to strengthen.
> Creatine in some abstracts, has been found to protect dopamine and tyrosine hyroxylase too.
>
> Do you know if the sulphation of dopamine is important in dopamine transport/storage?I don't see it that way. Not like DHEA-S. I think it's simply a way of inactivating dopamine from diet. 99% of the dopamine sulfation capacity in the periphery is in the intestinal wall. The only other place the enzyme is found is in accessory cells (glia, I think) in the brain. It mops up whatever amount of dopamine escapes MAO and COMT.
> Just seen a few references to free dopamine acting as an oxidant?
It might well be one, but there is so very little of it (free dopamine, as opposed to glucoronidated or sulfated (conjugated)), I think it's moot.
> Thanks,
>
> RayMy pleasure,
Lar
Posted by jujube on October 15, 2004, at 13:52:31
In reply to Re: CoQ10 » raybakes, posted by Larry Hoover on October 15, 2004, at 13:03:23
> > > Another question: Have you tried Co-enzyme Q10 for energy, etc.? I am thinking of trying a product that combines the Q10 with flaxseed oil. I really need something for energy that doesn't cause anxiety. But, I also tend to have low blood pressure, so I don't want anything that could significantly lower my blood pressure.
> >
> > I have taken Co Q10 in the past and got on really well with it - found different brands had different effects - some did absolutely nothing for me! Read a warning recently that Co Q10 can be toxic in low oxygen environments. The warning was in product info for a Co Q10 analogue called 'idebenone', that claims to not suffer the low oxygen toxicty of Co Q10. Flax sounds OK too, should be good to protect the mitochondrial membrane - flax is rich in 'lignans' too, which have immune balancing properties. If your uncle is taking statin drugs for his cholesterol, he might want to take Co Q10 too, as Co Q10 is made from cholesterol, and Co Q10 can get dangerously low when taking them.
>
> It's a fairly recent finding that CoQ10 uptake is highly dependent on fat, as it is not very water soluble. Considering the high price of this supp (expected to fall next year, as new supplies come on line), you'll get substantially more bang for the buck if you take CoQ10 that is in a fat base, such as rice bran oil (LEF brand), or this example of flax oil. You're really not taking it for the oil content (that's a bonus, if they use an oil that's good for you), you're taking it that way because uptake can be nearly 10 times as much as dry powders of equivalent dose.
>
> LarThanks Larry. I was debating whether to order just regular Q10 or the one with the flaxseed oil, and decided on the one with the flaxseed only because I had heard that flaxseed was good for you and felt it could be an added benefit. I'm glad I did.
Tamara
Posted by tealady on October 15, 2004, at 19:19:05
In reply to Re: brain fog and creatine/methylation » Larry Hoover, posted by raybakes on October 15, 2004, at 12:55:36
Hi Ray,
I haven't tried the methylation bit as yet.
What type of betaine do you take? I'll have to put an o'seas order in soon from somewhere as I've run out of P5P B6.
Only betaine I can get in Oz is Betaine HCL.
I used to take B12 as my blood levels were low..both needle form (hydroxycobalamin..the only type available in Oz besides cyanocobalamin)>sublingual B12, folinic acid and betaine
>
What is folinic acid..I gather some kind of folate...or why is it preferable to you?. I do take extra folate in addition to what's in my multi.Mine is called folic acid 550mcg. Its an oil based capsule. It doesn't appear to have much affect, then again it doesn't hurt. My folate blood levels before any supps were ABOVE range though...and so were my Mum's.
I ended up taking the additional folate as Lar mentioned something about falsely high blood levels maybe, but he couldn't remember the details I think.
Both my Mum's and my blood levels of B12 were low, and both had folate above range..Her B12 was lower than mine and folate higher...almost like our bodies try to replace the low B12 with folate?
I do notice my Mum has a far better memory after B12 needles (hydroxycobalamin), but she hasn't had any for a while. Before the needles it was difficult to hold conversation with her. So I'm pretty sure B12 can help with Alzheimer's type symptoms at least for some.
I couldn't get a homocysteine test. (local GP told me "homocysteine doesn't exist in Australia"..his exact words <g>)On B12 and me...I stopped taking it last February? My blood levels were fairly good then.
The reason I stopped taking it was I always had strange reactions to B12 needles, and to a lesser extent the methylcobalamin sublinguals. I've got some old posts on here about this I'll try to find as my memory is poor.
CoQ10..yeah I always knew about the oil based type being the only type to take. Maybe in Oz we are ahead in something!<g>
I took it religiously for a year but stopped a couple of weeks ago when I read something...it was probably that low oxygen connection thing you mentioned. Initially I think the CoQ10 really helped me as my gums used to bleed a lot despite VitC which did help a bit. My gums stopped bleeding, went a lot pinker and healthier looking....blaming the mercury here! And I think it helped with the energy too.
I've lost a lot of hair and my skin etc has wrinkled a lot in the past year though..looks like I've aged 20 years!
Partly this is to do with loss of excess weight..but I didn't have wrinkles before I blew up! So I'm concerned if any supps are speeding up the aging bit probably via low oxygen and oxidation..I get lost with this stuff still!
So after reading whatever it was about CoQ10 I stopped taking it and I think I improved. Can't really tell I guess.
Maybe one only needs to get it to a certain level or maybe I needed more of other nutrients for balance, but I'm not taking it again..,,at least until my gums start bleeding I think. At least I know its something I need then. and will help me.
Wish I could remember what is was I read too, maybe it was from you? *grins*
> Creatine in some abstracts, has been found to protect dopamine and tyrosine hyroxylase too.Interesting. Both dopamine and tyrosine hydroxalase with me appear to need a bit of a hand(I think). I thought it might be the P5P B6 here.
>
> Do you know if the sulphation of dopamine is important in dopamine transport/storage? Just seen a few references to free dopamine acting as an oxidant?Gee I really get lost trying to work out sulphation. I have an article on it I tried to work thru
http://edrv.endojournals.org/cgi/content/abstract/23/5/703
..but I figure maybe another year or two of study first! I suspect you are onto something here though.
I'm got interested as thyroid hormones also have a T3S ..no idea if any free part is measured when in the Ft3 levels or not.
Very confusing.
Also on allergy tests and elimination diets and retrials I am sensitive to sulphur preservatives. Maybe sensitive to sulphur based drugs too..at least I get nausea and feel dreadful after a few days, so I avoid them.
Because of this I've avoided any sulfate form of supps. Last month I did have a zinc sulfate (one capule..50 mg of zinc sulphate monohydrate) and soon after ended up vomiting, sweating ,shakin for about 30 mins or maybe an hour? Then I was OK. Any thoughts on this?
>
> Thanks,
Jan
Posted by raybakes on October 16, 2004, at 7:29:48
In reply to Re: brain fog and creatine/methylation » raybakes, posted by Larry Hoover on October 15, 2004, at 13:29:22
Hi Lar,
came across these two abstracts - the first one seems to suggest that dopamine degradation via the quinone pathway (monoamine oxidase?) is neurotoxic, but methylation of dopamine via COMT, bypasses that pathway.
Int J Mol Med. 2004 Mar;13(3):343-53. Related Articles, Links
CNS dopamine oxidation and catechol-O-methyltransferase: importance in the etiology, pharmacotherapy, and dietary prevention of Parkinson's disease.Zhu BT.
Department of Basic Pharmaceutical Sciences, College of Pharmacy, University of South Carolina, Columbia, SC 29208, USA. BTZhu@cop.sc.edu
In this article, a particular emphasis has been placed on the conceptual development and understanding of the unique pathogenic changes that are indigenous to the striatal dopaminergic neurons as an important etiological factor in human Parkinson's disease (PD) as well as on the understanding of their clinical implications. Specifically, I have discussed the etiological roles of central nervous system dopamine oxidation in PD, along with a critical review of the available evidence in support of the proposed hypotheses. The chemically-reactive dopamine quinone/semiquinone intermediates are known to be highly neurotoxic and potentially genotoxic. There is considerable evidence for the suggestion that the long-term use of levodopa accelerates the progression of PD. In comparison, centrally-acting non-catechol dopamine receptor agonists would be an excellent alternative to levodopa for the treatment of PD (particularly for late-stage PD) because these agents would not undergo redox cycling to cause oxidative neuronal damage. Catechol-O-methyltransferase (COMT)-mediated methylation metabolism of catecholamine neurotransmitters is a crucial first-line detoxification pathway, and its role in the causation and prevention of PD is also discussed. On the basis of the modulation of COMT-mediated methylation of catecholamines, it is mechanistically explained that hyperhomocysteinemia would be a pathogenic factor in PD whereas vitamins B6, B12, and folate would be a protective factor. Lastly, according to the mechanistic understanding developed here, a novel dietary strategy is proposed that is specifically tailored toward lowering the risk of human PD, which includes eating a nutritionally-balanced diet that contains adequate (but not excessive) amounts of fruits and vegetables, along with adequate dietary supplementation of S-adenosyl-L-methionine, vitamins C, B6, B12, and folate. It is believed that these conceptual developments would also aid in our better understanding of other age-related neurodegenerative disorders, such as Alzheimer's and Huntington's diseases.
The second one talks about biopterin and it's precursor possibly acting as anti-oxidants in dopaminergenic neurons..
J Neurochem. 2003 Apr;85(1):214-23. Related Articles, Links
Tetrahydrobiopterin precursor sepiapterin provides protection against neurotoxicity of 1-methyl-4-phenylpyridinium in nigral slice cultures.Madsen JT, Jansen P, Hesslinger C, Meyer M, Zimmer J, Gramsbergen JB.
Anatomy and Neurobiology, Institute of Medical Biology, University of Southern Denmark, Odense, Denmark.
Complex-I inhibition and oxidative processes have been implicated in the loss of nigral dopamine neurones in Parkinson's disease and the toxicity of MPTP and its metabolite MPP+. Tetrahydrobiopterin, an essential cofactor for tyrosine hydroxylase, may act as an antioxidant in dopaminergic neurones and protects against the toxic consequences of glutathione depletion. Here we studied the effects of manipulating tetrahydrobiopterin levels on MPP+ toxicity in organotypic, rat ventral mesencephalic slice cultures. In cultures exposed to 30 micro m MPP+ for 2 days, followed by 8 days 'recovery' in control medium, we measured dopamine and its metabolites in the tissue and culture medium by HPLC, lactate dehydrogenase release to the culture medium, cellular uptake of propidium iodide and counted the tyrosine hydroxylase-immunoreactive neurones. Inhibition of tetrahydrobiopterin synthesis by 2,4-diamino-6-hydroxypyrimidine had no significant synergistic effect on MPP+ toxicity. In contrast, the tetrahydrobiopterin precursor l-sepiapterin attenuated the MPP+-induced dopamine depletion and loss of tyrosine hydroxylase-positive cells in a dose-dependent manner with 40 micro m l-sepiapterin providing maximal protection. Accordingly, increasing intracellular tetrahydrobiopterin levels may protect against oxidative stress by complex-I inhibition
Posted by raybakes on October 17, 2004, at 6:31:25
In reply to creatine/methylation,B12, Folate, sulfation, CoQ10 » raybakes, posted by tealady on October 15, 2004, at 19:19:05
What type of betaine do you take?
Hi Jan, I take betaine by an english company called metabolics - betaine HCl does contain betaine but not enough to make much of a difference to methylation.
> >
> What is folinic acid..folinic acid is methyl tetrahydrofolate! It's the active form of folate - a lot of people have a genetic error that makes it difficult for them to activate folate - they can have plenty of folate, but very low active folate - which form of folate were you tested for?
My folate blood levels before any supps were ABOVE range though...and so were my Mum's.
>
might be because high because of the inability to activate it?> Both my Mum's and my blood levels of B12 were low, and both had folate above range..Her B12 was lower than mine and folate higher...almost like our bodies try to replace the low B12 with folate?
I've heard that sometimes one can mask a deficiency in the other too..
> I do notice my Mum has a far better memory after B12 needles (hydroxycobalamin), but she hasn't had any for a while. Before the needles it was difficult to hold conversation with her. So I'm pretty sure B12 can help with Alzheimer's type symptoms at least for some.
Homocysteine has been linked to alzheimers...
> I couldn't get a homocysteine test. (local GP told me "homocysteine doesn't exist in Australia"..his exact words <g>)
wouldn't trust ANYTHING this guy says!!!
>
> On B12 and me...I stopped taking it last February? My blood levels were fairly good then.
> The reason I stopped taking it was I always had strange reactions to B12 needles, and to a lesser extent the methylcobalamin sublinguals. I've got some old posts on here about this I'll try to find as my memory is poor.As my methylation is poor, any supplement that needs to be methylated i do badly with - if it's pre methylated, I'm much better... eg folate, DMG, lysine, choline, and will have to find some methylcobalmine(who's your's made by?)
>
>
> CoQ10..yeah I always knew about the oil based type being the only type to take. Maybe in Oz we are ahead in something!<g>Didn't know, but should have guessed!
> .
> Maybe one only needs to get it to a certain level or maybe I needed more of other nutrients for balance, but I'm not taking it againmight need to look at the electron transport chain in the mitochondria, to see what you need to balance - glutathione comes up again! - also radicals like superoxide.
>
> Interesting. Both dopamine and tyrosine hydroxalase with me appear to need a bit of a hand(I think). I thought it might be the P5P B6 here.p5p is for decarboxylase enzymes - dopa to dopamine, tyrosine to tyramine, 5 hydroxytryptophan to serotonin, glutamate to gaba, and histidine to histamine.
>
> Gee I really get lost trying to work out sulphation. I have an article on it I tried to work thruI'm still confused by sulphation too! sometimes it activates, sometimes deactivates, sometimes for transport, and sometimes structural!
> Also on allergy tests and elimination diets and retrials I am sensitive to sulphur preservatives. Maybe sensitive to sulphur based drugs too..at least I get nausea and feel dreadful after a few days, so I avoid them.
Think that's sulphites, they are metabolised to sulphate by 'sulphite oxidase'. Too much sulphite can destroy B1, B6, and folate.
> Because of this I've avoided any sulfate form of supps. Last month I did have a zinc sulfate (one capule..50 mg of zinc sulphate monohydrate) and soon after ended up vomiting, sweating ,shakin for about 30 mins or maybe an hour? Then I was OK. Any thoughts on this?Zinc sulphate might be a bit like taking epsom salts....will draw a lot of water into the gut...I've had a similar reaction too!
Hope that's helped!
Ray
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