Toxic chemicals in personal care products have been proven to have an accumulative affect in our bodies. For those with chronic illnesses, that burden becomes even greater. It is so important to avoid toxic chemicals as much as possible and lighten the load. Buy only natural, organic non-toxic products.
Measuring the Pollution in People
A number of striking studies (i) have shown that the man-made chemicals in our environment and in consumer products—including cosmetics—make their way into our bodies. Many of the chemicals found in cosmetics are absorbed by the skin into the body, and can be detected in blood or urine.
The length of time chemicals remain in the body varies from chemical to chemical and ranges from hours to decades. For chemicals that are excreted quickly, the fact that we can so consistently measure them indicates continual exposures that may have long-term effects on health.
Body Burden and Biomonitoring
Body burden refers to the levels of man-made chemicals in an individual’s body, generally measured through blood or urine. Large-scale biomonitoring programs that assess the levels of chemicals in a population or subset of a population would greatly support the ability of researchers to explore the links between exposures and disease. A gap in determining the long-term effects of chemical exposures upon disease has long been a lack of knowledge about chemical exposures and the intake of environmental toxins into the body. Ongoing biomonitoring programs would fill this vital data gap.
The Pollution in People
The largest U.S. body burden study to date measured the levels of 148 chemicals in approximately 3,000 people of varying ages, ethnicities and geographical locations (ii). This study, by the U.S. Centers for Disease Control, detected a common sunscreen ingredient, benzophenone-3 (BP-3) in 96.8 percent of individuals (iii), and triclosan, an antibacterial agent often used in antibacterial soaps, in 74.6 percent of individuals (iv). A CDC study found residues of four different phthalates in more than 75 percent of subjects (v). Phthalates are found in numerous cosmetics, often as a constituent ingredient of fragrances. A 2008 study of teen girls by the Environmental Working Group revealed 16 hormone-altering cosmetics chemicals in their young test subjects (vi).
The CDC tests of 148 chemicals represents a very small percentage of the over 80,000 chemicals manufactured and the approximately 10,000 chemicals used in cosmetic products. The next edition of the CDC report, anticipated in 2009, will include measurements of 250 chemicals, an increase that still doesn't approach the total number of chemicals in commerce. Nevertheless, this and other studies illustrate that chemicals we use in an array of consumer products make their way into our bodies (vii). This knowledge also furthers our understanding of the links between the chemicals we use, the absorption of these chemicals into our bodies, and the known and probable health effects of these chemicals.
i.Commonweal Biomonitoring Resource Center (2005). Taking It All In: Documenting Chemical Pollution in Californians through Biomonitoring. Available online at http://www.commonweal.org/programs/download/TIAI_1205.pdf. Accessed August 19, 2008.
Environmental Working Group (2006). Across Generations: Industrial Chemicals in Mothers and Daughters: The pollution we share and inherit. Available online at http://www.ewg.org/reports/generations/. Accessed August 19, 2008.
Environmental Working Group (2005). Body Burden: The Pollution in Newborns. Available online at: http://www.ewg.org/node/17686. Accessed August 19, 2008.
Environmental Working Group (2003). Body Burden: The Pollution in People. Available online at: http://archive.ewg.org/reports/bodyburden1/. Accessed August 19, 2008.
ii Centers for Disease Control and Prevention (CDC) (2005). Third National Report on Human Exposure to Environmental Chemicals. Available online at http://www.cdc.gov/exposurereport/. Accessed December 23, 2008.
iii Calafat AM, Wong LY, Ye X, Reidy JA, Needham LL. Concentrations of the Sunscreen Agent, Benzophenone-3, in Residents of the United States: National Health and Nutrition Examination Survey 2003-2004. Environ Health Perspect 116:893–897 (2008).
iv Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL. Urinary Concentrations of Triclosan in the U.S. Population: 2003–2004. Environmental Health Perspectives, 116:303–307 (2008).
v Silva MJ, Barr DB, Reidy JA, Malek NA, Hodge CC, Caudill SP, Brock JW, Needham LL, Calafat AM. “Urinary Levels of Seven Phthalate Metabolites in the U.S. Population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000,” Environmental Health Perspectives, 112(3): 331-338 (2004).
vi Sutton, R (2008). Teen Girls' Body Burden of Hormone-Altering Cosmetics Chemicals. Available online at http://www.ewg.org/reports/teens. Accessed October 10, 2008.
vii Commonweal and Breast Cancer Fund (2005). Taking It All In: Documenting Chemical Pollution in Californians through Biomonitoring. Available online at http://www.commonweal.org/programs/download/TIAI_1205.pdf. Accessed August 19, 2008.
Environmental Working Group (2006). Across Generations: Industrial Chemicals in Mothers and Daughters: The pollution we share and inherit. Available online at http://www.ewg.org/reports/generations/. Accessed August 19, 2008.
Environmental Working Group (2005). Body Burden: The Pollution in Newborns. Available online at: http://www.ewg.org/node/17686. Accessed August 19, 2008.
Environmental Working Group (2003). Body Burden: The Pollution in People. Available online at: http://archive.ewg.org/reports/bodyburden1/. Accessed August 19, 2008.
Monday, May 24, 2010
Monday, August 3, 2009
Ribose (Corvalen) - An Exciting New Treatment for Chronic Fatigue Syndrome and Fibromyalgia
Ribose (Corvalen) - An Exciting New Treatment for Chronic Fatigue Syndrome and Fibromyalgia
Can you really treat chronic fatigue syndrome and fibromyalgia with sugar?
Corvalen (D-Ribose) Valen Labs) is an outstanding new nutrient (a special sugar-even OK for those who need to avoid sugar!) for those of you who want a powerful energy boost! In addition to its role in making DNA and RNA, those of you familiar with biochemistry remember Ribose as the key building block for making energy. In fact, the main energy molecules (like “Energy dollars”) in your body (ATP, FADH, etc.) are made of ribose plus B vitamins/phosphate. That makes these energy molecules similar to the paper that money is printed on- kind of like being able to print your own energy currency!
Corvalen has many uses, including treating heart muscle weakness (Congestive Heart Failure). We were so impressed with this product that our research center we recently completed a research study reported on in the national news services using it in patients with chronic fatigue syndrome and fibromyalgia. Two thirds of these desperately ill patients improved, with an average increase in quality of life of ~30 improvement in energy. This is very dramatic for a single treatment/nutrient! In our study, pain, sleep, and “brain fog’ also improved.
The next study we hope to do will be a “Gold –standard” placebo controlled study on Ribose/Corvalen in CFS/FMS to follow up our initial pilot study. If you would like to be part of the study e-mail lgleason@bioenergy.com. You might want to let us know soon-our last study filled within 24 hours of our announcing it in our newsletter!
D-Ribose - Jump-Starting Your Body's Energy Furnaces
Before we begin the SHINE protocol, however, let's jump-start our energy and set ourselves up for success.
As we will discuss throughout this book, CFS and fibromyalgia reflect an energy crisis in your body. Although it can have numerous causes, the energy crisis will then trigger a host of downstream effects, including hypothalamic dysfunction ("blowing a fuse") which causes multiple other problems including, muscle pain, insomnia, hormonal deficiencies, infections, poor liver detoxification, decreased heart function, and more. Although going after these many triggers and problems is very important, it is also critical to also go to the heart of the problem and treat your body's "energy furnaces". Because of this, we will begin our discussion of treatments with those that directly increase energy production.
Each cell in your body contains structures called mitochondria. The mitochondria are the tiny furnaces in each cell that produce energy by burning calories. Many problems, including Epstein Barr viral infections, can suppress your energy furnaces.3 In this chapter, I will discuss treatments that can help your mitochondrial furnaces work properly, and explain how you can use this information to feel better.
The role of energy production
We simply can't overcome fatigue if the cells and tissues in our bodies don't have enough energy. Medical research shows there are many conditions that drain energy from the body, leaving us fatigued and with frequent complications such as muscle pain, heart problems, and even depression.
Of course athletes who participate in high-intensity, endurance type exercise often face the fatigue and muscle pain associated with energy depletion. Typically, a few days of rest will allow an athlete's muscles to recharge with energy. For the rest of us, however, the physiological factors that drain hearts and muscles of energy are not as easily overcome. It is amazing how a special simple sugar, called D-ribose, can help the body restore energy, giving hearts and muscles the power they need to fully recharge, so they can recover from fatigue and chronic muscle pain.
As we age, our bodies go through many changes that affect our ability to efficiently metabolize energy. For some, these changes occur more rapidly and are more pronounced, while for others the impact is seemingly absent. People with fibromyalgia and CFS have almost 20 percent less energy in their muscles than normal, and this lack of energy causes poor exercise tolerance and lack of endurance-making it hard to perform even the most basic of life's daily activities.4,5
The metabolic changes that occur in our bodies over time or with the onset of disease are varied. Many are found to have thickening of the walls of capillaries that feed blood to muscles. These thickened capillary walls make it harder for oxygen to move from the blood to the muscle tissue, reducing the oxygen tension of the muscle and slowing the rate of energy synthesis. 6,7
In others, the mitochondrial energy furnaces are found to be defective and cannot keep up with the energy demand of cells and tissues as they work through daily activities. 8-10 Still for others, cells and tissues are deficient in certain nutrients that are needed to process food into energy, leaving the tissues energy starved. 11-13 And in the most difficult conditions, the muscle itself is affected, leaking vital cellular constituents that include energy compounds and the fuels needed to restore energy levels in affected tissues.14
No matter the cause, the impact of energy depletion is to propel a downward spiral of fatigue, muscle pain, soreness and stiffness that will not stop until the energy in the affected tissue can be restored. As energy is used faster than it can be restored, muscles become more painful, stiff, and fatigued. This causes even more energy to be used as the muscle struggles to recover, causing even more fatigue, soreness and stiffness,15-17 and the cycle continues. If the conditions leading to energy depletion are not arrested in time, the fatigue can become overwhelming and debilitating-as occurs in CFS/FMS.
The Consequences of Mitochondrial Dysfunction
A large number of clinical findings common in CFS/FMS can be explained by mitochondrial furnace malfunction Hypothalamic suppression. Particularly severe changes in the hypothalamus have been seen in mitochondrial dysfunction syndromes.18 Brain fog. Mitochondrial dysfunction can cause decreases in levels of neurotransmitters in the brain, specifically low dopamine and acetylcholine, and possibly low serotonin.
Sensitivities and allergies. Decreased ability of the liver to eliminate toxins and medications could contribute to sensitivities to both medications and environmental factors.
Post-exertion fatigue. Low energy production and accumulation of excessive amounts of lactic acid in muscles would inhibit recovery after exercise.
• Poor digestion. Mitochondrial dysfunction would also cause related to the bowel problems that plague so many people with chronic fatigue and fibromyalgia.
Weak immune system. With problems in the mitochondria, you would expect to see poor white blood cell function and therefore a decreased ability to fight infection.
Heart dysfunction. Based on research by Dr. Paul Cheney, mitochondrial dysfunction may weaken the heart muscle, requiring increased anti-oxidant levels through supplementation.
Kidney function. Poor kidney function resulting from mitochondrial dysfunction may cause a defect in the filtration and detoxification process.
Thus, mitochondrial dysfunction might well be the root cause of-or at least a contributing factor to-the hypothalamic, immune, neurotransmitter, nutritional, detoxification, sleep and other disorders seen in CFS/FMS.
Improving Mitochondrial Function
If mitochondrial dysfunction is an underlying or contributing cause to CFS/FMS, the next question is whether anything can be done to make those cellular energy furnaces work better. A number of natural treatments are available to do just that. Let us now look at some of the treatments that can improve mitochondrial energy production. Let's begin with D-Ribose, the key to energy production.
D-Ribose-The Natural Body Energizer
In looking at energy production, it helps to look at the "energy molecules" such as ATP, NADH, and FADH. These represent the energy currency in your body, and are like the paper that money is printed on. You can have all the fuel you want, but if it cannot be converted to these molecules, it is useless!
For years, I talked about the importance of B vitamins, which are a key component of these molecules. These helped to a degree, but it was clear that a key component was missing. In looking at the biochemistry of these energy molecules, they are also made of 2 other key components-adenine and ribose. Adenine is plentiful in the body and supplementing with adenine did not help CFS. We then turned our attention to Ribose. Ribose is made in your body in a slow, laborious process and cannot be found in food. We knew that CFS/FMS causes your body to dump other key energy molecules like acetyl-l-carnitine. We then found that the body did the same with Ribose, making it hard to get your furnaces working again even after the other problems were treated.
This was like one of those "Eureka!" moments where things came together. Not having Ribose would be like trying to build a fire without kindling-nothing would happen. We wondered if giving Ribose to people with CFS would jump-start their energy furnaces. The answer was a resounding yes!
Our recently published study (see the study abstract in Appendix B) showed an average 44.7- remarkable results from a single nutrient! 19 The only significant side effects were that 2 people felt too energized and hyper/anxious on the ribose. This is simply dealt with by lowering the dose and/or taking it with food.
Several of the patients participating in the study have contacted me regarding the relief they found with ribose therapy. Most importantly, they speak to the profound joy they feel when they are able to begin living normal, active lives after sometimes years of fatigue, pain, and suffering. Here is a sample of what one patient, Julie (Minnesota), an elementary teacher, wrote: "I had so much pain and fatigue I thought I was going to have to quit teaching. When I take [ribose], I feel like a huge weight is being lifted from my chest, and I'm ready to take on those kids again!" The relief patients feel with ribose therapy is heartwarming, and goes directly to the dramatic impact ribose has on increasing energy, overcoming fatigue, enhancing exercise tolerance, and raising the patient's quality of life.
To further validate these findings, we are currently conducting a much larger placebo controlled study, and hope to have the results published in the coming year. Interestingly, one of our study patients had an abnormal heart rhythm called atrial fibrillation. Ribose is outstanding in the treatment of heart disease as well, because it restores energy production in the heart muscle. Because of this, it was not surprising that this man's atrial fibrillation also went away on the ribose and he was able to stop his heart medications as well! Because of its importance and the research showing marked heart muscle dysfunction (because of low energy) in CFS, let's look at
Ribose and the heart in more detail.
Ribose and the Fatigue Associated with Heart Disease
Decades of research have shown that ribose has a profound effect on heart function in patients with congestive heart failure, coronary artery disease, and cardiomyopathy (a weakened heart muscle). Like the muscles in patients with fibromyalgia, sick hearts are energy starved.24 This energy deprivation keeps the heart from relaxing between heartbeats, making it impossible for the heart to completely fill with blood 25 (it surprisingly takes more energy for the heart muscle to relax than contract). Because the heart does not fill completely, less blood is pumped to the body with each heartbeat. The heart then gets stiff and it strains to contract. Ultimately, the heart becomes enlarged, a condition known as hypertrophy, and it is unable to pump normally.
You can compare this to the effect of weight training on the muscles in the bicep of the upper arm. Over time, weight training against more and more weight makes the muscle larger and harder. Similarly, when the heart becomes stiff it is forced to contract against more and more pressure, making the heart muscle grow. While in the case of the bicep this may be a desirable outcome, in the heart it can be deadly. In contrast to the biceps muscle, hearts must remain supple so they can fill properly and empty fully with each contraction. If hearts cannot pump normal volumes of blood, muscles of the arms and legs and brain tissue become oxygen starved. The result is fatigue, pain on standing or walking, loss of interest in, or the ability to perform any physical activity, brain fog, and depression. In the end, the heart cannot pump enough blood to even supply itself with live-giving oxygen and a heart attack can be the result.
Using ribose to restore the energy level in the heart allows it to fully relax, fill, and empty completely to circulate blood to the outer reaches of the body.26 Circulating more blood means muscles in the arms and legs, and the tissues of the brain, get the oxygen they need to function normally. This result was made evident in several important studies in patients with congestive heart failure and angina.
In one study conducted at the University of Bonn in Germany, patients with congestive heart failure were treated with either 10-grams of ribose or a sugar placebo every day for three weeks.27 They were then tested for heart function, exercise tolerance (a measure of fatigue), and quality of life using a questionnaire designed for this purpose. In this study, ribose therapy had a significant effect on all measures of diastolic heart function, showing that increased energy in the heart allowed the heart to relax, fill, and pump more normally. Patients in the study were also much more tolerant to exercise when they were on ribose, and, through their responses to the questionnaire, showed they had a higher quality of life as a result.
Two additional studies went on to help explain how ribose therapy in congestive heart failure may affect fatigue and exercise tolerance.28,29 These studies showed that ribose treatment increased ventilatory and oxygen utilization efficiency, a medical way of saying that the patients were able to breathe better and use the oxygen they inhaled more efficiently. Improving the patient's ability to use oxygen means more oxygen is available to go into the blood and out to the tissues. Having more oxygen available allows the muscle to burn fuel more efficiently, helping it keep pace with its energy demand. The result is less fatigue, a greater ability to tolerate exercise, and a higher quality of life. An added benefit to improving ventilatory efficiency is that ventilatory efficiency is a dominant predictor of mortality in congestive heart failure. Increasing ventilatory efficiency with ribose therapy is, therefore, a direct correlate to prolonging life in this patient population.
There are very few nutritional therapies that can legitimately boast of having this profound of an effect on the tissues they target. None, other than ribose, can claim such an effect in cell or tissue energy metabolism. Ribose is a unique and powerful addition to our complement of metabolic therapies in that it is completely safe, proven by strong, well designed clinical and scientific evidence, natural, and fundamental to a vital metabolic process in the body.30-34 I have added a few more study references for those who would like more information about ribose. 35-56
Ribose regulates how much energy we have in our bodies, and for those suffering from fatigue, muscle soreness, stiffness, and a host of related medical complications, the relief found in energy restoration can be life changing. This is why I recommend that all CFS/FMS patients begin with D-Ribose 5 grams (1 scoop of Corvalen) 3 x day for 2-3 weeks then twice a day. It is critical to take the 3 scoops a day for the first few weeks to see the optimal effects. Although many of the treatments in this book take 6-12 weeks to start working, most people feel the difference by the end of a single 280 gm container. For the few who don't, retry it again once you are 12-16 weeks into the other treatments well discuss. You'll be glad you did!
Although Ribose is the most promising energy nutrient, others are also worth looking at as well. Most of these only need to be taken for 4-9 months; though some people choose to take them longer (I take my Ribose every day even though I feel great. It makes me feel even better!). You will know by how you feel on them.
Click here to listen to a lecture on D-Ribose by Dr. Teitelbaum.
These other energy boosters are discussed at length in the "web site notes" section and include:
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3-Vernon DC, et al. Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr Virus. BMC Infectious Diseases/ 2006, 6; 15 doi:10.1186/1471-2334-6-15, 31 January 2006.http://www.biomedcentral.com/1471-2334/6/15/abstract
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6. Lund N, A Bengtsson, P Thorborg. Muscle tissue oxygen in primary fibromyalgia. Scandinavian Journal of Rheumatology 1986;15(2):165-173.
7-Strobl ES, M Krapf, M Suckfull, W Bruckle, W Fleckenstein, W Muller. Tissue oxygen measurement and 31P magnetic resonance spectroscopy in patients with muscle tension and fibromyalgia. Rheumatology International 1997;16(5):175-180.
8.Douche-Aourik F, W Berlier, L Feasson, T Bourlet, R Harrath, S Omar, F Grattard, C Denis, B Pozzetto. Detection of enterovirus in human muscle from patients with chronic inflammatory muscle disease or fibromyalgia and healthy subjects. Journal of Medical Virology 2003;71(4):540-547.
9. Park JH, P Phothimat, CT Oates, M Hernanz-Schulman, NJ Olson. Use of P-31 magnetic resonance spectroscopy to detect metabolic abnormalities in muscles of patients with fibromyalgia. Arthritis and Rheumatology 1998;41(3):406-413.
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11. Bengtson A, KG Heriksson, J Larsson. Reduced high-energy phosphate levels in the painful muscles of patients with primary fibromyalgia. Arthritis and Rheumatology 1986;29(7):817-821.
12. Lund E, SA Kendall, B Janerot-Sjoberg, A Bengtsson. Muscle metabolism in fibromyalgia studied by P-31 magnetic resonance spectroscopy during aerobic and anaerobic exercise. Scandinavian Journal of Rheumatology 2003; 32(3):138-145.
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14. Jacobsen S, KE Jensen, C Thomsen, B Danneskiold-Samsoe, O Henriksen. Magnetic resonance spectroscopy in fibromyalgia. A study of phosphate-31 spectra from skeletal muscles during rest and after exercise. Ugeskr Laeger 1994;156(46):6841-6844.
15. Olson NJ, JH Park. Skeletal muscle abnormalities in patients with fibromyalgia. American Journal of Medical Science 1998;315(6):351-358.
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17. Krapf MW, S Muller, P Mennet, T Stratz, W Samborski, W Muller. Recording muscle spasms in the erector spinae using in vivo 31P magnetic resonance spectroscopy in patients with chronic lumbalgia and generalized tendomyopathies. Z Rheumatology 1992;51(5):229-237.
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22. Brault JJ, Terjung RL. Purine salvage to adenine nucleotides in different skeletal muscle fiber types. Journal of Applied Physiology 2001; 91: 231-238.
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24. 22. Ingwall JS. ATP and the Heart. Kluwer Academic Publishers, Boston, Massachusetts.
25. Reibel D, Rovetto M. Myocardial ATP Synthesis and Mechanical Function Following Oxygen Deficiency. American Journal of Physiology 1978; 234(5): H620-H624.
26. Zimmer HG, Ibel H, Suchner U. Ribose Intervention in the Cardiac Pentose Phosphate Pathway is Not Species-Specific. Science 1984; 223: 712-714.
27. Omran H, S Illien, D MacCarter, JA St. Cyr, B Luderitz. D-Ribose improves diastolic function and quality of life in congestive heart failure patients: A prospective feasibility study. European Journal of Heart Failure 2003; 5:615-619.
28. Vijay N, D MacCarter, M Washam, J St.Cyr. Ventilatory efficiency improves with d-ribose in congestive Heart Failure patients. Journal of Molecular and Cellular Cardiology 2005;38(5):820.
29. Carter O, D MacCarter, S Mannebach, J Biskupiak, G Stoddard, EM Gilbert, MA Munger. D-Ribose improves peak exercise capacity and ventilatory efficiency in heart failure patients. Journal of the American College of Cardiology 2005;45(3 Suppl A):185A.
30. Griffiths JC, JF Borzelleca, J St.Cyr. Lack of oral embryo toxicity/ teratogenicity with D-ribose in Wistar rats. Journal of Food and Chemical Toxicology 2007;45(3):388-395.
31. Griffiths JC, JF Borzelleca, J St. Cyr. Sub-chronic (13-week) oral toxicity study with D-ribose in Wistar rats. Journal of Food and Chemical Toxicology 2007:45(1):144-152.
32. Gross M, Dormann B, Zollner N. Ribose administration during exercise: effects on substrates and products of energy metabolism in healthy subjects and a patient with myoadenylate deaminase deficiency. Klin Wochenschr 1991; 69: 151-155.
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35. Guymer EK, KJ Clauw. Treatment of fatigue in fibromyalgia. Rheum Dis Clin North Am 2002;28(2):67-78.
36. Rooks DS, CB Silverman, FG Kantrowitz. The effects of progressive strength training and aerobic exercise on muscle strength and cardiovascular fitness in women with fibromyalgia: a pilot study. Arthritis Rheum 2002;47(1):22-28.
37. Geenen R, JW Jacobs, JW Bijlsma. Evaluation and management of endocrine dysfunction in fibromyalgia. Rheum Dis Clin North Am 2002;28(2):389-404.
38. Schachter CL, AJ Busch, PM Peloso, MS Shepard. Effects of short versus long bouts of aerobic exercise in sedentary women with fibromyalgia: a randomized controlled trial. Phys Ther 2003;83(4):340-358.
39. Williamson DL, PM Gallagher, MP Goddard, SW Trappe. Effects of ribose supplementation on adenine nucleotide concentration in skeletal muscle following high-intensity exercise. Med Sci Sport Exc 2001; 33(5 suppl).
40. Zollner N, Reiter S, Gross M, Pongratz D, Reimers CD, Gerbitz K, Paetzke I, Deufel T, Hubner G. Myoadenylate deaminase deficiency: successful symptomatic therapy by high dose oral administration of ribose. Klin Wochenschr 1986; 64: 1281-1290.
41. Patton BM. Beneficial effect of D-ribose in patients with myoadenylate deaminase deficiency. Lancet May 1982; 1701.
42. Salerno C, D'Eufermia P, Finocchiaro R, Celli M, Spalice A, Crifo C, Giardini O. Effect of D-ribose on purine synthesis and neurological symptoms in a patient with adenylsuccinase deficiency. Biochim Biophys Acta 1999; 1453: 135-140.
43. Salerno C, M Celli, R Finocchiaro, P D'Eufemia, P Iannetti, C Crifo, O Giardini. Effect of D-ribose administration to a patient with inherited defect of adenylosuccinase. Purine Metabolism in Man IX. Plenum Press, New York, 1998.
44. Pauly D, C Pepine. D-Ribose as a supplement for cardiac energy metabolism. J Cardiovasc Pharmacol Ther 2000;5(4):249-258.
45. Pauly D, C Johnson, JA St. Cyr. The benefits of ribose in cardiovascular disease. Med Hypoth 2003;60(2):149-151.
46. Pauly DF, CJ Pepine. Ischemic heart disease: Metabolic approaches to management. Clin Cardiol 2004;27(8):439-441.
47. Dodd SL, CA Johnson, K Fernholz, JA St.Cyr. The role of ribose in human skeletal muscle metabolism. Med Hypoth 2004;62(5):819-824.
48. Zarzeczny R, JJ Brault, KA Abraham, CR Hancock, RL Terjung. Influence of ribose on adenine salvage after intense muscle contractions. J Appl Physiol 2001;91:1775-1781.
49. Wallen JW, MP Belanger, C Wittnich. Preischemic administration of ribose to delay the onset of irreversible ischemic injury and improve function: studies in normal and hypertrophied hearts. Can J Physiol Pharmacol 2003;81:40-47.
50. Wilson R, D MacCarter, J St. Cyr. D-Ribose enhances the identification of hibernating myocardium. Heart Drug 2003:3:61-62.
51. Van Gammeren D, D Faulk, J Antonio. The effects of four weeks of ribose supplementation on body composition and exercise performance in healthy, young male recreational bodybuilders: A double-blind, placebo-controlled trial. Curr Ther Res 2002;63(8):486-495.
52. Sharma R, M Munger, S Litwin, O Vardeny, D MacCarter, JA St. Cyr. D-Ribose improves Doppler TEI myocardial performance index and maximal exercise capacity in stage C heart failure. J Mol Cell Cardiol 2005;38(5):853.
53. Pliml W, T von Arnim, A Stablein, H Hofmann, HG Zimmer, E Erdmann. Effects of ribose on exercise-induced ischaemia in stable coronary artery disease. Lancet 1992;340:507-510.
54. Perkowski D, S Wagner, A Marcus, J St. Cyr. D-Ribose improves cardiac indices in patients undergoing "off" pump coronary arterial revascularization. J Surg Res 2007;173(2):295.
55. Muller C, H Zimmer, M Gross, U Gresser, I Brotsack, M Wehling, W Pliml. Effect of ribose on cardiac adenine nucleotides in a donor model for heart transplantation. Eur J Med Res 1998;3:554-558.
56. Grant GF, RW Gracey. Therapeutic nutraceutical treatments for osteoarthritis and ischemia. Exp Opin Ther Patents 2000;10(1): 1-10.
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58. H. Kuratsune, K. Yamaguti, M. Takahashi, et al., "Acylcarnitine Deficiency in Chronic Fatigue Syndrome," Clinical Infectious Disease 18 (3 Supplement 1) (January 1994): S62-S67.
59. http://www.hsrmagazine.com/hotnews/66h21048207977.html)
60. Palan PR, Connell K, et al,"Effects of menopause and hormone replacement therapy on serum levels of coenzyme Q-10 and other lipid-soluble antioxidants," Biofactors, 2005; 25(1-4): 61-6.
61. Berthold HK, Naini A, et al, "Effect of ezetimibe and/or simvastatin on coenzyme Q10 levels in plasma: a randomised trial," Drug Saf, 2006; 29(8): 703-12.
62. Sander S, Coleman SI, et al, "The impact of coenzyme Q10 on systolic function in patients with chronic heart failure," Journal of Cardiac Failure, 2006; 12(6): 464-72.
63. Weant KA, Smith KM, "The role of coenzyme Q10 in heart failure," Ann Pharmacother, 2005; 39(9): 1522-6.)
64. K. Folkers, S. Shizukuishi, K. Takemura, et al., "Increase in Levels of IgG in Serum of Patients Treated with Coenzyme Q10," Research Communications in Chemical Pathology and Pharmacology 38 (2) (1982): 335-338.
65. K. Folkers, P. Langsjoen, Y. Nara, et al., "Biochemical Deficiencies of Coenzyme Q10 in HIV Infection and Exploratory Treatment," Biochemical and Biophysical Research Communications 153 (2) (1988): 888-896.
66. K. Lockwood, S. Moesgaadr, T. Hanoike, et al., "Apparent Partial Remission of Breast Cancer in "High Risk" Patients Supplemented with Nutritional Antioxidants, Essential Fatty Acids and Coenzyme Q10," Molecular Aspects of Medicine 15 (Supplement) (1994): S231-S240.
67. K. Lockwood, S. Moesgaard, T. Yamamoto, et al., "Progress on Therapy of Breast Cancer with Coenzyme Q10 and the Regression of Metastases," Biochemical and Biophysical Research Communications 212 (1) (6 July 1995): 172-177.
67A. Rusciani L, Proietti I, et al, "Low plasma coenzyme Q10 levels as an independent prognostic factor for melanoma progression," J Am Acad Dermatol, 2006; 54(2):234-41.)
68. P. Mayer, H. Hamberger, and J. Drew, "Differential Effects of Ubiquinone Q7 and Ubiquinone Analogs on Macrophage Activation and Experimental Infections in Granulocytopenic Mice," Infection 8 (1980): 256-261.
69. E. Bliznakov, A. Casey, and E. Premuzic, "Coenzymes Q: Stimulants of Phagocytic Activity in Rats and Immune Response in Mice," Experientia 26 (1970): 953-954.
70. L. Van Gaal, I.D. de Leeuw, S. Vadhanavikit, et al., "Exploratory Study of Coenzyme Q10 in Obesity," in K. Folkers and Y. Yamamura, eds., Biomedical and Clinical Aspects of Coenzyme Q, Vol. 4 (New York, NY: Elsevier Publishers, 1984), pp. 235-373.
71. Sandor PS, Di Clemente L, et al, "Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial," Neurology, 2005; 64(4): 713-5.
72. A. Gaby, "The Role of Coenzyme Q10 in Clinical Medicine. Part I," Alternative Medicine Review 1 (1) (1996): 11-17.
73. Y. Ishihara, Y. Uchida, S. Kitamura, et al., "Effect of Coenzyme Q10, a Quinone Derivative, on Guinea Pig Lung and Tracheal Tissue," Arzneimittelforschung 35 (1985): 929-933.
Can you really treat chronic fatigue syndrome and fibromyalgia with sugar?
Corvalen (D-Ribose) Valen Labs) is an outstanding new nutrient (a special sugar-even OK for those who need to avoid sugar!) for those of you who want a powerful energy boost! In addition to its role in making DNA and RNA, those of you familiar with biochemistry remember Ribose as the key building block for making energy. In fact, the main energy molecules (like “Energy dollars”) in your body (ATP, FADH, etc.) are made of ribose plus B vitamins/phosphate. That makes these energy molecules similar to the paper that money is printed on- kind of like being able to print your own energy currency!
Corvalen has many uses, including treating heart muscle weakness (Congestive Heart Failure). We were so impressed with this product that our research center we recently completed a research study reported on in the national news services using it in patients with chronic fatigue syndrome and fibromyalgia. Two thirds of these desperately ill patients improved, with an average increase in quality of life of ~30 improvement in energy. This is very dramatic for a single treatment/nutrient! In our study, pain, sleep, and “brain fog’ also improved.
The next study we hope to do will be a “Gold –standard” placebo controlled study on Ribose/Corvalen in CFS/FMS to follow up our initial pilot study. If you would like to be part of the study e-mail lgleason@bioenergy.com. You might want to let us know soon-our last study filled within 24 hours of our announcing it in our newsletter!
D-Ribose - Jump-Starting Your Body's Energy Furnaces
Before we begin the SHINE protocol, however, let's jump-start our energy and set ourselves up for success.
As we will discuss throughout this book, CFS and fibromyalgia reflect an energy crisis in your body. Although it can have numerous causes, the energy crisis will then trigger a host of downstream effects, including hypothalamic dysfunction ("blowing a fuse") which causes multiple other problems including, muscle pain, insomnia, hormonal deficiencies, infections, poor liver detoxification, decreased heart function, and more. Although going after these many triggers and problems is very important, it is also critical to also go to the heart of the problem and treat your body's "energy furnaces". Because of this, we will begin our discussion of treatments with those that directly increase energy production.
Each cell in your body contains structures called mitochondria. The mitochondria are the tiny furnaces in each cell that produce energy by burning calories. Many problems, including Epstein Barr viral infections, can suppress your energy furnaces.3 In this chapter, I will discuss treatments that can help your mitochondrial furnaces work properly, and explain how you can use this information to feel better.
The role of energy production
We simply can't overcome fatigue if the cells and tissues in our bodies don't have enough energy. Medical research shows there are many conditions that drain energy from the body, leaving us fatigued and with frequent complications such as muscle pain, heart problems, and even depression.
Of course athletes who participate in high-intensity, endurance type exercise often face the fatigue and muscle pain associated with energy depletion. Typically, a few days of rest will allow an athlete's muscles to recharge with energy. For the rest of us, however, the physiological factors that drain hearts and muscles of energy are not as easily overcome. It is amazing how a special simple sugar, called D-ribose, can help the body restore energy, giving hearts and muscles the power they need to fully recharge, so they can recover from fatigue and chronic muscle pain.
As we age, our bodies go through many changes that affect our ability to efficiently metabolize energy. For some, these changes occur more rapidly and are more pronounced, while for others the impact is seemingly absent. People with fibromyalgia and CFS have almost 20 percent less energy in their muscles than normal, and this lack of energy causes poor exercise tolerance and lack of endurance-making it hard to perform even the most basic of life's daily activities.4,5
The metabolic changes that occur in our bodies over time or with the onset of disease are varied. Many are found to have thickening of the walls of capillaries that feed blood to muscles. These thickened capillary walls make it harder for oxygen to move from the blood to the muscle tissue, reducing the oxygen tension of the muscle and slowing the rate of energy synthesis. 6,7
In others, the mitochondrial energy furnaces are found to be defective and cannot keep up with the energy demand of cells and tissues as they work through daily activities. 8-10 Still for others, cells and tissues are deficient in certain nutrients that are needed to process food into energy, leaving the tissues energy starved. 11-13 And in the most difficult conditions, the muscle itself is affected, leaking vital cellular constituents that include energy compounds and the fuels needed to restore energy levels in affected tissues.14
No matter the cause, the impact of energy depletion is to propel a downward spiral of fatigue, muscle pain, soreness and stiffness that will not stop until the energy in the affected tissue can be restored. As energy is used faster than it can be restored, muscles become more painful, stiff, and fatigued. This causes even more energy to be used as the muscle struggles to recover, causing even more fatigue, soreness and stiffness,15-17 and the cycle continues. If the conditions leading to energy depletion are not arrested in time, the fatigue can become overwhelming and debilitating-as occurs in CFS/FMS.
The Consequences of Mitochondrial Dysfunction
A large number of clinical findings common in CFS/FMS can be explained by mitochondrial furnace malfunction Hypothalamic suppression. Particularly severe changes in the hypothalamus have been seen in mitochondrial dysfunction syndromes.18 Brain fog. Mitochondrial dysfunction can cause decreases in levels of neurotransmitters in the brain, specifically low dopamine and acetylcholine, and possibly low serotonin.
Sensitivities and allergies. Decreased ability of the liver to eliminate toxins and medications could contribute to sensitivities to both medications and environmental factors.
Post-exertion fatigue. Low energy production and accumulation of excessive amounts of lactic acid in muscles would inhibit recovery after exercise.
• Poor digestion. Mitochondrial dysfunction would also cause related to the bowel problems that plague so many people with chronic fatigue and fibromyalgia.
Weak immune system. With problems in the mitochondria, you would expect to see poor white blood cell function and therefore a decreased ability to fight infection.
Heart dysfunction. Based on research by Dr. Paul Cheney, mitochondrial dysfunction may weaken the heart muscle, requiring increased anti-oxidant levels through supplementation.
Kidney function. Poor kidney function resulting from mitochondrial dysfunction may cause a defect in the filtration and detoxification process.
Thus, mitochondrial dysfunction might well be the root cause of-or at least a contributing factor to-the hypothalamic, immune, neurotransmitter, nutritional, detoxification, sleep and other disorders seen in CFS/FMS.
Improving Mitochondrial Function
If mitochondrial dysfunction is an underlying or contributing cause to CFS/FMS, the next question is whether anything can be done to make those cellular energy furnaces work better. A number of natural treatments are available to do just that. Let us now look at some of the treatments that can improve mitochondrial energy production. Let's begin with D-Ribose, the key to energy production.
D-Ribose-The Natural Body Energizer
In looking at energy production, it helps to look at the "energy molecules" such as ATP, NADH, and FADH. These represent the energy currency in your body, and are like the paper that money is printed on. You can have all the fuel you want, but if it cannot be converted to these molecules, it is useless!
For years, I talked about the importance of B vitamins, which are a key component of these molecules. These helped to a degree, but it was clear that a key component was missing. In looking at the biochemistry of these energy molecules, they are also made of 2 other key components-adenine and ribose. Adenine is plentiful in the body and supplementing with adenine did not help CFS. We then turned our attention to Ribose. Ribose is made in your body in a slow, laborious process and cannot be found in food. We knew that CFS/FMS causes your body to dump other key energy molecules like acetyl-l-carnitine. We then found that the body did the same with Ribose, making it hard to get your furnaces working again even after the other problems were treated.
This was like one of those "Eureka!" moments where things came together. Not having Ribose would be like trying to build a fire without kindling-nothing would happen. We wondered if giving Ribose to people with CFS would jump-start their energy furnaces. The answer was a resounding yes!
Our recently published study (see the study abstract in Appendix B) showed an average 44.7- remarkable results from a single nutrient! 19 The only significant side effects were that 2 people felt too energized and hyper/anxious on the ribose. This is simply dealt with by lowering the dose and/or taking it with food.
Several of the patients participating in the study have contacted me regarding the relief they found with ribose therapy. Most importantly, they speak to the profound joy they feel when they are able to begin living normal, active lives after sometimes years of fatigue, pain, and suffering. Here is a sample of what one patient, Julie (Minnesota), an elementary teacher, wrote: "I had so much pain and fatigue I thought I was going to have to quit teaching. When I take [ribose], I feel like a huge weight is being lifted from my chest, and I'm ready to take on those kids again!" The relief patients feel with ribose therapy is heartwarming, and goes directly to the dramatic impact ribose has on increasing energy, overcoming fatigue, enhancing exercise tolerance, and raising the patient's quality of life.
To further validate these findings, we are currently conducting a much larger placebo controlled study, and hope to have the results published in the coming year. Interestingly, one of our study patients had an abnormal heart rhythm called atrial fibrillation. Ribose is outstanding in the treatment of heart disease as well, because it restores energy production in the heart muscle. Because of this, it was not surprising that this man's atrial fibrillation also went away on the ribose and he was able to stop his heart medications as well! Because of its importance and the research showing marked heart muscle dysfunction (because of low energy) in CFS, let's look at
Ribose and the heart in more detail.
Ribose and the Fatigue Associated with Heart Disease
Decades of research have shown that ribose has a profound effect on heart function in patients with congestive heart failure, coronary artery disease, and cardiomyopathy (a weakened heart muscle). Like the muscles in patients with fibromyalgia, sick hearts are energy starved.24 This energy deprivation keeps the heart from relaxing between heartbeats, making it impossible for the heart to completely fill with blood 25 (it surprisingly takes more energy for the heart muscle to relax than contract). Because the heart does not fill completely, less blood is pumped to the body with each heartbeat. The heart then gets stiff and it strains to contract. Ultimately, the heart becomes enlarged, a condition known as hypertrophy, and it is unable to pump normally.
You can compare this to the effect of weight training on the muscles in the bicep of the upper arm. Over time, weight training against more and more weight makes the muscle larger and harder. Similarly, when the heart becomes stiff it is forced to contract against more and more pressure, making the heart muscle grow. While in the case of the bicep this may be a desirable outcome, in the heart it can be deadly. In contrast to the biceps muscle, hearts must remain supple so they can fill properly and empty fully with each contraction. If hearts cannot pump normal volumes of blood, muscles of the arms and legs and brain tissue become oxygen starved. The result is fatigue, pain on standing or walking, loss of interest in, or the ability to perform any physical activity, brain fog, and depression. In the end, the heart cannot pump enough blood to even supply itself with live-giving oxygen and a heart attack can be the result.
Using ribose to restore the energy level in the heart allows it to fully relax, fill, and empty completely to circulate blood to the outer reaches of the body.26 Circulating more blood means muscles in the arms and legs, and the tissues of the brain, get the oxygen they need to function normally. This result was made evident in several important studies in patients with congestive heart failure and angina.
In one study conducted at the University of Bonn in Germany, patients with congestive heart failure were treated with either 10-grams of ribose or a sugar placebo every day for three weeks.27 They were then tested for heart function, exercise tolerance (a measure of fatigue), and quality of life using a questionnaire designed for this purpose. In this study, ribose therapy had a significant effect on all measures of diastolic heart function, showing that increased energy in the heart allowed the heart to relax, fill, and pump more normally. Patients in the study were also much more tolerant to exercise when they were on ribose, and, through their responses to the questionnaire, showed they had a higher quality of life as a result.
Two additional studies went on to help explain how ribose therapy in congestive heart failure may affect fatigue and exercise tolerance.28,29 These studies showed that ribose treatment increased ventilatory and oxygen utilization efficiency, a medical way of saying that the patients were able to breathe better and use the oxygen they inhaled more efficiently. Improving the patient's ability to use oxygen means more oxygen is available to go into the blood and out to the tissues. Having more oxygen available allows the muscle to burn fuel more efficiently, helping it keep pace with its energy demand. The result is less fatigue, a greater ability to tolerate exercise, and a higher quality of life. An added benefit to improving ventilatory efficiency is that ventilatory efficiency is a dominant predictor of mortality in congestive heart failure. Increasing ventilatory efficiency with ribose therapy is, therefore, a direct correlate to prolonging life in this patient population.
There are very few nutritional therapies that can legitimately boast of having this profound of an effect on the tissues they target. None, other than ribose, can claim such an effect in cell or tissue energy metabolism. Ribose is a unique and powerful addition to our complement of metabolic therapies in that it is completely safe, proven by strong, well designed clinical and scientific evidence, natural, and fundamental to a vital metabolic process in the body.30-34 I have added a few more study references for those who would like more information about ribose. 35-56
Ribose regulates how much energy we have in our bodies, and for those suffering from fatigue, muscle soreness, stiffness, and a host of related medical complications, the relief found in energy restoration can be life changing. This is why I recommend that all CFS/FMS patients begin with D-Ribose 5 grams (1 scoop of Corvalen) 3 x day for 2-3 weeks then twice a day. It is critical to take the 3 scoops a day for the first few weeks to see the optimal effects. Although many of the treatments in this book take 6-12 weeks to start working, most people feel the difference by the end of a single 280 gm container. For the few who don't, retry it again once you are 12-16 weeks into the other treatments well discuss. You'll be glad you did!
Although Ribose is the most promising energy nutrient, others are also worth looking at as well. Most of these only need to be taken for 4-9 months; though some people choose to take them longer (I take my Ribose every day even though I feel great. It makes me feel even better!). You will know by how you feel on them.
Click here to listen to a lecture on D-Ribose by Dr. Teitelbaum.
These other energy boosters are discussed at length in the "web site notes" section and include:
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2. Teitelbaum JE, Bird B, "Effective Treatment of Severe Chronic Fatigue: A Report of a Series of 64 Patients," Journal of Musculoskeletal Pain 3 (4) (1995): 91-110.
3-Vernon DC, et al. Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr Virus. BMC Infectious Diseases/ 2006, 6; 15 doi:10.1186/1471-2334-6-15, 31 January 2006.http://www.biomedcentral.com/1471-2334/6/15/abstract
4-Eisinger J, A Plantamura, T Ayavou. Glycolysis abnormalities in fibromyalgia. Journal of the American College of Nutrition 1994;13(2):144-148.
5.Bengtsson A, KG Henriksson. The muscle in fibromyalgia - a review of Swedish studies. Journal of Rheumatology Supplement 1989;19:144-149.
6. Lund N, A Bengtsson, P Thorborg. Muscle tissue oxygen in primary fibromyalgia. Scandinavian Journal of Rheumatology 1986;15(2):165-173.
7-Strobl ES, M Krapf, M Suckfull, W Bruckle, W Fleckenstein, W Muller. Tissue oxygen measurement and 31P magnetic resonance spectroscopy in patients with muscle tension and fibromyalgia. Rheumatology International 1997;16(5):175-180.
8.Douche-Aourik F, W Berlier, L Feasson, T Bourlet, R Harrath, S Omar, F Grattard, C Denis, B Pozzetto. Detection of enterovirus in human muscle from patients with chronic inflammatory muscle disease or fibromyalgia and healthy subjects. Journal of Medical Virology 2003;71(4):540-547.
9. Park JH, P Phothimat, CT Oates, M Hernanz-Schulman, NJ Olson. Use of P-31 magnetic resonance spectroscopy to detect metabolic abnormalities in muscles of patients with fibromyalgia. Arthritis and Rheumatology 1998;41(3):406-413.
10.Kushmerick MJ. Muscle energy metabolism, nuclear magnetic resonance spectroscopy and their potential in the study of fibromyalgia. Journal of Rheumatology Supplement 1989;19:40-46.
11. Bengtson A, KG Heriksson, J Larsson. Reduced high-energy phosphate levels in the painful muscles of patients with primary fibromyalgia. Arthritis and Rheumatology 1986;29(7):817-821.
12. Lund E, SA Kendall, B Janerot-Sjoberg, A Bengtsson. Muscle metabolism in fibromyalgia studied by P-31 magnetic resonance spectroscopy during aerobic and anaerobic exercise. Scandinavian Journal of Rheumatology 2003; 32(3):138-145.
13. Eisinger J, D Bagneres, P Arroyo, A Plantamura, T Ayavou. Effects of magnesium, high-energy phosphates, piracetam and thiamin on erythrocyte transketolase. Magnetic Research 1994;7(1):59-61.
14. Jacobsen S, KE Jensen, C Thomsen, B Danneskiold-Samsoe, O Henriksen. Magnetic resonance spectroscopy in fibromyalgia. A study of phosphate-31 spectra from skeletal muscles during rest and after exercise. Ugeskr Laeger 1994;156(46):6841-6844.
15. Olson NJ, JH Park. Skeletal muscle abnormalities in patients with fibromyalgia. American Journal of Medical Science 1998;315(6):351-358.
16. Henriksson KG. Muscle pain in neuromuscular disorders and primary fibromyalgia. Neurologija 1989;38(3):213-221.
17. Krapf MW, S Muller, P Mennet, T Stratz, W Samborski, W Muller. Recording muscle spasms in the erector spinae using in vivo 31P magnetic resonance spectroscopy in patients with chronic lumbalgia and generalized tendomyopathies. Z Rheumatology 1992;51(5):229-237.
18. P.O. Behan, "Post-Viral Fatigue Syndrome Research," in The Clinical and Scientific Basis of Myalgic Encephalitis and Chronic Fatigue Syndrome, ed. Byron Hyde, Jay Goldstein, and Paul Levine (Ottawa, Ontario, Canada: Nightingale Research Foundation, 1992), p. 238.
19. Teitelbaum JE, JA St.Cyr, C Johnson. The use of D-ribose in chronic fatigue syndrome and fibromyalgia: a pilot study. J Alternative and Complementary Medicine 2006;12(9):857-862.
20. Hellsten Y, Skadgauge L, Bangsbo J. Effect of ribose supplementation on resynthesis of adenine nucleotides after intense intermittent training in humans. American Journal of Physiology 2004; 286(1): R182-R188.
21. Tullson PC, Terjung RL. Adenine nucleotide synthesis in exercising and endurance-trained skeletal muscle. American Journal of Physiology 1991; 261: C342-C347.
22. Brault JJ, Terjung RL. Purine salvage to adenine nucleotides in different skeletal muscle fiber types. Journal of Applied Physiology 2001; 91: 231-238.
23. Gebhart B, JA Jorgenson. Benefit of ribose in a patient with fibromyalgia. Pharmacotherapy 2004;24(11):1146-1648
24. 22. Ingwall JS. ATP and the Heart. Kluwer Academic Publishers, Boston, Massachusetts.
25. Reibel D, Rovetto M. Myocardial ATP Synthesis and Mechanical Function Following Oxygen Deficiency. American Journal of Physiology 1978; 234(5): H620-H624.
26. Zimmer HG, Ibel H, Suchner U. Ribose Intervention in the Cardiac Pentose Phosphate Pathway is Not Species-Specific. Science 1984; 223: 712-714.
27. Omran H, S Illien, D MacCarter, JA St. Cyr, B Luderitz. D-Ribose improves diastolic function and quality of life in congestive heart failure patients: A prospective feasibility study. European Journal of Heart Failure 2003; 5:615-619.
28. Vijay N, D MacCarter, M Washam, J St.Cyr. Ventilatory efficiency improves with d-ribose in congestive Heart Failure patients. Journal of Molecular and Cellular Cardiology 2005;38(5):820.
29. Carter O, D MacCarter, S Mannebach, J Biskupiak, G Stoddard, EM Gilbert, MA Munger. D-Ribose improves peak exercise capacity and ventilatory efficiency in heart failure patients. Journal of the American College of Cardiology 2005;45(3 Suppl A):185A.
30. Griffiths JC, JF Borzelleca, J St.Cyr. Lack of oral embryo toxicity/ teratogenicity with D-ribose in Wistar rats. Journal of Food and Chemical Toxicology 2007;45(3):388-395.
31. Griffiths JC, JF Borzelleca, J St. Cyr. Sub-chronic (13-week) oral toxicity study with D-ribose in Wistar rats. Journal of Food and Chemical Toxicology 2007:45(1):144-152.
32. Gross M, Dormann B, Zollner N. Ribose administration during exercise: effects on substrates and products of energy metabolism in healthy subjects and a patient with myoadenylate deaminase deficiency. Klin Wochenschr 1991; 69: 151-155.
33. Wagner DR, Gresser U, Zollner N. Effects of oral ribose on muscle metabolism during bicycle ergometer in AMPD-deficient patients. Annals of Nutrition and Metabolism 1991; 35: 297-302.
34. Gross M, S Reiter, N Zollner. Metabolism of D-ribose administered to healthy persons and to patients with myoadenylate deaminase deficiency. Klin Wochenschr 1989; 67: 1205-1213.
35. Guymer EK, KJ Clauw. Treatment of fatigue in fibromyalgia. Rheum Dis Clin North Am 2002;28(2):67-78.
36. Rooks DS, CB Silverman, FG Kantrowitz. The effects of progressive strength training and aerobic exercise on muscle strength and cardiovascular fitness in women with fibromyalgia: a pilot study. Arthritis Rheum 2002;47(1):22-28.
37. Geenen R, JW Jacobs, JW Bijlsma. Evaluation and management of endocrine dysfunction in fibromyalgia. Rheum Dis Clin North Am 2002;28(2):389-404.
38. Schachter CL, AJ Busch, PM Peloso, MS Shepard. Effects of short versus long bouts of aerobic exercise in sedentary women with fibromyalgia: a randomized controlled trial. Phys Ther 2003;83(4):340-358.
39. Williamson DL, PM Gallagher, MP Goddard, SW Trappe. Effects of ribose supplementation on adenine nucleotide concentration in skeletal muscle following high-intensity exercise. Med Sci Sport Exc 2001; 33(5 suppl).
40. Zollner N, Reiter S, Gross M, Pongratz D, Reimers CD, Gerbitz K, Paetzke I, Deufel T, Hubner G. Myoadenylate deaminase deficiency: successful symptomatic therapy by high dose oral administration of ribose. Klin Wochenschr 1986; 64: 1281-1290.
41. Patton BM. Beneficial effect of D-ribose in patients with myoadenylate deaminase deficiency. Lancet May 1982; 1701.
42. Salerno C, D'Eufermia P, Finocchiaro R, Celli M, Spalice A, Crifo C, Giardini O. Effect of D-ribose on purine synthesis and neurological symptoms in a patient with adenylsuccinase deficiency. Biochim Biophys Acta 1999; 1453: 135-140.
43. Salerno C, M Celli, R Finocchiaro, P D'Eufemia, P Iannetti, C Crifo, O Giardini. Effect of D-ribose administration to a patient with inherited defect of adenylosuccinase. Purine Metabolism in Man IX. Plenum Press, New York, 1998.
44. Pauly D, C Pepine. D-Ribose as a supplement for cardiac energy metabolism. J Cardiovasc Pharmacol Ther 2000;5(4):249-258.
45. Pauly D, C Johnson, JA St. Cyr. The benefits of ribose in cardiovascular disease. Med Hypoth 2003;60(2):149-151.
46. Pauly DF, CJ Pepine. Ischemic heart disease: Metabolic approaches to management. Clin Cardiol 2004;27(8):439-441.
47. Dodd SL, CA Johnson, K Fernholz, JA St.Cyr. The role of ribose in human skeletal muscle metabolism. Med Hypoth 2004;62(5):819-824.
48. Zarzeczny R, JJ Brault, KA Abraham, CR Hancock, RL Terjung. Influence of ribose on adenine salvage after intense muscle contractions. J Appl Physiol 2001;91:1775-1781.
49. Wallen JW, MP Belanger, C Wittnich. Preischemic administration of ribose to delay the onset of irreversible ischemic injury and improve function: studies in normal and hypertrophied hearts. Can J Physiol Pharmacol 2003;81:40-47.
50. Wilson R, D MacCarter, J St. Cyr. D-Ribose enhances the identification of hibernating myocardium. Heart Drug 2003:3:61-62.
51. Van Gammeren D, D Faulk, J Antonio. The effects of four weeks of ribose supplementation on body composition and exercise performance in healthy, young male recreational bodybuilders: A double-blind, placebo-controlled trial. Curr Ther Res 2002;63(8):486-495.
52. Sharma R, M Munger, S Litwin, O Vardeny, D MacCarter, JA St. Cyr. D-Ribose improves Doppler TEI myocardial performance index and maximal exercise capacity in stage C heart failure. J Mol Cell Cardiol 2005;38(5):853.
53. Pliml W, T von Arnim, A Stablein, H Hofmann, HG Zimmer, E Erdmann. Effects of ribose on exercise-induced ischaemia in stable coronary artery disease. Lancet 1992;340:507-510.
54. Perkowski D, S Wagner, A Marcus, J St. Cyr. D-Ribose improves cardiac indices in patients undergoing "off" pump coronary arterial revascularization. J Surg Res 2007;173(2):295.
55. Muller C, H Zimmer, M Gross, U Gresser, I Brotsack, M Wehling, W Pliml. Effect of ribose on cardiac adenine nucleotides in a donor model for heart transplantation. Eur J Med Res 1998;3:554-558.
56. Grant GF, RW Gracey. Therapeutic nutraceutical treatments for osteoarthritis and ischemia. Exp Opin Ther Patents 2000;10(1): 1-10.
57. A.V. Plioplys and S. Plioplys, "Amantadine and L-Carnitine Treatment of Chronic Fatigue Syndrome," Neuropsychobiology 35 (1) (1997): 16-23.
58. H. Kuratsune, K. Yamaguti, M. Takahashi, et al., "Acylcarnitine Deficiency in Chronic Fatigue Syndrome," Clinical Infectious Disease 18 (3 Supplement 1) (January 1994): S62-S67.
59. http://www.hsrmagazine.com/hotnews/66h21048207977.html)
60. Palan PR, Connell K, et al,"Effects of menopause and hormone replacement therapy on serum levels of coenzyme Q-10 and other lipid-soluble antioxidants," Biofactors, 2005; 25(1-4): 61-6.
61. Berthold HK, Naini A, et al, "Effect of ezetimibe and/or simvastatin on coenzyme Q10 levels in plasma: a randomised trial," Drug Saf, 2006; 29(8): 703-12.
62. Sander S, Coleman SI, et al, "The impact of coenzyme Q10 on systolic function in patients with chronic heart failure," Journal of Cardiac Failure, 2006; 12(6): 464-72.
63. Weant KA, Smith KM, "The role of coenzyme Q10 in heart failure," Ann Pharmacother, 2005; 39(9): 1522-6.)
64. K. Folkers, S. Shizukuishi, K. Takemura, et al., "Increase in Levels of IgG in Serum of Patients Treated with Coenzyme Q10," Research Communications in Chemical Pathology and Pharmacology 38 (2) (1982): 335-338.
65. K. Folkers, P. Langsjoen, Y. Nara, et al., "Biochemical Deficiencies of Coenzyme Q10 in HIV Infection and Exploratory Treatment," Biochemical and Biophysical Research Communications 153 (2) (1988): 888-896.
66. K. Lockwood, S. Moesgaadr, T. Hanoike, et al., "Apparent Partial Remission of Breast Cancer in "High Risk" Patients Supplemented with Nutritional Antioxidants, Essential Fatty Acids and Coenzyme Q10," Molecular Aspects of Medicine 15 (Supplement) (1994): S231-S240.
67. K. Lockwood, S. Moesgaard, T. Yamamoto, et al., "Progress on Therapy of Breast Cancer with Coenzyme Q10 and the Regression of Metastases," Biochemical and Biophysical Research Communications 212 (1) (6 July 1995): 172-177.
67A. Rusciani L, Proietti I, et al, "Low plasma coenzyme Q10 levels as an independent prognostic factor for melanoma progression," J Am Acad Dermatol, 2006; 54(2):234-41.)
68. P. Mayer, H. Hamberger, and J. Drew, "Differential Effects of Ubiquinone Q7 and Ubiquinone Analogs on Macrophage Activation and Experimental Infections in Granulocytopenic Mice," Infection 8 (1980): 256-261.
69. E. Bliznakov, A. Casey, and E. Premuzic, "Coenzymes Q: Stimulants of Phagocytic Activity in Rats and Immune Response in Mice," Experientia 26 (1970): 953-954.
70. L. Van Gaal, I.D. de Leeuw, S. Vadhanavikit, et al., "Exploratory Study of Coenzyme Q10 in Obesity," in K. Folkers and Y. Yamamura, eds., Biomedical and Clinical Aspects of Coenzyme Q, Vol. 4 (New York, NY: Elsevier Publishers, 1984), pp. 235-373.
71. Sandor PS, Di Clemente L, et al, "Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial," Neurology, 2005; 64(4): 713-5.
72. A. Gaby, "The Role of Coenzyme Q10 in Clinical Medicine. Part I," Alternative Medicine Review 1 (1) (1996): 11-17.
73. Y. Ishihara, Y. Uchida, S. Kitamura, et al., "Effect of Coenzyme Q10, a Quinone Derivative, on Guinea Pig Lung and Tracheal Tissue," Arzneimittelforschung 35 (1985): 929-933.
Monday, March 9, 2009
What is the difference between CORvalen and CorvalenM?
What is the difference between CORvalen and CorvalenM? Both products recommend 5 grams per serving, and both have the same number of servings of D-ribose the principal active ingredient. In addition, CorvalenM contains magnesium and malate, both shown to improve muscle metabolism and relaxation.
How do I know which is best for me? As a general rule, CORvalen is recommended for heart patients and athletic applications. CorvalenM is used more for muscle aches, pain, soreness, and stiffness. But there are many exceptions with each. Ask yourself, Does my diet need additional magnesium? Magnesium is important for over 200 chemical reactions in the body. Some say the American diet contains less and less natural magnesium because more of our food is processed and we drink more bottled water and beverages than a couple of generations ago.
Conversely, too much magnesium leads to loose stools and diarrhea. You can pick up magnesium from several sources vitamin pills and other supplements.
What are the ingredients for each product? CORvalen is 100% D-ribose. Each serving contains 5g of D-ribose. CORvalen M contains D-ribose, malate and magnesium. For each serving of CORvalen M, there is 5g D-ribose, 240mg Malate (or malic acid) and 800mg magnesium gluconate (the same as 40mg elemental magnesium). CORvalen Chewable Wafers each contain 1.67 grams D-ribose. Other ingredients include inulin, cocoa bean powder, mannitol, modified cellulose, safflower oil, coconut powder, stearic acid, silicon dioxide and natural flavors.
What is ribose? D-Ribose is a simple, 5-carbon monosaccharide, or pentose sugar. It is used by all the cells of the body and is an essential compound in energy metabolism. Ribose is also the carbohydrate backbone of genetic material, DNA and RNA, certain vitamins and other important cellular compounds.
Who needs CORvalen? Ribose is an essential ingredient in stimulating natural energy production. Research has shown that ribose promotes cardiovascular health, reduces cardiac stress associated with strenuous activity and helps athletes extend their exercise tolerance and accelerates recovery. Ribose helps hearts and muscles maximize energy recovery. Whether you are a trained athlete, a weekend warrior or are concerned about your cardiovascular health, ribose may help give the energy boost your body needs.
How is ribose made in the body? Most compounds necessary for life are made in the body through a series of complicated pathways. Ribose is no different. In the body, ribose is made from glucose (a simple 6-carbon sugar) through a pathway called the Pentose Phosphate Pathway (PPP). Eventually, adenosine triphosphate (ATP) is produced. ATP is the primary energy molecule in your body’s cells. Though your body makes ribose and ATP naturally, it produces it slowly. As a result, your heart and muscle tissues use their energy faster than they can restore it and the energy pools become depleted.
How does the body derive cellular energy from ribose? The physiologically functional form of ribose, called 5-phosphoribosyl-1-pyrophosphate (PRPP), regulates the metabolic pathway that synthesizes energy compounds in all living tissue. If this compound is not available in sufficient quantity, energy synthesis slows.
How does taking supplemental CORvalen aid in increasing cellular energy? If the cellular energy pool is depleted by disease or exercise, it must be replaced. PRPP is required to turn on the metabolic pathway used by the body to replenish these energy pools. Supplemental ribose bypasses the slow and rate-limiting enzymes in the Pentose Phosphate Pathway, forms PRPP, and quickly begins the process of energy synthesis.
What will CORvalen do for someone concerned about cardiovascular health? Numerous medical studies have shown that energy levels in the heart can be dramatically lowered by exercise or decreased blood flow associated with certain cardiac diseases. Depleted cardiac energy pools may be associated with increased cardiac stress, altered cardiac function, fatigue and decreased exercise tolerance. Ribose is the key nutrient for quickly restoring cardiac energy stores.
What is the recommended daily dosage of CORvalen? Usual dosage: 5g serving twice daily, taken with meals. A third serving may be added with a midday meal as needed.
Alternative dosage: 5g just before and just after exercise or physical activity.
Serving measurement: 5g of CORvalen powder is a rounded teaspoonful. A single dose measuring scoop is provided with each jar.
CORvalen may be dissolved in 2 oz. or more of juice, tea, or coffee or sprinkled over foods of choice (such as hot oatmeal, yogurt, cold cereal). CorvalenM has a more citrus flavor so it is best in juice, water or yogurt. CORvalen and CorvalenM should NOT be mixed into carbonated beverages.
To maximize athletic performance, or to keep energy pools high during strenuous activity, slightly larger doses may be required. CORvalen (D-ribose) should be taken just before and just after exercise or activity. For extended exercise, an additional 1 to 2 grams per hour of exercise or activity may be helpful.
When can I expect to feel results/benefits from taking CORvalen? Individual response varies widely, but relief from fatigue is often felt within the first 10 days of consistent use.
What can I mix with CORvalen? CORvalen may be mixed with water, juice, coffee, tea or sprinkled on cereal or fruit. It has a mild pleasant sweet taste and is very flexible.
Are there any side effects associated with taking ribose? CORvalen may lower blood sugar for 60 to 90 minutes after ingestion. This may cause one to feel very hungry or lightheaded. This can be avoided by taking with meals or with some form of a carbohydrate such as a juice.
What will ribose do for someone who exercises on a regular basis? Scientific research shows that three or four workouts per week may not allow enough rest time between sessions for heart and muscle energy pools to return to normal levels. Taking CORvalen (D-ribose) shortens the time needed by heart and muscle tissue to replace energy that is lost through vigorous exercise. Keeping energy pools full helps to keep hearts and muscles in good physiological condition, increase power and endurance, and reduce fatigue. Recent research has also shown that ribose supplementation during exercise manages free radical formation and lowers cardiac stress associated with hypoxia.
Does CORvalen conflict with any medications? There are no known interactions with drugs or other supplements.
Does ribose work with creatine or other supplements? Ribose can increase the effect of creatine and other energy supplements by keeping the energy pool at full capacity. Creatine works by recycling energy that is already present in the tissue. Another supplement, carnitine, aids in fatty acid metabolism. A third, pyruvate, also helps to recycle energy. Only ribose performs this important metabolic function. Without adequate levels of energy to work with, no other supplement can be fully effective.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
How do I know which is best for me? As a general rule, CORvalen is recommended for heart patients and athletic applications. CorvalenM is used more for muscle aches, pain, soreness, and stiffness. But there are many exceptions with each. Ask yourself, Does my diet need additional magnesium? Magnesium is important for over 200 chemical reactions in the body. Some say the American diet contains less and less natural magnesium because more of our food is processed and we drink more bottled water and beverages than a couple of generations ago.
Conversely, too much magnesium leads to loose stools and diarrhea. You can pick up magnesium from several sources vitamin pills and other supplements.
What are the ingredients for each product? CORvalen is 100% D-ribose. Each serving contains 5g of D-ribose. CORvalen M contains D-ribose, malate and magnesium. For each serving of CORvalen M, there is 5g D-ribose, 240mg Malate (or malic acid) and 800mg magnesium gluconate (the same as 40mg elemental magnesium). CORvalen Chewable Wafers each contain 1.67 grams D-ribose. Other ingredients include inulin, cocoa bean powder, mannitol, modified cellulose, safflower oil, coconut powder, stearic acid, silicon dioxide and natural flavors.
What is ribose? D-Ribose is a simple, 5-carbon monosaccharide, or pentose sugar. It is used by all the cells of the body and is an essential compound in energy metabolism. Ribose is also the carbohydrate backbone of genetic material, DNA and RNA, certain vitamins and other important cellular compounds.
Who needs CORvalen? Ribose is an essential ingredient in stimulating natural energy production. Research has shown that ribose promotes cardiovascular health, reduces cardiac stress associated with strenuous activity and helps athletes extend their exercise tolerance and accelerates recovery. Ribose helps hearts and muscles maximize energy recovery. Whether you are a trained athlete, a weekend warrior or are concerned about your cardiovascular health, ribose may help give the energy boost your body needs.
How is ribose made in the body? Most compounds necessary for life are made in the body through a series of complicated pathways. Ribose is no different. In the body, ribose is made from glucose (a simple 6-carbon sugar) through a pathway called the Pentose Phosphate Pathway (PPP). Eventually, adenosine triphosphate (ATP) is produced. ATP is the primary energy molecule in your body’s cells. Though your body makes ribose and ATP naturally, it produces it slowly. As a result, your heart and muscle tissues use their energy faster than they can restore it and the energy pools become depleted.
How does the body derive cellular energy from ribose? The physiologically functional form of ribose, called 5-phosphoribosyl-1-pyrophosphate (PRPP), regulates the metabolic pathway that synthesizes energy compounds in all living tissue. If this compound is not available in sufficient quantity, energy synthesis slows.
How does taking supplemental CORvalen aid in increasing cellular energy? If the cellular energy pool is depleted by disease or exercise, it must be replaced. PRPP is required to turn on the metabolic pathway used by the body to replenish these energy pools. Supplemental ribose bypasses the slow and rate-limiting enzymes in the Pentose Phosphate Pathway, forms PRPP, and quickly begins the process of energy synthesis.
What will CORvalen do for someone concerned about cardiovascular health? Numerous medical studies have shown that energy levels in the heart can be dramatically lowered by exercise or decreased blood flow associated with certain cardiac diseases. Depleted cardiac energy pools may be associated with increased cardiac stress, altered cardiac function, fatigue and decreased exercise tolerance. Ribose is the key nutrient for quickly restoring cardiac energy stores.
What is the recommended daily dosage of CORvalen? Usual dosage: 5g serving twice daily, taken with meals. A third serving may be added with a midday meal as needed.
Alternative dosage: 5g just before and just after exercise or physical activity.
Serving measurement: 5g of CORvalen powder is a rounded teaspoonful. A single dose measuring scoop is provided with each jar.
CORvalen may be dissolved in 2 oz. or more of juice, tea, or coffee or sprinkled over foods of choice (such as hot oatmeal, yogurt, cold cereal). CorvalenM has a more citrus flavor so it is best in juice, water or yogurt. CORvalen and CorvalenM should NOT be mixed into carbonated beverages.
To maximize athletic performance, or to keep energy pools high during strenuous activity, slightly larger doses may be required. CORvalen (D-ribose) should be taken just before and just after exercise or activity. For extended exercise, an additional 1 to 2 grams per hour of exercise or activity may be helpful.
When can I expect to feel results/benefits from taking CORvalen? Individual response varies widely, but relief from fatigue is often felt within the first 10 days of consistent use.
What can I mix with CORvalen? CORvalen may be mixed with water, juice, coffee, tea or sprinkled on cereal or fruit. It has a mild pleasant sweet taste and is very flexible.
Are there any side effects associated with taking ribose? CORvalen may lower blood sugar for 60 to 90 minutes after ingestion. This may cause one to feel very hungry or lightheaded. This can be avoided by taking with meals or with some form of a carbohydrate such as a juice.
What will ribose do for someone who exercises on a regular basis? Scientific research shows that three or four workouts per week may not allow enough rest time between sessions for heart and muscle energy pools to return to normal levels. Taking CORvalen (D-ribose) shortens the time needed by heart and muscle tissue to replace energy that is lost through vigorous exercise. Keeping energy pools full helps to keep hearts and muscles in good physiological condition, increase power and endurance, and reduce fatigue. Recent research has also shown that ribose supplementation during exercise manages free radical formation and lowers cardiac stress associated with hypoxia.
Does CORvalen conflict with any medications? There are no known interactions with drugs or other supplements.
Does ribose work with creatine or other supplements? Ribose can increase the effect of creatine and other energy supplements by keeping the energy pool at full capacity. Creatine works by recycling energy that is already present in the tissue. Another supplement, carnitine, aids in fatty acid metabolism. A third, pyruvate, also helps to recycle energy. Only ribose performs this important metabolic function. Without adequate levels of energy to work with, no other supplement can be fully effective.
These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
Wednesday, February 11, 2009
Microcrystalline Hydroxyapatite Concentrate (MCHC)
Microcrystalline hydroxyapatite concentrate (MCHC) is an excellent source of bioavailable calcium that is important for developing strong bones and teeth, preventing osteoporosis, and assisting with proper function of various body systems such as the heart, nerves, and muscles. MCHC is derived from whole bone and is complete with the minerals and organic factors naturally found in raw bone. In addition to calcium and the organic factors (mostly collagen protein and mucopolysaccharides), MCHC contains phosphorus, magnesium, fluoride, zinc, silicon, manganese, and other trace minerals in the same physiological proportions found in healthy bone. MCHC has been shown to be well-tolerated, even by small children, with no undesirable side effects.
In addition, MCHC has been shown to contain biologically active growth factors. Such growth factors are known to directly stimulate bone cell activity thereby enhancing bone formation.
With the rapid aging of the population, experts agree that prevention is the most effective method of dealing with osteoporosis. Along with regular exercise as well as a healthy diet and lifestyle, MCHC provides comprehensive bone nourishment which aims at preventing the onset of osteoporosis and many other health problems.
Uses
MCHC is available in tablet form. Be sure to drink 6 to 8 cups of water throughout the day to avoid constipation. Studies have shown that 500 mg of MCHC yield approximately 200 mg of elemental calcium and thus, MCHC should be taken according to the following guidelines:
In addition, MCHC has been shown to contain biologically active growth factors. Such growth factors are known to directly stimulate bone cell activity thereby enhancing bone formation.
With the rapid aging of the population, experts agree that prevention is the most effective method of dealing with osteoporosis. Along with regular exercise as well as a healthy diet and lifestyle, MCHC provides comprehensive bone nourishment which aims at preventing the onset of osteoporosis and many other health problems.
Uses
- Excellent source of bioavailable calcium.
- Provides a full complement of minerals that are important for healthy bone formation and metabolism such as phosphorus, fluoride, magnesium, silicon, iron, zinc, copper, and manganese.
- Contains intact organic factors that provide secondary support for healthy bone formation.
In several studies, MCHC has been shown to be highly successful in minimizing bone loss as well as positively affecting bone healing. This includes reducing the incidence of fractures as well as facilitating the healing of fractures.
MCHC is available in tablet form. Be sure to drink 6 to 8 cups of water throughout the day to avoid constipation. Studies have shown that 500 mg of MCHC yield approximately 200 mg of elemental calcium and thus, MCHC should be taken according to the following guidelines:
- Adults ages 19 to 50 need 2,500 mg per day of MCHC (1,000 mg of calcium). After age 50, adults need 3,000 mg per day of MCHC (1,200 mg of calcium).
- Adolescents ages 9 to 18 need 3,250 mg per day of MCHC (1,300 mg of calcium).
- Children ages 6 to 8 need 2,000 mg per day of MCHC (800 mg of calcium); children ages 1 to 5 need 1,250 mg per day of MCHC (500 mg of calcium).
Precautions
Talk with your healthcare provider about your calcium needs if you have any thyroid or kidney problems, or if you have hormone or vitamin deficiencies.
Be especially careful when choosing an MCHC product. It is important to realize that supplements that claim to contain MCHC may vary widely in purity, form, and effectiveness.
The sources of bone extract as well as the processing procedures are of utmost importance in determining the quality of MCHC. Some sources of MCHC may contain high levels of lead and other contaminants, or be tainted with cartilage and tendons. Certain processing procedures, such as high-heat and excessive grinding, can result in a product that is nothing more than bone meal. These products lack the full complement of minerals, organicfactors, and the microcrystalline structures that are characteristic of true MCHC.
Possible Interactions
Some foods, drinks, and medications can cause you to excrete MCHC. These include some soft drinks, aluminum-containing antacids, salt, sugar, saturated fat, caffeine, alcohol, and very high protein and fiber intake.
In addition, excessive amounts of some foods and drinks and regular use of some medications make it hard for your body to get the MCHC it needs. These include alcohol, aspirin, barbiturates, fiber, neomycin, strong sedatives, oxalic acid (found in chocolate, rhubarb, spinach, chard, sweet potatoes, and dried beans), phytic acid (found in grains), and uronic acid (a type of fiber found in fruits and vegetables).
Supporting Research
Epstein O, Kato Y, Dick R, et al. Vitamin D, hydroxyapatite and calcium gluconate in treatment of cortical bone thinning in postmenopausal women with primary biliary cirrhosis. Am J Clin Nutr 1982;36(3):426-30.
Fleming KH, Heimbach JT. Consumption of calcium in the U.S.: food sources and intake levels. J Nutr 1994;124(8 suppl):1426S-30S.
Pines A, Raafat H, Lynn AH, et al. Clinical trial of MCHC in the prevention of osteoporosis due to corticosteroid therapy. Curr Med Res Opin 1984:8(10):734-42.
Riggs BL, Melton LJ 3rd. Involutional osteoporosis. N Eng J Med 1986;314(26):1676-86.
Notelovitz M. Osteoporosis: screening, prevention and management. Fertil Steril 1993;59(4):707-25.
Ruegsegger P, Keller A, Dambacher MA. Comparison of the treatment effects of ossein-hydroxyapatite compound and calcium carbonate in osteoporotic females. Osteo Int 1995;5(1):30-34.
Stepan JJ, Pospichal J, Presl J, et al. Prospective trial of ossein-hydroxyapatite compound in surgically induced postmenopausal women. Bone 1989;10(3):179-85.
Windsor ACM, Misra DP, Loudon JM, et al. The effect of whole-bone extract on 47Ca absorption in the elderly. Age & Ageing 1973;2(4):230-34.
Advanced Nutrition Publications ©2002
Magnesium supplementation and osteoporosis
Although calcium has received most of the attention, there is growing evidence that magnesium is an important factor in maintaining optimal bone health. In fact, experts agree that adequate magnesium intake is necessary for the proper utilization of calcium, which is found in large quantities in bone.
According to researchers, "With this degree of supporting evidence, it is curious that magnesium supplementation has not been examined more frequently in studies of osteoporosis."
Osteoporosis is a reduction in bone mass that leads to an increased risk of bone fractures. In response to the lack of research on magnesium and osteoporosis, researchers reviewed a 2-year study performed on 31 osteoporotic postmenopausal women given magnesium. For the first 6 months, participants were treated with 250 to 750 mg per day of magnesium (depending upon individual tolerance). From month 6 to 24, treatment consisted of 250 mg per day of magnesium. An age-matched group consisting of 23 postmenopausal women with osteoporosis served as controls (untreated) for comparison. Bone mineral density tests were performed on all participants at the beginning of the study, after 1 year of treatment, and at the end of the 2-year study.
Researchers stated that, "At the end of the 2-year study, magnesium therapy [appeared] to have prevented fractures and resulted in a significant increase in bone density."
Researchers also claimed, "The finding that magnesium supplementation actually caused increased bone density rather than a stabilization of existing bone density is noteworthy. This has not been a finding of either calcium or estrogen intervention trials."
J. Sojka and colleagues concluded in Nutrition Reviews that "...magnesium intake should be measured when conducting studies investigating the importance of nutrients on the prevention or treatment of osteoporosis."
Nutr Rev 1995;53(3):71-80.
Advanced Nutrition Publications ©2002
Buy Magnesium Supplement - Quality - Highly Absorbable
According to researchers, "With this degree of supporting evidence, it is curious that magnesium supplementation has not been examined more frequently in studies of osteoporosis."
Osteoporosis is a reduction in bone mass that leads to an increased risk of bone fractures. In response to the lack of research on magnesium and osteoporosis, researchers reviewed a 2-year study performed on 31 osteoporotic postmenopausal women given magnesium. For the first 6 months, participants were treated with 250 to 750 mg per day of magnesium (depending upon individual tolerance). From month 6 to 24, treatment consisted of 250 mg per day of magnesium. An age-matched group consisting of 23 postmenopausal women with osteoporosis served as controls (untreated) for comparison. Bone mineral density tests were performed on all participants at the beginning of the study, after 1 year of treatment, and at the end of the 2-year study.
Researchers stated that, "At the end of the 2-year study, magnesium therapy [appeared] to have prevented fractures and resulted in a significant increase in bone density."
Researchers also claimed, "The finding that magnesium supplementation actually caused increased bone density rather than a stabilization of existing bone density is noteworthy. This has not been a finding of either calcium or estrogen intervention trials."
J. Sojka and colleagues concluded in Nutrition Reviews that "...magnesium intake should be measured when conducting studies investigating the importance of nutrients on the prevention or treatment of osteoporosis."
Nutr Rev 1995;53(3):71-80.
Advanced Nutrition Publications ©2002
Buy Magnesium Supplement - Quality - Highly Absorbable
Friday, January 23, 2009
High PCB exposure tied to diabetes risk
Last Updated: 2008-08-15 11:43:12 -0400 (Reuters Health)
NEW YORK (Reuters Health) - People who have been exposed to high levels of toxic polychlorinated biphenyls (PCBs) may face an elevated risk of type 2 diabetes, a new study shows.
The findings, reported in the journal Diabetes Care, come from a long-term study of Taiwanese adults who, in the 1970s, had been poisoned by cooking oil contaminated with PCB pollutants.
Once used in products ranging from fluorescent lights and appliances to insulation and insecticide, PCBs were banned in the late 1970s as carcinogens and general health hazards. They linger in the environment, however.
In the new study, Dr. Yueliang Leon Guo, from the National Taiwan University in Taipei, and colleagues examined the incidence of type 2 diabetes among 378 Taiwanese "oil disease" victims and 370 of their neighbors who had not been poisoned.
They found that women who had been exposed to the PCB-laced oil were twice as likely as other women to develop type 2 diabetes over 24 years. And women who had been most severely affected by the PCB exposure had a more than five-times higher diabetes risk.
There were no similar risks seen in men, however.
Other studies have found that people with diabetes tend to have relatively higher levels of organic pollutants, such as PCBs, in their blood. In comments to Reuters Health, Guo said that since "everyone" has detectable PCB levels in his or her body, it's possible that exposure to such pollutants has helped feed the widespread rise in diabetes in recent decades.
"The public health implication of these findings can be huge," Guo added, "considering the burden of diabetes and its multiple long-term complications."
.SOURCE: Diabetes Care 2008, August 2008.
NEW YORK (Reuters Health) - People who have been exposed to high levels of toxic polychlorinated biphenyls (PCBs) may face an elevated risk of type 2 diabetes, a new study shows.
The findings, reported in the journal Diabetes Care, come from a long-term study of Taiwanese adults who, in the 1970s, had been poisoned by cooking oil contaminated with PCB pollutants.
Once used in products ranging from fluorescent lights and appliances to insulation and insecticide, PCBs were banned in the late 1970s as carcinogens and general health hazards. They linger in the environment, however.
In the new study, Dr. Yueliang Leon Guo, from the National Taiwan University in Taipei, and colleagues examined the incidence of type 2 diabetes among 378 Taiwanese "oil disease" victims and 370 of their neighbors who had not been poisoned.
They found that women who had been exposed to the PCB-laced oil were twice as likely as other women to develop type 2 diabetes over 24 years. And women who had been most severely affected by the PCB exposure had a more than five-times higher diabetes risk.
There were no similar risks seen in men, however.
Other studies have found that people with diabetes tend to have relatively higher levels of organic pollutants, such as PCBs, in their blood. In comments to Reuters Health, Guo said that since "everyone" has detectable PCB levels in his or her body, it's possible that exposure to such pollutants has helped feed the widespread rise in diabetes in recent decades.
"The public health implication of these findings can be huge," Guo added, "considering the burden of diabetes and its multiple long-term complications."
.SOURCE: Diabetes Care 2008, August 2008.
Saturday, January 10, 2009
Using inositol for promoting brain wellness: an interview with Robert Belmaker, MD
Robert Crayhon: Joining us now to discuss his groundbreaking research on inositol and mental health is psychiatrist and researcher Robert H. Belmaker, MD. Dr. Belmaker, would you please give us your educational background?
Robert Belmaker: I received my Bachelors Degree in 1967 at Harvard University and my MD in 1971 at Duke University. I then started a psychiatric residency at Duke and then went to the National Institutes of Mental Health as a clinical associate from 1972-1974. I then came to Israel in 1974 and completed my psychiatric residency. Eventually, I became director of research at the Jerusalem Mental Health Center in Jerusalem. Later, I became in addition, an associate professor of psychiatry at the Hebrew University School of Medicine in Jerusalem. In 1985 I came to the new medical school in Beersheva at Ben Gurion University to become the Hoffer-Vickar Chair of Psychiatry.
RC: Can you just describe for us briefly, your daily duties?
RB: I am a professor of psychiatry; I am the assistant director of the Beersheva Mental Health Center, so I have administrative duties. Every Monday I have a full clinic day with my own patients. Sometimes with my own 30 patients. Two to three times a week I do rounds on inpatients with the residents as well. So I have clinical, teaching and research duties.
RC: What got you interested in the role of nutrition in brain function as a psychiatrist?
RB: I think it's partly derived from some skepticism about the pharmaceutical companies. It is also derived from the feeling that so much of what we ingest everyday is food, and that chemicals in food must have some effect on our brain, and perhaps some potential therapeutic effects on the brain. But actually the chair of psychiatry that I am incumbent of was endowed by a family that has been famous for their interest in nutrition and psychiatry. I haven't decided to this day whether they found me and endowed the chair, or whether the endowment of the chair influenced my thinking. But, of course, Abram Hoffer, MD, PhD, from Canada has been interested and influential in nutrition and psychiatry for fifty years now. He published in the 1950s about nutrition and psychiatry when it was very unpopular, and he very bravely continued.
RC: Is the connection between nutrition and psychiatry any more popular now in psychiatric circles?
RB: There is an increase in interest in nutrition and psychiatry. However, like the increased interest in nutrition and medicine, it goes with a healthy degree of skepticism. There are a fair number of people who are suspicious -- perhaps sometimes rightly so -- of excessive claims. Often people with severe mental illnesses reject any drug treatment. They do that partly because of their illness in their thinking. Sometimes they use arguments derived from the nutrition literature and don't get proper pharmaceutical treatment. This is a shame, and this makes some psychiatrists in this position skeptical about nutrition. Clearly, however, some patients with heart disease need surgery and sometimes need triple artery by-pass, and other patients with high blood pressure are clearly going to need hypertensive and anti-hypertensive medicine. All cardiologists today know and believe and preach the role of nutrition in preventing heart disease and high blood pressure. So, the two should not be seen as antagonistic. In psychiatry there is no question that the anti-psychotic drugs and the mood stabilizer drugs are effective. But I think perhaps we are a little behind cardiology and some of the papers show that folate supplementation can enhance the ability of lithium to prevent mood disorders and the ability of anti-psychotic drugs to reduce psychosis. These papers are not given as much publicity and as much acceptance as they really deserve. I don't know if it's because they do not have a pharmaceutical company pushing folate -- because it's too cheap -- or whether it's the skepticism that might be a result of excessive claims of the past. Or perhaps it is the skepticism that is coming as an antidote to the fact that some patients refuse pharmaceutical treatment, and only want natural treatment. Often those patients are too sick to be able to make a rational decision.
RC: Dr. Belmaker, do you feel the future of psychiatry is an intelligent integration of pharmaceuticals and nutrients? And, should nutrients be tried first?
RB: I think we have to answer that question empirically. There are going to have to be studies, like the ones we did with inositol. There is no way to know what comes first and what comes second. Certainly in most cases nutrients are milder. If a person finds changing his diet can prevent his headaches, we would like to see him do that before he tries a strong medicine like Valproate to prevent a headache. Ultimately, it has to be an empirical question. We have to do the studies.
RC: What got you interested in inositol?
RB: I had been interested previously in lithium and I am still interested in lithium. As you know, lithium is a very simple compound and a non-patented compound and a cheap compound. Those are some of the things that keep my interest. I have been interested in lithium for 30 years. Lithium has a major effect on inositol and the brain that was discovered by a wonderful man, name of Dr. Berridge from London, a Nobel prize candidate for that work. That work was done on flies, of the salivary gland of the fruit fly. For those people who sometimes make jokes about how animal research is not relevant, here is an example of how something that seems terribly funny, the salivary gland of the fruit fly, has become a major area of scientific research, with many important benefits for humanity. He discovered the whole cycle, the inositol cycle of the cell, and that lithium had an effect on it. So, as a lithium researcher, I read his papers and got interested in inositol. Professor Berridge was very interested in how inos itol can affect cell function. We were really the first to think that one could possibly give inositol as a nutrient in quantities that could get it to the brain.
RC: How does lithium affect inositol's function?
RB: It's a bit complicated, and there are still disagreements about it. Lithium inhibits a key enzyme called inositol mono-phosphatase. Some people say, as a result, inositol levels in some areas in the brain should go down. Other people believe because that enzyme is inhibited, the inositol phosphates actually go up, and we really don't know which of those two things are more important in lithium action.
RC: What is the difference between inositol and myo-inositol? Is there a difference? Is it just two terms for the same thing?
RB: For a biologist they are two terms for the same thing. The only inositol that exists naturally in the body of the human or any other mammal is called myo-inositol. For a chemist, inositol can exist in eight different forms that are mirror images of each other, although it might be hard to imagine how you can have eight different mirror images; but that's because there are eight different places on the inositol molecule that a carbon and a hydroxyl group can have a mirror image. But, only the myo-inositol is present naturally so when I talk about inositol as a medicine or a cell, I can just drop the myo and call it inositol, because that is the only one that we have.
RC: What happens when the human body is given inositol orally?
RB: It depends on the dose. The doses that we found are large enough to get inositol into the brain are the dose equivalent of 3 to 6 teaspoons a day. That's 12 to 18 grams. It could be teaspoons in tea or in juice. That's the quantities that we are talking about. In order for these doses to be effective, they need to be taken over a period of three to four weeks. We found those doses to be as beneficial as anti-depressants used in depression, panic disorders and in obsessive-compulsive disorders. We've done one study in normal volunteers, who were given a much larger dose at a single time in the morning in a large cup of juice. They were given 12 grams in one swallow and then every hour they were asked to fill out rating scales as to their tension, mood, feelings of relaxation, feeling of wellbeing, welfare, things that a normal person would write, called a profile of mood scale (the scale for normal mood), and we found that indeed, even a single dose peaking at about six hours reduced tension and increased feelings of well-being. In depressed patients we don't see those effects quite so early. Perhaps because the depression is strong enough to mask them, and in these patients, inositol did not work any faster than standard antidepressants. It only had a significant and beneficial effect after about three weeks.
RC: How does inositol work?
RB: That of course is a very good question. We have done quite a bit of animal work in rats to look at the mechanism and we think that the strongest findings relate to serotonin and particularly the 5HT2 serotonin receptor. In a rat if you drip serotonin on neurons with those receptors, and measure the response, after a while the nerve cell stops responding and if you add inositol it jumps up and starts responding again. So, it seems like cells can get depleted of inositol. Or, specific nerve cells might not have enough to be able to maintain neurotransmission in the serotonergic system. Of course, there are many things we have not investigated, but it could be that some patients have deficiencies in the brain of inositol to the point where their serotonin system cannot respond.
We did do a study with brains donated after death from patients with depression, manic-depression and other mental illnesses, and no illness. These were given to us by the Stanley Research Foundation in Washington DC, which was able to obtain these brains from people who consented before their death to donate their brains. They were diagnosed before their death as suffering from these diseases. We did find a group of patients especially with affective disorder with low, very low inositol levels in the brain.
RC: Is there a way for most people through their diet to get enough inositol? When you are talking about a therapeutic dose in the 12-18 gram range, I am wondering where someone may get a gram of inositol on a daily basis though food.
RB: The usual intake is about a gram a day through food. I think it would be really hard to get 12 grams a day through food, I think that is really a pharmacological dose. Of course, prevention of depression might require a lower dose, and we have been interested. I have a colleague now, a dietitian, whom I have asked to do some surveys of the diet of people who come complaining of depression, to see whether there are different amounts of inositol. We also have a study that will be published in May in the American Journal of Psychiatry on omega-3 fatty acids, another nutrient that we found to be anti-depressant in depressed patients, and on this we were not the first.
RC: Has there been an actual clinical trial of omega-3 fats in depression?
RB: Let me just say one thing about the omega-3s. There is one previous study by Andy Stull of Boston, a Clinical Trial with positive results. What I wanted to say is that the omega-3s also are given in much higher doses than are present in the usual diet, even though there have been reports of a correlation in the usual diet, such that the people who eat more omega-3s get depressed less. It might be with some of these nutrients you need more to correct real depression than you do to prevent it.
RC: Which will bring us back to a lesson taught to us by Abram Hoffer decades ago -- that is exactly the case. If you are missing a nutrient for decades you might need a lot more for the rest of your life to get back to normal. Regarding inositol and the diet, my understanding is that inositol in our food is largely in the form of inositol hexaphosphate, which is in a form of fiber that's hard to absorb. In other words, it might be in the food, but how well we absorb it, I think is perhaps open to question.
RB: I think you are asking a very good question, it's something I am just getting very interested in, and don't have the answer for you.
RC: Let's talk about inositol in some other applications, to say it's effective in depression at doses of 12-18 grams, but you've got to give it three weeks to really see the results?
RB: That's right.
RC: What about agoraphobia?
RB: We tend to call this panic disorder, with or without agoraphobia. Same doses seem to be effective, and also our statistical significant results occurred at three weeks. There was a strong trend before that, but our statistical significant results occurred at about three weeks.
RC: What about obsessive-compulsive disorder and inositol?
RB: In obsessive-compulsive disorder our studies use 18 grams. I can't say it doesn't work less than that, the way it works with depression with 12 grams, but we just haven't tried it. These people tend to be more ill -- and started with 18 grams. We've only seen statistically significant improvement by about six weeks, not before that. It does take longer, which is similar to drug treatment for obsessive-compulsive disorder.
RC: And only with inositol monotherapy, with no other nutrient or drug?
RB: That's right.
RC: Very impressive. Did you arrive at these doses by clinically examining the fact that the 3 and 6 grams doesn't work and then titrating upward to 18 grams?
RB: We arrived at the doses actually first with the pharmacokinetic studies. We tested to see what doses were necessary to get a good rise in inositol in human spinal fluid. Less than 12 grams a day didn't achieve much of a rise. At 12 grams a day, there is a 70% rise in human spinal fluid inositol levels. We have tried some patients in the early days more than now on lower doses, so we had some feeling of what the dose should be. I must say it has not been done in a systematic way because these kinds of controlled trials are expensive. We haven't had the funding that the pharmaceutical companies have. To really work up inositol in the way you are describing with very large trials in multiple doses -- is a one hundred million dollar project. No one would give us this to study a non-patentable compound. We had some grants from NIH and from the Stanley Foundation, but we have not done a good dose response study.
RC: What about SSRI medications and inositol, since they seem to be accentuating the same pathway. What if someone is taking a Zoloft or a Prozac and they ask their physician, "Can I take inositol at the same time?"
RB: We have studied that, and we have not had side effects with it. But, to our surprise and disappointment, we did not see synergism. We would have hoped for synergism, but it seems that inositol works and the SSRIs worked. If you put the two of them together it doesn't work any better than inositol alone or SSRIs alone. So that SSRIs in that sense are an alternative to inositol, or inositol is an alternative to SSRIs. We don't have reason to believe that it is a good addition to a SSRI non-responder, although we have not found it in any way unsafe if someone wants to try.
RC: What if someone wants to transition off of a SSRI? Would inositol be a logical stepping-stone to perhaps a more natural approach to accentuating serotonin metabolism?
RB: It is certainly an option, but we don't have data on that. We have data on people who have been treated in the past with SSRIs successfully and on their next depressive episode they were treated successfully with inositol. But we don't actually have people going from one to the other in the same depressive episode.
RC: Let's talk about inositol and safety. You've used doses of 18 grams in your trials and your practice. Any side effects from these doses?
RB: Well, people will have some loose stools and about the same with some of the SSRIs. I would say about quarter of the patients will move their bowels more frequently. We've had very few people who have to stop the medicine for that reason. We have not seen any significant changes. By now we've have a fairly large number of patients with hematological or chemical parameters. This is a large number of patients for a natural compound, but these are still fewer patients than would be expected, let's say for the FDA. If it were a new SSRI, they would want a considerably larger number of patients.
RC: Is there anyone who should not take inositol?
RB: I think it would make sense for someone who was diabetic to be careful. Someone with severe kidney disease or liver disease to be careful with inositol but I think this is a very general medical consideration.
RC: And that's because inositol has a molecular similarity to glucose and because of this theoretically could raise blood sugar in diabetics?
RB: That's right.
RC: Any other pearls here for nutritional pharmacology research? You spoke about folate and omega-3s, any other information you would like to share with our readers?
RB: Well, I think one of the most exciting things that we've been doing lately is with homocysteine. Homocysteine is the amino acid that's not used in protein synthesis and its been shown to be a risk factor for cardiovascular disease over the last few years. In more recent years it's been proven to be a risk factor for Alzheimer's and cerebral vascular disorders as well. We thought that this might mean that it's a risk factor for mental disorder and we have been surveying homocysteine levels in our patients and have found markedly elevated levels of homocysteine. We have begun a trial of folate, B12 and B6 in schizophrenic patients, because these are known to be homocysteine lowering vitamins that can lower homocysteine levels by up to 50% in combination. Homocysteine has been shown in a test tube to be neurotoxic, so we think we might be able to prevent the clinical deterioration and cognitive deterioration in schizophrenia with homocysteine lowering.
RC: Have you seen lowering homocysteine to be an effective strategy; perhaps in the treatment of depression?
RB: We have not looked at that.
RC: What happens when you give a patient a good-sized powder container of inositol and say "Take 6 teaspoons per day, please." Do they look at you and say "why is this doctor giving me a nutrient, and so much of it?"
RB: Well, I explain it. Most of the patients that consent to be on our program are people who are looking for this. That's how they get to us. So we find it very acceptable among patients, compliance is very high.
RC: Does it matter if inositol is taken with food or not?
RB: No it doesn't. It's absorbed very well. We recommend it be taken with some food
Metagenics Cenitol Powder with Inositiol
Robert Belmaker: I received my Bachelors Degree in 1967 at Harvard University and my MD in 1971 at Duke University. I then started a psychiatric residency at Duke and then went to the National Institutes of Mental Health as a clinical associate from 1972-1974. I then came to Israel in 1974 and completed my psychiatric residency. Eventually, I became director of research at the Jerusalem Mental Health Center in Jerusalem. Later, I became in addition, an associate professor of psychiatry at the Hebrew University School of Medicine in Jerusalem. In 1985 I came to the new medical school in Beersheva at Ben Gurion University to become the Hoffer-Vickar Chair of Psychiatry.
RC: Can you just describe for us briefly, your daily duties?
RB: I am a professor of psychiatry; I am the assistant director of the Beersheva Mental Health Center, so I have administrative duties. Every Monday I have a full clinic day with my own patients. Sometimes with my own 30 patients. Two to three times a week I do rounds on inpatients with the residents as well. So I have clinical, teaching and research duties.
RC: What got you interested in the role of nutrition in brain function as a psychiatrist?
RB: I think it's partly derived from some skepticism about the pharmaceutical companies. It is also derived from the feeling that so much of what we ingest everyday is food, and that chemicals in food must have some effect on our brain, and perhaps some potential therapeutic effects on the brain. But actually the chair of psychiatry that I am incumbent of was endowed by a family that has been famous for their interest in nutrition and psychiatry. I haven't decided to this day whether they found me and endowed the chair, or whether the endowment of the chair influenced my thinking. But, of course, Abram Hoffer, MD, PhD, from Canada has been interested and influential in nutrition and psychiatry for fifty years now. He published in the 1950s about nutrition and psychiatry when it was very unpopular, and he very bravely continued.
RC: Is the connection between nutrition and psychiatry any more popular now in psychiatric circles?
RB: There is an increase in interest in nutrition and psychiatry. However, like the increased interest in nutrition and medicine, it goes with a healthy degree of skepticism. There are a fair number of people who are suspicious -- perhaps sometimes rightly so -- of excessive claims. Often people with severe mental illnesses reject any drug treatment. They do that partly because of their illness in their thinking. Sometimes they use arguments derived from the nutrition literature and don't get proper pharmaceutical treatment. This is a shame, and this makes some psychiatrists in this position skeptical about nutrition. Clearly, however, some patients with heart disease need surgery and sometimes need triple artery by-pass, and other patients with high blood pressure are clearly going to need hypertensive and anti-hypertensive medicine. All cardiologists today know and believe and preach the role of nutrition in preventing heart disease and high blood pressure. So, the two should not be seen as antagonistic. In psychiatry there is no question that the anti-psychotic drugs and the mood stabilizer drugs are effective. But I think perhaps we are a little behind cardiology and some of the papers show that folate supplementation can enhance the ability of lithium to prevent mood disorders and the ability of anti-psychotic drugs to reduce psychosis. These papers are not given as much publicity and as much acceptance as they really deserve. I don't know if it's because they do not have a pharmaceutical company pushing folate -- because it's too cheap -- or whether it's the skepticism that might be a result of excessive claims of the past. Or perhaps it is the skepticism that is coming as an antidote to the fact that some patients refuse pharmaceutical treatment, and only want natural treatment. Often those patients are too sick to be able to make a rational decision.
RC: Dr. Belmaker, do you feel the future of psychiatry is an intelligent integration of pharmaceuticals and nutrients? And, should nutrients be tried first?
RB: I think we have to answer that question empirically. There are going to have to be studies, like the ones we did with inositol. There is no way to know what comes first and what comes second. Certainly in most cases nutrients are milder. If a person finds changing his diet can prevent his headaches, we would like to see him do that before he tries a strong medicine like Valproate to prevent a headache. Ultimately, it has to be an empirical question. We have to do the studies.
RC: What got you interested in inositol?
RB: I had been interested previously in lithium and I am still interested in lithium. As you know, lithium is a very simple compound and a non-patented compound and a cheap compound. Those are some of the things that keep my interest. I have been interested in lithium for 30 years. Lithium has a major effect on inositol and the brain that was discovered by a wonderful man, name of Dr. Berridge from London, a Nobel prize candidate for that work. That work was done on flies, of the salivary gland of the fruit fly. For those people who sometimes make jokes about how animal research is not relevant, here is an example of how something that seems terribly funny, the salivary gland of the fruit fly, has become a major area of scientific research, with many important benefits for humanity. He discovered the whole cycle, the inositol cycle of the cell, and that lithium had an effect on it. So, as a lithium researcher, I read his papers and got interested in inositol. Professor Berridge was very interested in how inos itol can affect cell function. We were really the first to think that one could possibly give inositol as a nutrient in quantities that could get it to the brain.
RC: How does lithium affect inositol's function?
RB: It's a bit complicated, and there are still disagreements about it. Lithium inhibits a key enzyme called inositol mono-phosphatase. Some people say, as a result, inositol levels in some areas in the brain should go down. Other people believe because that enzyme is inhibited, the inositol phosphates actually go up, and we really don't know which of those two things are more important in lithium action.
RC: What is the difference between inositol and myo-inositol? Is there a difference? Is it just two terms for the same thing?
RB: For a biologist they are two terms for the same thing. The only inositol that exists naturally in the body of the human or any other mammal is called myo-inositol. For a chemist, inositol can exist in eight different forms that are mirror images of each other, although it might be hard to imagine how you can have eight different mirror images; but that's because there are eight different places on the inositol molecule that a carbon and a hydroxyl group can have a mirror image. But, only the myo-inositol is present naturally so when I talk about inositol as a medicine or a cell, I can just drop the myo and call it inositol, because that is the only one that we have.
RC: What happens when the human body is given inositol orally?
RB: It depends on the dose. The doses that we found are large enough to get inositol into the brain are the dose equivalent of 3 to 6 teaspoons a day. That's 12 to 18 grams. It could be teaspoons in tea or in juice. That's the quantities that we are talking about. In order for these doses to be effective, they need to be taken over a period of three to four weeks. We found those doses to be as beneficial as anti-depressants used in depression, panic disorders and in obsessive-compulsive disorders. We've done one study in normal volunteers, who were given a much larger dose at a single time in the morning in a large cup of juice. They were given 12 grams in one swallow and then every hour they were asked to fill out rating scales as to their tension, mood, feelings of relaxation, feeling of wellbeing, welfare, things that a normal person would write, called a profile of mood scale (the scale for normal mood), and we found that indeed, even a single dose peaking at about six hours reduced tension and increased feelings of well-being. In depressed patients we don't see those effects quite so early. Perhaps because the depression is strong enough to mask them, and in these patients, inositol did not work any faster than standard antidepressants. It only had a significant and beneficial effect after about three weeks.
RC: How does inositol work?
RB: That of course is a very good question. We have done quite a bit of animal work in rats to look at the mechanism and we think that the strongest findings relate to serotonin and particularly the 5HT2 serotonin receptor. In a rat if you drip serotonin on neurons with those receptors, and measure the response, after a while the nerve cell stops responding and if you add inositol it jumps up and starts responding again. So, it seems like cells can get depleted of inositol. Or, specific nerve cells might not have enough to be able to maintain neurotransmission in the serotonergic system. Of course, there are many things we have not investigated, but it could be that some patients have deficiencies in the brain of inositol to the point where their serotonin system cannot respond.
We did do a study with brains donated after death from patients with depression, manic-depression and other mental illnesses, and no illness. These were given to us by the Stanley Research Foundation in Washington DC, which was able to obtain these brains from people who consented before their death to donate their brains. They were diagnosed before their death as suffering from these diseases. We did find a group of patients especially with affective disorder with low, very low inositol levels in the brain.
RC: Is there a way for most people through their diet to get enough inositol? When you are talking about a therapeutic dose in the 12-18 gram range, I am wondering where someone may get a gram of inositol on a daily basis though food.
RB: The usual intake is about a gram a day through food. I think it would be really hard to get 12 grams a day through food, I think that is really a pharmacological dose. Of course, prevention of depression might require a lower dose, and we have been interested. I have a colleague now, a dietitian, whom I have asked to do some surveys of the diet of people who come complaining of depression, to see whether there are different amounts of inositol. We also have a study that will be published in May in the American Journal of Psychiatry on omega-3 fatty acids, another nutrient that we found to be anti-depressant in depressed patients, and on this we were not the first.
RC: Has there been an actual clinical trial of omega-3 fats in depression?
RB: Let me just say one thing about the omega-3s. There is one previous study by Andy Stull of Boston, a Clinical Trial with positive results. What I wanted to say is that the omega-3s also are given in much higher doses than are present in the usual diet, even though there have been reports of a correlation in the usual diet, such that the people who eat more omega-3s get depressed less. It might be with some of these nutrients you need more to correct real depression than you do to prevent it.
RC: Which will bring us back to a lesson taught to us by Abram Hoffer decades ago -- that is exactly the case. If you are missing a nutrient for decades you might need a lot more for the rest of your life to get back to normal. Regarding inositol and the diet, my understanding is that inositol in our food is largely in the form of inositol hexaphosphate, which is in a form of fiber that's hard to absorb. In other words, it might be in the food, but how well we absorb it, I think is perhaps open to question.
RB: I think you are asking a very good question, it's something I am just getting very interested in, and don't have the answer for you.
RC: Let's talk about inositol in some other applications, to say it's effective in depression at doses of 12-18 grams, but you've got to give it three weeks to really see the results?
RB: That's right.
RC: What about agoraphobia?
RB: We tend to call this panic disorder, with or without agoraphobia. Same doses seem to be effective, and also our statistical significant results occurred at three weeks. There was a strong trend before that, but our statistical significant results occurred at about three weeks.
RC: What about obsessive-compulsive disorder and inositol?
RB: In obsessive-compulsive disorder our studies use 18 grams. I can't say it doesn't work less than that, the way it works with depression with 12 grams, but we just haven't tried it. These people tend to be more ill -- and started with 18 grams. We've only seen statistically significant improvement by about six weeks, not before that. It does take longer, which is similar to drug treatment for obsessive-compulsive disorder.
RC: And only with inositol monotherapy, with no other nutrient or drug?
RB: That's right.
RC: Very impressive. Did you arrive at these doses by clinically examining the fact that the 3 and 6 grams doesn't work and then titrating upward to 18 grams?
RB: We arrived at the doses actually first with the pharmacokinetic studies. We tested to see what doses were necessary to get a good rise in inositol in human spinal fluid. Less than 12 grams a day didn't achieve much of a rise. At 12 grams a day, there is a 70% rise in human spinal fluid inositol levels. We have tried some patients in the early days more than now on lower doses, so we had some feeling of what the dose should be. I must say it has not been done in a systematic way because these kinds of controlled trials are expensive. We haven't had the funding that the pharmaceutical companies have. To really work up inositol in the way you are describing with very large trials in multiple doses -- is a one hundred million dollar project. No one would give us this to study a non-patentable compound. We had some grants from NIH and from the Stanley Foundation, but we have not done a good dose response study.
RC: What about SSRI medications and inositol, since they seem to be accentuating the same pathway. What if someone is taking a Zoloft or a Prozac and they ask their physician, "Can I take inositol at the same time?"
RB: We have studied that, and we have not had side effects with it. But, to our surprise and disappointment, we did not see synergism. We would have hoped for synergism, but it seems that inositol works and the SSRIs worked. If you put the two of them together it doesn't work any better than inositol alone or SSRIs alone. So that SSRIs in that sense are an alternative to inositol, or inositol is an alternative to SSRIs. We don't have reason to believe that it is a good addition to a SSRI non-responder, although we have not found it in any way unsafe if someone wants to try.
RC: What if someone wants to transition off of a SSRI? Would inositol be a logical stepping-stone to perhaps a more natural approach to accentuating serotonin metabolism?
RB: It is certainly an option, but we don't have data on that. We have data on people who have been treated in the past with SSRIs successfully and on their next depressive episode they were treated successfully with inositol. But we don't actually have people going from one to the other in the same depressive episode.
RC: Let's talk about inositol and safety. You've used doses of 18 grams in your trials and your practice. Any side effects from these doses?
RB: Well, people will have some loose stools and about the same with some of the SSRIs. I would say about quarter of the patients will move their bowels more frequently. We've had very few people who have to stop the medicine for that reason. We have not seen any significant changes. By now we've have a fairly large number of patients with hematological or chemical parameters. This is a large number of patients for a natural compound, but these are still fewer patients than would be expected, let's say for the FDA. If it were a new SSRI, they would want a considerably larger number of patients.
RC: Is there anyone who should not take inositol?
RB: I think it would make sense for someone who was diabetic to be careful. Someone with severe kidney disease or liver disease to be careful with inositol but I think this is a very general medical consideration.
RC: And that's because inositol has a molecular similarity to glucose and because of this theoretically could raise blood sugar in diabetics?
RB: That's right.
RC: Any other pearls here for nutritional pharmacology research? You spoke about folate and omega-3s, any other information you would like to share with our readers?
RB: Well, I think one of the most exciting things that we've been doing lately is with homocysteine. Homocysteine is the amino acid that's not used in protein synthesis and its been shown to be a risk factor for cardiovascular disease over the last few years. In more recent years it's been proven to be a risk factor for Alzheimer's and cerebral vascular disorders as well. We thought that this might mean that it's a risk factor for mental disorder and we have been surveying homocysteine levels in our patients and have found markedly elevated levels of homocysteine. We have begun a trial of folate, B12 and B6 in schizophrenic patients, because these are known to be homocysteine lowering vitamins that can lower homocysteine levels by up to 50% in combination. Homocysteine has been shown in a test tube to be neurotoxic, so we think we might be able to prevent the clinical deterioration and cognitive deterioration in schizophrenia with homocysteine lowering.
RC: Have you seen lowering homocysteine to be an effective strategy; perhaps in the treatment of depression?
RB: We have not looked at that.
RC: What happens when you give a patient a good-sized powder container of inositol and say "Take 6 teaspoons per day, please." Do they look at you and say "why is this doctor giving me a nutrient, and so much of it?"
RB: Well, I explain it. Most of the patients that consent to be on our program are people who are looking for this. That's how they get to us. So we find it very acceptable among patients, compliance is very high.
RC: Does it matter if inositol is taken with food or not?
RB: No it doesn't. It's absorbed very well. We recommend it be taken with some food
Metagenics Cenitol Powder with Inositiol
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