knackers323
Senior Member
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Hi radio I am taking the propax and all I am seeing is bright yellow urine. How long did it take for you to notice a difference? Thanks
@Radio thanks for the link, once one gets low enough down in the study it appears to benefit mainly as a vaso-dilator. It would be interesting to know if it is degrading to AMP (this is a known vasodilator). Not sure how that would work out for those with POTS, but it's a new slant on ATP isn't it?Adenosine-5'-triphosphate (ATP) supplementation improves low peak muscle torque and torque fatigue during repeated high intensity exercise sets
http://www.jissn.com/content/9/1/48
Hi radio I am taking the propax and all I am seeing is bright yellow urine. How long did it take for you to notice a difference? Thanks
@Radio thanks for the link, once one gets low enough down in the study it appears to benefit mainly as a vaso-dilator. It would be interesting to know if it is degrading to AMP (this is a known vasodilator). Not sure how that would work out for those with POTS, but it's a new slant on ATP isn't it?
"Life is short, medicine is long"
The famous first aphorism of Hippocrates was long considered a perfect summary of medical ethics. Modern physicians find the words impossible to understand. But it can be interpreted as a fundamental insight into the ethical problems of modern medicine. The technology of modern scientific medicine can sustain life, even when life is losing its vitality.
http://www.ncbi.nlm.nih.gov/pubmed/17162734
DISCUSSION:
These data show that anthocyanins suppress MOS-induced apoptosis by preserving mitochondrial GSH and inhibiting cardiolipin oxidation and mitochondrial fragmentation. These nutraceutical antioxidants warrant further study as potential therapeutic agents for neurodegenerative diseases caused by MOS.
Neuroprotective effects of anthocyanins on apoptosis induced by mitochondrial oxidative stress.http://www.ncbi.nlm.nih.gov/pubmed/22053756
International Journal of Science and Technology Volume 2 No. 3, March, 2013
IJST © 2013 – IJST Publications UK. All rights reserved.
269
Anthocyanins in Red Beet Juice Act as Scavengers for Heavy Metals Ions such as Lead and Cadmium
Jaleel K. Ahmed, Husain A. M. Salih, Angham, G. Hadi
Babylon University ,Iraq
ABSTRACT
Recently many papers appeared on (Anthocyanins) as a complexing agent with metals ions.
The aim of this research is to fitting pollution and poisoning by metals and their ions by forming complexes.
Aqueous solution of anthocyanin from red beet is slightly acidic (pH 6.4) which attack metals slowly (oxidation process). As soon as metal ion forms the anthocyanin anion capture it and precipitate. Anthocyanin juice was shown a high antioxidant capacity in numerous studies. In this study anthocyanins are extracted and purified, then a series of complexes are prepared from reaction with the metal ions Pb(II) and Cd( II) after fixing the optimum conditions of (volume, concentration, temperature and pH). The UV-Vis spectra of these ions with pigment solution have been studied.
The formula of complexes is deduced according to the continuous variation method (Jobs method)
which is obtained from the spectrophotometric studies of the complex solution. The ratios of ligand: metal obtained are 2: 1 for all complexes under study (depending on the above job method). The solid complexes are indicated by UV-Vis spectra that showed red shift when it compared with pigment solution spectra. Also infrared spectra are studied and showed appearance and disappearance of some peaks.
The molar conductivity showed the absence of ionic property. The determination of magnetic susceptibility for all complexes showed that they have diamagnetic properties (i.e. all orbitals have pairs electrons). According to the results, molar conductivity, magnetic susceptility and electronic configuration support the structural formula of complexes that have a ratio of ligand: metal equal 2: 1 and the suggested structures are tetrahedral.
Vince Giuliano says:
Jim Watson has bought an additional piece of research to my attention suggesting that an additional health producing function of C-60 could be the enhancement of mitophagy. In the article above I pointed out how depolarization of the mitochondrial membrane is likely to be an impact of C-60, and this can lead to decrease or elimination of the production of superoxide with all its damaging impacts. The following publication suggests that a second benefit of such depolarization could be an enhancement of mitophagy. If this applies, C-60 might have three different positive effects: 1. direct antioxidant effect once it enters a mitochondrion, 2. reduction of the production of superoxide, and 3. enhancement of mitophagy. See Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by Parkin at
http://www.ncbi.nlm.nih.gov/m/pubmed/21173115/?i=4&from=/23620051/related
As explained in the blog entry, the same benefits might be realized from MitoQ.
New-form-of-CoQ10 / MitoQMitoQ is a mitochondria-targeted antioxidant designed to accumulate within mitochondria in vivo in order to protect against oxidative damage. It is the first molecule specifically designed to decrease mitochondrial oxidative damage to have undergone clinical trials in humans.[1][2][3] Mitochondria are an essential organelle within most cells that use oxygen to break down carbohydrates and fat to release energy in a form the cell can use. In doing this mitochondria release disruptive free radicals that contribute to oxidative damage in a wide range of diseases and pathologies. MitoQ is being evaluated as a therapy for some of these disorders. The molecule comprises a positively-charged lipophilic cation that drives its extensive accumulation within the negatively-charged mitochondria inside cells. The active antioxidant component of MitoQ is ubiquinone, which is identical to the active antioxidant in Coenzyme Q10. The lipophilic cation enables MitoQ to be accumulated selectively and extensively by mitochondria, in contrast to other antioxidants which distribute evenly throughout the cell. It is this approximately thousand-fold greater concentration of MitoQ within mitochondria that makes it more effective at preventing mitochondrial oxidative damage when compared to untargeted antioxidants such as Coenzyme Q10
MitoQ
http://en.wikipedia.org/wiki/MitoQ
The obvious question raised by the article is whether delivering a postive charge into the Mitchondria is a good idea? Should that negative internal charge be messed up then you also mess up the electric field across the mitochondrial transporters. Bonding the CQ10 to aspartic acid or malic acid would have achieved the same things without any such damage simply using the Mitos inherent transporters.Radio: Please check out C-60 / MitoQ updated info...
Update on C60 fullerenes in olive oil :
http://www.anti-agingfirewalls.com/2014/02/25/update-on-c60-fullerenes-in-olive-oil/
C60 Mitochondria Repair
http://forums.phoenixrising.me/index.php?threads/c60-mitochondria-repair.29355/
New-form-of-CoQ10 / MitoQ
http://www.nutraingredients-usa.com/Manufacturers/New-form-of-CoQ10-hits-supplement-market
MitoQ 5mg - Dietary Supplement. Capsules 60
http://www.amazon.com/MitoQ-5mg-Dietary-Supplement-Capsules/dp/B00H8MANVY
The Krebs’ cycle is an eloquent and essential system designed to generate large amounts of cellular energy required for life. Disruption of the Krebs’ cycle, whether caused by deficiencies in energy substrates, acquired or inherited disease states, or physical stress, leads to an inhibition of normal energy production and contributes to a wide range of metabolic disturbances and symptoms.
The use of supplemental Krebs’ cycle acids and anti-fatigue buffers can assist in the management of mitochondrial energy substrates and increase cellular energy production. Such a nutritional approach can be of benefit to athletes, anyone who is aging, as well as those suffering from metabolic disturbances caused by inherited mitochondrial diseases or acquired diseases, such as Alzheimer’s disease and Chronic Fatigue Syndrome (CFS). See more at: http://nutritionreview.org/2013/04/krebs-cycle-intermediates/
Maximizing Your Body’s Performance
By Ward Dean, MD and Jim English
Production and management of sustainable biological energy resources is of vital concern for everyone. Disruptions in the normal production of mitochondrial energy can contribute to a wide range of metabolic disturbances and symptoms, including fatigue, immune system dysfunction, dementia, depression, behavioral disturbances, attention deficiency, muscle weakness and pain, angina, heart disease, diabetes, skin rashes, and hair loss. These symptoms of metabolic impairment are also present in persons suffering from acquired diseases, such as Alzheimer’s disease and Chronic Fatigue Syndrome (CFS), and in those with inherited mitochondrial diseases, such as mitochondrial myopathy.
As these conditions share a common link in mechanisms of metabolic energy production, they may also benefit from nutritional strategies that optimize energy production and metabolic pathways.
The Krebs’ Cycle
All cells must produce energy to survive. Hans A. Krebs first elucidated the process of cells converting food into energy, the Citric Acid Cycle, in 1937. Krebs proposed a specific metabolic pathway within the cells to account for the oxidation of the basic components of food – carbohydrates, protein and fats – w for energy. The Krebs’ cycle takes place inside the mitochondria or ‘power plant’ of cells and provides energy required for the organism to function.
Mitochondria are found in all cells in the human body, with the exception of mature red blood cells. The primary function of these tiny organelles (each cell contains between 500 and 2,000 mitochondria) is to convert energy found in nutrient molecules and store it in the form of adenosine triphosphate (ATP). ATP is the universal energy-yielding molecule used by enzymes to perform a wide range of cellular functions. Humans cannot survive, even for a second, without a constant supply of ATP.
In order to carry out energy conversion, mitochondria require oxygen. The purpose of our respiratory and circulatory systems is to deliver oxygen to the tissues for use by mitochondria, and to eliminate carbon dioxide. The consumption of oxygen by mitochondria is called cellular respiration.
In simple terms, the Krebs’ cycle metabolizes acetyl coenzyme A into citric acid and then runs through a complex series of biological oxidations, producing free hydrogen ions. A net of two molecules of ATP is created at this stage in the Krebs’ cycle. The hydrogen ions then enter a biochemical chain, known as oxidative phosphorylation, which is a highly efficient aerobic energy generator. Oxidative phosphorylation generates 36 molecules of ATP during a sequence of steps that combine hydrogen electrons to molecular oxygen to form water. Therefore, each molecule of citric acid that rotates through the Krebs’ cycle, generates 38 molecules of ATP for tissue fuel. (1)
There are different points where metabolites enter the Krebs’ cycle. Most of the products of protein, carbohydrates and fat metabolism are reduced to the molecule acetyl coenzyme A that enters the Krebs’ cycle. Glucose, the primary fuel in the body, is first metabolized into pyruvic acid and then into acetyl coenzyme A. The breakdown of the glucose molecule forms two molecules of ATP for energy in the Embden Meyerhof pathway process of glycolysis. On the other hand, amino acids and some chained fatty acids can be metabolized into Krebs intermediates and enter the cycle at several points.
When oxygen is unavailable or the Krebs’ cycle is inhibited, the body shifts its energy production from the Krebs’ cycle to the Embden Meyerhof pathway of glycolysis, a very inefficient way of making energy.
As well as producing far less energy, glycolysis also produces lactic acid as a byproduct. Increased lactic acid is a common acidotic condition that can be caused by a variety of metabolic problems. Accumulation of lactic acid in muscle tissue produces the pain and inflammation we experience after exercising. While untrained individuals have a low lactate threshold, highly trained, elite athletes are extremely efficient at converting lactate to glucose and therefore have lower lactate levels. (2,3)
Step 1 The acetic acid subunit of acetyl CoA is combined with oxaloacetate to form a molecule of citrate. Acetyl coenzyme A acts only as a transporter of acetic acid from one enzyme to another. After Step 1, the coenzyme is released by hydrolysis to combine with another acetic acid molecule and begin the Krebs’ Cycle again.
Step 2 The citric acid molecule undergoes an isomerization. A hydroxyl group and a hydrogen molecule are removed from the citrate structure in the form of water. The two carbons form a double bond until the water molecule is added back. Only now, the hydroxyl group and hydrogen molecule are reversed with respect to the original structure of the citrate molecule. Thus, isocitrate is formed.
Step 3 The isocitrate molecule is oxidized by a NAD molecule. The NAD molecule is then reduced by the hydrogen atom and the hydroxyl group. The NAD binds with a hydrogen atom and carries off the other hydrogen atom leaving a carbonyl group. This structure is very unstable, so a molecule of CO2 is released, creating alpha-ketoglutarate.
Step 4 In this step, coenzyme A, returns to oxidize alpha-ketoglutarate. A molecule of NAD is reduced again to form NADH and leaves with another hydrogen. This instability causes a carbonyl group to be released as carbon dioxide and a thioester bond is formed in its place between the former alpha-ketoglutarate and coenzyme A to create a molecule of succinyl-coenzyme A complex.
Step 5 A water molecule sheds its hydrogen atoms to coenzyme A. Then, a free-floating phosphate group displaces coenzyme A and forms a bond with the succinyl complex. The phosphate is then transferred to a molecule of ADP to produce an energy molecule of ATP. It leaves behind a molecule of succinate.
Step 6 In this step, succinate is oxidized by a molecule of FAD (Flavin Adenine Dinucleotide). The FAD removes two hydrogen atoms from the succinate and forms a double bond between the two carbon atoms to create fumarate.
Step 7 An enzyme adds water to the fumarate molecule to form malate. The malate is created by adding one hydrogen atom to a carbon atom and then adding a hydroxyl group to a carbon next to a terminal carbonyl group.
Step 8 In this final step, the malate molecule is oxidized by a NAD molecule. The carbon that carried the hydroxyl group is now converted into a carbonyl group. The end product is oxaloacetate which can then combine with acetyl-coenzyme A and begin the Krebs’ Cycle all over again. See more at: http://nutritionreview.org/2013/04/krebs-cycle-intermediates/
That kitten is so cute, is it yours?Radio or anyone else, have you taken NTFactor? If so did it help? I have ordered Propax Gold.
Radio or anyone else, have you taken NTFactor? If so did it help? I have ordered Propax Gold.
An amazing story about Phosphatidyl-Choline, the cell membrane and lecithin. The story of PC has recently become quite amazing which involves 3 players, Dr Burzynski, Professor Barenholz and Dr Milz and a dynamic research with rat heart cell myocytes. The study describes the heart cells beating together in vitro at 160 beats per minute, then losing their beating rate with age, which was subsequently revived with the addition of phosphatidylcholine. An amazing story.
Click here to get our BodyBio Bulletin Article referred to in the video - titled Answers to Nature Article - http://www.bodybio.com/content.aspx?p...
Hi, SaintDear Radio,
I read that your health "turned the corner" while using certain supplements. You credit LRT from Body Bio. I've been scouring the net trying to find out if lecithin will work as well. One member here said Rich V. said it should, but not as well. I reacted badly to Holtdorf NT factor. Did a challenge & took next day & have bad headache ALL day. But can take lecithin granules.
Thought about trying BodyBio, but hate to put out more money, unless there is a money-back guarantee. Do you know anything about Allergy Research.phospholipid formula or anyone here who is hypersensitive who has taken it/ and/or what worked for them?
Also - anyone have any success with liposomal glutathione?
Any help appreciated.
saint@ has anyone here ever "recovered" from cfs/