terça-feira, 2 de junho de 2015

Congenital Muscular Torticollis

Congenital Muscular Torticollis

By Warren Hammer, MS, DC, DABCO
Congenital muscular torticollis (CMT) refers to a shortening of the sternocleidomastoid (SCM) muscle in an infant. It is a condition that responds very well to a stretching program and spinal adjustments. 
The most common causes are considered to be due to intrauterine malposition and/or birth trauma since CMT is more frequent after breech presentations1 and congenital hip dysplasias.2 In rare instances bony anomalies of the cervical spine such as Klippel-Feil syndrome3 or ocular imbalance might be causative. Other possibilities are spontaneous subluxation of a cervical vertebra, cervical adenitis secondary to upper respiratory tract infection, unilateral soft tissue infection, neck tumors, myositis or disease of the basal ganglia.3
Turek3 feels that every case of torticollis deserves roentgenographic study before treatment is instituted. Often a fibrous mass may be palpated in the SCM. The mass, which may the result of venous occlusion during the birth trauma, usually appears within three weeks after delivery and attains maximum size by one month.4 The infant will show the typical head position of head tilt toward the side of shortening and contralateral neck rotation. The face and even the skull may appear asymmetrical. While spontaneous recovery may occur, if left untreated, the cervical fascia and scaleni muscle may contract and a cervical and thoracic scoliosis may develop.3,5 Infants treated before one year of age had better results.6
Emery outlines a treatment method in an excellent article.7 She educates the parents to perform the stretching procedures. Two people take part in the procedure. If the infant's neck is laterally bent right and rotated left, with the infant in the prone position, one person holds the infant's shoulders while the other person performs the stretch standing at the head of the patient. The stretch is performed by cupping the left side of the infant's face with the left hand and supporting the skull under the occiput with the right hand. Use slight traction to gain relaxation and rotate the head to the right to achievable range of motion (ROM). Next, lateral bending stretch is done 10 degrees of right rotation. Now move the head laterally to the left and attempt to have the left ear reach the left shoulder. Hold both of the above stretches for 10 seconds and repeat five times each, twice a day. This treatment should be continued until full ROM is achieved. Adjustment of the spine for fixations wherever they exist is of course pertinent.
The parents are also educated7 about positions the infant may assume. For example, the child should play in a prone position with neck extended to encourage bilateral SCM muscle elongation. The infant can be placed in a crib in a position of being forced to look and lift the head toward the direction of correction.3
If at four months the head was still tilted, Emery7 used a method called lateral head righting to strengthened the opposite SCM. For example with the child sitting and tilted to the right the child is moved in a manner so its head will now tilt to the left. This "righting" motion could be used in rolling and side-lying maneuvers. If at four and one-half months the head tilt was six degrees or greater she used a tubular collar in which there were lateral uprights on one side to keep the head in a neutral position.8
References 
  1. Coventry MB and Harris LE. Congenital muscular torticollis in infancy: some observations regarding treatment. J Bone Joint Surg (Am). 41:815-822, 1959.

  2. Hummer CD and MacEwen GD. The coexistence of torticollis and congenital dysplasia of the hip. J Bone Joint (Am). 1972; 54:1255-1256.

  3. Turek SL. Orthopaedics: Principles & Their Application, fourth edition, Philadelphia: J.B. Lippincott Co. 1984:869.

  4. Bredenkamp JK, Hoover IA, Berke GS and Shaw A. Congenital muscular torticollis: a spectrum of disease. Arch Otolaryngol Head Neck Surg. 116:212-216, 1990.

  5. Tachdjian MO. Congenital muscular torticollis. J Pediatr Orthop. 1:65-73, 1972.

  6. Canale ST, Griffin DW and Hubbard CN. Congenital muscular torticollis: a long-term follow-up. J Bone Joint Surg (Am). 64:810-816, 1982.

  7. Emery C. The determinations of treatment duration for congenital muscular torticollis. Phys Ther 74:921-929, 1994.

  8. Emery, Carolyn: Personal communication, 10/94.

Nociception, Mechanoreception and Proprioception

Nociception, Mechanoreception and Proprioception ... What's the Difference and What Do They Have to Do with Subluxation?

By David Seaman, DC, MS, DABCN
This topic is a fruitful one for regular bloopers from BOOPers and nonBOOPers. A future breed of subluxation-oriented chiropractors, unlike us (their predecessors), will not be confused by these words. 
A future breed of chiropractors, perhaps the real doctors of the future, might also heed the words that have been attributed to Thomas Edison and "interest his patients in the care of the human frame, in diet, and in the cause and prevention of disease." Such a doctor would probably be a neuromusculoskeletal master, a nutritional biochemist, and public health specialist. No one in our profession can boast competency in all these areas. In fact, I do not know anyone who is a true expert in any one of these areas.
In the past two years, I have yet to meet one DC who truly comprehends the meanings and clinical consequences of nociception, mechanoreception, and proprioception, and probably none of us do. Nonetheless we must develop a working understanding of these different topics so we can better understand the science of chiropractic. The most common misconception that I come across is the idea that nociception and mechanoreception are the two subsets of proprioception. Nothing could be further from the truth.
Nociception is the process by which nociceptive receptors receive tissue damaging stimuli that is then carried into the CNS by nociceptive axons (A-delta and C fibers). Potential outcomes of nociceptive input to the cord include pain, autonomic symptoms, vasoconstriction and muscle spasm. Nociceptive input to the cord appears to be the driving force behind the pathogenesis of subluxation (see Figure A). We must remember that nociception and pain are two completely different animals. However, a devastating consequence of both pain and nociceptive stimulation of the hypothalamus, is the release of cortisol by the adrenal glands. Over time, elevated levels of cortisol will promote glucose intolerance, inhibit collagen formation, increase protein breakdown, inhibit secretory IgA output, and inhibit white blood cell function. Clearly, the clinical importance of pain and nociception should not be minimized.
Mechanoreception refers to the process by which tissue mechanoreceptors are stimulated by mechanical input such as touch, muscle stretching, and joint motion. A-alpha and A-beta fibers carry mechanoreceptive information into the CNS. Segmental reflex effects of mechanoreceptor input can excitatory and inhibitory. An important inhibitory effect is the presynaptic and postsynaptic inhibition of the nociceptive pathways. It is thought that the adjustment stimulates joint mechanoreceptors by increasing joint motion. There are also suprasegmental reflex effects of mechanoreceptor stimulation, which are proprioceptive in nature.
Proprioception refers to kinaesthetic awareness. Proprioception occurs as a consequence of the integration of vestibular input, visual input and tissue mechanoreceptor input to the cerebral cortex and cerebellum. It is thought that mechanoreceptor input is of the utmost importance for proprioception. Thus, mechanoreceptors give rise to local segmental reflexes and suprasegmental proprioceptive reflex effects. The word proprioceptor is a misnomer, as no somatosensory receptor functions solely in proprioceptive mechanisms.
Nociception, mechanoreception, and proprioception are all intimately associated with the normal and abnormal function of vertebral joints. In a nutshell, nociception induces subluxation which subsequently reduces mechanoreception and proprioception. The end result is individual-specific conditions and patients that go from doctor to doctor and get no relief until they visit a chiropractor.
The topics of nociception, mechanoreception, and proprioception are not well understood by many BOOPer and nonBOOPer DCs and thus, stand as fertile ground from which impersonal support of chiropractic might begin. It would be much easier to work together on reducing our collective ignorance in our severely deficient areas, rather than trying to defend and prove that a tenth of the truth is the whole truth.

Spondylolysis and Spondylolisthesis

By Deborah Pate, DC, DACBR
Spondylolysis and Spondylolisthesis often become confusing. Spondylolysis is a term used to describe a defect in the pars interarticularis or a break in the pars.
The most common level for a spondylolysis is L5.
It is rarely found in the cervical spine. It is unilateral in about 1/6 to 1/3 of cases. The cause of a spondylolysis is felt to be repeated trauma, as in a stress fracture, to a par interarticularis that has been inherently weakened by hypoplasia or dysplasia of the pars, most often developmental. The most accepted documented reason for a spondylolysis in young children is torsional stresses or repeated trauma to a hypoplastic or dysplastic pars, ultimately causing a stress fracture. There are however instances when a single traumatic event will cause a spondylolysis.
The best view to determine the presence of a spondylolysis in on the oblique view. If there is a question as to whether or not there is one present, a CT scan will demonstrate this region very clearly. If a possible recent fracture is suspected a bone will demonstrate whether or not the spondylolysis is recent.
Spondylolisthesis is defined as a subluxation of one vertebral body on another; displacement generally is understood that the superior vertebral body is displaced anterior in relationship to the inferior vertebral body.
Spondylolisthesis may be classified as isthmic, degenerative, dysplastic, traumatic or pathologic. In isthmic spondylolisthesis, the cause of the spondylolisthesis is due to a spondylolysis of the pars, and therefore allows the anterior slippage of one vertebrae on another. Dysplastic spondylolisthesis is often due to developmental hypoplasia of the pars, which may be elongated, allowing for the anterior slippage of one vertebrae on another. Traumatic spondylolisthesis is almost always due to a fracture of the posterior arch which allows for slippage of the fractured vertebrae on the adjacent segment. The best example is the "hangman's fracture." Degenerative spondylolisthesis is due to alteration in the biomechanics of the facets, which generally demonstrated marked degenerative changes and allow for the spillage of one vertebrae on another. Neoplastic processes can cause destruction of a vertebral body, again allowing for the displacement of one vertebrae on another, which is termed a pathologic spondylolisthesis.
It is important to note what type of spondylolisthesis is present for clinical management of the patient. There is also a grading system for determining the stability of a spondylolisthesis. This system I am sure everyone is aware of, however, it is more important to determine if there is in fact a progression of the anterior slippage. Any progression of the anterior slippage is even more important than the grade of spondyloslisthesis. If there is radiographic evidence of an increase in the anterior displacement, that alone is enough to document instability.
Grading of degree of spondylolisthesis - Copyright – Stock Photo / Register Mark
Grading of degree of spondylolisthesis by dividing the sacral surface in four equal parts. A) first degree; B) second degree; C) third degree; D) fourth degree. From: Meyerding HW. Spondylolisthesis. Surg Gyn Obstet 54: 371-377, 1932. By permission of Surgery, Gynecology & Obstetrics.

Glucosamine Review

By G. Douglas Andersen, DC, DACBSP, CCN
In the summer of 1993 I was accumulating literature and preparing a three part series on glucosamine when I got scooped by my own publication. The September 12, 1993, issue of Dynamic Chiropractic contains an excellent article by Michael Murray, ND, on the treatment of osteoarthritis with glucosamine. 
I urge any readers who want in-depth information on glucosamine (definitions, biochemical action, and references) to read this article.
In the last few years, interest in glucosamine has been on the rise. The majority of positive studies occurred in the late 1970s and early 1980s and were published outside the U.S. Maybe that's why it took almost a decade to catch on in America. These foreign studies show that ingestion of the sulfate form of glucosamine: 
  1. is well-absorbed when taken by mouth;

  2. stimulates the synthesis and repair of connective tissue and cartilage;

  3. blocks the breakdown of cartilage;

  4. relieves joint pain and inflammation;

  5. increases range of motion;

  6. continues to suppress symptoms weeks after administration is discontinued;

  7. does not have side effects (a refreshing alternative to the abdominal pain, dyspepsia, diarrhea, and peptic ulcers caused by nonsteroidal anti-inflammatories);

  8. is dosed at 500 mg three times per day for eight weeks, away from food (occasionally patients may have gastrointestinal complaints; in the event this occurs, try dosing with meals);

  9. takes two to six weeks for patients to "feel the effects";

  10. the only anatomic regions specifically mentioned in studies were the knee and hip. I did not see any studies that were limited to arthritis of the spine.

All the studies with glucosamine utilized the sulfate form. Glucosamine hydrochloride and N acetyl glucosamine are also on the market. Companies selling these forms make good arguments that they work. However, there have been no human studies with arthritic patients -- positive or negative -- utilizing these forms of glucosamine. The hydrochloride and N acetyl forms are less expensive than the sulfate variety. If you decide to try one of these untested forms, I would appreciate any feedback, good or bad. There have also not been any studies on glucosamine for conditions such as whiplash, sprains, and disc problems. However, a substance that can stimulate proteoglycan and glycosaminoglycan production should be considered for any serious musculoskeletal problem.
After discontinuing oral glucosamine sulfate therapy, symptoms did eventually return in patients with osteoarthritis. In my personal practice, after eight weeks of 1500 mg of glucosamine sulfate a day (10 mg per pound for larger and obese individuals), I have not been discontinuing therapy, but instead reducing doses to 500 mg per day. When initiating glucosamine therapy, patients should be informed that glucosamine treats a cause rather than a symptom and therefore, they will not have the immediate reduction in pain that nonsteroidal anti-inflammatories produce. I show my patients summaries of studies where arthritic people who take glucosamine sulfate orally eventually feel better than those on anti-inflammatory medication. In my practice, I have observed favorable results with glucosamine therapy.

Smoking and Low Back Pain

By Ronald L. Rupert
The statement, "things never stay the same," certainly applies to biomedical information. It is estimated that there are now over 7,000 science articles published daily. We need only look at the rapid growth in the number of chiropractic publications to see this trend. 
Subscribing to several of the quality peer-reviewed chiropractic journals is an indispensable step in staying informed. However, because subscribing to and reading thousands of journals isn't compatible with practice, it is important to develop online search skills that permit use of indexes which direct the busy practitioner to additional information.
Information actually changes so rapidly that your education is dated if you didn't begin reading and continuing the learning process on the day after graduating from chiropractic college. If you don't make time to read, you create unnecessary risks for your patient, decrease the quality of diagnostic and therapeutic services you perform, and create a legal risk for yourself. There are hundreds of examples that much of what was learned 10, five, or even as little as one year ago is no longer the most expeditious or effective diagnostic or therapeutic approach. As an example of how knowledge changes, we will explore the research relating to smoking. This information should impact the daily practice of every chiropractor. We will search the Medline and Chirolars databases for information from the last decade about cigarette smoking as it relates to low back pain. At the same time the indexing concept of "subheading" will be explained.
While a growing number of chiropractors are becoming familiar with the Medical Subject Headings (MeSH) used by virtually all chiropractic and biomedical indexes, most are not as familiar with the distinction between heading and subheading. A heading is a major topic i.e., smoking, low back pain, headache, neoplasms, etc. They usually relate to diseases, injuries, anatomical structures, diagnostic equipment, chemicals, organisms, etc. The subheading is used to modify the heading. In most online searches if a heading alone is used, there will be too many articles to retrieve. For example, there are thousands of articles on low back pain. There are several ways to reduce this number to a reasonable amount including limiting the number of years for your search, restricting the search to a specific age group, country, etc. The most common strategy is to use a subheading to focus on the specific aspect of low back pain desired. MeSH only permits a limited number of subheadings to be used for each headings. Some of the commonly used subheadings permitted for low back pain are as follows:
HeadingFull Subheading
Low Back Pain/clClassification
Low Back Pain/diDiagnosis
Low Back Pain/dhDiet Therapy
Low Back Pain/dtDrug Therapy
Low Back Pain/ecEconomics
Low Back Pain/epEpidemiology
Low Back Pain/etEtiology
Low Back Pain/ppPhysiopathology
Low Back Pain/pcPrevention & Control
Low Back Pain/pxPsychology
Low Back Pain/suSurgery
Low Back Pain/thTherapy
An online retrieval through Medline and Chirolars could use the heading "low back pain" with subheadings "etiology" and "physiopathology" and the additional heading "smoking." By structuring the argument in this way we can see if smoking impacts the cause or abnormal physiology involved in low back pain. Such a search yields a number of important articles.
For decades we have told our patients about the adverse effects of smoking as it relates to lung cancer and many other health problems. But as neuromusculoskeletal specialists, have we kept abreast of the research linking smoking with low back pain? During the early 1980s, a number of studies began to look for risk factors associated with low back pain. 
  • Frymoyer et al.,1 noted that "low back pain sufferers were likely to be smokers particularly when smoking was accompanied by a chronic cough." His work in 1984 emphasized that knowing the risk factors of low back pain permits us to prevent the problem.2 This study also associated smoking and backache.

  • In 1984, Kelsey et al.,3 noted: "Cigarette smoking in the past year was associated with an increased risk for prolapsed disc."

  • In 18 year old men Hellsing et al.,4 found that "smoking more than 20 cigarettes a day showed a predictive value of 23%" for developing back pain.

  • Dwyer5 again suggested that smoking cessation was an important "preventive measure" for back pain.

  • Several chiropractic studies, including the study by Cox and Trier6 in 1987, also link smoking and low back pain.

In the last few years there is a growing body of evidence that the adverse effects of smoking are not only from the mechanical stress of coughing, but smoking's direct destructive effect on connective tissue. The 1991 Value Award in Clinical Sciences was given to Battie, et al.,7 for studying disc degeneration in identical twins (one a smoker, one a nonsmoker) using MRI. Smokers had a marked increase in disc degeneration.
Recent studies demonstrate biochemical changes due to smoking, e.g., altered body pH and other variables. These changes have potential adverse effects on all body connective tissue. Research in 1993 by Boshuyen, et al.,8 found that: "Pain in the extremities turned out to be related more clearly to smoking than to pain in the neck or back."
This is only a sample of the many fascinating studies that implicate smoking in ways you may never have learned in school. It is the kind of information that all chiropractors should know thoroughly. After all, don't we treat musculoskeletal symptoms? Don't we advocate prevention?
The most recent information is not available in textbooks because it is too new. By the time the average text is written, printed, and distributed, even the most recent references are several years old. Many of the most important supporting studies may be omitted. The only way to stay informed and clinically competent is to use primary source material. This means subscribing to several research oriented journals and developing the skills to use online indexes.
References 
  1. Frymoyer, J, et al. Epidemiologic Studies of Low Back Pain. Spine, 5(5):419-23, 1980.

  2. Frymoyer, J, et al. Helping Your Patients Avoid Low Back Pain. Journal of Musculoskeletal Medicine, 1:65-74, 1984.

  3. Kelsey, J, et al. Acute Prolapsed Lumbar Intervertebral Disc: An Epidemiologic Study with Special Reference to Driving Automobiles and Cigarette Smoking. Spine, 9(6):608-13, 1984.

  4. Hellsing, A, et al. Individual Predictability of Back Trouble in 18-Year-Old Men. Manual Medicine, 2(3):72-6, 1986.

  5. Dwyer, A. Backache and Its Prevention. Clinical Orthopaedics and Related Research, 222: 35-43, 1987.

  6. Cox, J and Trier, K. Exercise and Smoking Habits in Patients With and Without Low Back and Leg Pain. Journal of Manipulative and Physiological Therapeutics, 10(5):239-45, 1987.

  7. Battie, M, et al. 1991 Volvo Award in Clinical Sciences. Spine, 16(9):1015-21, 1991.

  8. Boshuizen, H, et al. Do Smokers Get More Back Pain? Spine, 18(1):35-40, 1993.

Burning Fat

By G. Douglas Andersen, DC, DACBSP, CCN
In a recent study, scientists looked at the question, "If you are in good aerobic condition, will you burn fat at a higher rate than people who are not aerobically fit?" The answer in this study was a surprising "No." Researchers gave 50 gm of fat for breakfast to trained and untrained individuals. 
They then measured energy use and fat oxidation postprandial. There was no difference. There was also no difference between the two groups at 6 hours and at 18 hours after the meal. The authors did not rule out the possibility of a long-term difference.1
Comment: It should be noted that this study group was small. It would be interesting to have the authors repeat this study with a larger sample size over a longer period of time. Until proven otherwise, the message to your patients should be: Whether you are in shape or not, if you eat more fat than your body needs, your body will most likely store it.
Creatine
Creatine is a hot, new ergogenic aid. Like so many other miracle substances, companies marketing creatine have been very enthusiastic and have been very liberal with their claims. I wrote an article on creatine in the April 8, 1994 issue of Dynamic Chiropractic. At the time, I had not found any published data using creatine on healthy, weightlifting humans. This double-blind, placebo-controlled study involved five subjects who were given four, 5 gm servings of creatine orally or a placebo. Before and after each blinded administration, the subjects did five sets of 30 repetitions of single leg knee extensions. The results: Peak torque production was greater in those subjects who took creatine in the second, third, and fourth sets, as well as parts of the first and fifth sets. Creatine ingestion also lowered plasma ammonia levels. The authors concluded that oral creatine could reduce fatigue in repeated sets of an aerobic exercise. They postulated that the fatigue reduction could be due to one or a combination of the following: a) increase in pre-exercise phosphocreatine levels; b) increase in muscle buffering capacity (although no blood lactate changes were found in this study); c) increase in phosphocreatine resynthesis; d) all of the above could potentially stimulate ATP resynthesis.2
Comment: One small study is certainly not the final answer, but it does make it easier to recommend creatine on a trial basis to your patients involved in heavy weightlifting who are looking for a natural advantage. Remember too that the results in this study were with a whopping 20 gm per day dose -- an amount that challenges even your most compliant patients.
Magnesium
Magnesium is an amazing mineral. Some day I am going to write a series of articles on magnesium, but keeping with today's sports theme, we will focus on a study looking at its ergogenic effects. Twenty-six untrained people were put on a weightlifting program and given either 150 percent of the RDA of magnesium or 70 percent of the RDA of magnesium. After seven weeks of training, three times per week, the subjects were tested. Strength gains in the magnesium 150 percent group were significantly greater than in the group that received magnesium levels at 70 percent of RDA.3
Comment: My recommendation is if you have patients who are engaged in a rigorous exercise program, you should examine their nutrient intakes carefully and not be afraid to place them on levels greater than the RDAs. A logical follow-up to this study would be a repeat study using the same parameters but with well-trained individuals.
Protein
I will conclude our update by reviewing three studies that involve sports and protein. The first involved postexercise feeding for glycogen replacement. After endurance exercise, muscle glycogen levels are low. This study compared carbohydrate, protein, and a carbohydrate-protein mixture after exhaustive exercise to see which helped the body to restore muscle glycogen levels. Plasma analysis after supplementation showed higher glucose levels after carbohydrate ingestion. Plasma insulin was highest after the protein-carbohydrate combination. Plasma insulin, not glucose, is the metabolite we want to see elevated because of its strong stimulating effect on muscle glycogen storage. Muscle biopsies revealed that the carbohydrate-protein supplement combination had faster rates of muscle glycogen repletion than the carbohydrate group alone, which had significantly greater impact on glycogen repletion than the protein only group, which was a distant third.4
In the second study, researchers looked at plasma amino acid changes after endurance exercise to exhaustion in 11 triathletes. The diets included a level of protein that was 1.6 gm/kg of body weight, which is significantly higher than the RDA of 0.8 gm/kg of body weight. Carbohydrates made up 65 percent of the total caloric intake. After in-depth analysis (which will not be reviewed due to space requirements), the researchers concluded that protein requirements of athletes participating in exhaustive endurance activities should be substantially higher than the RDA. They stated that precise recommendations required further study.5
Our final protein study looked at protein requirements and muscle mass and strength changes during intensive training in novice male body builders. Using a double blind, crossover format, 12 men in their early 20s were put on a six-day-a-week, intensive, weight lifting program. Researchers found that to maintain nitrogen balance, protein needs were 1.6 to 1.7 gm/kg of body weight, which is more than double the RDA.6
Comment: It is interesting that for years athletes in the body building, Olympic lifting, and power lifting communities have ingested amounts of protein that traditional medical practitioners and dietitians have said was of no benefit to them. I expect that if studies of this nature continue, we will receive further evidence that athletes who train intensely, whether it be in aerobic or anaerobic sports, have protein requirements greater than the general public. The rule of thumb I use for my patients is as follows: In times of illness, injury, stress, or intense training, the requirements for nutrient-dense foods, macronutrients, and micronutrients all increase. I am confident we will continue to see research that validates this principle.
References 
  1. Bennett, Reed, et al. Short-term effects of dietary fat ingestion on energy expenditure and nutrient balance. American Journal of Clinical Nutrition. 55:1071-1077, 1992.

  2. Greenhaff, Casey, et al. Influence of oral creatine supplementation on muscle torque during repeated bouts of maximal voluntary exercise in humans. Clinical Science. 84:555-571, 1993.

  3. Brilla and Haley. Effect of magnesium supplementation on strength training in humans. Journal of American College of Nutrition. 11:326-329, 1992.

  4. Zawadski, Yaspelkis, and Ivy. Carbohydrate-protein conflict increases rate of muscle glycogen storage after exercise. Journal of Applied Physiology. 72:1854-1859, 1992.

  5. Bazzare and Merdoch, et al. Plasma amino acid responses of trained athletes to successive exhaustion trials with and without interim carbohydrate feeding. Journal of the American College of Nutrition. 11:501-511, 1992.

  6. Lemon, et al. Protein requirements and muscle mass/strength changes during intensive training in novice body builders. Journal of Applied Physiology. 73:767-775, 1992.

Hypochondriasis: An Intrapsychic Phenomenon

By Abne Eisenberg
From a clinical perspective, hypochondriasis is described as a neurotic disorder characterized by a preoccupation with bodily functions and a morbid fear that one is suffering from serious disease. 
Paul Mac Lean, MD, describes such a psychosomatic condition as follows: "Emotional feelings, instead of finding expression and discharge in the symbolic use of words and appropriate behavior, must be conceived as being translated into a kind of "organ language." As such, the diagnostician must be on constant alert for nonverbal signs; e.g., hypertension, gastrointestinal distress, vertigo, cephalagia, etc. A plethora of symptoms may be elicited by a patient suffering from hypochondriasis -- all are expressions of what is being referred to here as "organ language."
When both sender and receiver occupy the same body, it is called intrapsychic communication (IPC), also referred to in communication theory as intrapersonal communication. Consciously or unconsciously, we all communicate with ourselves on a verbal, nonverbal, and vocal level. When we think, write in a diary, meditate, or rehearse a speech, it is called verbal IPC. When we make faces in a mirror, exercise, or pace back and forth, it is called nonverbal IPC. When we moan, groan, cry, laugh or sigh, it is called vocal IPC. When we bite our nails, rub a sore muscle, or pick particles of food from between our teeth, it is called tactile IPC. When we check to see if our underarm deodorant is working, it is called olfactory IPC. Each of the aforementioned employs a sensory pathway enabling us to experience a sense of self.
In an age where stress has become a household word, and practically everyone has experienced it to some extent, it is essential that we understand which biologic system it preempts -- especially, when it is taken to an extreme. The symptoms a patient manifests will depend upon which system is selected as a channel for the expression vehicle for stress. Some break out in a rash, others develop diarrhea, while still others get light-headed and faint. Only a small proportion of our thoughts find their way into verbal or iconic form; the greater percentage are internally retained and stored as memory.
Becoming sensitive to one's own nonverbal IPC can be an asset or a liability. In the case of hypochondriasis, it is a liability. Acting as an asset, it enables us to enjoy a more total sense of self. We constantly get feedback from all parts of our body. The professional athlete, in particular, depends upon such feedback for maximum muscle coordination and split second timing.
When you awoke this morning, how did you know you were awake and that everything was OK? Autonomically, a routine check was made to determine whether all of your senses were in good working order and that your muscles will obey the commands they are given by your brain: all of this accomplished through feedback.
For a dramatic example of negative intrapsychic feedback, we must think of the first-time speechmaker. Stage fright almost invariably evokes such reactions as dryness in the mouth, weakness in the knees, profuse sweating, and the proverbial lump in the throat. Any of these symptoms, taken to an extreme, characterizes the behavior of a hypochondriac -- someone who works himself up into an inappropriate state of anxiety and apprehension. The reason they give may be real or imagined.
Perhaps you know people who have a perpetual need to know how they look. They spend inordinate amounts of time in front of a mirror. With meticulous care, they examine themselves in great detail. Then there are those whose preoccupation is with movable body parts; they habitually wiggle their fingers, shrug their shoulders, and stretch. Fortunately, the majority of us require only a modest amount of such nonverbal intrapsychic feedback to have a sense of well-being. Only when this need becomes distorted, or exaggerated, is there a basis for concern.
Abraham Kaplan's Law of the Instrument states: "Give a small boy a hammer and he will find that everything he encounters needs pounding." This penchant for hammering could be analogous to Pasteur's germ theory. Prior to 1868, before bacteria became the target for organized medicine, humors of the body received their undivided attention. Then came the microbe hunters; with few exceptions, a search for the offending organism was on. In 1895, D.D. Palmer gave birth to subluxation hunters; with few exceptions, a search for the offending subluxation was on. In both instances, the axiom: one-cause, one-cure, prevailed. Only the more sophisticated in each profession approached disease from a more holistic (multi-dimensional) perspective.
It is fitting that we now address something called somatization, the phenomenon whereby cognitive imprints experientially generate inimical symptoms in various body parts. Once these noxious impressions manifest themselves in the musculoskeletal system, neural feedback via proprioceptors qualify as an integral part of the intrapsychic communication network.
Regardless of which culprit health care professions choose to single out as their prime suspect, susceptible patients in each field quickly become habituated. Talk to anyone who has been in analysis for years; their rhetoric is often stereotypical. The same indictment may also be applied to medicine as well as chiropractic. People have a compelling need to know what is causing their discomfort or disease. Whenever an etiology is unknown, rather than simply admitting ignorance, the tendency is to say something -- regardless of whether or not it is clinically valid.
Carl Jung suggests that the "self" is the product of intrapsychic communication, or the behavioral result of a dialogue between unconscious values and conscious experience that is going on within every person. It is with this perception of self that the hypochondriac has difficulty: that is, a problem keeping the self-image intact.
To the hypochondriac, symptoms are very real. Although objective findings are not always available to validate a given complaint, there are cases in which physical manifestations leave doctors in a quandary. Pseudocyesis is one such phenomenon. It is seen in women who fantasize that they are pregnant and present a visibly enlarged abdomen. Under anesthesia, however, the enlargement disappears.
The placebo effect is also known in therapeutic circles. Numerous studies have reported its effectiveness under controlled circumstances. Henry K. Beecher studied the effects of placebos on patients suffering from conditions including postoperative pain, angina pectoris and the common cold. He estimated that placebos achieve satisfactory relief for about 35 percent of the patients surveyed. In view of this, isn't it ironic that, according to Sissela Bok, a sample of 19 recent textbooks in medicine, pediatrics, surgery, anesthesia, obstetrics and gynecology, only three even mention placebos and none of them deal with either the medical or ethical dilemmas placebos present? I myself, have never encountered a discussion of the placebo-effect as it relates to the adjustment in any chiropractic textbook.
Thorough studies have estimated that as many as 35-45 percent of all prescriptions are for substances that are incapable of having an effect on the condition for which they are prescribed. Can a similar statistic be posited for the adjustment; what percentage of adjustments actually produce the biodynamic effect they profess to deliver? The age old question is begged: To what extent does a patient's mental attitude toward a particular form of treatment mediate its effectiveness?
In his book, "Language, thought, and reality," Benjamin Whorf describes us as cutting up Nature, organizing it into concepts and ascribing significances as we do, largely because we are parties to an agreement to organize it in a certain way. It is staggering to think that the pattern of living each of us embraces grows out of approximately the 100 million nerve impulses pouring into our nervous system every second of the day. In all probability, the hypochondriac organizes aspects of Nature, especially as it applies to the self, in a slightly different manner.
As we listen to our patients on a daily basis, patterns of communicative expression begin to emerge. Patients think and talk about their bodies differently. Opera singers, for example, when referring to their voice will say "the voice" rather than "my voice." Or, a patient with acute sciatica will say, "The leg is bothering me today," rather than "my leg." They tend to disown the offending part and repossess it when it is well.
How people perceive or misperceive themselves is a reality with which the physician must come to terms. Using both quantitative and qualitative language, patients describe their symptoms in various ways; they either exaggerate, understate, or distort what they think or feel. We, as doctors, can neither confirm nor deny subjective symptoms. Unlike body temperature or blood pressure, they cannot be measured with a thermometer or sphygmomanometer. We are obliged to accept what we are told on faith. Fortunately, experience teaches us to discriminate -- to discern whether what a patient tells us makes sense and is consistent with what we know about the body.
This should be our approach to hypochondriasis: First, we must recognize that it is a breakdown in intrapsychic communication (a mismanagement of the self). Second, that mind does influence body. Third, that we have a responsibility to acknowledge and therapeutically address the clinically significant nonverbal as well as the verbal messages the body transmits.
We all hear that inner voice telling us right from wrong, steering us in a particular direction, warning us of impending danger, and inspiring us to try something new. Whether we identify this source of information as coming from the id, superego, unconscious, innate or good old fashion instinct, the messages we get act like a compass or guidepost. The important thing is to develop an ability to distinguish between which messages to honor and which ones to ignore. Trial and error makes this differentiation possible.
Let me recapitulate by saying that we all talk to ourselves; it is perfectly normal. Every patient, on the way to your office engages in the practice. They ask themselves whether they really need to go, whether what they are feeling is really serious, or whether the treatment they are about to receive will make them feel better. This intrapsychic communication deserves both your respect and attention. Why? Because it will act as a baseline, a springboard for your ultimate evaluation of the patient's mental and physical condition. Once you have trained yourself to clinically recognize the allowable parameters for normal intrapsychic or intrapersonal communication, you will be better able to recognize the abnormal, i.e., the hypochondrical patient.
In closing, I propose that the extent to which mind affects body may also include something as final as death, i.e., that we choose "when" to die. Just as the hypochondriac chooses what, where, and how to feel, death may be but another choice.
Dr. David P. Phillips, a sociologist at the University of California, conducted a very interesting study. He sought to determine whether men or women who were gravely ill gave up the ghost before or after their upcoming birthday. The conclusion reached was that, in women, three percent more deaths than expected occurred in the week after their birthday than before it. Among men, however, death peaked just before their birthday.
Dr. Phillips theorized that more men died before their birthday because it may be perceived as a time of taking stock; with less successful men, deciding against living another year. Women, on the other hand, may be more family-connected and, therefore, take a more positive stand. It should also be noted that these attitudes are not restricted to birthdays, but to any other personally meaningful occasion, e.g., a son or daughter graduating from college, and anniversary, or the completion of some special project.
Whether one is speaking of the hypochondrical or ordinary patient, the bottom line is how they communicate intrapsychically -- the messages they send back and forth from mind to body. Careful clinical attention must be paid by every physician, both medical and chiropractic, to how patients talk about their bodies, i.e., whether the voice from within produces biologic harmony or discord (dis-ease) between their inner and outer worlds.

What is a Subluxation?

What is a Subluxation?

By Joseph Siragusa, DC
What is a subluxation? Wouldn't that be a great question for John Stossel (of "20/20" fame) to ask 10 chiropractors at random? The answers could range from the most scientific to the most unusual. 
Could it be that in our attempt to overcome a professional inferiority complex, we've overcompensated by reaching for the "golden definition" that shields us from the inevitable criticisms? Could it be that in an attempt to "try harder because we're #2," that we have lost sight of the common sense approach to explaining chiropractic?
Let's take a scenario where a "typical" chiropractic low back and leg pain patient is examined by an orthopedic surgeon. When Dr. Orthopod examines our patient, he often will find evidence of restricted motion. He will make a note of restricted range of motion and may place significance on it. He may find weakness of the extensor hallicus and/or loss of sensation to pinprick. He also will usually make note of muscle spasm, which is typically interpreted as an indication for the prescription of muscle relaxers. On x-ray the orthopod may observe disc degeneration and spurring which his literature will tell him is normal aging. And when the patient mentions concurrent constipation, it my be interpreted as a mere coincidence with no connection to the chief complaint of back and leg pain.
This scenario is not presented to pass judgment, but simply to recount what most chiropractors hear from patients on a weekly, if not a daily basis.
Can we blame third-party payers and employers for being confused when the very same patient gets examined by a chiropractor and the exam yields a different diagnosis, treatment plan, and prognosis? And then the 10 chiropractors don't agree on what a subluxation is, or what technique is best.
So much for identifying the problem. What can we do to solve it? Actually I think the answer is closer than we think and simply requires the application of that good old common sense.
First let me suggest that we adopt a model of the subluxation that acts as an "umbrella" or "syndrome" which consists of five individual components. Those components have already been identified by our orthopedist. When he found decreased range of motion he was identifying the first component of the subluxation complex: spinal kinesiopathology. Of course a chiropractor could document this even better with static and motion palpation and stress x-rays. When he determined that there was weakness of the extensor hallicus, he was documenting the second component of the subluxation complex: neuropathophysiology. The finding of muscle spasm was the documenting of myopathology and would be recognized by a chiropractor as the body's natural protective mechanism: in other words an effect of the problem, not the problem itself. The degeneration on x-ray was evidence of histopathology and would be interpreted by chiropractors (as well as researchers like Kirkaldy-Willis) to be the result of prolonged dysfunction (spinal kinesiopathology), not normal aging. Chiropractors would place significance on the constipation because of the relationship of the lumbosacral spine to the colon. This is the fifth component of the subluxation complex: pathophysiology.
So what we have is a syndrome that both professions recognize by individual components. One profession sees only the individual components, the other sees the components as part of a bigger picture. Chiropractors have the subluxation as part of their heritage. Attempts at defining a subluxation by individual "technique gurus" have been less than successful, and we have as many definitions as we have techniques. The solution has to be a broader definition to include all techniques and all variations of subluxations.
Using the subluxation complex as a syndrome of component parts will facilitate this goal. Our Dr. Orthopod found all the components of the subluxation syndrome. Only because of our chiropractic heritage can we as chiropractors recognize, interpret, and appreciate the significance of the presence of all the components in the patient.
Additionally, the chosen technique is a matter of preference. After all, dentists don't argue over what a cavity is, and they don't argue over the best type of drill to use. As long as the lesion (cavity or subluxation complex) is corrected, the use of a given technique is not important. Research within this model would allow evaluation of techniques and procedures as well. If Gonstead doctors enter the model by emphasizing the kinesiopathology component and successfully reduce the subluxation complex, the technique is valid. If an activator or applied kinesiology doctor enters the model through the neuropathophysiology or myopathology components and reduce the subluxation complex, their technique is valid. If the latest "whop 'em on the head" technique doesn't affect the components of the subluxation complex, then it should not be considered mainstream chiropractic and should be investigated further before it is promoted to the profession.
If would be wonderful to have a common terminology to use even among doctors from different schools and different techniques. We could describe patients such as: "I have a patient with a subluxation complex. There is a major kinesiopathological component at C7, with a weakness of the finger extensors indicating neuropathophysiology, a trigger point in the right trapezius representing a myopathology, and disc degeneration at C6-C7 representing histopathology." That would leave room for the individual doctors to determine their technique of choice, yet vividly communicate the condition.
The subluxation does exist. No, you won't see it on an x-ray. You find the subluxation complex on a patient. The only difference between the exam by the orthopod and the chiropractic exam is that the chiropractor recognized the individual isolated findings as part of a larger syndrome which our profession has chosen to call the subluxation.
If we define the subluxation this way, and if we explain the semantic use of our word "subluxation" to the medical profession and insurance industry, communication will have to improve. I encourage you to examine for the components, x-ray for the components, diagnose by the components, and adjust to reduce the components. In other words, manage your patients based on the components. Notice I didn't mention only adjusting patients who are in pain.
I ask you to review your practice paradigm and either present a better model that will be as inclusive as the one I've presented, or join the movement to present a rational unified voice that still respects your individual practice style.
Adopt the component model into your practice. There are hundreds of literature citations that support this concept. Practicing this way, and educating my patients this way has been the best thing I ever did for my personal practice and, I believe, the best thing I could do to promote chiropractic health care to the people who don't understand the value of a chiropractic adjustment.

Conservative Management of Causalgia

Conservative Management of Causalgia

(Reflex Sympathetic Dystrophy)

By R. Vincent Davis, DC, PT, DNBPM
Causalgia may be described as an uncommon pain syndrome characterized by posttraumatic pain most commonly affecting the upper or lower extremities. Clinically, the presenting pain is usually paroxysmally produced by local friction, or even air currents, which affect the nerve supply innervating that given region where the pain syndrome is symptomatically manifested.
This pain phenomenon varies in its clinical presentation from immediately post-injury to several weeks later. The character of the injury may be as trivial as a sprain but any type of trauma may be etiological. Although the etiology is idiopathic, it is most often due to complete, or incomplete, laceration of the nerve, or plexus, involved.
The cardinal symptom is severe burning pain of paroxysmal character. There may be an intolerance to dryness in the area of pain and possible cutaneous coolness, color changes involving redness, or cyanosis, with glossiness, and edema. The pain is commonly exquisitely hyperalgesic. The symptoms may not present for several weeks following the etiological event, but gradually cutaneous symptoms indicative of vasodilation appear. Later, the skin may become cold, cyanotic, pale, diaphoretic, thin, and glossy with brittle and ridged nails. These cutaneous arteriovenous characteristics usually exist even in the presence of blood flow studies which show equality with the uninvolved extremity. These findings suggest that such nerve damage may affect surface vasodilatation without influencing larger deep vessels. Reduction, or complete elimination, of the pain by sympathetic block is diagnostic.
Since it has been shown clinically that the pain may spread to the opposite extremity, or to the cephalad, or caudal, cord, it is imperative to treat this clinical entity in a timely manner. If it went untreated, the probability is that it would reach a point in its progress where treatment would become unresponsive. Theoretically, the spread of this pain may take place in the internuncial pool.
Therapeutically, thermal agents in the form of hydrocollator packs, or silicone gel packs applied directly to the symptomatic region using a moist form of treatment to achieve the effect of convection, are desired for the vasoconstrictor type of pain. Application should be for 25 minutes p.r.n. with at least 10 minute intermissions between applications. Erythema ab igne must be avoided.
Moist cool packs in the form of ice packs, or silicone gel packs, may be applied to relieve the pain of the vasodilator type. Application should be for 10 minutes, directly to the symptomatic area, ensuring the absence of cyanotic increase due to percutaneous temperature effects. Pallor may be expected. The hyperemia and edema may be reduced by rest and elevation of the affected area.
Lidocaine (2.5 percent) phonophoresis over the area respective to the anatomical site of the perispinal sympathetic trunk on the ipsilateral side may be a helpful therapeutic aid in the treatment of the upper extremity. Application may be b.i.d., t.i.d., or p.r.n. pain. Treating the lower extremity would involve directing the cone of the ultrasonic beam at the sympathetic trunk between the first two pair of lumbar vertebrae with the same frequency of administration. Of course, phono-phoretic transfer is by pulsed waveform in this process.
In the event of the presence, or development, of trophic changes in the symptomatic area, referral to a neurosurgeon, or orthopedic surgeon, is mandatory to avoid the development of permanent trophic changes, or deformity. If conservative care is not providing for resolution of symptoms within two weeks, the patient should be referred, either for consult, or other treatment.
References
Davis RV: Therapeutic Modalities for the Clinical Health Sciences, 2nd ed. 1989. Library of Congress Card #TXU, 389-661
Griffin JE, Karselis TC: Physical Agents for Physical Therapists, 2nd ed. Springfield: Charles C. Thomas, 1982
Krupp, Chatton: Current Medical Diagnosis & Treatment. Lange Publishers, 1980.
Krusen, Kottke, Ellwood: Handbook of Physical Medicine & Rehabilitation, 2nd ed. Philadelphia: W.B. Saunders Company, 1982.
Schriber WA: A Manual of Electrotherapy, 4th ed. Philadelphia: Lea & Febiger Publishers, 1975.
Turek: Orthopedics, Their Principles and Application, 3rd ed. Lippincott.

Osteonecrosis of the Hip

By Deborah Pate, DC, DACBR
Osteonecrosis of bone can occur anywhere in the skeletal system, however the most common areas affected are the femoral head, medial condyle of the distal femur and the scaphoid. Osteonecrosis can occur due to vasocclusive disorders or causes unknown. 
The most common predisposing factors associated with osteonecrosis are trauma, cortiosteroids, radiation, alcoholism, and collagen vascular diseases. The early changes are not readily apparent on x-rays and can be easily missed.
The earliest radiographic feature of osteonecrosis is a radiolucent line inferior to the subchondral bone adjacent to the articular cartilage. This represents the crescent sign. It is due to the collapse of necroticsubchondral bone and is visualized as a narrow radiolucent line parallel to the articular surface of the bone. It is best seen in the hip on the frogleg view. Later radiographic signs are associated with continued collapse of the dying bone. As the bone continues to collapse, varying degrees of sclerosis and cystic radiolucencies appear, mainly in the superior aspect of the femur head, the weightbearing portion. Occasionally this area can become completely sclerotic. Later the subchondral bone will fracture and fragment, causing the femoral head to become displaced, generally laterally. The end result is severe degenerative joint disease, which requires a prosthesis.
The clinical history of patient with osteonecrosis of the femoral head and medial condyle are usually patients in the 50 to 70 age group. Symptoms usually are vague initially, consisting of pain in the buttock, groin, thigh or knee. Usually there is a gradual increase in intensity of pain and a decrease in range of motion. This can occur over a period of years and associated with a limp and muscle atrophy. If the patient has a previous history of coricosteriod therapy, radiation therapy, alcoholism, one should consider the possibility of osteonecrosis of the hip. If the patient has a history of a hemoglobinopathy such as sickle cell anemia, Gaucher's disease or a collagen vascular disease such as lupus erythematosus, and rheumatoid arthritis, osteonecrosis must be ruled out. Most of these patients have a very high incidence of osteonecrosis in multiple areas, particularly the hips.
If the osteonecrosis is recognized early before there is any collapse of the femoral head, a transtrochanteric anterior rotational osteotomy can be performed to save the femoral head. This is particularly important with patients under the age of 60 as most hip replacements will only last 10 to 15 years, 20 tops. If collapse of the femoral head can be avoided the degenerative arthrosis which usually follows will not occur and a hip replacement can be avoided.
If osteonecrosis in the hip is suspected it can be confirmed with a MRI scan or a bone scan. The MRI study will detect a vascularity a few weeks to a few months sooner than the bone scan. Both studies will be positive long before the changes are seen on plain x-rays.
If any of your patients have a possibility of osteonecrosis of the femoral head, make certain that this disorder is ruled out with a MRI if radiographic findings are equivocal. You may save a patient from having to undergo a hip replacement.

Subluxations, Inflammation, and Zinc

By Anthony Cichoke, MA, DC, DACBN
John is 42-years-old and works in a warehouse, lifting heavy boxes, loading and unloading trucks. Last week, while bending over to pick up a heavy box, he felt a sudden, sharp, stabbing pain across his low back. 
Repeated trips to the chiropractor have produced only temporary relief, although John is receiving the full range of chiropractic care, including nutritional supplements. John not only has a subluxation, but also inflammation, and zinc could be the answer.
Probably the most frequent reason a patient comes to the chiropractor's office is pain -- pain somewhere in the body's joints or soft tissue, that is, subluxations, strains, and sprains. Pain, along with swelling, heat, redness, and loss of function are the cardinal signs of inflammation. Zinc, as an antioxidant, fights inflammation.
Inflammation is a serious problem with subluxations, sprains, strains, myofascial pain syndrome, and systemic problems. Free radicals and cross-linked tissues are a major problem in inflammatory conditions of the joints and connective tissue fibers.
In a subluxation, the ligament/joint facets (as well as the surrounding connective tissue) can be stretched or torn. Scar tissue is formed as a result of injury, inflammation, and repair. Cross-linking and free radical formation of the injured fibers are a part of this process with resulting decrease in flexibility. This same sequence of events occurs in any subluxation, strain, or sprain. Antioxidents, such as zinc, can help fight cross-linking and free radicals.
Collagen is the main protein component in skin and connective tissue. Its molecules can be fused together or cross-linked by free radicals. When this occurs, connective tissue becomes leathery and rigid.
Free radicals are highly reactive molecules that destroy cell membranes and damage DNA. They are formed during the processes of cellular metabolism, and are normally detoxified by the body's free radical defense system. Free radicals cause proteins to be incorrectly synthesized and can lead to cell death.
Zinc as an Antioxidant
As an antioxidant, zinc has at least four roles: 1) protects vital biomolecules (sulfhydryl compounds) from oxidation; 2) competes with pro-oxident metals (iron and copper) for binding sites, thus decreasing their ability to form free radicals; 3) limits production of free radicals, such as superoxide and malondialdehyde (MDA), produced naturally by the body; 4) essential part of potent antioxidant enzymes zinc metallothionein, and superoxide dismutase (SOD). In fact, results from a recent study at the University of California, Davis, indicated that zinc monomethionine (a potent new form of zinc) reduced excessive levels of superoxide free radicals produced by white blood cells.
Zinc plays many vital roles in human nutrition, including: 
  • antioxidant capability
  • eye health (preventing macular degeneration)
  • growth and development
  • hair and skin health
  • immune function, especially white cell development
  • free radical fighter
  • sexual development and reproduction
  • wound healing
  • sense of taste and appetite
  • fights aging

What can affect zinc status in the body? Before his injury, our worker John, had been in top physical condition. He ran, lifted weights, and exercised daily. However, he had just gone through a very sticky divorce and was recovering from a prolonged bout of bronchitis. Further, he had a high cholesterol level and had gone on a low fat, vegetarian diet. John was a walking zinc deficiency and an accident waiting to happen.
As we know, zinc deficiencies are most frequently caused by: 
  • stress
  • diets high in fiber and phytate (compounds present in fruits, vegetables, and grain that actually inhibit zinc absorption -- a definite problem with vegetarians)
  • illness, disease, or other inflammatory reactions
  • exercise

Vitamins A, E, C, plus selenium, are most frequently used as antioxidants, but zinc is also extremely effective.
What Is the RDA of Zinc?
Zinc RDA for adult men is 15 mg./day and 12 mg. for nonpregnant women (15 mg. when pregnant, 19 mg. during the first six months of lactation, and 16 mg. during the second six months of lactation). Infants and children are 5 mg. and 10 mg. respectively. Studies show many people consume less than RDA levels and that marginal zinc deficiencies are quite frequent. Studies show many people consume less than RDA levels and that marginal zinc deficiencies are quite frequent.
Zinc Supplements
Unfortunately, the best sources of zinc (red meat, liver, eggs, and oysters) also tend to be high in cholesterol and fat. Because of depleted soil, environmental and food pollution, food additives, preservatives, etc., we can't get adequate zinc in our diet. Therefore, supplementation seems to be the answer.
Inorganic zinc supplements (i.e., zinc oxide and zinc sulfate) are poorly absorbed. However, chelated forms, such as zinc monomethionine, are much more bioavailable. In fact, a recent University of Illinois study has shown that the bioavailability of zinc monomethionine (when compared to ordinary zinc supplements) increased as the phytate/fiber content of the diet increased.
Zinc Safety
Research has shown that an excessive amount of zinc can decrease immune function and block copper absorption. Therefore, doses of zinc should be limited to 50 mg. per day. Further certain zinc ligands may pose a safety hazard. A recent report indicates that citric acid, the ligand in zinc citrate, increases the uptake of lead (a toxic metal). And picolinic acid, the ligand in zinc picolinate, removes iron from cells. In one report, elderly people taking RDA-levels of zinc picolinate developed anemia.
Neither lead uptake, nor anemia, are caused by zinc monomethionine. In addition, methionine, the ligand in zinc monomethionine, provides potent antioxidant protection.
Zinc Highlights
Therefore, it seems that adequate levels of zinc are critical for the successful, long-term treatment of subluxation, plus connective tissue problems, such as strains and sprains. As an antioxidant and free radical fighter, zinc works in many ways, helping to "hold" the adjustment. Although we think we have adequate intakes of zinc daily, we are most likely deficient. Diet won't do it, thus supplements appear necessary. Of all the zinc supplements, zinc monomethionine seems to be the most effective, helping the chiropractic treatments in rehabilitating injured patients, such as John.