Low energy is probably the No. I complaint I hear from my patients. But in many cases, the underlying problem may be more serious than “just getting older.” It can actually reflect reduced energy in the cells, much like a battery wearing down and needing to be recharged. And the key to boosting cellular energy is to provide the cells with the fuel they need to function at peak performance, the enzyme adenosine triphosphate (ATP). How? With a simple five-carbon sugar found in every cell of the body called D-ribose, or simply “ribose,” the cellular battery recharger.
Ribose’s main function is to regulate the production of ATP– major source of energy for all your cells. This action makes it useful for all sorts of conditions, including heart disease, congestive heart failure, and fibromyalgia. It’s even good for supplying extra energy for workouts, and restoring energy after sustained exertion.
Ribose can be made naturally in the body, but it’s a slow process limited by several enzymes that are lacking in heart and muscle cells. There are no foods containing ribose in any substantial amounts. Still, under normal circumstances getting enough ribose isn’t a problem. But when the heart or our muscles are challenged from stress or lack of oxygen for any number of reasons, they need an extra ribose boost to restore ATP levels.
Two weeks of treatment erases debilitating pain and fatigue
Take fibromyalgia for example. It’s often difficult both to diagnose and to treat. Until now, there have been few tools to help these patients. However, we’ve found that ribose can provide significant improvement, as seen in the following case study published last year in the journal Pharmacotherapy.
At 37, Kris, a veterinary surgeon and researcher at a major university, became so debilitated from fibromyalgia she had to give up her practice.
But then she joined a clinical study on fibromyalgia and began taking 5 grams of ribose two times per day (10 grams per day) Within a week, she felt better. Within two weeks, she was back at work in the operating room.
Over the course of the following month, she continued to improve. After a month, however, Kris stopped her treatment. Ten days later, she was totally debilitated again and could no longer perform surgery. So she began ribose treatment for a second time, again with dramatically positive results, and has remained symptom-free as long as she takes the supplement regularly.
While there’s no official explanation as to why ribose is so effective for fibromyalgia, it could go back to its roots in ATP production. People with fibromyalgia have lower levels of ATP and a reduced capacity to make ATP in their muscles
There are other nutrients that, like ribose, are necessary for ATP production. One is malic acid, which also helps to combat fibromyalgia’s chronic muscle soreness. I have been recommending it along with magnesium to my fibromyalgia patients for years with relatively good success.
Ribose and the heart
Researchers have seen similarly remarkable results in people with heart problems. Heart disease, heart attack, heart surgery, and organ transplants can all lead to restricted blood flow, called ischemia in which your cells don’t get the oxygen they need to properly burn for energy
In addition, individuals who are on inotropic drugs to make the heart beat harder then have an additional strain on the heart’s energy production.
So it is especially important that patients with congestive heart failure, chronic coronary artery disease, or cardiomyopathy take extra ribose to offset their energy-draining effects.
Research shows that supplementation with ribose can offset this energy drain without interfering with the effects of any other medication the person might be taking.
D-Ribose in Fibromyalgia and Neuromuscular Disease
Fibromyalgia is a common, nonarticular, rheumatic syndrome that affects the upper and lower body, right and left sides. Concrete diagnosis of fibromyalgia is difficult since many other diseases and conditions present with similar symptoms and there are no laboratory tests that can be used as a primary diagnosis. As a result, accurate diagnosis must be made by excluding these other diseases or conditions. The American College of Rheumatology has defined the clinical diagnosis of fibromyalgia following two criteria:
1) widespread musculoskeletal pain in all four quadrants of the body for at least three months, and
2) tenderness at 11 or more of 18 specific tender points (or trigger points) located on the upper back and chest, insides of the elbows, lower back, upper thighs and front of knees.
Pathophysiology of Fibromyalgia
Patients suffering with fibromyalgia suffer from constant pain, sleep disturbances, overwhelming fatigue, weakness, muscle stiffness and soreness, headaches, irritable bowel, anxiety and depression. The condition is most commonly diagnosed in females, aged 20 to 50 years, and is generally treated by analgesic drugs and antidepressants.
The cause of fibromyalgia is unknown, but it has been associated with stress, tension, trauma, overexertion, hormone deficiency diseases (particularly thyroid disease), alterations in brain chemistry, anemia, parasites, and viral infections. Conditions that may be associated with, or mimic, fibromyalgia include chronic fatigue syndrome, myofascial pain syndrome, carpal tunnel syndrome, mitral valve prolapse, Raynaud’s syndrome and rheumatic disease.
While a great deal of popular press can be found discussing the disease, scientific research is, in large part, lacking. However, many conclusions can be drawn from the scientific press.
Controlled examination of the vastus lateralis muscle of the quadriceps group, trapezius and brachioradial muscle has shown that the blood flow to the tissue is lower in fibromyalgia patients than normal controls leading to low tissue oxygenation levels. Electron microscopic evaluation of the capillaries supplying the trapezius showed thickening and derangement of the capillary wall. Further, examination of muscle fibers revealed mitochondrial derangement in fibromyalgia patients. These small muscle fibers were not found in normal subjects. Reduced blood flow, changes in capillary wall thickness and structural changes to the mitochondria contribute to hypoxia, decreased oxidative phosphorylation, lower ATP synthesis and reduced levels of adenine nucleotides; in fibromyalgic muscle. Since it is postulated that the pain associated with fibromyalgia is of nociceptor origin , the primary hypothesis is that any condition that could lead to constant muscle hypoxia, and prolonged energy deficiency might be a cause of fibromyalgic pain.
The poor bioenergetic status of muscles in fibromyalgia may be due to reduced blood flow to affected tissue and thickening of capillary walls, leading directly to reduced levels of ATP, lower energy reserves and oxidative capacity (Vmax) and abnormal levels of phosphodiesters in the muscle. The additional complication of impaired oxidative phosphorylation in the mitochondria and diminished glucose metabolism, both lowering ATP turnover, suggests that fibromyalgic muscle is energy starved. Decreased levels of ATP and changes in energy metabolism have also been found in the red blood cells of fibromyalgia patients, suggesting that fibromyalgia may be a more general and systemic problem than originally thought, possibly impinging on other organ systems.
The metabolic abnormalities in fibromyalgic muscle have been well established and show multiple interactions that may impact on the clinical symptoms. Decreased numbers of capillaries that reduce oxidative capacity may increase pain, while thickened capillary walls lowering oxygen delivery and abnormal mitochondria lead to fatigue and weakness. All are associated with reduced levels of ATP and energy metabolism that, in turn, leads to disruptions in calcium stasis, muscle soreness and stiffness. At the same time, these metabolic changes force morphological changes in the muscle that continue to exacerbate the problem with metabolism.
Ribose in Maintaining Tissue Energy Stasis
Tissue hypoxia leads to a progressive depression of the cellular purine nucleotide pool creating an energy deficit. The adenine nucleotide ATP is the primary energy source of all living cells. In tissues suffering the metabolic stress of hypoxia or ischemia, ATP is broken down and the metabolic machinery to recycle expended energy is disrupted. As such, adenosine diphosphate (ADP) levels accumulate leading to a series of reactions undertaken by the cell to balance ATP/ADP ratios and maintain energy stasis. These reactions ultimately lead to increased concentrations of adenosine monophosphate (AMP) in the cell. In a further effort to control energy balance, heart cells catabolize AMP, in reactions catalyzed by 5′-nucleotidase and AMP deaminase, to form inosine, hypoxanthine and adenine. These catabolic end products are washed out of the cell netting a reduction in the total pool of adenine nucleotides available to the tissue and lowering its phosphorylation potential. Up to 90% of these catabolites can be biochemically salvaged and recycled.
The availability of phosphoribosyl-5-pyrophosphate (PRPP) is rate limiting in adenine nucleotide synthesis and salvage pathways required to restore nucleotide pools and rebuild cellular energy stores. PRPP is formed through a pyrophosphorylation reaction from ribose-5-phosphate that is, in turn, synthesized from glucose via the Pentose Phosphate Pathway (PPP; or Hexose Monophosphate Shunt). The activity of the PPP varies between organs, with those synthesizing fatty acids and sterols being most active. The rate limiting enzymes in the PPP, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, have limited expression in muscle. As such, energy production in muscle via this mechanism is delayed and cannot be relied upon to replenish depressed adenine nucleotide pools during or following a metabolic insult, such as prolonged periods of hypoxia.
The rate of recovery of depressed energy levels following ischemia and/or hypoxia is important for functional recovery of muscle providing adequate levels of AMP and ADP necessary for complete repletion of ATP. Blocking the degradation of adenine nucleotides, or by providing metabolic supplementation to enhance nucleotide recovery via the salvage or de novo pathways are potential solutions to maintaining energy stasis. Exogenous ribose administration provides the metabolic support required to bypass the rate limiting enzymes of the PPP, form PRPP and restore energy stasis in metabolically stressed muscle.
Ribose has been extensively studied in both hearts and muscles. Safety data is well accepted, with no noted significant adverse reactions. Experiments on the use of ribose to enhance myocardial and skeletal muscle adenine nucleotide synthesis and salvage have involved both animal and human investigations and the effects of ribose in hearts are not species specific. The low activity of glucose-6-phosphate dehydrogenase is in the same order of magnitude in human, rat, guinea pig and dog hearts.
The effect of ribose treatment in myoadenylate deaminase deficiency (AMP deaminase deficiency) and adenylosuccinase deficiency has been well documented. Like fibromyalgia, these conditions lead to progressive depletion of cellular energy pools, leading to muscle pain, soreness and stiffness. The beneficial role in energy recovery in these disease conditions with ribose treatment is suggestive of its potential role in energy recovery in fibromyalgia. As in the case of myoadenylate deaminase deficiency, anecdotal reports from fibromyalgia patients indicate a reduction in fatigue, muscle soreness and stiffness associated with the condition. While further research continues, it is apparent that ribose can play a beneficial role as an adjunctive, metabolic treatment for fibromyalgia.
A simple 5-carbon sugar, carbohydrate (pentose)
* found in most foods & in each cell of body
* early 1990’s began use for heart problems
* mildly sweet & easily dissolves in water
* easily absorbed from GI tract & get high blood levels
Main Biological Function: rebuilds the ATP energy pool
* only compound in body that rebuilds-recharges ATP energy stores
* raises hypoxic thresholds & improves athletic performance
* builds lean mm mass
* reduces cramps & soreness
* reduces exercise-induces joint swelling
* after short-burst exercise, ribose helps to restore energy levels in 12 to 36 hours compared with the body’s natural rate of 7 to 10 days.
* synergestic effect with Creatine & CoEnzyme Q
* enhances immune function
* helps to produce DNA & RNA
* coronary artery disease, angina, congestive heart failure, arrhythmias, peripheral vascular disease & general ischemias
* Chronic Fatigue Syndrome
* and other myopathies
Side Effects: > 60gm per day with no reported problems; when reported — mild loose stool & light headedness (hypoglycemia??)