Saturday, September 8, 2012

VITAMIN C AND CARDIOVASCULAR DISEASE


VITAMIN C AND CARDIOVASCULAR DISEASEA Personal Viewpoint by Alan Spencer and Andrew W. Saul

(OMNS, June 22, 2010) Linus Pauling was aware that studies of the animal kingdom showed that most animals have the ability to manufacture vitamin C in their bodies. Humans cannot. Furthermore, on average, mammals make 5,400mg daily when adjusted for body weight, and make more (often considerably more) when under stress or ill. This is about 100 times as much as the 50mg we get from a typical modern diet. It prompts the question, why do animals make so much vitamin C, and what purpose does it serve in the body.
A small number of animals which are known to share our inability to make vitamin C include the apes, the guinea pig, the fruit bat, and some birds, all of which will normally get a lot of vitamin C from their food. If you deprive a guinea pig of vitamin C it soon develops a form of cardiovascular disease (damage to its arteries showing within a few weeks). Similarly, studies of genetically modified mice have shown that if you switch off the gene that enables a mouse to produce vitamin C it will also soon show signs of heart disease. Re-introduction of a high vitamin C diet enables the damage to be reversed. While heart disease is rare in the animal kingdom, it is becoming a problem for apes in zoos where their diets are perhaps not as rich in vitamin C as when they are in the wild.
Collagen
A very important function of vitamin C in the body is its role in the production of collagen. Collagen is the most abundant protein in the body, and forms into fibres which are stronger than iron wire of comparable size. These fibres provide strength and stability to all body tissues, including the arteries. Vitamin C is absolutely essential for the production and repair of collagen, and is destroyed during the process, so a regular supply of vitamin C is necessary to maintain the strength of body tissues. Severe deficiency of vitamin C causes the total breakdown of body tissue witnessed in scurvy. Linus Pauling believed that whilst humans normally obtain sufficient vitamin C to prevent full-blown scurvy, we do not consume enough to maintain the strength of the walls of the arteries. He suggested that of all the structural tissues in the body, the walls of the arteries around the heart are subject to the greatest continual stress. Every time the heart beats the arteries are flattened and stretched, and this has been likened to standing on a garden hose thousands of times a day. Many tiny cracks and lesions develop and the artery walls become inflamed.
Dr. Pauling believed that in the presence of adequate supplies of vitamin C this damage can be readily repaired and heart disease is avoided. However, in the absence of adequate levels of vitamin C, the body attempts to repair the arteries using alternative materials: cholesterol and other fatty substances, which attach to the artery wall. (1-8)
Cholesterol and Lipoprotein (a), Lp(a)
The most abundant amino acids (protein building blocks) in collagen are lysine and proline, and when collagen strands are damaged lysine and proline become exposed. A special kind of cholesterol, lipoprotein(a), is attracted to lysine and proline and will attach itself to the exposed damaged collagen strands. It is an attempt by the body to repair damage to the collagen of the artery walls in the absence of adequate levels of vitamin C. Unfortunately the repair is not ideal and over many years repeated deposits can cause the artery to become narrow and inflamed. Heart attack or stroke is likely to follow (usually caused by a clot forming at the site of the narrowed artery, or by a piece of plaque breaking off and blocking a smaller vessel downstream). When vitamin C levels are low, the body manufactures more cholesterol, especially Lp(a). Conversely, when vitamin C levels are high the body makes less cholesterol.
If high blood cholesterol were the primary cause of heart disease, all bears and other hibernating animals would have become extinct long ago. They naturally have high cholesterol levels. One reason bears are still with us is simple: they produce large amounts of vitamin C in their bodies, which stabilises the artery walls, and there is therefore no tendency to develop cholesterol deposits or plaque.
Keeping healthy
The low levels of vitamin C that are available through diet are inadequate to prevent many people developing arterial plaques, and over time this may result in cardiovascular disease. Post mortem examinations showed that 77% of young American soldiers killed in the Korean war (average age 22) already had well-advanced atherosclerosis (heart disease), and post mortem studies from the Vietnam war gave similar results. Heart disease is not just a disease of the elderly, although it does not usually become life threatening until later in life.
How can we prevent it? Pauling believed that once we start taking high levels of vitamin C, the disease process is halted, or at least slowed, as Lp(a) cholesterol is no longer needed as a repair material. He also believed that when we take adequate levels of vitamin C, existing arterial plaques may start to be removed from the arteries. He found that the removal of plaques is more rapid if the amino acid lysine is taken along with vitamin C. Lysine appears to attach to the Lp(a) in existing plaque deposits and helps to loosen them. Linus Pauling recommended at least 3000mg of vitamin C per day as a preventive dose, and significantly higher levels of both vitamin C and lysine for the treatment of existing heart disease. Dosage is a key factor: low doses are ineffective.
Retention in the body
Another important point is that a single dose of vitamin C is not retained in the body for very long. This fact has been used for a long time by those who do not support the use of high doses of vitamin C as evidence that the body does not need and cannot use large doses. After a single large dose of vitamin C, the blood level quite soon returns to a low level. A lot is excreted, the high blood level only remaining for a few hours.
The key factor here is that the body is not designed to function with just a single large dose of vitamin C once a day. Animals are able to manufacture vitamin C in their bodies and do so continuously throughout the day. They have an enzyme which converts glucose to vitamin C, and each day they produce on the order of a hundred times more vitamin C than we are able to get from even a good diet. When animals are ill they manufacture even more, perhaps thousands of times more than we can get from our diet.
How much should we take?
For people who are essentially fit and well, the Vitamin C Foundation recommends perhaps 3,000mg of vitamin C per day, taken in divided doses as 500mg every four hours, as a protection against the development of heart disease. The problem with even this protective dose is that taking a tablet every four hours is not something that many people would want to adopt as part of their daily routine. But there is good evidence to suggest that this level of intake will help maintain the strength of the arteries and prevent the build up of cholesterol plaques. If everybody were to do this, perhaps heart disease would become a largely a thing of the past (as might many other chronic diseases).
When treating illness, "bowel tolerance" is the indicator of dosage level that should be used. This means taking just under the level of vitamin C (in divided doses) that results in loose stools. Everyone is different. Note that while a few 1,000mg doses a day might make you loose when you are fit and well, your "bowel tolerance" might increase to ten or even a hundred times this when very ill. So, for illness, the levels suggested by the Vitamin C Foundation are 6,000mg to 18,000mg of vitamin C per day (or up to bowel tolerance) plus 2,000mg to 6,000mg of lysine. These vitamin C levels may seem high, but are perhaps not particularly large when compared with levels seen in the animal kingdom. A substantial amount of lysine may be obtained from diet. For example, one may obtain 3,000 to 4,000 milligrams of lysine from about can and a half of beans. Supplementation reduces the need to consume that much.
Controversy
"Even though some physicians had observed forty or fifty years ago that amounts of vitamin C a hundred to a thousand times larger (than the RDA) have value in controlling various diseases, the medical profession and most scientists ignored this evidence." (Linus Pauling, How to Live Longer and Feel Better)
In medical circles, Pauling's recommendations remain controversial. However, his theory seems reasonable, and the implications are so significant that some major scientific trials should have been undertaken to assess it. This has not happened. Supporters of high-dose vitamin C have had their applications for research funding denied repeatedly, and have had to be content with carrying out small scale research projects and case studies. These have been very positive. Over the past fifteen years, Pauling therapy advocates have received hundreds of reports from heart patients who have self administered the therapy. It is reported that these people typically recover within 30 days, and the majority experience significant relief within as little as a week or two. In 1994, Linus Pauling wrote, "I think we can get almost complete control of cardiovascular disease, heart attacks and strokes by the proper use of vitamin C and lysine. It can prevent cardiovascular disease and even cure it. If you are at risk of heart disease, or if there is a history of heart disease in your family, if your father or other members of the family died of a heart attack or stroke or whatever, or if you have a mild heart attack yourself, then you had better be taking vitamin C and lysine."

References:
 (1) Rath M, Pauling L. Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. Proc Natl Acad Sci U S A. 1990 Dec;87(23):9388-90. PMID: 2147514. Free full text download: http://www.pnas.org/content/87/23/9388.full.pdf
(2) Rath M, Pauling L. Hypothesis: lipoprotein(a) is a surrogate for ascorbate. Proc Natl Acad Sci U S A. 1990 Aug;87(16):6204-7. [Erratum in: Proc Natl Acad Sci U S A 1991 Dec 5;88(24):11588.] PMID: 2143582. Free full text download: http://www.pnas.org/content/87/16/6204.full.pdf
(3) Rath M, Pauling L. Solution To the Puzzle of Human Cardiovascular Disease: Its Primary Cause Is Ascorbate Deficiency Leading to the Deposition of Lipoprotein(a) and Fibrinogen/Fibrin in the Vascular Wall. J Orthomolecular Med, Vol 6, 3&4th Quarters, 1991, p 125. Free full text download:http://orthomolecular.org/library/jom/1991/pdf/1991-v06n03&04-p125.pdf
(4) Pauling L, Rath M. An Orthomolecular Theory of Human Health and Disease. J Orthomolecular Med, Vol 6, 3&4th Quarters, 1991, p 135. Free full text download:http://orthomolecular.org/library/jom/1991/pdf/1991-v06n03&04-p135.pdf
(5) Rath M, Pauling L. Apoprotein(a) Is An Adhesive Protein. J Orthomolecular Med, Vol 6, 3&4th Quarters, 1991, p 139. Free full text download: http://orthomolecular.org/library/jom/1991/pdf/1991-v06n03&04-p139.pdf
(6) Rath M, Pauling L. Case Report: Lysine/Ascorbate Related Amelioration of Angina Pectoris. J Orthomolecular Med, Vol 6, 3&4th Quarters, 1991, p 144. Free full text download:http://orthomolecular.org/library/jom/1991/pdf/1991-v06n03&04-p144.pdf
(7) Rath M, Pauling L. A Unified theory of Human Cardiovascular Disease Leading the Way To the Abolition of This Diseases As A Cause for Human Mortality. J Orthomolecular Med, Vol 7, First Quarter 1992, p 5. Free full text download: http://orthomolecular.org/library/jom/1992/pdf/1992-v07n01-p005.pdf
(8) Rath M, Pauling L. Plasmin-induced Proteolysis and the Role of Apoprotein(a), Lysine and Synthetic Lysine Analogs. J Orthomolecular Med, Vol 7, First Quarter 1992, p 17. Free full text download:http://orthomolecular.org/library/jom/1992/pdf/1992-v07n01-p017.pdf
For More Information:
Fonorow O. Practicing Medicine Without a License? The Story of the Linus Pauling Therapy for Heart Disease. 2008. Lulu.com. ISBN-10: 1435712935; ISBN-13: 978-1435712935. Reviewed in J Orthomolecular Med, 2009. Vol 24, No 1, p 51-5.
Hickey S and Roberts H. Ascorbate: The Science of Vitamin C. 2004. ISBN-10: 1411607244; ISBN-13: 978-1411607248. Lulu.com. This book contains 575 references, and is reviewed athttp://www.doctoryourself.com/ascorbate.html
Hickey S, Saul AW. Vitamin C: The Real Story. Laguna Beach, CA: Basic Health Publications, 2008. ISBN: 978-1-59120-223-3. This book contains 387 references, and is reviewed athttp://www.doctoryourself.com/realstory.html
Levy TE. Stop America's #1 Killer: Reversible vitamin deficiency found to be the origin of all coronary heart disease. 2006. ISBN-10: 0977952002; ISBN-13: 978-0977952007. (Dr. Levy is a board-certified cardiologist.) Reviewed in J Orthomolecular Med, 2006. Vol 21, No 3, p 177-178. This book contains 60 pages of references. To download the review: http://orthomolecular.org/library/jom/2006/pdf/2006-v21n03-p175.pdf
Pauling L. How to Live Longer and Feel Better (Revised edition). Oregon State University Press, 2006. ISBN-10: 0870710966; ISBN-13: 978-0870710964. Reviewed in J Orthomolecular Med, 2006. Vol 21, No 3, p 175-177. To download the review: http://orthomolecular.org/library/jom/2006/pdf/2006-v21n03-p175.pdf
On the Web:
The Vitamin C Foundation http://www.vitamincfoundation.org
AscorbateWeb, a historical compendium of 20th-Century medical and scientific literature demonstrating the efficacy of vitamin C. http://www.seanet.com/~alexs/ascorbate/
Putting the "C" in Cure: Quantity and frequency are the keys to ascorbate therapy.http://orthomolecular.org/resources/omns/v05n11.shtml
RDA for Vitamin C is 10% of USDA Standard for Guinea Pigs.http://orthomolecular.org/resources/omns/v06n08.shtml

Nutritional Medicine is Orthomolecular Medicine
Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information:http://www.orthomolecular.org
The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.

Editorial Review Board:
Ralph K. Campbell, M.D. (USA)
Carolyn Dean, M.D., N.D. (Canada)
Damien Downing, M.D. (United Kingdom)
Michael Ellis, M.D. (Australia)
Michael Gonzalez, D.Sc., Ph.D. (Puerto Rico)
Steve Hickey, Ph.D. (United Kingdom)
James A. Jackson, Ph.D. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Thomas Levy, M.D., J.D. (USA)
Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)
Erik Paterson, M.D. (Canada)
Gert E. Shuitemaker, Ph.D. (Netherlands)
Andrew W. Saul, Ph.D. (USA), Editor and contact person. Email: omns@orthomolecular.org

Lemon, raw, without peel : nutrition Facts

Lemon, raw, without peel
Nutritional value per 100 g (3.5 oz)
Energy121 kJ (29 kcal)
Carbohydrates9.32 g
Sugars2.50 g
Dietary fiber2.8 g
Fat0.30 g
Protein1.10 g
Thiamine (vit. B1)0.040 mg (3%)
Riboflavin (vit. B2)0.020 mg (2%)
Niacin (vit. B3)0.100 mg (1%)
Pantothenic acid (B5)0.190 mg (4%)
Vitamin B60.080 mg (6%)
Folate (vit. B9)11 μg (3%)
Vitamin C53.0 mg (64%)
Calcium26 mg (3%)
Iron0.60 mg (5%)
Magnesium8 mg (2%)
Phosphorus16 mg (2%)
Potassium138 mg (3%)
Zinc0.06 mg (1%)
Percentages are relative to
US recommendations for adults.
Source: USDA Nutrient Database

A bee on a Meyer lemon flower

Tuesday, May 8, 2012

Janda Syndromes

Janda Syndromes

Janda’s Crossed Syndromes
Over time, these imbalances will spread throughout the muscular system in a predictable manner. Janda has classified these patterns as “Upper Crossed Syndrome” (UCS), “Lower Crossed Syndrome” (LCS), and “Layer Syndrome” (LS) (Janda, 1987, 1988). [UCS is also known as “cervical crossed syndrome”; LCS is also known as “pelvic crossed syndrome; and LS is also known as “stratification syndrome.”] Crossed syndromes are characterized by alternating sides of inhibition and facilitation in the upper quarter and lower quarter. Layer syndrome, essentially a combination of UCS and LCS is characterized by alternating patterns of tightness and weakness, indicating long-standing muscle imbalance pathology. Janda’s syndromes are summarized in Figure 1.
Janda's Crossed Syndromes
Upper crossed syndrome is characterized by facilitation of the upper trapezius, levator, sternocleidomastoid, and pectoralis muscles, as well as inhibition of the deep cervical flexors, lower trapezius, and serratus anterior. Lower crossed syndrome is characterized by facilitation of the thoraco-lumbar extensors, rectus femoris, and iliopsoas, as well as inhibition of the abdominals (particularly transversus abdominus) and the gluteal muscles.
By using Janda’s classification, clinicians can begin to predict patterns of tightness and weakness in the sensorimotor system’s attempt to reach homeostasis. Janda noted that these changes in muscular tone create a muscle imbalance, which leads to movement dysfunction. Muscles prone to tightness generally have a “lowered irritability threshold” and are readily activated with any movement, thus creating abnormal movement patterns. These imbalances and movement dysfunctions may have direct effect on joint surfaces, thus potentially leading to joint degeneration. In some cases, joint degeneration may be a direct source of pain, but the actual cause of pain is often secondary to muscle imbalance. Therefore, clinicians should find and treat the cause of the pain rather than focus on the source of the pain.


Janda Evaluation

Systematic evaluation of muscular imbalance begins with static postural assessment, observing muscles for characteristic signs of hypertonicity or hypotonicity. This is followed by observation of single leg stance and gait. Static posture, gait and balance often give the best indication of the status of the sensorimotor system. Computerized force plate posturography is often valuable in quantifying sensory and motor deficits. Next, characteristic movement patterns are assessed, and specific muscles are tested for tightness or shortness. Surface electromyography is useful in quantifying muscle activation patterns. All the above information collected provides the clinician a system to determine or rule out the presence of muscle imbalance syndromes. Furthermore, identification of specific patterns and syndromes of imbalance also provides the clinician to choose appropriate interventions to address the cause of the dysfunction.

Janda Treatment

Janda’s Approach to Treatment
1. Normalize the periphery. The Janda approach to treatment of musculoskeletal pain follows several steps. Treatment of muscle imbalance and movement impairment begins with normalizing afferent information entering the sensorimotor system. This includes providing an optimal environment for healing (by reducing effusion and protection of healing tissues, restoring proper postural alignment (through postural and ergonomic education), and correcting the biomechanics of a peripheral joint (through manual therapy techniques).
2. Restore Muscle Balance. Once peripheral structures are normalized, muscle balance is restored. Normal muscle tone surrounding joints must be restored. Sherrington’s law of reciprocal inhibition (Sherrington, 1907) states that a hypertonic antagonist muscle may be reflexively inhibiting their agonist. Therefore, in the presence of tight and/or short antagonistic muscles, restoring normal muscle tone and/or length must first be addressed before attempting to strengthen a weakened or inhibited muscle. Techniques to decrease tone must be specific to the cause of the hypertonicity. These include post-isometric relaxation (PIR) (Lewit, 1994) and post-facilitation stretch (PFS) (Janda, 1988).
Muscles that have been reflexively inhibited by tight antagonists often recover spontaneously after addressing the tightness. In the Janda approach, the coordinated firing patterns of muscle are more important than the absolute strength of muscles. The strongest muscle is not functional if it cannot contract quickly and in coordination with other muscles; therefore, isolated muscle strengthening is not emphasized in the Janda approach. Instead, muscles are facilitated to contract at the proper time during coordinated movement patterns to provide reflexive joint stabilization.
3. Increase afferent input to facilitate reflexive stabilization. Once muscle balance has been addressed, Janda stresses increasing proprioceptive input into the CNS with a specific exercise program, “Sensorimotor Training” (SMT) (Janda & Vavrova, 1996). This program increases afferent information entering the subcortical pathways (including spinocerebellar, spinothalamic, and vestibulocerebellar pathways) to facilitate automatic coordinated movements. SMT involves progressive stimulation through specific exercises with increasing level of challenge to the sensorimotor system. SMT has been proven to improve proprioception, strength, and postural stability in ankle instability (Freeman et al. 1965), knee instability (Ihara & Nakayam, 1996), and after ACL reconstruction (Pavlu & Novosadova, 2001).
4. Increase endurance in coordinated movement patterns. Finally, endurance is increased through repetitive, coordinated movement patterns. Since fatigue is a predisposing factor to compensated movement patterns, endurance is also more important than absolute strength. Exercises are performed at low intensities and high volumes to simulate activities of daily living.
The Janda approach is valuable in today’s managed care environment. Once these patterns and syndromes are identified, specific treatment can be implemented without expensive equipment. Early detection of these causes of chronic pain allows the clinician to treat the patient with fewer visits and less expensive equipment compared to traditional interventions that emphasize modalities and passive treatments. The key to the Janda approach is in the home exercise program. Inexpensive home exercise equipment such as wobble boards, elastic bands, and foam pads are used with a specific progression of exercises as the patient improves in function.
Summary
In summary, the Janda approach emphasizes the importance of the CNS in the sensorimotor system, and its role in the pathogenesis in musculoskeletal pain. In particular: the neurological pre-disposition of muscles to exhibit predictable changes in tone, and the importance of proprioception and afferent information in the regulation of muscle tone and movement. Therefore, assessment and treatment focus on the sensorimotor system, rather than the musculoskeletal system itself. Using a functional, rather than a structural approach, the cause of musculoskeletal pain can be quickly identified and addressed. The Janda approach can be a valuable tool for the clinician in the evaluation and treatment of chronic musculoskeletal pain.

Janda Philosophy

Janda Philosophy

Janda’s approach to the evaluation and management of chronic musculoskeletal pain focuses on the importance of the central nervous system in mediating chronic pain through neuromuscular imbalance.
Structure vs. Function

In musculoskeletal medicine, there are two main schools of thought, that is, a structural or functional approach. In the structural approach, the pathology of specific static structures is emphasized; this is the typical orthopaedic approach that emphasizes diagnosis based on localized evaluation and special tests (X-Ray, MRI, CT Scan, etc). On the other hand, the functional approach recognizes the function of all processes and systems within the body, rather than focusing on a single site of pathology. While the structural approach is necessary and valuable for acute injury or exacerbation, the functional approach is preferable when addressing chronic musculoskeletal pain.
The Sensorimotor System
In chronic pain, special diagnostic tests of localized areas (for example, low back radiographs) are often normal, although the patient complains of pain. The site of pain is often not the cause of the pain. Recent evidence by supports the fact that chronic pain is centrally-mediated (Staud et al. 2001). Similarly, research on the efficacy of different modes of exercise management of chronic pain has shown a central effect of exercise in decreasing chronic low back pain (Mannion et al. 1999). This research supports the basis of Janda’s approach: the interdependence of the musculoskeletal and central nervous system. Janda states that these two anatomical systems cannot be separated functionally. Therefore, the term “sensorimotor” system is used to define the functional system of human movement. In addition, changes within one part of the system will be reflected by compensations or adaptations elsewhere within the system because of the body’s attempt at homeostasis (Panjabi, 1992).
The muscular system often reflects the status of the sensorimotor system, as it receives information from both the musculoskeletal and central nervous systems. Changes in tone within the muscle are the first responses to nociception by the sensorimotor system. This has been supported by various studies demonstrating the effect of joint pathology on muscle tone. For example, the presence of knee effusion causes reflex inhibition of the vastus medialis (Stokes & Young, 1984). The multifidus has been shown to atrophy in patients with chronic low back pain (Hides et al. 1994), and muscles demonstrate increased latency after ankle sprains (Konradsen & Raven, 1990) and ACL tears (Ihara & Nakayama, 1986). The global effect of joint pathology on the sensorimotor system was demonstrated by Bullock-Saxton (1994). She noted a delay in firing patterns of the hip muscles and decreased vibratory sensation in patients with ankle sprains.
Because of the involvement of the CNS in muscle imbalance and pain, Janda emphasizes the importance of the afferent proprioceptive system. A reflex loop from the joint capsular mechanoreceptors and the muscles surrounding the joint is responsible for reflexive joint stabilization (Guanche et al. 1995; Tsuda et al. 2001). In chronic instability, deafferentation (the loss of proper afferent information from a joint) is often responsible for poor joint stabilization (Freeman et al. 1965).
Tonic and Phasic Muscle Systems
Janda identified two groups of muscles based on their phylogenetic development (Janda, 1987). Functionally, muscles can be classified as “tonic” or “phasic”. The tonic system consists of the “flexors”, and is phylogenetically older and dominant. These muscles are involved in repetitive or rhythmic activity (Umphred, 2001), and are activated in flexor synergies. The phasic system consists of the “extensors”, and emerges shortly after birth. These muscles work eccentrically against the force of gravity and emerge in extensor synergies (Umphred, 2001).
Janda noted that the tonic system muscles are prone to tightness or shortness, and the phasic system muscles are prone to weakness or inhibition (Table 1). Based on his clinical observations of orthopedic and neurological patients, Janda found that this response is based on the neurological response of nociception in the muscular system. For example, following structural lesions in the central nervous systems (such cerebral palsy or cerebrovascular accident), the tonic flexor muscles tend to be spastic and the phasic extensor muscles tend to be flaccid. Therefore, patterns of muscle imbalance may be due to CNS influence, rather than structural changes within the muscle itself.
It’s important to note that this classification is not rigid, in that some muscles may exhibit both tonic and phasic characteristics. It should also be noted that in addition to neurological predisposition to tightness or weakness, structural changes within the muscle also contribute to muscle imbalance. However, in chronic pain that is centralized within the CNS, patterns of muscle imbalance are often a result of neurological influence rather than structural changes.
Tonic Muscles
Prone to Tightness or Shortness
Phasic MusclesProne to Weakness or Inhibition
Gastroc-SoleusTibialis Posterior Hip Adductors
Hamstrings
Rectus Femoris
Iliopsoas
Tensor Fascia Lata
Piriformis
Thoraco-lumbar extensors
Quadratus Lumborum
Pectoralis Major
Upper Trapezius
Levator Scapulae
Scalenes
Sternocleidomastoid
Upper limb flexors
Peroneus Longus, BrevisTibialis Anterior Vastus Medialis, Lateralis
Gluteus Maximus, Medius, Minimus
Rectus Abdominus
Serratus Anterior
Rhomboids
Lower Trapezius
Deep neck flexors
Upper limb extensors
Table 1: Tonic & Phasic Muscles

About Dr. Janda

About Dr. Janda

Dr. Vladimir JandaExcerpted from Assessment and Treatment of Muscle Imbalance: The Janda Approach
Vladimir Janda was born in 1928. At the age of 15, he contracted polio. He was paralyzed as a quadriplegic and unable to walk for 2 years. He eventually recovered walking function, but developed post-polio syndrome and was forced to use a walker until the end of his life in 2002.
As a physician, he focused on post-polio patients early on. One of his early influences was Sister Kinney in 1947, who introduced the treatment of polio in Czechoslovakia. He served as an interpreter for Sister Kinney as a first year medical student, and decided to pursue an interest in physiotherapy after medical school. He received the “Kinney Physiotherapist” certificate after graduation from medical school. He was one of the first physicians to combine therapy and medicine in a ‘hands-on’ approach, becoming one of the earliest to practice physical medicine and rehabilitation.
He became more interested in pain syndromes of the locomotor system. His first book in 1949 at the age of 21 was on muscle testing and function, which was the first of its kind in Czech. He continued as a prolific researcher and writer; before his death, he published over 16 books and over 200 papers on muscle function.
At the age of 24, he was working in a rehabilitation center for post-polio patients. He was interested in evaluating the claims from muscle testing textbooks at the time. Using EMG, he began studying the muscle activity of the hip joint in physiotherapist students. He found muscles that weren’t supposed to be activated actually were, noting the accessory role of muscles outside of their primary movements. Specifically, he found subjects without activity in the gluteus maximus during hip extension movements used an increased pelvic tilt to accomplish the extension. This led to his lifelong passion to study movements, rather than individual muscles as was common at the time of the polio era. He recognized the importance of testing muscle function rather than strength. This was the beginning of thinking globally rather than locally in terms of muscle function.
In the 1960s, Freeman and Wyke published several papers on the importance of afferent input and mechanoreceptors. They described the use of wobble boards in the treatment of chronic ankle instability. Janda noted a connection between chronic ankle instability and chronic low back pain: proprioception. This led to Janda’s development of “Sensorimotor Training”, a progressive exercise program using simple exercises and unstable surfaces. He rarely recommended strengthening exercises, instead focusing on balance and function. This was in contrast to the traditional rehabilitation approach in the 60’s and 70’s emphasizing strength training.
Janda completed his thesis in 1964 on patients with sacroiliac dysfunction, finding weakness and inhibition of the gluteus maximus, even in the absence of pain. He recognized that certain other muscles were prone to weakness. Janda subsequently defined movement patterns to estimate the quality of movement. He discovered that muscle imbalance was systematic, predictable, and involved the entire body.
In 1979, he defined his “crossed syndromes”: Upper crossed, lower crossed, and layer syndrome. He subsequently noted that his crossed syndromes were his only ‘discovery’; he always gave credit to others influencing his approach. Janda had a wide range of influences that provided him a comprehensive viewpoint:
  • Berta Botath, a physiotherapist and her husband Karel Bobath, a neurophysiologist from London, who were leaders in neurodevelopmental principles and treatment in physiotherapy
  • Austrian physician Hans Kraus, who first described “hypokinetic disease” in low back pain before the second world war, which as noted as a “lack of movement.”
  • His colleague and lifelong friend, Karel Lewit MD, who practiced with Janda in Prague for many years and shared his expertise on manual therapy and the locomotor system.
  • Vaclav Vojta MD, a Czech physician who described the influence of developmental kinesiology in human movement and pathology.
  • Alois Brugger MD, A Swiss neurologist who described the neurologic basis muscle imbalance.
  • Florence Kendall PT, who first influenced Janda on the concept of muscle imbalances.
  • John Basmajian MD, a Canadian expert in EMG analysis who lead Janda’s postdoctoral studies
  • David Simons MD, an expert in trigger points and muscle pain
Janda was an avid reader and collector of books and papers on muscles. His ability to fluently speak as many as 5 different languages gave him the ability to read and learn more from all over the world.  His international influence continued to spread as a consultant to the World Health Organization in the 1960s and 70s.
Janda founded the Department of Rehabilitation Medicine and directed the physiotherapy school at the Charles University Third School of Medicine, where he continued to practice until his death on November 25, 2002.  The authors of this text had the opportunity to be with him three months prior on his last visit to North America. The “Father of Czech Rehabilitation” will continue to be missed by many. For an excellent review of Janda’s life and contributions, read the paper by Morris and colleagues, Vladimir Janda, MD, DSc: tribute to a master of rehabilitation. (Spine. 2006 Apr 20;31(9):1060-4.)

Know your food!

Know your food!

Food Groups: Base of the food balance

You are what you eat. Everything that you eat and drink has an effect on your body. Nutrition is the basic prerequisite to sustain a healthy life. All the food that we eat provides us with a range of nutrients, each with its own role to play. Eating a balanced, varied diet everyday ensures that you have everything you need for a good health. Our diet must provide all the essential nutrients in the right amounts. To perform various functions normally you need a complete range of nutrients from various food groups. Broadly there are 7 food groups which have been grouped together as they share similar nutritional properties. These food groups are:

  1. Cereals:Cereals form the staple diet in India, e.g., rice, wheat, maize. Cereals are the main source of energy, contributing 60-70% of daily energy needs. Cereals are a source of protein, calcium, iron and B-complex vitamins. Whole-grains (grains with the intact outer layer like in brown rice, corn) are a good source of fibre and B-complex vitamins and should be included in daily diet.
  2. Pulses (legumes):Pulses are a rich source of proteins (up to 22%) and meet the protein requirement of the vegetarians. They are also rich in B complex vitamins. Germination (sprouting) of pulses increases the vitamin C and B group vitamins and also improves the digestibility.
  3. Milk and Milk Products:
    This category includes liquid and powdered milk, paneer, curd, buttermilk etc. They are not only a good source of quality protein but also calcium and riboflavin. These should be a part of everyday’s diet and especially essential for children as they support healthy growth.
  4. Fruits and Vegetables: these include
    1. Roots and Tubers: these are rich in carbohydrates and are good sources of energy and calcium. Root vegetables like carrots are a good source of vitamin A.
    2. Vegetables and Green Leafy Vegetables (GLV’s): vegetables add both color and variety to the diet. They provide minerals, vitamins and fiber (which add bulk to the diet). GLV’s are a rich source of calcium iron, vitamin A (β-carotene), vitamin C, folic acid.
    3. Fruits: these provide vitamins and fiber. Green, Yellow and Orange fruits are a rich source of beta carotene. Citrus fruits, amla, and guava are rich in vitamin C. dried fruits like dates supply iron. Seasonal fruits should be encouraged. Fruits also contain pectins which provide bulk to the diet and helps bowel movement.
  5. Animal Foods:This category includes eggs, chicken, meat, fish etc. They are a good source of high quality protein and other important nutrients. Fish is rich in omega-3 PUFA which is protective against cardiovascular diseases and calcium as well. A special feature in flesh foods is the presence of vitamin B12, which is absent in plant foods.
  6. Fats, Nuts and Oils:
    These are calorie-rich foods, and are useful for increasing the energy density of foods. Fats can be the visible fats (ghee, butter, oil) or the invisible fats (present inherently in each food). They are required in moderate quantities in the daily diet as they provide essential fatty acids and promote absorption of fat soluble vitamins along with improving the palatability of the food. However, the total calories from fat should not exceed 10-15%.
  7. Sugars:
    This group includes table sugar, jaggery, honey, syrups etc which are energy concentrates. They are the sweetening agents which should be consumed in moderation as they provide calories but not much in the way of nutrition. Also excessive sugar consumption has been linked to weight gain.