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Assessment and Treatment of Tensor Fascia Lata

Assessment and Treatment of Tensor Fascia Lata

These assessment and treatment recommendations represent a synthesis of information derived from personal clinical experience and from the numerous sources which are cited, or are based on the work of researchers, clinicians and therapists who are named (Basmajian 1974, Cailliet 1962, Dvorak & Dvorak 1984, Fryette 1954, Greenman 1989, 1996, Janda 1983, Lewit 1992, 1999, Mennell 1964, Rolf 1977, Williams 1965).

 

Clinical Application of Neuromuscular Techniques: Tensor Fascia Lata

 

�Assessment of shortness in tensor fascia lata (TFL)

 

The test recommended is a modified form of Ober�s test (see Fig. 4.14).

 

Figure 4 14 Assessment for Shortness of TFL Modified Obers Test Image 1

 

Figure 4.14 Assessment for shortness of TFL � modified Ober�s test. When the hand supporting the flexed knee is removed the thigh should fall to the table if TFL is not short.

 

Patient is side-lying with back close to the edge of the table. The practitioner stands behind the patient, whose lower leg is flexed at hip and knee and held in this position, by the patient, for stability. The tested leg is supported by the practitioner, who must ensure that there is no hip flexion, which would nullify the test.

 

The leg is extended only to the point where the iliotibial band lies over the greater trochanter. The tested leg is held by the practitioner at ankle and knee, with the whole leg in its anatomical position, neither abducted nor adducted and not forward or backward of the body.

 

Box 4.5 Notes on TFL

 

  • Mennell (1964) and Liebenson (1996) say that TFL shortness can produce all the symptoms of acute and chronic sacroiliac problems.
  • Pain from TFL shortness can be localised to the posterior superior iliac spine (PSIS), radiating to the groin or down any aspect of the thigh to the knee.
  • Although the pain may arise in the sacroiliac (SI) joint, dysfunction in the joint may be caused and maintained by taut TFL structures.
  • Pain from the band itself can be felt in the lateral thigh, with referral to hip or knee.
  • TFL can be �riddled� with sensitive fibrotic deposits and trigger point activity.
  • There is commonly a posteriority of the ilium associated with short TFL.
  • TFL�s prime phasic activity (all postural structures also have some phasic function) is to assist the gluteals in abduction of the thigh.
  • If TFL and psoas are short they may, according to Janda, �dominate� the gluteals on abduction of the thigh, so that a degree of lateral rotation and flexion of the hip will be produced, rotating the pelvis backwards.
  • Rolf (1977) points out that persistent exercise such as cycling will shorten and toughen the fascial iliotibial band �until it becomes reminiscent of a steel cable�. This band crosses both hip and knee, and spatial compression allows it to squeeze and compress cartilaginous elements such as the menisci. Ultimately, it will no longer be able to compress, and rotational displacement at knee and hip will take place.

 

The practitioner carefully introduces flexion at the knee to 90�, without allowing the hip to flex, and then, holding just the ankle, allows the knee to fall towards the table. If TFL is normal, the thigh and knee will fall easily, with the knee contacting the table surface (unless unusual hip width, or thigh length prevent this).

 

If the upper leg remains aloft, with little sign of �falling� towards the table, then either the patient is not letting go or the TFL is short and does not allow it to fall. As a rule the band will palpate as tender under such conditions.

 

Lewit�s TFL Palpation

(Lewit 1999; see also functional assessment method in Ch. 5)

 

Patient is side-lying and practitioner stands facing the patient�s front, at hip level. The practitioner�s cephalad hand rests over the anterior superior iliac spine (ASIS) so that it can also palpate over the trochanter. It should be placed so that the fingers rest on the TFL and trochanter with the thumb on gluteus medius. The caudad hand rests on the mid-thigh to apply slight resistance to the patient�s effort to abduct the leg.

 

The patient�s table-side leg is slightly flexed to provide stability, and there should be a vertical line to the table between one ASIS and the other (i.e. no forwards or backwards �roll� of the pelvis). The patient abducts the upper leg (which should be extended at the knee and slightly hyperextended at the hip) and the practitioner should feel the trochanter �slip away� as this is done.

 

If, however, the whole pelvis is felt to move rather than just the trochanter, there is inappropriate muscular imbalance. (In balanced abduction gluteus comes into action at the beginning of the movement, with TFL operating later in the pure abduction of the leg. If there is an overactivity (and therefore shortness) of TFL, then there will be pelvic movement on the abduction, and TFL will be felt to come into play before gluteus.)

 

The abduction of the thigh movement will then be modified to include external rotation and flexion of the thigh (Janda 1996). This confirms a stressed postural structure (TFL), which implies shortness.

 

It is possible to increase the number of palpation elements involved by having the cephalad hand also palpate (with an extended small finger) quadratus lumborum during leg abduction. In a balanced muscular effort to lift the leg sideways, quadratus should not become active until the leg has been abducted to around 25�30�. When quadratus is overactive it will often start the abduction along with TFL, thus producing a pelvic tilt.�(See also Fig. 5.11A and B)

 

Method (a) Supine MET treatment of shortened TFL (Fig. 4.15) The patient lies supine with the unaffected leg flexed at hip and knee. The affected side leg is adducted to its barrier which necessitates it being brought under the opposite leg/foot.

 

Figure 4 15 MET Treatment of TFL Image 2

 

Figure 4.15 MET treatment of TFL (see Fig. 1.4 for description of isolytic variation). If a standard MET method is being used, the stretch will follow the isometric contraction in which the patient will attempt to move the right leg to the right against sustained resistance. It is important for the practitioner to maintain stability of the pelvis during the procedure. Note: the hand positions in this figure are a variation of those described in the text.

 

Using guidelines for acute and chronic problems, the structure will either be treated at, or short of, the barrier of resistance, using light or fairly strong isometric contractions for short (7 second) or long (up to 20 seconds) durations, using appropriate breathing patterns as described earlier in this chapter (Box 4.2).

 

The practitioner uses his trunk to stabilise the patient�s pelvis by leaning against the flexed (nonaffected side) knee. The practitioner�s caudad arm supports the affected leg so that the knee is stabilised by the hand. The other hand maintains a stabilising contact on the affected side ASIS.

 

The patient is asked to abduct the leg against resistance using minimal force. After the contraction ceases and the patient has relaxed using appropriate breathing patterns, the leg is taken to or through the new restriction barrier (into adduction past the barrier) to stretch the muscular fibres of TFL (the upper third of the structure).

 

Care should be taken to ensure that the pelvis is not tilted during the stretch. Stability is achieved by the practitioner increasing pressure against the flexed knee/thigh. This whole process is repeated until no further gain is possible.

 

Method (b) Alternative supine MET treatment of shortened TFL (Fig. 4.16) The patient adopts the same position as for psoas assessment, lying at the end of the table with non-tested side leg in full hip flexion and held by the patient, with the tested leg hanging freely, knee flexed.

 

Figure 4 16 MET Treatment of Psoas Using Grieves Method Image 3

 

Figure 4.16 MET treatment of psoas using Grieve�s method, in which there is placement of the patient�s foot, inverted, against the operator�s thigh. This allows a more precise focus of contraction into psoas when the hip is flexed against resistance.

 

The practitioner stands at the end of the table facing the patient so that his left lower leg (for a right-sided TFL treatment) can contact the patient�s foot. The practitioner�s left hand is placed on the patient�s distal femur and with this he introduces internal rotation of the thigh, and external rotation of the tibia (by means of light pressure on the distal foot from his lower leg).

 

During this process the practitioner senses for resistance (the movement should have an easy �springy� feel, not wooden or harsh) and observes for a characteristic depression or groove on the lateral thigh, indicating shortness of TFL.

 

This resistance barrier is identified and the leg held just short of it for a chronic problem, as the patient is asked to externally rotate the tibia, and to adduct the femur, against resistance, for 7�10 seconds. Following this the practitioner eases the leg into a greater degree of internal hip rotation and external tibial rotation, and holds this stretch for 10�30 seconds.

 

Method (c) Isolytic variation If an isolytic contraction is introduced in order to stretch actively the interface between elastic and non-elastic tissues, then there is a need to stabilise the pelvis more efficiently, either by use of wide straps or another pair of hands holding the ASIS downwards towards the table during the stretch.

 

The procedure consists of the patient attempting to abduct the leg as the practitioner overcomes the muscular effort, forcing the leg into adduction. The contraction/stretch should be rapid (2�3 seconds at most to complete). Repeat several times.

 

Method (d) Side-lying MET treatment of TFL The patient lies on the affected TFL side with the upper leg flexed at hip and knee and resting forward of the affected leg. The practitioner stands behind patient and uses caudad hand and arm to raise the affected leg (which is on the table) while stabilising the pelvis with the cephalad hand, or uses both hands to raise the affected leg into slight adduction (appropriate if strapping used to hold pelvis to table).

 

The patient contracts the muscle against resistance by trying to take the leg into abduction (towards the table) using breathing assistance as appropriate (see notes on breathing, Box 4.2). After the effort, on an exhalation, the practitioner lifts the leg into adduction beyond the barrier to stretch the interface between elastic and non-elastic tissues. Repeat as appropriate or modify to use as an isolytic contraction by stretching the structure past the barrier during the contraction.

 

Additional TFL Methods

 

Mennell has described superb soft tissue stretching techniques for releasing TFL. These involve a series of snapping actions applied by thumbs to the anterior fibres with patient side-lying, followed by a series of heel of hand thrusts across the long axis of the posterior TFL fibres.

 

Additional release of TFL contractions is possible by use of elbow or heel of hand �stripping� of the structure, neuromuscular deep tissue approaches (using thumb or a rubber-tipped T-bar) applied to the upper fibres and those around the knee, and specific deep tissue release methods. Most of these are distinctly uncomfortable and all require expert tuition.

 

Self-Treatment and Maintenance

 

The patient lies on her side, on a bed or table, with the affected leg uppermost and hanging over the edge (lower leg comfortably flexed). The patient may then introduce an isometric contraction by slightly lifting the hanging leg a few centimeters, and holding this position for 10 seconds, before slowly releasing and allowing gravity to take the leg towards the floor, so introducing a greater degree of stretch.

 

This is held for up to 30 seconds and the process is then repeated several times in order to achieve the maximum available stretch in the tight soft tissues. The counterforce in this isometric exercise is gravity.

 

Dr. Alex Jimenez offers an additional assessment and treatment of the hip flexors as a part of a referenced clinical application of neuromuscular techniques by Leon Chaitow and Judith Walker DeLany. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

By Dr. Alex Jimenez

 

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Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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WELLNESS TOPIC: EXTRA EXTRA: Managing Workplace Stress

 

 

Suffer From Sciatica: Chiropractic Care Reduces Pain, Promotes Healing

Suffer From Sciatica: Chiropractic Care Reduces Pain, Promotes Healing

Suffer Sciatica: Are you experiencing pain along one side of your body from your lower back down through your hip and the back of your leg? If so, you could be suffering from a condition called sciatica.

According to the Mayo Clinic, sciatica can best be described as “most commonly occurring when a herniated disk or a bone spur on the spine compresses part of the nerve. This causes inflammation, pain and often some numbness in the affected leg.”

A variety of issues weigh in on an individual’s likelihood of ending up with sciatica. Most of them deal with increased pressure on the spine.

Suffer Sciatica: Causes

Obesity: carrying too much weight is instrumental in bringing on a number of health related issues. Extra pounds overload the spine, causing damage that results in sciatica.

Improper Lifting: Individuals who frequently twist the bodies and lift heavy loads are more likely to suffer from sciatica. Certain jobs that require these movements are a key cause of the condition.

Sedentary Lifestyle. A person’s job does not have to involve lifting to be responsible for this condition. Sitting for extended periods without stretching or standing puts excess pressure on the spine and can cause sciatica.

Too Many Birthdays. Getting older can affect all of our body’s joints and bones in a negative manner, especially if we never committed to an exercise routing. An individual’s back often deteriorates with age, causing bone spurs and herniated disks that sometimes result in sciatica.

Treatment options for sciatica are varied, and the choice depends on the severity of the condition.

Pain Medication: A common and easy way to treat sciatica is with drug therapy. Anti-inflammatory drugs are frequently used to reduce�the inflammation around the nerve, which is a big contributor of the pain. Over-the-counter pain medicines, as well as codeine, may also help with pain management.

suffer medical diagnosis of a pinched nerve

Acupuncture. Alternative therapies like acupuncture have shown positive results in the treatment of sciatica. If a drug-free treatment option appeals to you, find an experienced acupuncturist in your area and talk to them about treatment options.

Strengthening Exercises. A consistent exercise program strengthens your muscles and helps the body function effectively. Ask your doctor which exercises assist the body with bouncing back from sciatica.

Supplements. Supplying the body with vital vitamins and minerals assists in overall health in general, including improvement from sciatica. Daily doses of supplements such as calcium, magnesium, St. John’s Wort, and Vitamin B12 have shown to treat sciatica effectively.

Chiropractic Care. Chiropractors understand all things spine-related, and work with the body as a whole to help it heal itself. Chiropractic treatment for sciatica works to align the spine and reduce the stress to the lower back. Treatment helps alleviate the underlying causes of the condition, and shows positive results in a short amount of time.

Cortisone Injections. Most of the time, sciatica can be treated by the less invasive measures mentioned above. However, severe bouts of sciatica may require a shot of cortisone directly into the inflamed area. Individuals generally choose this option when other treatments have garnered no relief.

Dealing with sciatica is painful and irritating, as the condition often sidelines the sufferer from daily activities. By knowing the treatment options that are effective in combating both the underlying causes and the pain of sciatica, sufferers can begin a regimen that will help them get back on their feet, pain-free in the shortest period of time possible and no longer have to suffer.

If you are suffering from sciatica and would like to talk to an experienced chiropractor about how to treat the condition, contact us today.

Sciatica

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Environmental Factors for Autoimmune Diseases

Environmental Factors for Autoimmune Diseases

It has currently been accepted that the interaction between environmental factors, and that of certain genes, can influence the destructive immune response characterized in many autoimmune diseases. As a matter of fact, approximately less than 10 percent of those people with a higher genetic susceptibility to disease may actually develop autoimmunity. This implies a solid environmental cause behind the beginning of the autoimmune process. Environmental factors have also been believed to likely affect the results of the process as well as the rate of development of autoimmune diseases. One theory is that intestinal luminal antigens absorbed through the gut might be involved in the pathogenesis of autoimmune diseases. The intestinal epithelium is the largest mucosal surface in the human body and it provides a connection between the external environment and the mammalian host.

 

What environmental factors cause autoimmune diseases?

 

Healthy, mature intestinal mucosa with its absolute tight junctions, or TJs, is the most significant barrier for the passage of macromolecules, as seen on Figure 1. In a physiological state, quantitatively small but immunologically active antigens can cross the mucosal barrier. These antigens are absorbed through the mucosa via two practical paths. The massive collection of absorbed proteins, amounting to about 90 percent, cross the intestinal barrier throughout the transcellular pathway followed by lysosomal degradation which converts the proteins into smaller, non-immunogenic peptides. The remaining proteins are then carried as entire proteins, causing antigen-specific immune responses in the body. This occurrence utilizes the Microfold (M) cell pathway or the paracellular pathway, which requires a subtle but complex balance of intercellular TJs that can result in antigenic tolerance.

 

Figure 1 Macroscopic Arrangement and Microscopic Composition of Intercellular Tight Junctions Image 1

Figure 1

 

After the integrity of the intestinal barrier are compromised, best known as TJ disassembly, an immune response to environmental antigens that spanned the gut mucosa can grow, leading to autoimmune diseases or allergies. The cells that play a vital part in this immune response lie in close proximity to the intestinal epithelial barrier. Another critical component for this immune response is the human leukocyte antigen, or HLA, system. HLA class I and II genes encode the antigen presenting cell (APC) glycoprotein receptors that present antigens to T cells in the intestinal mucosa. Susceptibility to up to 50 diseases, such as celiac disease, or CD, and type 1 diabetes, or T1D, has been associated with certain HLA class I or class II alleles. A typical denominator of these diseases is the occurrence of numerous preexisting conditions which can lead to autoimmunity. The first is a hereditary susceptibility for the host immune system to recognize, and potentially misinterpret, an environmental antigen introduced within the gastrointestinal tract, or GI tract. Second, the host needs to be exposed to the antigen. Finally, the antigen needs to be introduced into the gastrointestinal mucosal immune system, following its M-cell passage or paracellular passage, usually blocked by TJ competency, from the intestinal lumen to acquire the intestine submucosa. In most instances, higher intestinal permeability precedes disease and triggers an abnormality in antigen delivery which triggers an immune response, ultimately causing autoimmunity. Researchers have therefore hypothesized that genes, environment, and decreased intestinal barrier function are all critical to develop autoimmune diseases, especially CD and T1D.

 

Gliadin as an Environmental Factor of Autoimmune Diseases

 

Celiac Disease

 

Gluten is a well-known environmental factor that triggers celiac disease. It is the gliadin fraction of wheat germ and equal alcohol-soluble proteins in distinct grains, known as prolamins, which are connected to the growth of intestinal damage. A standard characteristic of the prolamins of wheat, rye, and barley is a greater content of glutamine (>30%) and proline (>15%), whereas the non-toxic prolamins of rice and corn have decreased glutamine and proline content. However, the environmental factor that influenced the development CD is complex and unknown. Some aspects of gluten consumption might help determine the risk of CD incidence, particularly in: the amount of gluten intake, the higher the amount, the larger the risk; the caliber of consumed gluten, a few grains contain more hazardous epitopes than others; and the pattern/timing of infant feeding. Recent research studies suggest that the pattern of infant nutrition might have a very important role on the development of the CD as well as that of other autoimmune diseases. Breastfeeding is believed to delay or reduce the possibility of developing CD. The positive effects of breast milk may be attributed to its influence on the microbial colonization procedure for the own newborn’s intestine. The genus Bifidobacterium is predominant in the feces of breast-fed infants, while a larger variety of bacterial groups, including Bacteroides, Streptococcus, Clostridium, etc., are found in the fecal microbiota of all formula-fed infants. Changes in the composition of the intestinal microbiota also occur as a consequence of the following changes from breastfeeding or formula feeding to weaning and even the introduction of solid food. Alterations in the intestinal balance between favorable and possibly harmful bacteria have also been associated with allergy symptoms, type 1 diabetes and inflammatory bowel diseases, among others.

 

Type 1 Diabetes

 

It is believed that genetically predisposed individuals develop T1D after encountering one or more environmental factors of the disease. Fast improvements could be made in disease prevention and treatment if these environmental factors were identified. Amongst the others, gliadin has only been the subject of a series of research studies that aim at establishing its part in the pathogenesis of type 1 diabetes. Early introduction of gliadin-containing cereals were reported to raise the prospect of islet cell autoimmunity in humans. Gliadin-specific, lamina propria-derived T cells play an important role in the pathogenesis of CD. The same HLA class II haplotype, DQ (? 1 * 0501, �1 * 0201), that can be connected with gliadin peptides in CD is also one of two HLA class II haplotypes inherited most frequently by people with T1D. There are also signs of immunological activity in the intestine of T1D patients: jejunal specimens from T1D patients have been found to consist of much higher doses of interferon gamma (IFN?)- and tumor necrosis factor-alpha (TNF-?) positive cells in contrast to people with healthy controls, suggesting an inflammatory response. Still another study found substantially increased manifestation of HLA-DR and HLA-DP molecules on intestinal villi of jejunal specimens from T1D patients in comparison with specimens from healthy controls. Recent evidence confirmed these findings by assessing the mucosal immune response to gliadin in the jejunum of patients with T1D. Small intestinal biopsies from children with T1D were cultured with gliadin and evaluated for epithelial infiltration and lamina propria T-cell activation. The caliber of intraepithelial CD3+ cells and of lamina propria CD25+ mononuclear cells has been higher in jejunal biopsies from T1D patients versus control subjects. In the patients’ biopsies cultured with enzymatically treated gliadin, there was epithelial infiltration by CD3 cells, a more significant growth in lamina propria CD25+ and CD80+ cells, enhanced manifestation of lamina propria cells favorable into ligand and receptor molecules ?4/?7 and ICAM 1, along with enhanced expression of CD54 and crypt HLA-DR. Also, ?4 positive T cells have been recovered in the pancreatic islets of an T1D person, providing an immediate connection between gliadin-activated T cells and destruction of pancreatic islet cells.

 

Findings from research studies using non-obese diabetic, or NOD, mice in addition to the BioBreeding diabetes-prone, or BBDP, rats have also implicated wheat gliadin as a nutritional supplement diabetogen. In BBDP rats, gliadin vulnerability is accompanied by increased intestinal permeability, and changes in gut microbiota composition, as seen on Figure 2., presumably allow food antigens to grow in contact with all the underlying lamina propria. Feeding NOD mice and BBDP rats a gluten free hydrolyzed casein diet resulted in a delay and decline in T1D development. Interestingly, these T1D animal models additionally demonstrated the moment of exposure to wheat proteins is quite important to the development of T1D. Delaying the vulnerability of diabetogenic wheat proteins by prolonging the breastfeeding period decreased T1D expansion from the BBDP rats. What is more, exposing neonatal rats or mice to diabetogenic wheat components or bacterial antigens diminished T1D incidence, which is perhaps due to the induction of immunological tolerance.

 

Figure 2 Postulated Mechanism of Action of Gluten in T1D Pathogenesis Image 2

Figure 2

 

Rats that were fed corn protein-based diets developed T1D and demonstrated a moderate celiac-like enteropathy. Mesenteric lymph nodes, or MLNs, which drain the gut, are the substantial inductive site where dietary antigens are famous in the gut-associated connective tissue. The authors described an increase in the expression ratio of T-bet:Gata3, master transcription factors for Th1 and Th2 cytokines, respectively, in the MLN by wheat-fed BBDP rats compared to this by BBDR rats, mainly due to diminished Gata3 expression. Also, CD3+CD4+IFN?+ T cells were prevalent in the MLN of wheat-fed BBDP rats, but remained at control levels in BBDP rats fed with a diabetes-retardant wheat-free diet. BioBreeding diabetes-prone MLN cells increased quickly in response to wheat protein antigens in a particular, dose-dependent manner, and 93 percent of cells were CD3+CD4+ T cells. This proliferation was connected using a minimum proportion of CD4+CD25+ T cells and a greater proportion of dendritic cells in the MLN of BBDP rats. These results suggest that, before insulitis is established, the MLNs of wheat-fed BBDP rats contain a remarkably large proportion of Th1 cells that rapidly increased particularly in response to wheat protein antigens. Collectively, these research studies suggest a deranged mucosal immune response to gliadin in T1D and a direct connection between gliadin-induced stimulation of gut mucosal T cells and abuse of pancreatic islet cells, as seen on Figure 2.

 

Link between Gliadin, Zonulin & Increased Intestinal Permeability in Autoimmune Diseases

 

Researchers have generated enough evidence to support that gliadin can induce increased intestinal permeability by releasing preformed zonulin. Intestinal cell lines exposed to gliadin released zonulin from the cell medium with subsequent zonulin binding to the cell surface, rearrangement of the cell cytoskeleton, loss of occludin-ZO1 protein interaction, and increased monolayer permeability. Pre-treatment with all of the zonulin antagonist AT1001 blocked these alterations without affecting zonulin release. When exposed to luminal gliadin, intestinal biopsies from patients with celiac disease in remission expressed a continuous luminal zonulin discharge and increase in intestinal permeability. On the contrary, biopsies from non-CD patients showed a limited, transient zonulin release, which was paralleled by a decline in intestinal permeability that had not reached the level of permeability found in celiac disease cells. As a matter of fact, when gliadin was added to the basolateral side of cell lines or intestinal biopsies, no zonulin release was detected. The latter finding indicates that gliadin interacts using an intestinal luminal receptor, which encouraged researchers to comprehend this issue. In vitro experiments revealed specific colocalization of gliadin along with the chemokine receptor CXCR3 expressed in human and mouse intestinal epithelium and lamina propria. Gliadin vulnerability led to a tangible establishment of CXCR3 and MyD88. Ex vivo experiments revealed that gliadin exposure to intestinal segments from wild-type mice increased zonulin terminal and intestinal permeability, whereas CXCR3 intestinal segments failed to respond to gliadin. The increased intestinal permeability appeared cause a specific impact for gliadin, because the subsequent CXCR3 ligand, IP-10, did not affect intestinal barrier function. Based on these figures, researchers suggested that gliadin contrasts to CXCR3 additionally lead to stimulation of the zonulin pathway and improved intestinal permeability in a MyD88-dependent manner.

 

Conclusive Remarks

 

The classical paradigm of the pathogenesis of autoimmune diseases involving certain receptor makeup and exposure to environmental factors was contested with the addition of a third component, the decrease of intestinal barrier function. Genetic predisposition, miscommunication between innate and adaptive immunity, exposure to environmental factors and loss in intestinal barrier function secondary to the breakdown of intercellular tight junctions, or TJs, seem to be vital components in the pathogenesis of autoimmune disorders. Both in CD and T1D gliadin may play a role in inducing loss of intestinal barrier function or inducing the gastrointestinal response in genetically predisposed individuals. This new hypothesis suggests that after the digestive process is triggered, it is not auto-perpetuating, but rather, it might be balanced or reversed by preventing the continuous interaction between genes and the environment. Since TJ dysfunction allows this interaction, new treatment procedures targeted at re-establishing the intestinal barrier function supply innovative, unexplored procedures for caring for autoimmune diseases. Information referenced from the National Center for Biotechnology Information (NCBI) and the National University of Health Sciences. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

By Dr. Alex Jimenez

 

Green-Call-Now-Button-24H-150x150-2-3.png

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

blog picture of cartoon paperboy big news

 

WELLNESS TOPIC: EXTRA EXTRA: Managing Workplace Stress

 

 

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Expectant Mothers Benefit From Chiropractic Care

Expectant Mothers Benefit From Chiropractic Care

Expectant Mothers: Pregnancy is an exciting, precious time in a woman’s life, full of new experiences. Unfortunately, the baby’s development brings about bodily changes that often wreak havoc on the back and joints, and end up causing pain. These issues also frequently cause issues during delivery, and increase the time it takes for the body to recover post-pregnancy.

Expectant moms benefit from chiropractic care in a number of ways. Here are five key ways chiropractic care helps alleviate the toll pregnancy takes on a woman’s body.

#1: Expectant Mothers: Chiropractic Keeps The Spine In Alignment.

Pregnancy adds significant additional weight to a woman’s body in a short amount of time. This change bears on the spine, frequently pulling it out of alignment.

When this happens, the pain can be quite severe. Chiropractic care during pregnancy works to keep the spine in alignment and all supporting tendons working optimally, to be better prepared and able to adequately support the extra weight.

#2: Chiropractic Reduces Need For Pain Relievers.

Most times, individuals experiencing moderate pain pop a couple of over the counter pain relievers and think nothing of it. However, pregnant women strive to avoid medications when possible.

Chiropractic adjustments decrease the underlying issues that cause pain, so the patient relies less on medications. Experiencing less pain as well as eliminating the need for pain killers is a win-win situation for expectant mothers.

expectant#3: Chiropractic Strengthens And Repairs Joints.

Pregnancy really beats up an expectant mothers joints. Chiropractic care for expectant mothers is a productive way to minimize the effect the large, protruding abdomen has on her hips, legs, and ankles.

Treating the body as a whole, chiropractic treatment works to strengthen the body and promotes healing of injured or strained areas.

#4: Chiropractic Helps Achieve Pelvic Alignment.

An aligned pelvis is critical to the birthing process, and increases the chances of being able to give birth naturally. According to the American Pregnancy Association,

“When the pelvis is misaligned it may reduce the amount of room available for the developing baby. This restriction is called intrauterine constraint. A misaligned pelvis may also make it difficult for the baby to get into the best possible position for delivery. This can affect the mother�s ability to have a natural, non-invasive birth.”

An experienced chiropractor can effectively align the pelvis before delivery, so the mother is able to deliver with little incident.

#5: Chiropractic Increases The Body’s Ability To Bounce Back.

Let’s face it, every pregnant woman thinks “will I ever fit in the clingy red dress again?” The healthier and stronger a woman’s body is before and during pregnancy, the easier it is to get back into shape once the baby is born. Eating right and safely exercising are effective ways to accomplish this.

Chiropractic care is also a valuable component to fitness. Expectant mothers who choose chiropractic enjoy better posture, less pain, and increased mobility, especially late in the third trimester.

This allows them to maintain exercise routines and be active longer than those suffering from back pain and achy joints. After the delivery, it’s easier to get back into a fitness routine, and into that red dress, if the new mother’s joints, back, and hips are aligned and functioning properly.

Chiropractic care can serve to reduce pain and increase the overall heath of expectant mothers, letting her relax and focus on the more pleasant aspects of pregnancy. Expecting women who commit to chiropractic care can look forward to a stronger body, the chances of a smoother delivery, and an easier recovery after the baby comes.

Pregnancy & Chiropractic Care

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Chronic Ear Infections And Children: The Chiropractic Answer

Chronic Ear Infections And Children: The Chiropractic Answer

Ear Infections: “Mom, it hurts. It hurts!”

Parents of children suffering from ear infections are all too familiar with this cry. Tugging at their ears, crying, and trouble sleeping are all signs of an ear infection in your little one.

Children are more susceptible to ear infections than adults because of their smaller Eustachian tubes, and their less effective immune systems. Unfortunately, chronic ear infections can quickly become a painful, ongoing problem.

Parents have a variety of options at their disposal to treat their child’s ear infections. Drops, antibiotics, and ventilation tubes placed by surgical procedure are all commonly used treatments for chronic infections. Chiropractic care is another option available and is rapidly gaining acceptance and popularity for the effective treatment of ear infections.

According to HealthyChild.com, ear infections are the reason for 35% of pediatrician visits, and ear pain is the number one reason a child visits a chiropractor. Children who suffer from recurring ear infections benefit from chiropractic care in several ways that are not available through other, more traditional forms of treatment.

Here are a few of the benefits chiropractic care offer for ear infections are:

Ear Infections: It Is Non-Invasive

Unlike the surgical procedure that is often used to combat ear infections by inserting tubes in the child’s ears, chiropractic adjustments provide a non-invasive form of treatment.

This treatment option works well because a little one’s spine may be moved out of alignment from the birthing process, or from any number of spills he or she makes learning to walk, run, or navigate stairs. An experienced chiropractor can map out a treatment plan that includes gentle adjustments of the child’s neck and spine. The goal is to decrease fluid build up within the ear canals that bring on ear infections and pain.

It Is A Painless Option Of Treatment

The last thing parents want in any medical treatment is to cause their child more pain. A negative experience at a doctor’s office can create a fear that lasts for years to come.

Children with ear infections have nothing to fear from visiting a chiropractor. During a chiropractic visit, the child will participate in adjustments that are pain free. The treatments will be able to reduce the pain in a short amount of time in many instances, and reduce the chance of dealing with another ear infection down the road.

ear infectionsIt Treats The Underlying Cause

Other options of treatment may decrease the symptoms of an ear infection, but never get to the actual root issue. Chiropractic care strives to return the body in its entirety to its normal function.

This is the main building block concept for chiropractic in general. By re-aligning the spine, the body as a whole can be healthier and more resistant to infection and disease. Chiropractic care helps adjust the child’s body back to a normal state, thus providing a way for it to heal itself and fight off future ear (and other) infections better than simply using drops and antibiotics.

If your child is susceptible to ear infections, there are steps you can take to minimize the chances of an occurrence in the first place. Frequent hand washing to prevent the spread of germs and avoiding cigarette smoke are two simple ways to combat ear infections.

Chiropractic treatment continues to show promise in treating the underlying issues that cause a child to suffer from ear infections. If you are looking for a treatment that is pain free, not intimidating to the child, and an alternative to invasive surgery, enlisting the help of a chiropractor is a fantastic option.

So if your child is experiencing chronic ear infections, give us a call. Our Doctor of Chiropractic is here to help!

Doctors Of Chiropractic Ensure Patients Have Strong Posture

This article is copyrighted by Blogging Chiros LLC for its Doctor of Chiropractic members and may not be copied or duplicated in any manner including printed or electronic media, regardless of whether for a fee or gratis without the prior written permission of Blogging Chiros, LLC.

Muscle Energy Techniques (MET): Introduction

Muscle Energy Techniques (MET): Introduction

Muscle Energy Techniques: A revolution has taken place in manipulative therapy involving a movement away from high velocity/low amplitude thrusts (HVT � now commonly known as �mobilization with impulse� and characteristic of most chiropractic and, until recently, much osteopathic manipulation) towards gentler methods which take far more account of the soft tissue component (DiGiovanna 1991, Lewit 1999, Travell & Simons 1992).

Greenman (1996) states that: �Early [osteopathic] techniques did speak of muscle relaxation with soft tissue procedures, but specific manipulative approaches to muscle appear to be 20th century phenomena.� One such approach � which targets the soft tissues primarily, although it also makes a major contribution towards joint mobilization � has been termed muscle energy technique (MET) in osteopathic medicine. There are a variety of other terms used to describe this approach, the most general (and descriptively accurate) of which was that used by chiropractor Craig Liebenson (1989, 1990) when he described muscle energy techniques as �active muscular relaxation techniques�. Muscle energy techniques evolved out of osteopathic procedures developed by pioneer practitioners such as T. J. Ruddy (1961), who termed his approach �resistive duction�, and Fred Mitchell Snr (1967). As will become clear in this chapter, there also exists a commonality between Muscle energy techniques and various procedures used in orthopaedic and physiotherapy methodology, such as proprioceptive neuromuscular facilitation (PNF). Largely due to the work of experts in physical medicine such as Karel Lewit (1999), MET has evolved and been refined, and now crosses all interdisciplinary boundaries.

MET has as one of its objectives the induced relaxation of hypertonic musculature and, where�appropriate (see below), the subsequent stretching of the muscle. This objective is shared with a number of �stretching� systems, and it is necessary to examine and to compare the potential benefits and drawbacks of these various methods (see Box 1.1).

MET, as presented in this book, owes most of its development to osteopathic clinicians such as T. J. Ruddy (1961) and Fred Mitchell Snr (1967), with more recent refinements deriving from the work of people such as Karel Lewit (1986, 1999) and Vladimir Janda (1989) of the former Czechoslovakia, both of whose work will be referred to many times in this text.

T. J. Ruddy (1961)

In the 1940s and 50s, osteopathic physician T. J. Ruddy developed a treatment method involving patient-induced, rapid, pulsating contractions against resistance which he termed �rapid resistive duction�. It was in part this work which Fred Mitchell Snr used as the basis for the evolution of MET (along with PNF methodology, see Box 1.1). Ruddy�s method called for a series of rapid, low amplitude muscle contractions against resistance, at a rate a little faster than the pulse rate. This approach is now known as pulsed MET, rather than the tongue-twisting �Ruddy�s rapid resistive duction�.

As a rule, at least initially, these patient-directed pulsating contractions involve an effort towards the barrier, using antagonists to shortened structures. This approach can be applied in all areas where sustained contraction muscle energy technique procedures are appropriate, and is particularly useful for self-treatment, following instruction from a skilled practitioner. Ruddy suggests that the effects include improved local oxygenation, venous and lymphatic circulation, as well as a positive influence on both static and kinetic posture, because of the effects on proprioceptive and interoceptive afferent pathways.

Ruddy�s work formed part of the base on which Mitchell Snr and others constructed MET and aspects of its clinical application are described in Chapter 3.

Fred Mitchell Snr

No single individual was alone responsible for MET, but its inception into osteopathic work must be credited to F. L. Mitchell Snr, in 1958. Since then his son F. Mitchell Jnr (Mitchell et al 1979) and many others have evolved a highly sophisticated system of manipulative methods (F. Mitchell Jnr, tutorial on biomechanical procedures, American Academy of Osteopathy, 1976) in which the patient �uses his/her muscles, on request, from a precisely controlled position in a specific direction, against a distinctly executed counterforce�.

Philip Greenman

Professor of biomechanics Philip Greenman (1996) states that:

The function of any articulation of the body which can be moved by voluntary muscle action, either directly or indirectly, can be influenced by muscle energy procedures … . Muscle energy techniques can be used to lengthen a shortened, contractured or spastic muscle; to strengthen a physiologically weakened muscle or group of muscles; to reduce localized edema, to relieve passive congestion, and to mobilize an articulation with restricted mobility.

Sandra Yale

Osteopathic physician Sandra Yale (in DiGiovanna 1991) extols MET�s potential in even fragile and severely ill patients:

Muscle energy techniques are particularly effective in patients who have severe pain from acute somatic dysfunction, such as those with a whiplash injury from a car accident, or a patient with severe muscle spasm from a fall. MET methods are also an excellent treatment modality for hospitalized or bedridden patients. They can be used in older patients who may have severely restricted motion from arthritis, or who have brittle osteoporotic bones.

muscle energy techniquesEdward Stiles

Among the key MET clinicians is Edward Stiles, who elaborates on the theme of the wide range of MET application (Stiles 1984a, 1984b). He states that:

Basic science data suggests the musculoskeletal system plays an important role in the function of other systems. Research indicates that segmentally related somatic and visceral structures may affect one another directly, via viscerosomatic and somaticovisceral reflex pathways. Somatic dysfunction may increase energy demands, and it can affect a wide variety of bodily processes; vasomotor control, nerve impulse patterns (in facilitation), axionic flow of neurotrophic proteins, venous and lymphatic circulation and ventilation. The impact of somatic dysfunction on various combinations of these functions may be associated with myriad symptoms and signs. A possibility which could account for some of the observed clinical effects of manipulation.

As to the methods of manipulation he now uses clinically, Stiles states that he employs muscle energy methods on about 80% of his patients, and functional techniques (such as strain/counterstrain) on 15�20%. He uses high velocity thrusts on very few cases. The most useful manipulative tool available is, he maintains, muscle energy techniques.

J. Goodridge and W. Kuchera

Modern osteopathic refinements of MET � for example the emphasis on very light contractions which has strongly influenced this text � owe much to physicians such as John Goodridge and William Kuchera, who consider that (Goodridge & Kuchera 1997):

Localization of force is more important than intensity. Localization depends on palpatory proprioceptive perception of movement (or resistance to movement) at or about a specific articulation … . Monitoring and confining forces to the muscle group or level of somatic dysfunction involved are important for achieving desirable changes. Poor results are most often due to improperly localized forces, often with excessive patient effort.

Early Sources Of Muscle Energy Techniques

MET emerged squarely out of osteopathic tradition, although a synchronous evolution of treatment methods, involving isometric contraction and stretching, was taking place independently in physical therapy, called PNF (see Box 1.1).

Fred Mitchell Snr (1958) quoted the words of the developer of osteopathy, Andrew Taylor Still: �The attempt to restore joint integrity before soothingly restoring muscle and ligamentous normality was putting the cart before the horse.� As stated earlier, Mitchell�s work drew on the methods developed by Ruddy; however, it is unclear whether Mitchell Snr, when he was refining MET methodology in the early 1950s, had any awareness of proprioceptive neuromuscular facilitation (PNF), a method which had been developed a few years earlier, in the late 1940s, in a physical therapy context (Knott & Voss 1968).

PNF method tended to stress the importance of rotational components in the function of joints and muscles, and employed these using resisted (isometric) forces, usually involving extremely strong contractions. Initially, the focus of PNF related to the strengthening of neurologically weakened muscles, with attention to the release of muscle spasticity following on from this, as well as to improving range of motion at intervertebral levels (Kabat 1959, Levine et al 1954) (see Box 1.1).

Postisometric Relaxation & Reciprocal Inhibition: Two Forms Of MET (Box 1.2)

A term much used in more recent developments of muscle energy techniques is postisometric relaxation (PIR), especially in relation to the work of Karel Lewit (1999). The term postisometric relaxation refers to the effect of the subsequent reduction in tone experienced by a muscle, or group of muscles, after brief periods during which an isometric contraction has been performed.

The terms proprioceptive neuromuscular facilitation (PNF) and postisometric relaxation (PIR) (the latent hypotonic state of a muscle following isometric activity) therefore represent variations on the same theme. A further variation involves the physiological response of the antagonists of a muscle which has been isometrically contracted � reciprocal inhibition (RI).

muscle energy techniques

When a muscle is isometrically contracted, its antagonist will be inhibited, and will demonstrate reduced tone immediately following this. Thus the antagonist of a shortened muscle, or group of muscles, may be isometrically contracted in order to achieve a degree of ease and additional movement potential in the shortened tissues.

Sandra Yale (in DiGiovanna 1991) acknowledges that, apart from the well understood processes of reciprocal inhibition, the precise reasons for the effectiveness of MET remain unclear � although in achieving PIR the effect of a sustained contraction on the Golgi tendon organs seems pivotal, since their response to such a contraction seems to be to set the tendon and the muscle to a new length by inhibiting it (Moritan 1987). Other variations on this same theme include �hold�relax� and �contract�relax� techniques (see Box 1.1).

Lewit & Simons (1984) agree that while reciprocal inhibition is a factor in some forms of therapy related to postisometric relaxation techniques, it is not a factor in PIR itself, which is a phenomenon resulting from a neurological loop, probably involving the Golgi tendon organs (see Figs 1.1 and 1.2).

muscle energy techniquesmuscle energy techniquesLiebenson (1996) discusses both the benefits of, and the mechanisms involved in, use of muscle energy techniques (which he terms �manual resistance techniques�, or MRT):

Two aspects to MRT [i.e. MET by another name] are their ability to relax an overactive muscle … and their ability to enhance stretch of a shortened muscle or its associated fascia when connective tissue or viscoelastic changes have occurred.

Two fundamental neurophysiological principles account for the neuromuscular inhibition that occurs during application of these techniques. The first is postcontraction inhibition [also known as postisometric relaxation, or PIR], which states that after a muscle is contracted, it is automatically in a relaxed state for a brief, latent, period. The second is reciprocal inhibition (RI) which states that when one muscle is contracted, its antagonist is automatically inhibited.

Liebenson suggests that there is evidence that the receptors responsible for PIR lie within the muscle and not in the skin or associated joints (Robinson 1982).

Where pain of an acute or chronic nature makes controlled contraction of the muscles involved difficult, the therapeutic use of the antagonists can patently be of value. Thus modern MET incorporates both postisometric relaxation and reciprocal inhibition methods, as well as aspects unique to itself, such as isokinetic techniques, described later.

A number of researchers, including Karel Lewit of Prague (Lewit 1999), have reported on the usefulness of aspects of MET in the treatment of trigger points, and this is seen by many to be an excellent method of treating these myofascial states, and of achieving the restoration of a situation where the muscle in which the trigger lies is once more capable of achieving its full resting length, with no evidence of shortening.

Travell & Simons (1992) mistakenly credited Lewit with developing MET, stating that �The concept of applying post-isometric relaxation in the treatment of myofascial pain was presented for the first time in a North American journal in 1984 [by Lewit]�. In fact Mitchell Snr had described the method some 25 years previously, a fact acknowledged by Lewit (Lewit & Simons 1984).

Key Points About Modern Muscle Energy Techniques

MET methods all employ variations on a basic theme. This primarily involves the use of the patient�s own muscular efforts in one of a number of ways, usually in association with the efforts of the therapist:

1. The operator�s force may exactly match the effort of the patient (so producing an isometric contraction) allowing no movement to occur � and producing as a result a physiological neurological response (via the Golgi tendon organs) involving a combination of:

� reciprocal inhibition of the antagonist(s) of the muscle(s) being contracted, as well as

� postisometric relaxation of the muscle(s) which are being contracted.

  1. The operator�s force may overcome the effort of the patient, thus moving the area or joint in the direction opposite to that in which the patient is attempting to move it (this is an isotonic eccentric contraction, also known as an isolytic contraction).
  2. The operator may partially match the effort of the patient, thus allowing, although slightly retarding, the patient�s effort (and so producing an isotonic concentric, isokinetic, contraction).

Other variables may be also introduced, for example involving:

l Whether the contraction should commence with the muscle or joint held at the resistance barrier or short of it � a factor decided largely on the basis of the degree of chronicity or acuteness of the tissues involved

  • How much effort the patient uses � say, 20% of strength, or more, or less
  • The length of time the effort is held � 7�10 seconds, or more, or less (Lewit (1999) favours 7� 10 seconds; Greenman (1989), Goodridge & Kuchera (1997) all favour 3�5 seconds)
  • Whether, instead of a single maintained contraction, to use a series of rapid, low amplitude contractions (Ruddy�s rhythmic resisted duction method, also known as pulsed muscle energy techniques)
  • The number of times the isometric contraction (or its variant) is repeated � three repetitions are thought to be optimal (Goodridge & Kuchera 1997)
  • The direction in which the effort is made � towards the resistance barrier or away from it, thus involving either the antagonists to the muscles or the actual muscles (agonists) which require �release� and subsequent stretching (these variations are also known as �direct� and �indirect� approaches, see p. 8)
  • Whether to incorporate a held breath and/or specific eye movements to enhance the effects of the contraction � desirable if possible, it is suggested (Goodridge & Kuchera 1997, Lewit 1999)
  • What sort of resistance is offered (for example by the operator, by gravity, by the patient, or by an immovable object)
  • Whether the patient�s effort is matched, overcome or not quite matched � a decision based on the precise needs of the tissues � to achieve relaxation, reduction in fibrosis or tonifying/ reeducation
  • Whether to take the muscle or joint to its new barrier following the contraction, or whether or not to stretch the area/muscle(s) beyond the barrier � this decision is based on the nature of�the problem being addressed (does it involve shortening? fibrosis?) and its degree of chronicity
  • Whether any subsequent (to a contraction) stretch is totally passive, or whether the patient should participate in the movement, the latter being thought by many to be desirable in order to reduce danger of stretch reflex activation (Mattes 1995)
  • Whether to utilize Muscle energy techniques alone, or in a sequence with other modalities such as the positional release methods of strain/counterstrain, or the ischaemic compression/inhibitory pressure techniques of neuromuscular technique (NMT) � such decisions will depend upon the type of problem being addressed, with myofascial trigger point treatment frequently benefiting from such combinations (see description of integrated neuromuscular inhibition (INIT), p. 197 (Chaitow 1993)).

Greenman summarises the requirements for the successful use of MET in osteopathic situations as �control, balance and localisation�. His suggested basic elements of MET include the following:

  • A patient/active muscle contraction, which
    � commences from a controlled position
    � is in a specific direction (towards or away from a restriction barrier)
  • The operator applies distinct counterforce (to meet, not meet, or to overcome the patient�s force)
  • The degree of effort is controlled (sufficient to obtain an effect but not great enough to induce trauma or difficulty in controlling the effort).

What is done subsequent to the contraction may involve any of a number of variables, as will be explained.

The essence of MET then is that it uses the energy of the patient, and that it may be employed in one or other of the manners described above with any combination of variables depending upon the particular needs of the case. Goodridge (one of the first osteopaths to train with Mitchell Snr in 1970) summarises as follows: �Good results [with MET] depend on accurate diagnosis, appropriate levels of force, and sufficient localization. Poor results are most often caused by inaccurate diagnosis, improperly localized forces, or forces that are too strong� (Goodridge & Kuchera 1997) (see also Box 1.3).

muscle energy techniquesUsing agonist or antagonist? (Box 1.4)

As mentioned, a critical consideration in MET, apart from degree of effort, duration and frequency of use, involves the direction in which the effort is made. This may be varied, so that the operator�s�force is directed towards overcoming the restrictive barrier (created by a shortened muscle, restricted joint, etc.); or indeed opposite forces may be used, in which the operator�s counter-effort is directed away from the barrier.

There is general consensus among the various osteopathic experts already quoted that the use of postisometric relaxation is more useful than reciprocal inhibition in normalizing hypertonic musculature. This, however, is not generally held to be the case by experts such as Lewit and Janda, who see specific roles for the reciprocal inhibition variation.

muscle energy techniques

Osteopathic clinicians such as Stiles and Greenman believe that the muscle which requires stretching (the agonist) should be the main source of �energy� for the isometric contraction, and suggest that this achieves a more significant degree of relaxation, and so a more useful ability to subsequently stretch the muscle, than would be the case were the relaxation effect being achieved via use of the antagonist (i.e. using reciprocal inhibition).

Following on from an isometric contraction � whether agonist or antagonist is being used � there is a refractory, or latency, period of approximately 15 seconds during which there can be an easier (due to reduced tone) movement towards the new position (new resistance barrier) of a joint or muscle.

Variations On The Muscle Energy Techniques Theme

Liebenson (1989, 1990) describes three basic variations which are used by Lewit and Janda as well as by himself in a chiropractic rehabilitation setting.

Lewit�s (1999) modification of MET, which he calls postisometric relaxation, is directed towards relaxation of hypertonic muscle, especially if this relates to reflex contraction or the involvement of myofascial trigger points. Liebenson (1996) notes that �this is also a suitable method for joint mobilisation when a thrust is not desirable�.

Lewit�s postisometric relaxation method

(Lewit 1999)

  1. The hypertonic muscle is taken, without force or �bounce�, to a length just short of pain, or to the point where resistance to movement is first noted (Fig. 1.3).
  2. The patient gently contracts the affected hypertonic muscle away from the barrier (i.e. the agonist is used) for between 5 and 10 seconds, while the effort is resisted with an exactly equal counterforce. Lewit usually has the patient inhale during this effort.
  3. This resistance involves the operator holding the contracting muscle in a direction which would stretch it, were resistance not being offered.
  4. The degree of effort, in Lewit�s method, is minimal. The patient may be instructed to think in terms of using only 10 or 20% of his available strength, so that the manoeuvre is never allowed to develop into a contest of strength between the operator and the patient.
  5. After the effort, the patient is asked to exhale and to let go completely, and only when this is achieved is the muscle taken to a new barrier with all slack removed but no stretch � to the extent that the relaxation of the hypertonic muscles will now allow.
  6. Starting from this new barrier, the procedure is repeated two or three times.
  7. In order to facilitate the process, especially where trunk and spinal muscles are involved, Lewit usually asks the patient to assist by looking with his eyes in the direction of the contraction during the contracting phase, and in the direction of stretch during the stretching phase of the procedure.

The key elements in this approach, as in most MET, involve precise positioning, as well as taking out slack and using the barrier as the starting and ending points of each contraction.

muscle energy techniquesWhat Is Happening?

Karel Lewit, discussing MET methods (Lewit 1999), states that medullary inhibition is not capable of explaining their effectiveness. He considers that the predictable results obtained may relate to the following facts:

  • During resistance using minimal force (isometric contraction) only a very few fibers are active, the others being inhibited
  • During relaxation (in which the shortened musculature is taken gently to its new limit without stretching) the stretch reflex is avoided � a reflex which may be brought about even by passive and non-painful stretch (see Mattes� views p. 3).

He concludes that this method demonstrates the close connection between tension and pain, and between relaxation and analgesia.

The use of eye movements as part of the methodology is based on research by Gaymans (1980) which indicates, for example, that flexion is enhanced by the patient looking downwards, and extension by the patient looking upwards. Similarly, sidebending is facilitated by looking towards the side involved. These ideas are easily proved by self-experiment: an attempt to flex the spine while maintaining the eyes in an upwards (towards the forehead) looking direction will be found to be less successful than an attempt made to flex while looking downwards. These eye-direction aids are also useful in manipulation of the joints.

Effects of Muscle energy techniques

Lewit (1999) discusses the element of passive muscular stretch in MET and maintains that this factor does not always seem to be essential. In some areas, self-treatment, using gravity as the resistance factor, is effective, and such cases sometimes involve no element of stretch of the muscles in question. Stretching of muscles during MET, according to Lewit (1999), is only required when contracture due to fibrotic change has occurred, and is not necessary if there is simply a disturbance in function. He quotes results in one series of patients in his own clinic in which 351 painful muscle groups, or muscle attachments, were treated by MET (using postisometric�relaxation) in 244 patients. Analgesia was immediately achieved in 330 cases and there was no effect in only 21 cases. These are remarkable results by any standards.

Lewit suggests, as do many others, that trigger points and �fibrositic� changes in muscle will often disappear after MET contraction methods. He further suggests that referred local pain points, resulting from problems elsewhere, will also disappear more effectively than where local anaesthesia or needling (acupuncture) methods are employed.

Janda�s postfacilitation stretch method

Janda�s variation on this approach (Janda 1993), known as �postfacilitation stretch�, uses a different starting position for the contraction and also a far stronger isometric contraction than that suggested by Lewit and most osteopathic users of Muscle energy techniques:

  1. The shortened muscle is placed in a mid-range position about halfway between a fully stretched and a fully relaxed state.
  2. The patient contracts the muscle isometrically, using a maximum degree of effort for 5�10 seconds while the effort is resisted completely.
  3. On release of the effort, a rapid stretch is made to a new barrier, without any �bounce�, and this is held for at least 10 seconds.
  4. The patient relaxes for approximately 20 seconds and the procedure is repeated between three and five times more.

Some sensations of warmth and weakness may be anticipated for a short while following this more vigorous approach.

Reciprocal inhibition variation

This method, which forms a component of PNF methodology (see Box 1.1) and Muscle energy techniques, is mainly used in acute settings, where tissue damage or pain precludes the use of the more usual agonist contraction, and also commonly as an addition to such methods, often to conclude a series of stretches whatever other forms of MET have been used (Evjenth & Hamberg 1984):

  1. The affected muscle is placed in a mid-range position.
  2. The patient is asked to push firmly towards the restriction barrier and the operator either completely resists this effort (isometric) or allows a movement towards it (isotonic). Some degree of rotational or diagonal movement may be incorporated into the procedure.
  3. On ceasing the effort, the patient inhales and exhales fully, at which time the muscle is passively lengthened.

Liebenson notes that �a resisted isotonic effort towards the barrier is an excellent way in which to facilitate afferent pathways at the conclusion of treatment with active muscular relaxation techniques or an adjustment (joint). This can help reprogram muscle and joint proprioceptors and thus re-educate movement patterns.� (See Box 1.2.)

Strengthening variation

Another major muscle energy variation is to use what has been called isokinetic contraction (also known as progressive resisted exercise). In this the patient starts with a weak effort but rapidly progresses to a maximal contraction of the affected muscle(s), introducing a degree of resistance to the operator�s effort to put the joint, or area, through a full range of motion. The use of isokinetic contraction is reported to be a most effective method of building strength, and to be superior to high repetition, lower resistance exercises (Blood 1980). It is also felt that a limited range of motion, with good muscle tone, is preferable (to the patient) to having a normal range with limited power. Thus the strengthening of weak musculature in areas of permanent limitation of mobility is seen as�an important contribution in which isokinetic contractions may assist.

Isokinetic contractions not only strengthen the fibres which are involved, but also have a training effect which enables them to operate in a more coordinated manner. There is often a very rapid increase in strength. Because of neuromuscular recruitment, there is a progressively stronger muscular effort as this method is repeated. Isokinetic contractions, and accompanying mobilisation of the region, should take no more than 4 seconds at each contraction in order to achieve maximum benefit with as little fatiguing as possible, either of the patient or the operator. Prolonged contractions should be avoided. The simplest, safest, and easiest-to-handle use of isokinetic methods involves small joints, such as those in the extremities. Spinal joints may be more difficult to mobilise while muscular resistance is being fully applied.

The options available in achieving increased strength via these methods therefore involve a choice between either a partially resisted isotonic contraction, or the overcoming of such a contraction, at the same time as the full range of movement is being introduced (note that both isotonic concentric and eccentric contractions will take place during the isokinetic movement of a joint). Both of these options should involve maximum contraction of the muscles by the patient. Home treatment of such conditions is possible, via self-treatment, as in other MET methods.

Isolytic Muscle Energy Techniques

Another application of the use of isotonic contraction occurs when a direct contraction is resisted and overcome by the operator (Fig. 1.4). This has been termed isolytic contraction, in that it involves the stretching, and sometimes the breaking down, of fibrotic tissue present in the affected muscles. Adhesions of this type are reduced by the application of force by the operator which is just greater than that being exerted by the patient. This procedure can be uncomfortable, and the patient should be advised of this. Limited degrees of effort are therefore called for at the outset of isolytic contractions. This is an isotonic eccentric contraction, in that the origins and insertions of the muscles involved will become further separated, despite the patient�s effort to approximate them. In order to achieve the greatest degree of stretch (in the condition of myofascial fibrosis, for example), it is necessary for the largest number of fibers possible to be involved in the isotonic contraction. Thus there is a contradiction in that, in order to achieve this large involvement, the degree of contraction should be a maximal one, and yet this is likely to produce pain, which is contraindicated. It may also, in many instances, be impossible for the operator to overcome.

muscle energy techniquesThis stretches the muscles which are contracting (TFL shown in example) thereby inducing a degree of controlled microtrauma, with the aim of increasing the elastic potential of shortened or fibrosed tissues.

The patient should be instructed to use about 20% of possible strength on the first contraction, which is resisted and overcome by the operator, in a contraction lasting 3�4 seconds. This is then repeated, but with an increased degree of effort on the part of the patient (assuming the first effort was relatively painless). This continuing increase in the amount of force employed in the contracting musculature may be continued until, hopefully, a maximum contraction effort is possible, again to be overcome by the operator. In some muscles, of course, this may require a heroic degree of effort on the part of the operator, and alternative methods are therefore desirable. Deep tissue techniques, such as neuromuscular technique, would seem to offer such an alternative. The isolytic manoeuvre should have as its ultimate aim a fully relaxed muscle, although this will not always be possible.

Why Fibrosis Occurs Naturally

An article in the Journal of the Royal Society of Medicine (Royal Society of Medicine 1983) discusses connective tissue changes:

Aging affects the function of connective tissue more obviously than almost any organ system. Collagen fibrils thicken, and the amounts of soluble polymer decrease. The connective tissue cells tend to decline in number, and die off. Cartilages become less elastic, and their complement of proteoglycans changes both quantitatively and qualitatively. The interesting question is how many of these processes are normal, that contribute blindly and automatically, beyond the point at which they are useful? Does prevention of aging, in connective tissues, simply imply inhibition of cross linking in collagen fibrils, and a slight stimulation of the production of chondroitin sulphate proteoglycan?

The effects of various soft tissue approaches such as NMT and Muscle energy techniques will impact directly on these tissues as well as on the circulation and drainage of the affected structures, which suggests that the ageing process can be influenced. Destruction of collagen fibrils, however, is a serious matter (for example when using isolytic stretches), and although the fibrous tissue may be replaced in the process of healing, scar-tissue formation is possible, and this makes repair inferior to the original tissues, both in functional and structural terms. An isolytic contraction has the ability to break down tight, shortened tissues and the replacement of these with superior material will depend, to a large extent, on the subsequent use of the area (exercise, etc.), as well as the nutritive status of the individual. Collagen formation is dependent on adequate vitamin C, and a plentiful supply of amino acids such as proline, hydroxyproline and arginine. Manipulation, aimed at the restoration of a degree of normality in connective tissues, should therefore take careful account of nutritional requirements.

The range of choices in stretching, irrespective of the form of prelude to this � strong or mild isometric contraction, starting at or short of the barrier � therefore covers the spectrum from all- passive to all-active, with many variables in between.

Putting It Together

Many may prefer to use the variations, as described above, within individual settings. The recommendation of this text, however, is that they should be �mixed and matched� so that elements of all of them may be used in any given setting, as appropriate. Lewit�s (1999) approach seems ideal for more acute and less chronic conditions, while Janda�s (1989) more vigorous methods seem�ideal for hardy patients with chronic muscle shortening.

Muscle energy techniques offers a spectrum of approaches which range from those involving hardly any active contraction at all, relying on the extreme gentleness of mild isometric contractions induced by breath-holding and eye movements only, all the way to the other extreme of full-blooded, total- strength contractions. Subsequent to isometric contractions � whether strong or mild � there is an equally sensitive range of choices, involving either energetic stretching or very gentle movement to a new restriction. We can see why Sandra Yale (in DiGiovanna 1991) speaks of the usefulness of MET in treating extremely ill patients.

Many patients present with a combination of recent dysfunction (acute in terms of time, if not in degree of pain or dysfunction) overlaid on chronic changes which have set the scene for their acute current problems. It seems perfectly appropriate to use methods which will deal gently with hypertonicity, and more vigorous methods which will help to resolve fibrotic change, in the same patient, at the same time, using different variations on the theme of MET. Other variables can be used which focus on joint restriction, or which utilise RI should conditions be too sensitive to allow PIR methods, or variations on Janda�s more vigorous stretch methods (see Box 1.1).

Discussion of common errors in application of Muscle energy techniques will help to clarify these thoughts.

Why Muscle Energy Techniques Might Be Ineffective At Times

Poor results from use of Muscle energy techniques may relate to an inability to localize muscular effort sufficiently, since unless local muscle tension is produced in the precise region of the soft tissue dysfunction, the method is likely to fail to achieve its objectives. Also, of course, underlying pathological changes may have taken place, in joints or elsewhere, which make such an approach of short-term value only, since such changes will ensure recurrence of muscular spasms, sometimes almost immediately.

MET will be ineffective, or cause irritation, if excessive force is used in either the contraction phase or the stretching phase.

The keys to successful application of Muscle energy techniques therefore lie in a precise focusing of muscular activity, with an appropriate degree of effort used in the isometric contraction, for an adequate length of time, followed by a safe movement through the previous restriction barrier, usually with patient assistance.

Use of variations such as stretching chronic fibrotic conditions following an isometric contraction and use of the integrated approach (INIT) mentioned earlier in this chapter represent two examples of further adaptations of Lewit�s basic approach which, as described above, is ideal for acute situations of spasm and pain.

To Stretch Or To Strengthen?

Marvin Solit (1963), a former pupil of Ida Rolf, describes a common error in application of Muscle energy techniques � treating the �wrong� muscles the �wrong� way:

As one looks at a patient�s protruding abdomen, one might think that the abdominal muscles are weak, and that treatment should be geared towards strengthening them. By palpating the abdomen, however, one would not feel flabby, atonic muscles which would be the evidence of weakness; rather, the muscles are tight, bunched and shortened. This should not be surprising because here is an example of muscle working overtime maintaining body equilibrium. In addition these muscles are supporting the sagging viscera, which normally would be supported by their individual ligaments. As�the abdominal muscles are freed and lengthened, there is a general elevation of the rib cage, which in turn elevates the head and neck.

Attention to tightening and hardening these supposedly weak muscles via exercise, observes Solit, results in no improvement in posture, and no reduction in the �pot-bellied� appearance. Rather, the effect is to further depress the thoracic structures, since the attachments of the abdominal muscles, superiorly, are largely onto the relatively mobile, and unstable, bones of the rib cage. Shortening these muscles simply achieves a degree of pull on these structures towards the stable pelvic attachments below.

The approach to this problem adopted by Rolfers is to free and loosen these overworked and only apparently weakened tissues. This allows for a return to some degree of normality, freeing the tethered thoracic structures, and thus correcting the postural imbalance. Attention to the shortened, tight musculature, which will also be inhibiting their antagonist muscles, should be the primary aim. Exercise is not suitable at the outset, before this primary goal is achieved.

The common tendency in some schools of therapy to encourage the strengthening of weakened muscle groups in order to normalise postural and functional problems is also discussed by Vladimir Janda (1978). He expresses the reasons why this approach is �putting the cart before the horse�: �In pathogenesis, as well as in treatment of muscle imbalance and back problems, tight muscles play a more important, and perhaps even primary, role in comparison to weak muscles� (Fig. 1.5). He continues with the following observation:

Clinical experience, and especially therapeutic results, support the assumption that (according to Sherrington�s law of reciprocal innervation) tight muscles act in an inhibitory way on their antagonists. Therefore, it does not seem reasonable to start with strengthening of the weakened muscles, as most exercise programmes do. It has been clinically proved that it is better to stretch tight muscles first. It is not exceptional that, after stretching of the tight muscles, the strength of the weakened antagonists improves spontaneously, sometimes immediately, sometimes within a few days, without any additional treatment.

This sound, well-reasoned, clinical and scientific observation, which directs our attention and efforts towards the stretching and normalizing of those tissues which have shortened and tightened, seems irrefutable, and this theme will be pursued further in Chapter 2.

muscle energy techniquesMuscle energy techniques are designed to assist in this endeavor and, as discussed above, also provides an excellent method for assisting in the toning of weak musculature, should this still be required, after the stretching of the shortened antagonists, by use of isotonic methods.

Tendons

Aspects of the physiology of muscles and tendons are worthy of a degree of review, in so far as Muscle energy techniques and its effects are concerned (see also Box 1.5). The tone of muscle is largely the job of the Golgi tendon organs. These detect the load applied to the tendon, via muscular contraction. Reflex effects, in the appropriate muscles, are the result of this information being passed from the Golgi tendon organ back along the cord. The reflex is an inhibitory one, and thus differs from the muscle spindle stretch reflex. Sandler (1983) describes some of the processes involved:

When the tension on the muscles, and hence the tendon, becomes extreme, the inhibitory effect from the tendon organ can be so great that there is sudden relaxation of the entire muscle under stretch. This effect is called the lengthening reaction, and is probably a protective reaction to the force which, if unprotected, can tear the tendon from its bony attachments. Since the Golgi tendon organs, unlike the [muscle] spindles, are in series with the muscle fibres, they are stimulated by both passive and active contractions of the muscles.

Pointing out that muscles can either contract with constant length and varied tone (isometrically), or with constant tone and varied length (isotonically), he continues: �In the same way as the gamma efferent system operates as a feedback to control the length of muscle fibers, the tendon reflex serves as a reflex to control the muscle tone�.

muscle energy techniquesThe relevance of this to soft tissue techniques is explained as follows:

In terms of longitudinal soft tissue massage, these organs are very interesting indeed, and it is perhaps the reason why articulation of a joint, passively, to stretch the tendons that pass over the joint, is often as effective in relaxing the soft tissues as direct massage of the muscles themselves. Indeed, in some cases, where the muscle is actively in spasm, and is likely to object to being pummelled directly, articulation, muscle energy techniques, or functional balance techniques, that make use of the tendon organ reflexes, can be most effective.

The use of this knowledge in therapy is obvious and Sandler explains part of the effect of massage on muscle: �The [muscle] spindle and its reflex connections constitute a feedback device which can�operate to maintain constant muscle length, as in posture; if the muscle is stretched the spindle discharges increase, but if the muscle is shortened, without a change in the rate of gamma discharge, then the spindle discharge will decrease, and the muscle will relax.�

Sandler believes that massage techniques cause a decrease in the sensitivity of the gamma efferent, and thus increase the length of the muscle fibers rather than a further shortening of them; this produces the desired relaxation of the muscle. Muscle energy techniques provides for the ability to influence both the muscle spindles and also the Golgi tendon organs.

Joints & Muscle Energy Techniques

Bourdillon (1982) tells us that shortening of muscle seems to be a self-perpetuating phenomenon which results from an over-reaction of the gamma-neuron system. It seems that the muscle is incapable of returning to a normal resting length as long as this continues. While the effective length of the muscle is thus shortened, it is nevertheless capable of shortening further. The pain factor seems related to the muscle�s inability thereafter to be restored to its anatomically desirable length. The conclusion is that much joint restriction is a result of muscular tightness and shortening. The opposite may also apply where damage to the soft or hard tissues of a joint is a factor. In such cases the periarticular and osteophytic changes, all too apparent in degenerative conditions, are the major limiting factor in joint restrictions. In both situations, however, Muscle energy techniques may be useful, although more useful where muscle shortening is the primary factor.

The restriction which takes place as a result of tight, shortened muscles is usually accompanied by some degree of lengthening and weakening of the antagonists. A wide variety of possible permutations exists in any given condition involving muscular shortening which may be initiating, or be secondary to, joint dysfunction combined with weakness of antagonists. A combination of isometric and isotonic methods can effectively be employed to lengthen and stretch the shortened groups, and to strengthen and shorten the weak, overlong muscles.

Paul Williams (1965) stated a basic truth which is often neglected by the professions which deal with musculoskeletal dysfunction:

The health of any joint is dependent upon a balance in the strength of its opposing muscles. If for any reason a flexor group loses part, or all of its function, its opposing tensor group will draw the joint into a hyperextended position, with abnormal stress on the joint margins. This situation exists in the lumbar spine of modern man.

Lack of attention to the muscular component of joints in general, and spinal joints in particular, results in frequent inappropriate treatment of the joints thus affected. Correct understanding of the role of the supporting musculature would frequently lead to normalisation of these tissues, without the need for heroic manipulative efforts. Muscle energy techniques and other soft tissue approaches focus attention on these structures and offer the opportunity to correct both the weakened musculature and the shortened, often fibrotic, antagonists.

More recently, Norris (1999) has pointed out that:

The mixture of tightness and weakness seen in the muscle imbalance process alters body segment alignment and changes the equilibrium point of a joint. Normally the equal resting tone of the agonist and antagonist muscles allows the joint to take up a balanced position where the joint surfaces are evenly loaded and the inert tissues of the joint are not excessively stressed. However if the muscles on one side of a joint are tight and the opposing muscles relax, the joint will be pulled out of alignment towards the tight muscle(s).

Such alignment changes produce weight-bearing stresses on joint surfaces, and result also in shortened soft tissues chronically contracting over time. Additionally such imbalances result in reduced segmental control with chain reactions of compensation emerging (see Ch. 2).

Several studies will be detailed (Chs 5 and 8) showing the effectiveness of Muscle energy techniques application in diverse population groups, including a Polish study on the benefits of Muscle energy techniques in joints damaged by haemophilia, and a Swedish study on the effects of Muscle energy techniques in treating lumbar spine dysfunction, as well as an American/Czech study involving myofascial pain problems. In the main, the results indicate a universal role in providing resolution or relief of such problems by means of the application of safe and effective muscle energy techniques.

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Close Accordion
Cancer: A Preventable Disease

Cancer: A Preventable Disease

Cancer:�Abstract

This year, more than 1 million Americans and more than 10 million people worldwide are expected to be diagnosed with cancer, a disease commonly believed to be preventable. Only 5�10% of all cancer cases can be attributed to genetic defects, whereas the remaining 90�95% have their roots in the environment and lifestyle. The lifestyle factors include cigarette smoking, diet (fried foods, red meat), alcohol, sun exposure, environmental pollutants, infections, stress, obesity, and physical inactivity. The evidence indicates that of all cancer-related deaths, almost 25�30% are due to tobacco, as many as 30� 35% are linked to diet, about 15�20% are due to infections, and the remaining percentage are due to other factors like radiation, stress, physical activity, environmental pollutants etc. Therefore, cancer prevention requires smoking cessation, increased ingestion of fruits and vegetables, moderate use of alcohol, caloric restriction, exercise, avoidance of direct exposure to sunlight, minimal meat consumption, use of whole grains, use of vaccinations, and regular check-ups. In this review, we present evidence that inflammation is the link between the agents/factors that cause cancer and the agents that prevent it. In addition, we provide evidence that cancer is a preventable disease that requires major lifestyle changes.

KEY WORDS: cancer; environmental risk factors; genetic risk factors; prevention.

INTRODUCTION

After sequencing his own genome, pioneer genomic researcher Craig Venter remarked at a leadership for the twenty-first century conference, �Human biology is actually far more complicated than we imagine. Everybody talks about the genes that they received from their mother and father, for this trait or the other. But in reality, those genes have very little impact on life outcomes. Our biology is way too complicated for that and deals with hundreds of thousands of independent factors. Genes are absolutely not our fate. They can give us useful information about the increased risk of a disease, but in most cases they will not determine the actual cause of the disease, or the actual incidence of somebody getting it. Most biology will come from the complex interaction of all the proteins and cells working with environmental factors, not driven directly by the genetic code� (indiatoday.digitalto day.in/index.php?option=com_content&task=view&isseid= 48&id=6022&sectionid=30&Itemid=1).

This statement is very important because looking to the human genome for solutions to most chronic illnesses, including the diagnosis, prevention, and treatment of cancer, is overemphasized in today�s world. Observational studies, however, have indicated that as we migrate from one country to another, our chances of being diagnosed with most chronic illnesses are determined not by the country we come from but by the country we migrate to (1�4). In addition, studies with identical twins have suggested that genes are not the source of most chronic illnesses. For instance, the concordance between identical twins for breast cancer was found to be only 20% (5). Instead of our genes, our lifestyle and environment account for 90�95% of our most chronic illnesses.

Cancer continues to be a worldwide killer, despite the enormous amount of research and rapid developments seen during the past decade. According to recent statistics, cancer accounts for about 23% of the total deaths in the USA and is the second most common cause of death after heart disease (6). Death rates for heart disease, however, have been steeply decreasing in both older and younger populations in the USA from 1975 through 2002. In contrast, no appreciable differences in death rates for cancer have been observed in the United States (6).

By 2020, the world population is expected to have increased to 7.5 billion; of this number, approximately 15 million new cancer cases will be diagnosed, and 12 million cancer patients will die (7). These trends of cancer incidence and death rates again remind us of Dr. John Bailer�s May 1985 judgment of the US national cancer program as a �qualified failure,� a judgment made 14 years after President Nixon�s official declaration of the �War on Cancer.� Even after an additional quarter century of extensive research, researchers are still trying to determine whether cancer is preventable and are asking �If it is preventable, why are we losing the war on cancer?� In this review, we attempt to answer this question by analyzing the potential risk factors of cancer and explore our options for modulating these risk factors.

Cancer is caused by both internal factors (such as inherited mutations, hormones, and immune conditions) and environmental/acquired factors (such as tobacco, diet, radiation, and infectious organisms; Fig. 1). The link between diet and cancer is revealed by the large variation in rates of specific cancers in various countries and by the observed changes in the incidence of cancer in migrating. For example, Asians have been shown to have a 25 times lower incidence of prostate cancer and a ten times lower incidence of breast cancer than do residents of Western countries, and the rates for these cancers increase substantially after Asians migrate to the West (www.dietandcancerreportorg/?p=ER).

The importance of lifestyle factors in the development of cancer was also shown in studies of monozygotic twins (8). Only 5�10% of all cancers are due to an inherited gene defect. Various cancers that have been linked to genetic defects are shown in Fig. 2. Although all cancers are a result of multiple mutations (9, 10), these mutations are due to interaction with the environment (11, 12).

These observations indicate that most cancers are not of hereditary origin and that lifestyle factors, such as dietary habits, smoking, alcohol consumption, and infections, have a profound influence on their development (13). Although the hereditary factors cannot be modified, the lifestyle and environmental factors are potentially modifiable. The lesser hereditary influence of cancer and the modifiable nature of the environmental factors point to the preventability of cancer. The important lifestyle factors that affect the incidence and mortality of cancer include tobacco, alcohol, diet, obesity, infectious agents, environmental pollutants, and radiation.

RISK FACTORS OF CANCER: Tobacco

Smoking was identified in 1964 as the primary cause of lung cancer in the US Surgeon General�s Advisory Commission Report (profiles.nlm.nih.gov/NN/Views/Alpha Chron/date/10006/05/01/2008), and ever since, efforts have been ongoing to reduce tobacco use. Tobacco use increases the risk of developing at least 14 types of cancer (Fig. 3). In addition, it accounts for about 25�30% of all deaths from cancer and 87% of deaths from lung cancer. Compared with nonsmokers, male smokers are 23 times and female smokers 17 times more likely to develop lung cancer. (www. cancer.org/docroot/STT/content/STT_1x_Cancer_Facts_and_ Figures_2008.asp accessed on 05/01/2008)

The carcinogenic effects of active smoking are well documented; the U. S. Environmental Protection Agency, for example, in 1993 classified environmental tobacco smoke (from passive smoking) as a known (Group A) human lung carcinogen (cfpub2.epa.gov/ncea/cfm/recordisplay.cfm?deid=2835 accessed on 05/01/2008). Tobacco contains at least 50 carcinogens. For example, one tobacco metabolite, benzopyrenediol epoxide, has a direct etiologic association with lung cancer (14). Among all developed countries considered in total, the prevalence of smoking has been slowly declining; however, in the developing countries where 85% of the world�s population resides, the prevalence of smoking is increasing. According to studies of recent trends in tobacco usage, developing countries will consume 71% of the world�s tobacco by 2010, with 80% increased usage projected for East Asia (www.fao.org/DOCREP/006/Y4956E/Y4956E00. HTM accessed on 01/11/08). The use of accelerated tobacco- control programs, with an emphasis in areas where usage is increasing, will be the only way to reduce the rates of tobacco-related cancer mortality.

How smoking contributes to cancer is not fully understood. We do know that smoking can alter a large number of cell- signaling pathways. Results from studies in our group have established a link between cigarette smoke and inflammation. Specifically, we showed that tobacco smoke can induce activation of NF-?B, an inflammatory marker (15,16). Thus, anti- inflammatory agents that can suppress NF-?B activation may have potential applications against cigarette smoke.

We also showed that curcumin, derived from the dietary spice turmeric, can block the NF-?B induced by cigarette smoke (15). In addition to curcumin, we discovered that several natural phytochemicals also inhibit the NF-?B induced by various carcinogens (17). Thus, the carcinogenic effects of tobacco appear to be reduced by these dietary agents. A more detailed discussion of dietary agents that can block inflammation and thereby provide chemopreventive effects is presented in the following section.

Alcohol

The first report of the association between alcohol and an increased risk of esophageal cancer was published in 1910 (18). Since then, a number of studies have revealed that chronic alcohol consumption is a risk factor for cancers of the upper aerodigestive tract, including cancers of the oral cavity, pharynx, hypopharynx, larynx, and esophagus (18�21), as well as for cancers of the liver, pancreas, mouth, and breast (Fig. 3). Williams and Horn (22), for example, reported an increased risk of breast cancer due to alcohol. In addition, a collaborative group who studied hormonal factors in breast cancer published their findings from a reanalysis of more than 80% of individual epidemiological studies that had been conducted worldwide on the association between alcohol and breast cancer risk in women. Their analysis showed a 7.1% increase in relative risk of breast cancer for each additional 10 g/day intake of alcohol (23). In another study, Longnecker et al., (24) showed that 4% of all newly diagnosed cases of breast cancer in the USA are due to alcohol use. In addition to it being a risk factor for breast cancer, heavy intake of alcohol (more than 50�70 g/day) is a well-established risk factor for liver (25) and colorectal (26,27) cancers.

There is also evidence of a synergistic effect between heavy alcohol ingestion and hepatitis C virus (HCV) or hepatitis B virus (HBV), which presumably increases the risk of hepatocellular carcinoma (HCC) by more actively promoting cirrhosis. For example, Donato et al. (28) reported that among alcohol drinkers, HCC risk increased linearly with a daily intake of more than 60 g. However, with the concomitant presence of HCV infection, the risk of HCC was two times greater than that observed with alcohol use alone (i.e., a positive synergistic effect). The relationship between alcohol and inflammation has also been well established, especially in terms of alcohol-induced inflammation of the liver.

How alcohol contributes to carcinogenesis is not fully understood but ethanol may play a role. Study findings suggest that ethanol is not a carcinogen but is a cocarcinogen (29). Specifically, when ethanol is metabolized, acetaldehyde and free radicals are generated; free radicals are believed to be predominantly responsible for alcohol-associated carcinogenesis through their binding to DNA and proteins, which destroys folate and results in secondary hyperproliferation. Other mechanisms by which alcohol stimulates carcinogenesis include the induction of cytochrome P-4502E1, which is associated with enhanced production of free radicals and enhanced activation of various procarcinogens present in alcoholic beverages; a change in metabolism and in the distribution of carcinogens, in association with tobacco smoke and diet; alterations in cell-cycle behavior such as cell-cycle duration leading to hyperproliferation; nutritional deficiencies, for example, of methyl, vitamin E, folate, pyridoxal phosphate, zinc, and selenium; and alterations of the immune system. Tissue injury, such as that occurring with cirrhosis of the liver, is a major prerequisite to HCC. In addition, alcohol can activate the NF-?B proinflammatory pathway (30), which can also contribute to tumorigenesis (31). Furthermore, it has been shown that benzopyrene, a cigarette smoke carcinogen, can penetrate the esophagus when combined with ethanol (32). Thus anti-inflammatory agents may be effective for the treatment of alcohol-induced toxicity.

In the upper aerodigestive tract, 25�68% of cancers are attributable to alcohol, and up to 80% of these tumors can be prevented by abstaining from alcohol and smoking (33). Globally, the attributable fraction of cancer deaths due to alcohol drinking is reported to be 3.5% (34). The number of deaths from cancers known to be related to alcohol consumption in the USA could be as low as 6% (as in Utah) or as high as 28% (as in Puerto Rico). These numbers vary from country to country, and in France have approached 20% in males (18).

Diet

In 1981, Doll and Peto (21) estimated that approximately 30�35% of cancer deaths in the USA were linked to diet (Fig. 4). The extent to which diet contributes to cancer deaths varies a great deal, according to the type of cancer (35). For example, diet is linked to cancer deaths in as many as 70% of colorectal cancer cases. How diet contributes to cancer is not fully understood. Most carcinogens that are ingested, such as nitrates, nitrosamines, pesticides, and dioxins, come from food or food additives or from cooking.

Heavy consumption of red meat is a risk factor for several cancers, especially for those of the gastrointestinal tract, but also for colorectal (36�38), prostate (39), bladder (40), breast (41), gastric (42), pancreatic, and oral (43) cancers. Although a study by Dosil-Diaz et al., (44) showed that meat consumption reduced the risk of lung cancer, such consumption is commonly regarded as a risk for cancer for the following reasons. The heterocyclic amines produced during the cooking of meat are carcinogens. Charcoal cooking and/or smoke curing of meat produces harmful carbon compounds such as pyrolysates and amino acids, which have a strong cancerous effect. For instance, PhIP (2-amino-1- methyl-6-phenyl-imidazo[4,5-b]pyridine) is the most abundant mutagen by mass in cooked beef and is responsible for ~20% of the total mutagenicity found in fried beef. Daily intake of PhIP among Americans is estimated to be 280� 460 ng/day per person (45).

Nitrites and nitrates are used in meat because they bind to myoglobin, inhibiting botulinum exotoxin production; however, they are powerful carcinogens (46). Long-term exposure to food additives such as nitrite preservatives and azo dyes has been associated with the induction of carcinogenesis (47). Furthermore, bisphenol from plastic food containers can migrate into food and may increase the risk of breast (48) and prostate (49) cancers. Ingestion of arsenic may increase the risk of bladder, kidney, liver, and lung cancers (50). Saturated fatty acids, trans fatty acids, and refined sugars and flour present in most foods have also been associated with various cancers. Several food carcinogens have been shown to activate inflammatory pathways.

Obesity

According to an American Cancer Society study (51), obesity has been associated with increased mortality from cancers of the colon, breast (in postmenopausal women), endometrium, kidneys (renal cell), esophagus (adenocarcinoma), gastric cardia, pancreas, prostate, gallbladder, and liver (Fig. 5). Findings from this study suggest that of all deaths from cancer in the United States, 14% in men and 20% in women are attributable to excess weight or obesity. Increased modernization and a Westernized diet and lifestyle have been associated with an increased prevalence of overweight people in many developing countries (52).

Studies have shown that the common denominators between obesity and cancer include neurochemicals; hormones such as insulin like growth factor 1 (IGF-1), insulin, leptin; sex steroids; adiposity; insulin resistance; and inflammation (53).

Involvement of signaling pathways such as the IGF/ insulin/Akt signaling pathway, the leptin/JAK/STAT pathway, and other inflammatory cascades have also been linked with both obesity and cancer (53). For instance, hyperglycemia, has been shown to activate NF-?B (54), which could link obesity with cancer. Also known to activate NF-?B are several cytokines produced by adipocytes, such as leptin, tumor necrosis factor (TNF), and interleukin-1 (IL-1) (55). Energy balance and carcinogenesis has been closely linked (53). However, whether inhibitors of these signaling cascades can reduce obesity-related cancer risk remains unanswered. Because of the involvement of multiple signaling pathways, a potential multitargeting agent will likely be needed to reduce obesity-related cancer risk.

Infectious Agents

Worldwide, an estimated 17.8% of neoplasms are associated with infections; this percentage ranges from less than 10% in high-income countries to 25% in African countries (56, 57). Viruses account for most infection-caused cancers (Fig. 6). Human papillomavirus, Epstein Barr virus, Kaposi�s sarcoma- associated herpes virus, human T-lymphotropic virus 1, HIV, HBV, and HCV are associated with risks for cervical cancer, anogenital cancer, skin cancer, nasopharyngeal cancer, Bur- kitt�s lymphoma, Hodgkin�s lymphoma, Kaposi�s sarcoma, adult T-cell leukemia, B-cell lymphoma, and liver cancer.

In Western developed countries, human papillomavirus and HBV are the most frequently encountered oncogenic DNA viruses. Human papillomavirus is directly mutagenic by inducing the viral genes E6 and E7 (58), whereas HBV is believed to be indirectly mutagenic by generating reactive oxygen species through chronic inflammation (59�61). Human T-lymphotropic virus is directly mutagenic, whereas HCV (like HBV) is believed to produce oxidative stress in infected cells and thus to act indirectly through chronic inflammation (62, 63). However, other microorganisms, including selected parasites such as Opisthorchis viverrini or Schistosoma haematobium and bacteria such as Helicobacter pylori, may also be involved, acting as cofactors and/or carcinogens (64).

The mechanisms by which infectious agents promote cancer are becoming increasingly evident. Infection-related inflammation is the major risk factor for cancer, and almost all viruses linked to cancer have been shown to activate the inflammatory marker, NF-?B (65). Similarly, components of Helicobacter pylori have been shown to activate NF-?B (66). Thus, agents that can block chronic inflammation should be effective in treating these conditions.

Environmental Pollution

Environmental pollution has been linked to various cancers (Fig. 7). It includes outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons (PAHs); indoor air pollution by environmental tobacco smoke, formaldehyde, and volatile organic compounds such as benzene and 1,3-butadiene (which may particularly affect children); food pollution by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins, and other organochlorines; carcinogenic metals and metalloids; pharmaceutical medicines; and cosmetics (64).

Numerous outdoor air pollutants such as PAHs increase the risk of cancers, especially lung cancer. PAHs can adhere to fine carbon particles in the atmosphere and thus penetrate our bodies primarily through breathing. Long-term exposure to PAH-containing air in polluted cities was found to increase the risk of lung cancer deaths. Aside from PAHs and other fine carbon particles, another environmental pollutant, nitric oxide, was found to increase the risk of lung cancer in a European population of nonsmokers. Other studies have shown that nitric oxide can induce lung cancer and promote metastasis. The increased risk of childhood leukemia associated with exposure to motor vehicle exhaust was also reported (64).

Indoor air pollutants such as volatile organic compounds and pesticides increase the risk of childhood leukemia and lymphoma, and children as well as adults exposed to pesticides have increased risk of brain tumors, Wilm�s tumors, Ewing�s sarcoma, and germ cell tumors. In utero exposure to environmental organic pollutants was found to increase the risk for testicular cancer. In addition, dioxan, an environmental pollutant from incinerators, was found to increase the risk of sarcoma and lymphoma.

Long-term exposure to chlorinated drinking water has been associated with increased risk of cancer. Nitrates, in drinking water, can transform to mutagenic N-nitroso compounds, which increase the risk of lymphoma, leukemia, colorectal cancer, and bladder cancer (64).

Radiation

Up to 10% of total cancer cases may be induced by radiation (64), both ionizing and nonionizing, typically from radioactive substances and ultraviolet (UV), pulsed electro- magnetic fields. Cancers induced by radiation include some types of leukemia, lymphoma, thyroid cancers, skin cancers, sarcomas, lung and breast carcinomas. One of the best examples of increased risk of cancer after exposure to radiation is the increased incidence of total malignancies observed in Sweden after exposure to radioactive fallout from the Chernobyl nuclear power plant. Radon and radon decay products in the home and/or at workplaces (such as mines) are the most common sources of exposure to ionizing radiation. The presence of radioactive nuclei from radon, radium, and uranium was found to increase the risk of gastric cancer in rats. Another source of radiation exposure is x-rays used in medical settings for diagnostic or therapeutic purposes. In fact, the risk of breast cancer from x-rays is highest among girls exposed to chest irradiation at puberty, a time of intense breast development. Other factors associated with radiation-induced cancers in humans are patient age and physiological state, synergistic interactions between radiation and carcinogens, and genetic susceptibility toward radiation.

Nonionizing radiation derived primarily from sunlight includes UV rays, which are carcinogenic to humans. Exposure to UV radiation is a major risk for various types of skin cancers including basal cell carcinoma, squamous cell carcinoma, and melanoma. Along with UV exposure from sunlight, UV exposure from sunbeds for cosmetic tanning may account for the growing incidence of melanoma. Depletion of the ozone layer in the stratosphere can augment the dose-intensity of UVB and UVC, which can further increase the incidence of skin cancer.

Low-frequency electromagnetic fields can cause clasto- genic DNA damage. The sources of electromagnetic field exposure are high-voltage power lines, transformers, electric train engines, and more generally, all types of electrical equipments. An increased risk of cancers such as childhood leukemia, brain tumors and breast cancer has been attributed to electromagnetic field exposure. For instance, children living within 200 m of high-voltage power lines have a relative risk of leukemia of 69%, whereas those living between 200 and 600 m from these power lines have a relative risk of 23%. In addition, a recent meta-analysis of all available epidemi- ologic data showed that daily prolonged use of mobile phones for 10 years or more showed a consistent pattern of an increased risk of brain tumors (64).

PREVENTION OF CANCER

The fact that only 5�10% of all cancer cases are due to genetic defects and that the remaining 90�95% are due to environment and lifestyle provides major opportunities for preventing cancer. Because tobacco, diet, infection, obesity, and other factors contribute approximately 25�30%, 30�35%, 15�20%, 10�20%, and 10�15%, respectively, to the incidence of all cancer deaths in the USA, it is clear how we can prevent cancer. Almost 90% of patients diagnosed with lung cancer are cigarette smokers; and cigarette smoking combined with alcohol intake can synergistically contribute to tumorigenesis. Similarly, smokeless tobacco is responsible for 400,000 cases (4% of all cancers) of oral cancer worldwide. Thus avoidance of tobacco products and minimization of alcohol consumption would likely have a major effect on cancer incidence.

Infection by various bacteria and viruses (Fig. 6) is another very prominent cause of various cancers. Vaccines for cervical cancer and HCC should help prevent some of these cancers, and a cleaner environment and modified lifestyle behavior would be even more helpful in preventing infection- caused cancers.

The first FDA approved chemopreventive agent was tamoxifen, for reducing the risk of breast cancer. This agent was found to reduce the breast cancer incidence by 50% in women at high risk. With tamoxifen, there is an increased risk of serious side effects such as uterine cancer, blood clots, ocular disturbances, hypercalcemia, and stroke (www.fda.gov/ cder/foi/appletter/1998/17970s40.pdf). Recently it has been shown that a osteoporosis drug raloxifene is as effective as tamoxifen in preventing estrogen-receptor-positive, invasive breast cancer but had fewer side effects than tamoxifen. Though it is better than tamoxifen with respect to side effects, it can cause blood clots and stroke. Other potential side effects of raloxifene include hot flashes, leg cramps, swelling of the legs and feet, flu-like symptoms, joint pain, and sweating (www.fda.gov/bbs/topics/NEWS/2007/NEW01698.html).

The second chemopreventive agent to reach to clinic was finasteride, for prostate cancer, which was found to reduce incidence by 25% in men at high risk. The recognized side effects of this agent include erectile dysfunction, lowered sexual desire, impotence and gynecomastia (www. cancer.org/docroot/cri/content/cri_2_4_2x_can_prostate_can cer_be_prevented_36.asp). Celecoxib, a COX-2 inhibitor is another approved agent for prevention of familial adenomatous polyposis (FAP). However, the chemopreventive benefit of celecoxib is at the cost of its serious cardiovascular harm (www.fda.gov/cder/drug/infopage/cox2/NSAIDdecision Memo.pdf).

The serious side effects of the FDA approved chemopreventive drugs is an issue of particular concern when considering long-term administration of a drug to healthy people who may or may not develop cancer. This clearly indicates the need for agents, which are safe and efficacious in preventing cancer. Diet derived natural products will be potential candidates for this purpose. Diet, obesity, and metabolic syndrome are very much linked to various cancers and may account for as much as 30� 35% of cancer deaths, indicating that a reasonably good fraction of cancer deaths can be prevented by modifying the diet. Extensive research has revealed that a diet consisting of fruits, vegetables, spices, and grains has the potential to prevent cancer (Fig. 8). The specific substances in these dietary foods that are responsible for preventing cancer and the mechanisms by which they achieve this have also been examined extensively. Various phytochemicals have been identified in fruits, vegetables, spices, and grains that exhibit chemopreventive potential (Fig. 9), and numerous studies have shown that a proper diet can help protect against cancer (46, 67�69). Below is a description of selected dietary agents and diet-derived phytochemicals that have been studied extensively to determine their role in cancer prevention.

Fruits & Vegetables

The protective role of fruits and vegetables against cancers that occur in various anatomical sites is now well supported (46,69). In 1966, Wattenberg (70) proposed for the first time that the regular consumption of certain constituents in fruits and vegetables might provide protection from cancer. Doll and Peto (21) showed that 75�80% of cancer cases diagnosed in the USA in 1981 might have been prevented by lifestyle changes. According to a 1997 estimate, approximately 30�40% of cancer cases worldwide were preventable by feasible dietary means (www.dietandcancerreportorg/?p=ER). Several studies have addressed the cancer chemopreventive effects of the active components derived from fruits and vegetables.

More than 25,000 different phytochemicals have been identified that may have potential against various cancers. These phytochemicals have advantages because they are safe and usually target multiple cell-signaling pathways (71). Major chemopreventive compounds identified from fruits and vegetables includes carotenoids, vitamins, resveratrol, quercetin, silymarin, sulphoraphane and indole-3-carbinol.

Carotenoids

Various natural carotenoids present in fruits and vegetables were reported to have anti-inflammatory and anticarcinogenic activity. Lycopene is one of the main carotenoids in the regional Mediterranean diet and can account for 50% of the carotenoids in human serum. Lycopene is present in fruits, including watermelon, apricots, pink guava, grapefruit, rosehip, and tomatoes. A wide variety of processed tomato- based products account for more than 85% of dietary lycopene. The anticancer activity of lycopene has been demonstrated in both in vitro and in vivo tumor models as well as in humans. The proposed mechanisms for the anticancer effect of lycopene involve ROS scavenging, up- regulation of detoxification systems, interference with cell proliferation, induction of gap-junctional communication, inhibition of cell-cycle progression, and modulation of signal transduction pathways. Other carotenoids reported to have anticancer activity include beta-carotene, alpha-carotene, lutein, zeaxanthin, beta-cryptoxanthin, fucoxanthin, astaxanthin, capsanthin, crocetin, and phytoene (72).

Resveratrol

The stilbene resveratrol has been found in fruits such as grapes, peanuts, and berries. Resveratrol exhibits anticancer properties against a wide variety of tumors, including lymphoid and myeloid cancers, multiple myeloma, and cancers of the breast, prostate, stomach, colon, and pancreas. The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; induction of apoptosis via Fas/ CD95, p53, ceramide activation, tubulin polymerization, mitochondrial and adenylyl cyclase pathways; up-regulation of p21 p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL, and cellular inhibitor of apoptosis proteins; activation of caspases; suppression of nitric oxide synthase; suppression of transcription factors such as NF-?B, AP-1, and early growth response-1; inhibition of cyclooxyge- nase-2 (COX-2) and lipoxygenase; suppression of adhesion molecules; and inhibition of angiogenesis, invasion, and metastasis. Limited data in humans have revealed that resver- atrol is pharmacologically safe. As a nutraceutical, resveratrol is commercially available in the USA and Europe in 50 ?g to 60 mg doses. Currently, structural analogues of resveratrol with improved bioavailability are being pursued as potential chemo- preventive and therapeutic agents for cancer (73).

Quercetin

The flavone quercetin (3,3?,4?,5,7-pentahydroxyflavone), one of the major dietary flavonoids, is found in a broad range of fruits, vegetables, and beverages such as tea and wine, with a daily intake in Western countries of 25�30 mg. The antioxidant, anti-inflammatory, antiproliferative, and apoptotic effects of the molecule have been largely analyzed in cell culture models, and it is known to block NF-?B activation. In animal models, quercetin has been shown to inhibit inflammation and prevent colon and lung cancer. A phase 1 clinical trial indicated that the molecule can be safely administered and that its plasma levels are sufficient to inhibit lymphocyte tyrosine kinase activity. Consumption of quercetin in onions and apples was found to be inversely associated with lung cancer risk in Hawaii. The effect of onions was particularly strong against squamous cell carcinoma. In another study, an increased plasma level of quercetin after a meal of onions was accompanied by increased resistance to strand breakage in lymphocytic DNA and decreased levels of some oxidative metabolites in the urine (74).

Silymarin

The flavonoid silymarin (silybin, isosilybin, silychristin, silydianin, and taxifolin) is commonly found in the dried fruit of the milk thistle plant Silybum marianum. Although silymarin�s role as an antioxidant and hepatoprotective agent is well known, its role as an anticancer agent is just emerging. The anti-inflammatory effects of silymarin are mediated through suppression of NF-?B-regulated gene products, in- cluding COX-2, lipoxygenase (LOX), inducible NO synthase, TNF, and IL-1. Numerous studies have indicated that silymarin is a chemopreventive agent in vivo against various carcinogens/tumor promoters, including UV light, 7,12-dime- thylbenz(a)anthracene (DMBA), phorbol 12-myristate 13-acetate, and others. Silymarin has also been shown to sensitize tumors to chemotherapeutic agents through down- regulation of the MDR protein and other mechanisms. It binds to both estrogen and androgen receptors and down- regulates prostate specific antigen. In addition to its chemo- preventive effects, silymarin exhibits activity against tumors (e.g., prostate and ovary) in rodents. Various clinical trials have indicated that silymarin is bioavailable and pharmaco- logically safe. Studies are now in progress to demonstrate the clinical efficacy of silymarin against various cancers (75).

Indole-3-Carbinol

The flavonoid indole-3-carbinol (I3C) is present in vegetables such as cabbage, broccoli, brussels sprout, cauli- flower, and daikon artichoke. The hydrolysis product of I3C metabolizes to a variety of products, including the dimer 3,3?- diindolylmethane. Both I3C and 3,3?-diindolylmethane exert a variety of biological and biochemical effects, most of which appear to occur because I3C modulates several nuclear transcription factors. I3C induces phase 1 and phase 2 enzymes that metabolize carcinogens, including estrogens. I3C has also been found to be effective in treating some cases of recurrent respiratory papillomatosis and may have other clinical uses (76).

Sulforaphane

Sulforaphane (SFN) is an isothiothiocyanate found in cruciferous vegetables such as broccoli. Its chemopreventive effects have been established in both in vitro and in vivo studies. The mechanisms of action of SFN include inhibition of phase 1 enzymes, induction of phase 2 enzymes to detoxify carcinogens, cell-cycle arrest, induction of apoptosis, inhibi- tion of histone deacetylase, modulation of the MAPK pathway, inhibition of NF-?B, and production of ROS. Preclinical and clinical studies of this compound have suggested its chemopreventive effects at several stages of carcinogenesis. In a clinical trial, SFN was given to eight healthy women an hour before they underwent elective reduction mammoplasty. Induction in NAD(P)H/quinone oxidoreductase and heme oxygenase-1 was observed in the breast tissue of all patients, indicating the anticancer effect of SFN (77).

Teas & Spices

Spices are used all over the world to add flavor, taste, and nutritional value to food. A growing body of research has demonstrated that phytochemicals such as catechins (green tea), curcumin (turmeric), diallyldisulfide (garlic), thymoquinone (black cumin) capsaicin (red chili), gingerol (ginger), anethole (licorice), diosgenin (fenugreek) and eugenol (clove, cinnamon) possess therapeutic and preventive potential against cancers of various anatomical origins. Other phytochemicals with this potential include ellagic acid (clove), ferulic acid (fennel, mustard, sesame), apigenin (coriander, parsley), betulinic acid (rosemary), kaempferol (clove, fenugreek), sesamin (sesame), piperine (pepper), limonene (rose- mary), and gambogic acid (kokum). Below is a description of some important phytochemicals associated with cancer.

Catechins

More than 3,000 studies have shown that catechins derived from green and black teas have potential against various cancers. A limited amount of data are also available from green tea polyphenol chemoprevention trials. Phase 1 trials of healthy volunteers have defined the basic biodistribution patterns, pharmacokinetic parameters, and preliminary safety profiles for short-term oral administration of various green tea preparations. The consumption of green tea appears to be relatively safe. Among patients with established premalignant conditions, green tea derivatives have shown potential efficacy against cervical, prostate, and hepatic malignancies without inducing major toxic effects. One novel study determined that even persons with solid tumors could safely consume up to 1 g of green tea solids, the equivalent of approximately 900 ml of green tea, three times daily. This observation supports the use of green tea for both cancer prevention and treatment (78).

Curcumin

Curcumin is one of the most extensively studied com- pounds isolated from dietary sources for inhibition of inflammation and cancer chemoprevention, as indicated by almost 3000 published studies. Studies from our laboratory showed that curcumin inhibited NF-?B and NF-?B-regulated gene expression in various cancer cell lines. In vitro and in vivo studies showed that this phytochemical inhibited inflammation and carcinogenesis in animal models, including breast, esophageal, stomach, and colon cancer models. Other studies showed that curcumin inhibited ulcerative proctitis and Crohn�s disease, and one showed that curcumin inhibited ulcerative colitis in humans. Another study evaluated the effect of a combination of curcumin and piperine in patients with tropical pancreatitis. One study conducted in patients with familial adenomatous polyposis showed that curcumin has a potential role in inhibiting this condition. In that study, all five patients were treated with curcumin and quercetin for a mean of 6 months and had a decreased polyp number (60.4%) and size (50.9%) from baseline with minimal adverse effects and no laboratory-determined abnormalities.

The pharmacodynamic and pharmacokinetic effects of oral Curcuma extract in patients with colorectal cancer have also been studied. In a study of patients with advanced colorectal cancer refractory to standard chemotherapies, 15 patients received Curcuma extract daily for up to 4 months. Results showed that oral Curcuma extract was well tolerated, and dose-limiting toxic effects were not observed. Another study showed that in patients with advanced colorectal cancer, a daily dose of 3.6 g of curcumin engendered a 62% decrease in inducible prostaglandin E2 production on day 1 and a 57% decrease on day 29 in blood samples taken 1 h after dose administration.

An early clinical trial with 62 cancer patients with external cancerous lesions at various sites (breast, 37; vulva, 4; oral, 7; skin, 7; and others, 11) reported reductions in the sense of smell (90% of patients), itching (almost all patients), lesion size and pain (10% of patients), and exudates (70% of patients) after topical application of an ointment containing curcumin. In a phase 1 clinical trial, a daily dose of 8,000 mg of curcumin taken by mouth for 3 months resulted in histologic improvement of precancerous lesions in patients with uterine cervical intraepithelial neoplasm (one of four patients), intestinal metaplasia (one of six patients), bladder cancer (one of two patients), and oral leukoplakia (two of seven patients).

Results from another study conducted by our group showed that curcumin inhibited constitutive activation of NF- ?B, COX-2, and STAT3 in peripheral blood mononuclear cells from the 29 multiple myeloma patients enrolled in this study. Curcumin was given in doses of 2, 4, 8, or 12 g/day orally. Treatment with curcumin was well tolerated with no adverse events. Of the 29 patients, 12 underwent treatment for 12 weeks and 5 completed 1 year of treatment with stable disease. Other studies from our group showed that curcumin inhibited pancreatic cancer. Curcumin down-regulated the expression of NF-?B, COX-2, and phosphorylated STAT3 in peripheral blood mononuclear cells from patients (most of whom had baseline levels considerably higher than those found in healthy volunteers). These studies showed that curcumin is a potent anti-inflammatory and chemopreventive agent. A detailed description of curcumin and its anticancer properties can be found in one of our recent reviews (79).

Diallyldisulfide

Diallyldisulfide, isolated from garlic, inhibits the growth and proliferation of a number of cancer cell lines including colon, breast, glioblastoma, melanoma, and neuroblastoma cell lines. Recent studies showed that this compound induces apoptosis in Colo 320 DM human colon cancer cells by inhibiting COX-2, NF-?B, and ERK-2. It has been shown to inhibit a number of cancers including dimethylhydrazine-induced colon cancer, benzo[a]pyrene-induced neoplasia, and glutathione S-transferase activity in mice; benzo[a]pyrene-induced skin carcinogenesis in mice; N-nitrosomethylbenzylamine-induced esophageal cancer in rats; N-nitrosodiethylamine-induced forestomach neoplasia in female A/J mice; aristolochic acid-induced forestomach carcinogenesis in rats; diethylnitrosamine-induced glutathione S-transferase positive foci in rat liver; 2-amino- 3-methylimidazo[4,5-f]quinoline-induced hepatocarcinogen- esis in rats; and diethylnitrosamine-induced liver foci and hepatocellular adenomas in C3H mice. Diallyldisulfide has also been shown to inhibit mutagenesis or tumorigenesis induced by vinyl carbamate and N-nitrosodimethylamine; aflatoxin B1-induced and N-nitrosodiethylamine-induced liver preneoplastic foci in rats; arylamine N-acetyltransfer- ase activity and 2-aminofluorene-DNA adducts in human promyelocytic leukemia cells; DMBA-induced mouse skin tumors; N-nitrosomethylbenzylamine-induced mutation in rat esophagus; and diethylstilbesterol-induced DNA ad- ducts in the breasts of female ACI rats.

Diallyldisulfide is believed to bring about an anticarcino- genic effect through a number of mechanisms, such as scavenging of radicals; increasing gluathione levels; increasing the activities of enzymes such as glutathione S-transferase and catalase; inhibiting cytochrome p4502E1 and DNA repair mechanisms; and preventing chromosomal damage (80).

Thymoquinone

The chemotherapeutic and chemoprotective agents from black cumin include thymoquinone (TQ), dithymoquinone (DTQ), and thymohydroquinone, which are present in the oil of this seed. TQ has antineoplastic activity against various tumor cells. DTQ also contributes to the chemotherapeutic effects of Nigella sativa. In vitro study results indicated that DTQ and TQ are equally cytotoxic to several parental cell lines and to their corresponding multidrug-resistant human tumor cell lines. TQ induces apoptosis by p53-dependent and p53-independent pathways in cancer cell lines. It also induces cell-cycle arrest and modulates the levels of inflammatory mediators. To date, the chemotherapeutic potential of TQ has not been tested, but numerous studies have shown its promising anticancer effects in animal models. TQ suppresses carcinogen-induced forestomach and skin tumor formation in mice and acts as a chemopreventive agent at the early stage of skin tumorigenesis. Moreover, the combination of TQ and clinically used anticancer drugs has been shown to improve the drug�s therapeutic index, prevents nontumor tissues from sustaining chemotherapy-induced damage, and enhances the antitumor activity of drugs such as cisplatin and ifosfamide. A very recent report from our own group established that TQ affects the NF-?B signaling pathway by suppressing NF-?B and NF-?B-regulated gene products (81).

Capsaicin

The phenolic compound capsaicin (t8-methyl-N-vanillyl- 6-nonenamide), a component of red chili, has been extensively studied. Although capsaicin has been suspected to be a carcinogen, a considerable amount of evidence suggests that it has chemopreventive effects. The antioxidant, anti-inflammatory, and antitumor properties of capsaicin have been established in both in vitro and in vivo systems. For example, showed that capsaicin can suppress the TPA-stimulated activation of NF-?B and AP-1 in cultured HL-60 cells. In addition, capsaicin inhibited the constitutive activation of NF-?B in malignant melanoma cells. Furthermore, capsaicin strongly suppressed the TPA-stimulated activation of NF-?B and the epidermal activation of AP-1 in mice. Another proposed mechanism of action of capsaicin is its interaction with xenobiotic metaboliz- ing enzymes, involved in the activation and detoxification of various chemical carcinogens and mutagens. Metabolism of capsaicin by hepatic enzymes produces reactive phenoxy radical intermediates capable of binding to the active sites of enzymes and tissue macromolecules.

Capsaicin can inhibit platelet aggregation and suppress calcium-ionophore�stimulated proinflammatory responses, such as the generation of superoxide anion, phospholipase A2 activity, and membrane lipid peroxidation in macro- phages. It acts as an antioxidant in various organs of laboratory animals. Anti-inflammatory properties of capsaicin against carcinogen-induced inflammation have also been reported in rats and mice. Capsaicin has exerted protective effects against ethanol-induced gastric mucosal injury, hem- orrhagic erosion, lipid peroxidation, and myeloperoxidase activity in rats that was associated with suppression of COX- 2. While lacking intrinsic tumor-promoting activity, capsaicin inhibited TPA-promoted mouse skin papillomagenesis (82).

Gingerol

Gingerol, a phenolic substance mainly present in the spice ginger (Zingiber officinale Roscoe), has diverse pharmacologic effects including antioxidant, antiapoptotic, and anti-inflammatory effects. Gingerol has been shown to have anticancer and chemopreventive properties, and the proposed mechanisms of action include the inhibition of COX-2 expression by blocking of the p38 MAPK�NF-?B signaling pathway. A detailed report on the cancer-preventive ability of gingerol was presented in a recent review by Shukla and Singh (83).

Anethole

Anethole, the principal active component of the spice fennel, has shown anticancer activity. In 1995, Al-Harbi et al. (84) studied the antitumor activity of anethole against Ehrlich ascites carcinoma induced in a tumor model in mice. The study revealed that anethole increased survival time, reduced tumor weight, and reduced the volume and body weight of the EAT-bearing mice. It also produced a significant cytotoxic effect in the EAT cells in the paw, reduced the levels of nucleic acids and MDA, and increased NP-SH concentrations.

The histopathological changes observed after treatment with anethole were comparable to those after treatment with the standard cytotoxic drug cyclophosphamide. The frequency of micronuclei occurrence and the ratio of polychromatic erythrocytes to normochromatic erythrocytes showed anethole to be mitodepressive and nonclastogenic in the femoral cells of mice. In 1996, Sen et al., (85) studied the NF-?B inhibitory activity of a derivative of anethole and anetholdithiolthione. Their study results showed that anethole inhibited H2O2, phorbol myristate acetate or TNF alpha induced NF-?B activation in human jurkat T-cells (86) studied the anticarcino- genic activity of anethole trithione against DMBA induced in a rat mammary cancer model. The study results showed that this phytochemical inhibited mammary tumor growth in a dose- dependent manner.

Nakagawa and Suzuki (87) studied the metabolism and mechanism of action of trans-anethole (anethole) and the estrogenlike activity of the compound and its metabolites in freshly isolated rat hepatocytes and cultured MCF-7 human breast cancer cells. The results suggested that the biotransformation of anethole induces a cytotoxic effect at higher concentrations in rat hepatocytes and an estrogenic effect at lower concentrations in MCF-7 cells on the basis of the concentrations of the hydroxylated intermediate, 4OHPB. Results from preclinical studies have suggested that the organosulfur compound anethole dithiolethione may be an effective chemopreventive agent against lung cancer. Lam et al, (88) conducted a phase 2b trial of anethole dithiolethione in smokers with bronchial dysplasia. The results of this clinical trial suggested that anethole dithiolethione is a potentially efficacious chemopreventive agent against lung cancer.

Diosgenin

Diosgenin, a steroidal saponin present in fenugreek, has been shown to suppress inflammation, inhibit proliferation, and induce apoptosis in various tumor cells. Research during the past decade has shown that diosgenin suppresses prolif- eration and induces apoptosis in a wide variety of cancer cells lines. Antiproliferative effects of diosgenin are mediated through cell-cycle arrest, disruption of Ca2+ homeostasis, activation of p53, release of apoptosis-inducing factor, and modulation of caspase-3 activity. Diosgenin also inhibits azoxymethane-induced aberrant colon crypt foci, has been shown to inhibit intestinal inflammation, and modulates the activity of LOX and COX-2. Diosgenin has also been shown to bind to the chemokine receptor CXCR3, which mediates inflammatory responses. Results from our own laboratory have shown that diosgenin inhibits osteoclastogenesis, cell invasion, and cell proliferation through Akt down-regulation, I?B kinase activation, and NF-?B-regulated gene expression (89).

Eugenol

Eugenol is one of the active components of cloves. Studies conducted by Ghosh et al. (90) showed that eugenol suppressed the proliferation of melanoma cells. In a B16 xenograft study, eugenol treatment produced a significant tumor growth delay, an almost 40% decrease in tumor size, and a 19% increase in the median time to end point. Of more importance, 50% of the animals in the control group died of metastatic growth, whereas none in the eugenol treatment group showed any signs of cell invasion or metastasis. In 1994, Sukumaran et al. (91) showed that eugenol DMBA induced skin tumors in mice. The same study showed that eugenol inhibited superoxide formation and lipid peroxidation and the radical scavenging activity that may be responsible for its chemopreventive action. Studies conducted by Imaida et al. (92) showed that eugenol enhanced the development of 1,2- dimethylhydrazine-induced hyperplasia and papillomas in the forestomach but decreased the incidence of 1-methyl-1-nitro- sourea-induced kidney nephroblastomas in F344 male rats.

Another study conducted by Pisano et al. (93) demonstrated that eugenol and related biphenyl (S)-6,6?-dibromo-dehydrodieugenol elicit specific antiproliferative activity on neuroectodermal tumor cells, partially triggering apoptosis. In 2003, Kim et al. (94) showed that eugenol suppresses COX-2 mRNA expression (one of the main genes implicated in the processes of inflammation and carcinogenesis) in HT-29 cells and lipopolysaccharide-stimulated mouse macrophage RAW264.7 cells. Another study by Deigner et al. (95) showed that 1?-hydroxyeugenol is a good inhibitor of 5-lipoxygenase and Cu(2+)-mediated low-density lipoprotein oxidation. The studies by Rompelberg et al. (96) showed that in vivo treatment of rats with eugenol reduced the mutagenicity of benzopyrene in the Salmonella typhimurium mutagenicity assay, whereas in vitro treatment of cultured cells with eugenol increased the genotoxicity of benzopyrene.

Wholegrain Foods

The major wholegrain foods are wheat, rice, and maize; the minor ones are barley, sorghum, millet, rye, and oats. Grains form the dietary staple for most cultures, but most are eaten as refined-grain products in Westernized countries (97). Whole grains contain chemopreventive antioxidants such as vitamin E, tocotrienols, phenolic acids, lignans, and phytic acid. The antioxidant content of whole grains is less than that of some berries but is greater than that of common fruits or vegetables (98). The refining process concentrates the carbo- hydrate and reduces the amount of other macronutrients, vitamins, and minerals because the outer layers are removed. In fact, all nutrients with potential preventive actions against cancer are reduced. For example, vitamin E is reduced by as much as 92% (99).

Wholegrain intake was found to reduce the risk of several cancers including those of the oral cavity, pharynx, esophagus, gallbladder, larynx, bowel, colorectum, upper digestive tract, breasts, liver, endometrium, ovaries, prostate gland, bladder, kidneys, and thyroid gland, as well as lymphomas, leukemias, and myeloma (100,101). Intake of wholegrain foods in these studies reduced the risk of cancers by 30�70% (102).

How do whole grains reduce the risk of cancer? Several potential mechanisms have been described. For instance, insoluble fibers, a major constituent of whole grains, can reduce the risk of bowel cancer (103). Additionally, insoluble fiber undergoes fermentation, thus producing short-chain fatty acids such as butyrate, which is an important suppressor of tumor formation (104). Whole grains also mediate favorable glucose response, which is protective against breast and colon cancers (105). Also, several phytochemicals from grains and pulses were reported to have chemopreventive action against a wide variety of cancers. For example, isoflavones (including daidzein, genistein, and equol) are nonsteroidal diphenolic com- pounds that are found in leguminous plants and have antiproliferative activities. Findings from several, but not all, studies have shown significant correlations between an isoflavone-rich soy-based diet and reduced incidence of cancer or mortality from cancer in humans. Our laboratory has shown that tocotrienols, but not tocopherols, can suppress NF-?B activation induced by most carcinogens, thus leading to suppression of various genes linked with proliferation, survival, invasion, and angiogenesis of tumors (106).

Observational studies have suggested that a diet rich in soy isoflavones (such as the typical Asian diet) is one of the most significant contributing factors for the lower observed incidence and mortality of prostate cancers in Asia. On the basis of findings about diet and of urinary excretion levels associated with daidzein, genistein, and equol in Japanese subjects compared with findings in American or European subjects, the isoflavonoids in soy products were proposed to be the agents responsible for reduced cancer risk. In addition to its effect on breast cancer, genistein and related isoflavones also inhibit cell growth or the development of chemically induced cancers in the stomach, bladder, lung, prostate, and blood (107).

Vitamins

Although controversial, the role of vitamins in cancer chemoprevention is being evaluated increasingly. Fruits and vegetables are the primary dietary sources of vitamins except for vitamin D. Vitamins, especially vitamins C, D, and E, are reported to have cancer chemopreventive activity without apparent toxicity.

Epidemiologic study findings suggest that the anticancer/ chemopreventive effects of vitamin C against various types of cancers correlate with its antioxidant activities and with the inhibition of inflammation and gap junction intercellular communication. Findings from a recent epidemiologic study showed that a high vitamin C concentration in plasma had an inverse relationship with cancer-related mortality. In 1997, expert panels at the World Cancer Research Fund and the American Institute for Cancer Research estimated that vitamin C can reduce the risk of cancers of the stomach, mouth, pharynx, esophagus, lung, pancreas, and cervix (108).

The protective effects of vitamin D result from its role as a nuclear transcription factor that regulates cell growth, differentiation, apoptosis, and a wide range of cellular mechanisms central to the development of cancer (109).

Exercise/Physical Activity

There is extensive evidence suggesting that regular physical exercise may reduce the incidence of various cancers. A sedentary lifestyle has been associated with most chronic illnesses. Physical inactivity has been linked with increased risk of cancer of the breast, colon, prostate, and pancreas and of melanoma (110). The increased risk of breast cancer among sedentary women that has been shown to be due to lack of exercise has been associated with a higher serum concentration of estradiol, lower concentration of hormone- binding globulin, larger fat masses, and higher serum insulin levels. Physical inactivity can also increase the risk of colon cancer (most likely because of an increase in GI transit time, thereby increasing the duration of contact with potential carcinogens), increase the circulating levels of insulin (pro- mote proliferation of colonic epithelial cells), alter prosta- glandin levels, depress the immune function, and modify bile acid metabolism. Additionally, men with a low level of physical activity and women with a larger body mass index were more likely to have a Ki-ras mutation in their tumors, which occurs in 30�50% of colon cancers. A reduction of almost 50% in the incidence of colon cancer was observed among those with the highest levels of physical activity (111). Similarly, higher blood testosterone and IGF-1 levels and suppressed immunity due to lack of exercise may increase the incidence of prostate cancer. One study indicated that sedentary men had a 56% and women a 72% higher incidence of melanoma than did those exercising 5�7 days per week (112).

Caloric Restrictions

Fasting is a type of caloric restriction (CR) that is prescribed in most cultures. Perhaps one of the first reports that CR can influence cancer incidence was published in 1940 on the formation of skin tumors and hepatoma in mice (113, 114). Since then, several reports on this subject have been published (115, 116). Dietary restriction, especially CR, is a major modifier in experimental carcinogenesis and is known to significantly decrease the incidence of neoplasms. Gross and Dreyfuss reported that a 36% restriction in caloric intake dramatically decreased radiation-induced solid tumors and/or leukemias (117, 118). Yoshida et al. (119) also showed that CR reduces the incidence of myeloid leukemia induced by a single treatment with whole-body irradiation in mice.

How CR reduces the incidence of cancer is not fully understood. CR in rodents decreases the levels of plasma glucose and IGF-1 and postpones or attenuates cancer and inflammation without irreversible adverse effects (120). Most of the studies done on the effect of CR in rodents are long- term; however, that is not possible in humans, who routinely practice transient CR. The effect that transient CR has on cancer in humans is unclear.

Conclusions

On the basis of the studies described above, we propose a unifying hypothesis that all lifestyle factors that cause cancer (carcinogenic agents) and all agents that prevent cancer (chemopreventive agents) are linked through chronic inflammation (Fig. 10). The fact that chronic inflammation is closely linked to the tumorigenic pathway is evident from numerous lines of evidence.

First, inflammatory markers such as cytokines (such as TNF, IL-1, IL-6, and chemokines), enzymes (such as COX-2, 5-LOX, and matrix metalloproteinase-9 [MMP-9]), and adhesion molecules (such as intercellular adhesion molecule 1, endothelium leukocyte adhesion molecule 1, and vascular cell adhesion molecule 1) have been closely linked with tumorigenesis. Second, all of these inflammatory gene products have been shown to be regulated by the nuclear transcription factor, NF-?B. Third, NF-?B has been shown to control the expression of other gene products linked with tumorigenesis such as tumor cell survival or antiapoptosis (Bcl-2, Bcl-xL, IAP-1, IAP-2, XIAP, survivin, cFLIP, and TRAF-1), proliferation (such as c-myc and cyclin D1), invasion (MMP-9), and angiogenesis (vascular endothelial growth factor). Fourth, in most cancers, chronic inflammation precedes tumorigenesis.

Fifth, most carcinogens and other risk factors for cancer, including cigarette smoke, obesity, alcohol, hyperglycemia, infectious agents, sunlight, stress, food carcinogens, and environmental pollutants, have been shown to activate NF- ?B. Sixth, constitutive NF-?B activation has been encountered in most types of cancers. Seventh, most chemotherapeutic agents and ?-radiation, used for the treatment of cancers, lead to activation of NF-?B. Eighth, activation of NF-?B has been linked with chemoresistance and radioresistance. Ninth, sup- pression of NF-?B inhibits the proliferation of tumors, leads to apoptosis, inhibits invasion, and suppresses angiogenesis. Tenth, polymorphisms of TNF, IL-1, IL-6, and cyclin D1 genes encountered in various cancers are all regulated by NF-?B. Also, mutations in genes encoding for inhibitors of NF-?B have been found in certain cancers. Eleventh, almost all chemopreventive agents described above have been shown to suppress NF-?B activation. In summary, this review outlines the preventability of cancer based on the major risk factors for cancer. The percentage of cancer-related deaths attributable to diet and tobacco is as high as 60�70% worldwide.

ACKNOWLEDGEMENT

This research was supported by The Clayton Foundation for Research (to B.B.A.).

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Clinical Evaluation and Treatment for Inflammatory Bowel Disease

Clinical Evaluation and Treatment for Inflammatory Bowel Disease

Inflammatory Bowel Disease: The gastrointestinal mucosal barrier is an effective and powerful defense and repair mechanism, which allows for the proper absorption of energy, nutrients and water when we eat. The functioning of the digestive system with its balanced gut microbiota depends on the function of the mucosal barrier. The intestinal barrier has to be permeable to allow the passage of nutrients, however, when this permeability increases beyond what is necessary, it can lead to a variety of issues, in some instances, even causing disease.

 

What’s the connection between intestinal permeability and IBD?

 

Intestinal barrier dysfunction has been determined in a variety of gastrointestinal diseases, or GI diseases, such as inflammatory bowel disease, or IBD. It has now become more accepted that proper gastrointestinal mucosal barrier function plays a major role in the pathophysiology of inflammatory bowel disease. However, further understanding as well as research data is required to determine treatment and therapy options for such gastrointestinal diseases, particularly IBD.

Clinical Evaluation of Intestinal Permeability in Inflammatory Bowel Disease

 

Changes to intestinal permeability generally manifest early in the development of intestinal inflammation due to Crohn’s disease and other gastrointestinal diseases. Several risk factors, including the conditions themselves, may even exacerbate intestinal inflammation through increased intestinal permeability. According to recent research studies, nonsteroidal anti-inflammatory drugs, or NSAIDs, and stress can also induce symptoms of inflammation through increased gastrointestinal, or GI, mucosal permeability and the release of corticotropin-released factors. Additionally, changes to intestinal permeability can determine a patient’s risk of relapsing Crohn’s disease. Patients who’ve had an altered lactulose/mannitol test, or L/M test, are often 8 times more at risk of relapsing, even when asymptomatic and results demonstrate normal biochemical indices.

 

The lactulose/mannitol test is specifically used to evaluate small intestinal permeability by measuring urinary excretion after oral administration of these sugars. Lactulose�is a large sized oligosaccharide that generally doesn’t carry out paracellular transport and can be adsorbed in the instance of leaky intercellular junctions while mannitol is a smaller molecule that can freely move across the intestinal epithelium. Both probes are equally affected by gastrointestinal dilution, motility, bacterial degradation, and renal function; consequently, the ratio allows for the correction of possible confounding factors. The lactulose/mannitol test is utilized in clinical practice because of its noninvasiveness, its high sensitivity in detecting active inflammatory bowel disease, or IBD, and its ability to distinguish functional versus organic GI disease, or gastrointestinal disease. An altered L/M test has been reported in approximately 50 percent of patients with Crohn’s disease. Other sugars have also been routinely used to evaluate the upper gastrointestinal tract, for instance, sucrose which has been degraded by duodenal sucrase, may indicate the permeability of the stomach and the proximal duodenum. Accordingly, multisugar tests have been developed, with the latest inclusion of sucralose, which can be barely absorbed through the human intestine, allowing a functional assessment of the entire gastrointestinal tract, extending its use for ulcerative colitis as well.

 

Other functional tests, such as 51Cr-EDTA or the Ussing chambers, have demonstrated great precision in diagnosing gastrointestinal disease, however, their invasiveness and complex detection methods make their use impossible in humans. Whereas promising results have been demonstrated by novel imaging techniques, particularly confocal laser endomicroscopy. This endoscopic technique allows an in vivo evaluation of the epithelial lining and vasculature with the use of intravenous fluorescein as a molecular contrast agent, which generally doesn’t carry out paracellular transport. Confocal laser endomicroscopy is currently widely utilized to identify and classify gastrointestinal tumors but it has also been used in nonneoplastic conditions, such as celiac disease, collagenous colitis, and irritable bowel syndrome, or IBS. Discovering cellular and subcellular changes, such as cell shedding, is possible through this procedure, which makes it a highly effective technique for the imaging of intestinal barrier dysfunction in inflammatory bowel disease, or IBD. Confocal laser endomicroscopy demonstrated increased density of mucosal gaps after cell shedding in the small intestine of patients with Crohn’s disease as well as in macroscopically normal duodenum in both Crohn’s disease and ulcerative colitis. These alterations could represent impairment of intestinal permeability possibly predicting subsequent clinical relapse. Recently, confocal laser endomicroscopy has been utilized in patients with ulcerative colitis, demonstrating that the occurrence of crypt architectural abnormalities may predict disease relapse in patients with noticeable endoscopic remission, as seen on Figure 1.

 

Confocal Laser Endomicroscopy Images Figure 2

Figure 1: Confocal laser endomicroscopy images from a healthy subject (a) and an ulcerative colitis (UC) patient with inactive disease (b). UC patients display increased crypt diameter, intercryptic distance, and perivascular fluorescence.

 

Intestinal Permeability Treatment for Inflammatory Bowel Disease

 

Agents routinely used in the therapeutic armamentarium of inflammatory bowel disease, or IBD, may cause and maintain mucosal remission not only for their immunomodulating effect, but also through the recovery of epithelial integrity and permeability, as was demonstrated for anti-TNF-? drugs and medications in Crohn’s disease. Since similar effects are obtained using elemental diets for Crohn’s disease, raising interest is based on dietary strategies with the use of immunomodulatory nutrients and probiotics.

 

Western diets, with its high content of fat and refined sugars, is a risk factor for the growth of Crohn’s disease, where they’re believed to induce a low-grade inflammation through gut dysbiosis and increased intestinal permeability. Furthermore, there is increasing concern about the use of industrial food additives towards promoting immune-related diseases. A recent research study demonstrated how additives can increase intestinal permeability by interfering with the tight junctions, or TJs, increasing the passage of immunogenic antigens. In addition, certain fatty acids, such as propionate, acetate, butyrate, omega-3, and conjugated linoleic acid, amino acids, such as glutamine, arginine, tryptophan, and citrulline, and oligoelements, which are essential for intestinal surface integrity, when supplemented to experimental subjects with gastrointestinal diseases, GI diseases, can decrease inflammation and restore gastrointestinal mucosal permeability. However, their therapeutic effectiveness, especially in inflammatory bowel disease, remains debatable: butyrate, zinc, and probiotics have the strongest evidence in this aspect.

 

Butyrate is a short chain fatty acid produced by intestinal microbial fermentation of dietary fibers, which in experimental versions, stimulate mucus production and expression of tight junctions, or TJs, in vitro but a broader selection of action is anticipated. It’s essential for the overall homeostasis of enterocytes that its lack, measured as faecal concentrations, has been taken as an indirect indicator of altered intestinal barrier function. In clinical practice topical butyrate had demonstrated effectiveness in refractory distal ulcerative colitis. Other fatty acids with similar properties have also been proposed as an adjuvant treatment in inflammatory bowel disease, namely, omega-3 and phosphatidylcholine, but their usage in clinical practice remains limited. Zinc is a trace element essential for cell turnover and repair systems. Inflammatory conditions and malnutrition have been known to be risk factors for zinc deficiency and many research studies demonstrated the effectiveness of its supplementation during acute diarrhoea and experimental colitis. Oral zinc treatment may restore intestinal permeability in patients with Crohn’s disease, perhaps through its capacity to regulate tight junctions, or TJs, both in the small and the large intestines.

 

The reason for the use of probiotics in inflammatory bowel disease is for the above mentioned dysbiosis that characterizes these GI diseases, or gastrointestinal diseases. Several trials have tested the effectiveness of various species of probiotics in inflammatory bowel disease, or IBD, with contradicting results. Those which have demonstrated to be effective are Escherichia coli Nissle 1917, Bifidobacterium, Lactobacillus rhamnosus GG, or the multispecies VSL#3, which consists of eight unique probiotics. Nevertheless, their use remains confined to ulcerative colitis and are frequently aimed at maintaining remission rather than treating the active disease, as emphasized by the meta evaluation by Jonkers et al.. The mechanisms of their effect in ulcerative colitis have yet to be fully understood but likely, together with direct anti-inflammatory effects, they can restore the intestinal barrier and decrease intestinal permeability, regulating tight junction, or TJ, proteins. The favorable effect of probiotics in pouchitis seems to be about the improvement of gastrointestinal mucosal barrier function. Another potential mechanism of action is the recovery of butyrate-producing bacteria: patients with ulcerative colitis have decreased bacterial species like Faecalibacterium prausnitzii, but supplementation with butyrate-producing species or probiotics together with preformed butyrate demonstrated effectiveness in experimental models.

 

Finally, vitamin D can also be involved to preserve intestinal barrier function. Polymorphisms of its own receptor have been related to the development of inflammatory bowel disease, or IBD. While the expression of vitamin D receptor on intestinal epithelium prevents inflammation-induced apoptosis, its removal contributes to faulty autophagy that boosts experimental colitis. But, additional data and clinical trials are needed to rationalize vitamin D use in inflammatory bowel disease management.

 

Conclusion

 

The impairment of intestinal barrier function is just one of the critical events in the pathogenesis of inflammatory bowel disease, or IBD. Whether it precedes and predisposes disease development remains under analysis, particularly in Crohn’s disease, but it perpetuates and enriches chronic mucosal inflammation by increasing paracellular transport of luminal pathogens. Novel imaging and functional techniques allow us to assess intestinal permeability in vivo and help identify patients at risk of relapse guiding therapeutic management. Manipulation of intestinal permeability is a fascinating therapeutic approach but more research on its effectiveness and safety are required before nutritional immune-modulators may be utilized in clinical practice. Information referenced from the National Center for Biotechnology Information (NCBI) and the National University of Health Sciences. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

By Dr. Alex Jimenez

 

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Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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ADDITIONAL TOPIC: EXTRA EXTRA: Treating Back Pain

 

 

Nutritional Strategies For Skeletal And Cardiovascular Health

Nutritional Strategies For Skeletal And Cardiovascular Health

Nutritional Strategies:� Hard Bones, Soft Arteries, Rather Than Vice Versa

ABSTRACT

nutritional strategiesNutritional Strategies: The focus of this paper is to explore better strategies for optimizing bone strength and reducing risk of fracture, while at the same time decreasing risk of cardiovascular disease. The majority of Americans do not consume the current recommended dietary allowance for calcium, and the lifetime risk of osteoporosis is about 50%. However, traditional mono-nutrient calcium supplements may not be ideal. We comprehensively and systematically reviewed the scientific literature in order to determine the optimal dietary nutritional strategies and nutritional supplements for long- term skeletal health and cardiovascular health. To summarize, the following steps may be helpful for building strong bones while maintaining soft and supple arteries: (1) calcium is best obtained from dietary sources rather than supplements; (2) ensure that adequate animal protein intake is coupled with calcium intake of 1000 mg/day; (3) maintain vitamin D levels in the normal range; (4) increase intake of fruits and vegetables to alkalinize the system and promote bone health; (5) concomitantly increase potassium consumption while reducing sodium intake; (6) consider increasing the intake of foods rich in vitamins K1 and K2; (7) consider including bones in the diet; they are a rich source of calcium-hydroxyapatite and many other nutrients needed for building bone.

INTRODUCTION: Nutritional Strategies

Calcium: General Physiology Andepidemiology

Calcium is the most ubiquitous mineral in the human body. An average-sized adult body contains approximately 1000 to 1200 g of calcium, which is predominately incorporated into bones and teeth in the form of calcium-hydroxyapatite (Ca10(PO4)6(OH)2) crystals. The remainder circulates throughout the blood and soft tissues, and plays fundamental roles in cell conduction, muscle function, hormone regulation, vitamin (Vit) K-dependent pathways, and cardiac and blood vessel function.1

Some studies indicate only 30% of the US population consumes the Recommended

Dietary Allowance of calcium, which is 1000� 1200 mg daily.1 Furthermore, humans absorb only about 30% of calcium from foods depend- ing on the specific source.1 The body will demineralize its own skeletal system to maintain serum calcium levels in situations where dietary calcium is insufficient and/or absorption is decreased, and/or excretion is increased.2

Osteopenia/Osteoporosis:�An Epidemic

Starting at about age 50 years, postmenopausal women lose about 0.7�2% of their bone mass each year, while men over age 50 years lose 0.5�0.7% yearly. Between ages 45 and 75years, women, on average, lose 30% of their bone mass, whereas men lose 15%.

According to the US Surgeon General�s Report, 1 in 2 Americans over age 50 years is expected to have or to be at risk of develop- ing osteoporosis.3 Osteoporosis causes 8.9 million fractures annually, with an estimated cumulative cost of incident fractures predicted at US$474 billion over the next�20 years in the USA.3�6 Among adult women over age 45 years, osteoporosis accounts for more days spent in hospital than many other diseases such as diabetes, myocardial infarction (MI), chronic obstructive airway disease and breast cancer.3 Fragility fractures are the primary cause of hospitalization and/or death for US adults ? age 65 years and older; and 44% of nursing home admissions are due to fractures.3

A Mayo Clinic study reported that compared to 30 years ago, forearm fractures have risen more than 32% in boys and 56% in girls. The authors concluded that dietary changes, including insufficient calcium and excess phosphate, were significantly associated with increased fractures.7 Public health approaches are crucial to prevent symptomatic bone disease, but widespread pharmacological prophylaxis is prohibitively expensive and carries potential serious adverse effects.

Cardiovascular Disease & Bone Mineral Disease: A Calcium Nexus

Strong epidemiological associations exist between decreased bone mineral density (BMD) and increased risk of both cardiovascular (CV) disease and CV death.8 For example, individuals with osteoporosis have a higher risk of coronary artery disease, and vice versa. This problem will be magnified if the therapies for osteoporosis (eg, calcium supplements) independently increase risk of MI.

Issues With Dairy As Primary Source Of Calcium

Dairy foods and beverages account for about 70% of all dietary calcium intake among Americans. Dozens of epidemiological and randomized controlled trials in adults and children have used dairy products as the principal source of calcium, and have credited dairy intake with preventive benefits on study end points including bone mass, fractures and osteoporosis. A recent meta-analysis of over 270 000 people showed a strong trend for dairy intake protecting against hip fracture; the relative risk (RR) of hip fracture per daily glass of milk was 0.91, 95% CI 0.81 to 1.01.9

In many industrialized nations, milk is often the most cost-effective strategy for achieving recommended levels of calcium intake at a population level. Yet, legitimate concerns exist regarding potential deleterious effects of chronic dairy intake on health.10�16 Dairy foods, on an evolutionary time scale, are relative �new-comers� to the hominin diet.17 Domestication of cattle, sheep and goats first occurred approximately 11 000�10 000 years Before Present.17 Furthermore, it appears that an estimated 65% of the worldwide population expresses the phenotype of lactase non-persistence.18

Consumption of cow�s milk has been inconsistently associated with cataracts, ovarian and prostate cancers, and Parkinson�s disease, and it has been implicated in certain autoimmune diseases, such as type 1 diabetes and multiple sclerosis. Overall, the evidence for dairy-induced human disease appears to be most consistent for prostate cancer and for type 1 diabetes.19

A recent study of over 106 000 adults followed for 20 years showed that drinking three or more glasses of milk per day was associated with increased risks for bone fracture and higher mortality rates compared with drink- ing not more than one glass of milk per day.20 By contrast, for the women in that study, each daily serving of cheese and/or other fermented milk products such as yogurt was associated with a 10�15% decrease in the rates of mortality and hip fractures (p<0.001). However, this was an observational study with inherent limitations such as residual confounding and reverse causation, and thus, firm conclusions cannot be drawn from the data.

The sugar in milk, lactose, is broken down in the gastrointestinal tract to d-galactose and d-glucose. d-Galactose has been found to increase inflammation and oxidation in adult humans, and in adult animals this sugar triggers accelerated aging, neurodegeneration, and a shortened life span.20

Thus, cow�s milk, though rich in many nutrients, including calcium, has issues that render it less than ideal as a dietary staple for many adults. On the contrary, fermented dairy foods, such as yogurt and cheese, appear to be safer than milk, possibly because the most or all of d-galactose has been metabolized by bacteria.20

Plant-Based Dietary Sources Of Calcium & Protein: Effects On Bone Health

nutritional strategiesMost vegetarians, especially vegans, appear to absorb less calcium because of the oxalic and phytic acid contained in many plant, grain and legume products.1 Indeed, several studies have reported that risks of bone fracture are higher in vegans�likely due, at least in part, to their lower dietary calcium intake, and/or poor absorption of this key mineral (table 1).21

Dietary Protein, Calcium And Bone Health

Evolutionary evidence suggests that preagricultural diets were net base-yielding, and contributed to the robust�bone health generally seen among hunter-gatherers.10 17�By contrast, processed foods displace base-yielding fruits�and vegetables, thereby shifting to a net acid-yielding diet.2 22�24

Increased protein intake can raise levels of insulin-like growth factor 1, which is anabolic, and contributes to bone building. Experts currently agree that diets moderate in protein (?1.0�1.5 g/kg/day) are associated with normal calcium metabolism, and do not adversely alter bone metabolism; however, at lower protein intakes (<0.8 g/kg/day), intestinal calcium absorption is reduced and levels of parathyroid hormone rise, causing the mobilization of calcium from bone.25 26

 

A growing body of evidence indicates that diets higher in animal protein associate with greater bone mass and fewer fractures, particularly if the calcium intake is also sufficient (approximately 1000 mg of calcium/day) (figure 1).26�28 Thus, a diet providing ample dietary calcium, along with alkalizing nutrients, such as fruits and vegetables, and possibly also alkaline mineral waters, may create a milieu where moderate intake of animal protein contributes favorably to bone health. Additionally, intake of protein plus calcium with Vitamin D may reduce fracture rates through mechanisms independent of bone density.29

nutritional strategies

Magnesium

nutritional strategiesMaintaining replete magnesium status may reduce risk for the metabolic syndrome, diabetes, hypertension and MI.30 Circumstantial and experimental evidence has also implicated magnesium deficiency in osteoporosis.31�34 Optimal dietary magnesium intake is about 7�10 mg/ kg/day, preferably in the context of a net base-yielding diet, since a net acid-yielding diet increases excretion of both magnesium and calcium (table 2).

Potassium/Sodium Ratio Affects Calcium Metabolism

A potassium/sodium ratio of 1.0 or higher is associated with a 50% lower risk of CVD and total mortality com- pared with a ratio under 1.0.35 Reducing excessive sodium intake is also associated with resultant decreased urinary calcium excretion, which may help to prevent against bone demineralization.36 The average potassium content (about 2600 mg/day) of the typical US diet is substantially lower than its sodium content (about 3300 mg/day).35 Approximately 77% of dietary sodium chloride is consumed in the form of processed foods. By contrast, potassium is naturally abundant in many unprocessed foods, especially vegetables, fruits, tubers, nuts, legumes, fish and seafood. In fact, a high potassium/sodium ratio is a reliable marker for high intake of plant foods and lower intake of processed foods.35 High dietary sodium intake has been associated with endothelial damage, arterial stiffness, decreased nitric�oxide production and increased levels of transforming growth factor ?; whereas, high potassium dietary intake can counteract these effects.35 36

Evidence indicates that the lowest CV event rates occur in the moderate sodium excretion and high potassium excretion groups.37 Thus, it appears that a moderate sodium diet (2800�3300 mg/day) in conjunction with a high potassium intake (>3000 mg/day) might confer the optimal CV benefits for the general population.37

Vitamin K & Bone Health

Emerging evidence suggests that Vitamin K may confer protective effects for both the skeletal and CV systems. Vitamin K operates in the context of other fat-soluble vitamins, such as A and D, all of which are involved in maintenance of serum calcium concentration, along with the manipulation of materials leading to bone morphogenesis and maintenance of bone tissue.38 Specifically, the oxidation of Vitamin K results in activation/carboxylation of matrix Gla protein (MGP) which is partially responsible for mineralizing bone.39

Also, Vit K is required for the activation (?-carboxylation) of osteocalcin; the inactivated form, or per cent of undercaboxylated-osteocalcin (%ucOC), has been found to be a sensitive indicator of Vitamin K nutrition status.38 In cross-sectional and prospective analyses, elevated %ucOC, which occurs when Vitamin K status is low, is a marker of increased risk for hip fracture in the elderly.38

Several large observational studies appear to support the benefits of Vitamin K on bone health.38 A meta-analysis concluded that while supplementation with phytonadione (Vitamin K1) improved bone health, Vitamin K2 was even more effective in this regard.40 This large and statistically rigorous meta-analysis concluded that high Vitamin K2 levels were associated with reduced vertebral fractures by approximately 60% (95% CI 0.25% to 0.65%), hip fractures by 77% (95% CI 0.12% to 0.47%), and all non- vertebral fractures by approximately 81% (95% CI 0.11% to 0.35%). Moreover, the benefit of Vitamin K on bone may not be due to its ability to increase BMD, but rather to its effects at increasing bone strength.41

Vitamin K Benefits In CV Health

Mounting evidence suggests vascular calcification whether in the coronary or peripheral arteries is a powerful predictor of CV morbidity and all-cause mortal- ity.42 Prevention of vascular calcification is therefore important as an early intervention to potentially improve long-term CV prognosis.

A major calcification inhibitory factor, is a Vitamin K-dependent protein synthesized by vascular smooth muscle cells.42 Increased

nutritional strategiesVitamin K2 intake has been associated with decreased arterial calcium deposition and the ability to reverse vascular calcification in animal models. Vitamin K2 prevents pathological calcification in soft tissues via the carboxylation of protective MGP. The undercarboxylated (inactive) species of MGP is formed during inadequate Vitamin K status, or as a result of Vitamin K�antagonists.42 Low Vitamin K status is associated with increased vascular calcifications, and can be improved by effective Vitamin K supplementation (table 3).43 44 In two different randomized, double-blind controlled trials, supplemental Vitamin K has been shown to significantly delay both the development of coronary artery calcification and the deterioration of arterial elasticity.45 46

Dietary Vitamin K exists as two major forms: phylloquinone (K1) and menaquinones (MK-n). K1, the predominant dietary form of Vitamin K, is abundant in dark-green leafy vegetables and seeds. The main dietary sources for MK-n in Western populations are fermented foods, especially natto, cheese and curds (mainly MK-8 and MK-9).47

Calcium Supplementation & Bone Health

A recent large meta-analysis of 26 randomized controlled trials reported that calcium supplements lowered the risk of any fracture by a modest but statistically significant 11% (n=58 573; RR 0.89, 95% CI 0.81 to 0.96).48 Even so, the authors concluded that the evidence for calcium supplements on bone health was weak and inconsistent.

Other large meta-analyses found that calcium supplementation was most effective for preventing hip fractures when it was combined with Vitamin D.49�51 Indeed Vitamin D plays a major role in intestinal calcium absorption and bone health (figure 2).52 Additionally, calcium absorption is, in part, dependent on adequate stomach acid, and both these parameters tend to decrease with age. Drugs that markedly reduce stomach acid, such as proton pump inhibitors, have been shown to reduce calcium absorption and increase risk of osteoporosis and fractures.53

nutritional strategies

A large meta-analysis focusing on calcium intake and fracture risk found that in women (seven prospective cohort studies=170 991 women, 2954 hip fractures), there was no association between total calcium intake and hip fracture risk (pooled RR per 300 mg total=1.01; 95% CI 0.97 to 1.05).50 In men (five prospective cohort studies= 68 606 men, 214 hip fractures), the pooled RR per 300 mg of calcium daily was 0.92 (95% CI 0.82 to 1.03).

Monosupplementation with calcium, especially using the most commonly prescribed formulations (calcium carbonate and calcium citrate) might drive down the absorption of phosphate, thereby contributing to bone demineralization secondary to abnormal calcium to phosphate ratios.54 The recently updated US Preventive Services Task Force (USPSTF) has stated that there is insufficient evidence that calcium and Vitamin D prevent fractures in premenopausal women or in men who have not experienced a prior fracture. Indeed, the USPSTF now recommends against daily calcium supplementation for primary prevention of fragility fractures; stating, �the balance of benefits and harms cannot be determined�.55

Calcium Supplementation & Arterial Health

The Women�s Health Initiative, a 7-year, placebo- controlled randomized trial involving 36 282 participants, found that calcium supplementation with Vitamin D�(1000 mg/400 IU daily) had a neutral effect on coronary risk and cerebrovascular risk.56 By contrast, some subsequent publications have reported data challenging the CV safety of calcium supplementation.57�60

One meta-analysis of placebo-controlled trials involving 28 000 participants reported that a daily calcium supplement was associated with an increased risk of MI (HR 1.24, 95% CI 1.07 to 1.45, p=0.004).58 A prospective study of 388229 men and women with a 12-year follow-up showed that calcium supplementation was associated with elevated risk of heart disease death in men, but not in women.61 Yet, only one randomized controlled trial of calcium supplementation using adverse cardiac events as the primary end point has been published. In that study, daily supplementation using 1200 mg of calcium carbonate did not increase the risk of CV death or hospitalization for 1460 women (mean age 75 years).62

nutritional strategies

In a prospective cohort study with a mean follow-up of 19 years, both�high and low dietary calcium intakes were associated with increased CV disease and higher all-cause mortality (figure 3).51 Importantly, a low dietary calcium intake with or without calcium supplementation is also associated with higher CV morbidity and mortality rates.51

Other possible mechanisms that have linked calcium supplements with CV disease include coronary artery calcification, impaired vasodilation, increased arterial stiffness, and hypercoagulability.51 66

Nutritional Strategies: Food As The Ideal Source Of Calcium

The traditional focus in nutritional strategies based on supplementation of single isolated nutrients may be especially mis- guided in the case of calcium and bone health. A diet supplemented with calcium as a mononutrient pill is not ideal for promoting bone health, and may instead accelerate arterial plaque growth and vascular calcification, and increase risk of MI. Food-based solutions place evidence-based emphasis on finding the admixture of foods that balance the acid�base status of the body, and that most favorably impact the body�s calcium metabolism and bone health.

A plant-rich, grain-free diet alters the acid�base status so as to be slightly alkaline, which is conducive for bone health. However, plants are relatively poor sources of calcium compared to animal sources such as dairy pro- ducts and animal bones. We suspect that milk, though an excellent source of bioavailable calcium, has potential adverse health effects for some individuals. Additionally, 65% of the world�s population show some decrease in lactase activity during adulthood. Importantly, fermented dairy has been linked to favorable outcomes for bone health and mortality risk.

Benefits Of Consuming Bones Or Bone Meal

Ethnographic and anthropological studies indicate that adult human hunter-gatherers consumed most of their calcium in the form of bones from animals, such as small and large mammals, birds, fish and reptiles.67 68 Indeed through millions of years of evolution, we are genetically adapted to consume a large proportion of our dietary calcium from bones, where calcium is absorbed along with a matrix of nutrients including magnesium, phosphorus, strontium, zinc, iron, copper, collagen protein, aminoglycans and osteocalcin�all of which also support robust bone formation.68 69 Theoretically, including animal bones (sardines, salmon, soft chicken bones, bone broths, etc) may be an effective dietary strategy to ensure adequate calcium intake and to optimize long-term bone health.

Mineral supplements made from bone meal, when taken with food, theoretically might provide a more practical means to ensure

nutritional strategiesadequate calcium intake without predisposing to CVD risk. Ingestion of micro- crystalline hydroxyapatite (the form of calcium found in bone) produces less of an acute spike in blood calcium levels compared to soluble calcium salts typically used in standard supplements, and thus may be less likely to increase vascular calcification and coronary risk.65 Hydroxyapatite also stimulates bone osteoblast cells and contains virtually all the essential building blocks needed to construct bone tissue. In a small placebo- controlled randomized trial, women who took 1000 mg of calcium in the form of hydroxyapatite in conjunction with oral Vitamin D showed a significant increase in bone thickness, whereas those who took 1000 mg of a standard calcium carbonate supplement did not (figure 4).70 Another double-blind placebo-controlled study found�that supplementing with hydroxyapatite and Vitamin D3 significantly improved serological markers of bone health.15

In theory, the addition of Vitamin K2 and magnesium to an organic bone meal supplement might further enhance its effectiveness and reduce the risk of soft tissue calcification. However, the quantity and quality of the experimental data testing the effects of Vitamin D and calcium on bone health dwarfs the data for bone meal supplementation. Much larger randomized trials will be needed to firmly establish the safety and effectiveness of bone meal as well as Vitamin K and magnesium as supplements for building bone without increasing vascular calcification.

Conclusion: Nutritional Strategies

It is becoming increasingly clear that the fundamental unit for nutrition is the food (eg, milk, nuts, eggs), not the nutrient (eg, calcium, saturated fat, cholesterol). A nutrient perceived as beneficial, such as calcium, may be unhealthy if the parent food, say milk, contains other nutrients, such as galactose, that on the balance might stimulate adverse effects in the body. In theory, consuming calcium-rich foods such as bones, fermented dairy (eg, unsweetened yogurt, kefir, cheese), leafy greens, almonds, and chia seeds may be an effective strategy for improving both calcium intake and long-term health.

James H O�Keefe,1 Nathaniel Bergman,2 Pedro Carrera-Bastos,3 Mae?lan Fontes-Villalba,3 James J DiNicolantonio,1 Loren Cordain4

 

Twitter Follow Maela?n Fontes-Villalba at @maelanfontes

Contributors NB, PC-B and MF-V assisted with the gathering and review of the data; JD, LC and JHO reviewed the data; NB, PC-B, MF-V, JD, LC and JHO assisted in the concept and design of the manuscript. JHO, NB and PC-B wrote, rewrote and finalised the manuscript.

Funding This manuscript received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. This paper was not commissioned.

Competing interests JHO is Chief Medical Officer and has an ownership interest in CardioTabs, a nutraceutical company that markets products containing vitamins and minerals.

Provenance and peer review Not commissioned; externally peer reviewed.

Data sharing statement No additional data are available.

Open Access This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non- commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http:// creativecommons.org/licenses/by-nc/4.0/

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Inflammatory Bowel Disease and Intestinal Permeability

Inflammatory Bowel Disease and Intestinal Permeability

The pathogenesis of inflammatory bowel disease, or IBD, suggests that interrupted interactions between the gastrointestinal tract, or GI tract, and the gut microbiota can often be the cause behind the development of the disease. A damaged or unhealthy gastric mucosal barrier may result in increased intestinal permeability which can cause an immunological reaction and result in symptoms of inflammation. Individuals diagnosed with inflammatory bowel disease present several defects in the many specialized components of mucosal barrier function, from the mucous coating makeup to the adhesion molecules that regulate paracellular permeability. These alterations may represent a primary dysfunction in Crohn’s disease, but they may also cause chronic mucosal inflammation in ulcerative colitis.

 

How does inflammatory bowel disease affect intestinal permeability?

 

In clinical practice as well as experimental testings, many research studies have reported that changes in intestinal permeability can predict the development of inflammatory bowel disease, or IBD. Functional evaluations, such as the sugar absorption test or the novel imaging technique using confocal laser endomicroscopy, allow an in vivo assessment of intestinal barrier integrity. Antitumor necrosis factor-? (TNF-?) therapy reduces mucosal inflammation and soothes intestinal permeability from IBD patients. Butyrate, zinc, and some probiotics also ameliorate mucosal barrier dysfunction but their use is still limited and further research is required before suggesting permeability manipulation as a therapeutic goal in inflammatory bowel disease.

 

The gut plays a major role in food digestion and absorption of nutrients as well as in maintaining the overall homeostasis. It is estimated that the entire bacterial count in our entire body exceeds ten times the entire amount of individual cells in it, with more than one million species found in the gastrointestinal tract. The gut microbiota, whose genome includes 100 times more genes in relation to the entire human genome, also plays an important role in nutrition, energy metabolism, host defense, and immune system development. However, modified microbiota has been connected to, not just gastrointestinal disorders, but also to the pathogenesis of systemic conditions, such as obesity and metabolic syndrome. Therefore, the expression “mucosal barrier” seems to properly highlight the critical role of the gut and its interaction with microbiota: it is not a static shield but an active apparatus with specialized components. According to Bischoff et al. “permeability” is described as a functional feature of this barrier which allows the coexistence of bacteria required by our organism and prevents luminal penetration of macromolecules and pathogens. Altered intestinal permeability was documented during several diseases, including, acute pancreatitis, multiple organ failure, major surgery, and severe trauma, and may also explain the high incidence of Gram-negative sepsis and related mortality in critically ill patients. Furthermore, perturbation of the complex mechanism of permeability has been connected to the development of irritable bowel syndrome and steatohepatitis, or NASH.

 

The pathogenesis of inflammatory bowel disease, or IBD, remains unclear but it most likely is multifactorial and driven by an exaggerated immune response towards the gastrointestinal microbiome in a genetically susceptible host. Increasing evidence suggests that intestinal permeability may be critical and some authors even considered inflammatory bowel disease, or IBD, as a disease, primarily caused by intestinal barrier dysfunction.

 

Intestinal Barrier Dysfunction in Inflammatory Bowel Disease

 

The main component of the mucosal barrier is represented by the intestinal epithelium, which is made up of one layer of various subtypes of cells, including the enterocytes, goblet cells, Paneth cells, and enteroendocrine cells, as well as immune cells, such as intraepithelial lymphocytes and dendritic cells, as seen on Figure 1. The regulation of paracellular permeability of ions and tiny molecules is provided by three kinds of junctional complexes: the tight junctions, or TJs, adherence junctions, and desmosomes.

 

Components of the mucosal barrier in a healthy gut and inflammatory bowel disease.

Figure 1

 

Individuals with IBD present enhanced paracellular permeability with TJ abnormalities, according to several research studies. These are complex multiprotein structures with an extracellular portion, a transmembrane domain and an intracellular association with the cytoskeleton, referenced from Figure 1. A decreased expression and redistribution of the components, such as occludins, claudins, and junctional adhesion molecules, abbreviated as JAM, have all been demonstrated in IBD, where a current experiment found that eliminating claudin-7 can cause colonic inflammation. In addition, tumour necrosis factor-? (TNF-?), one of the main factors behind IBD inflammation, may regulate the transcription of TJ proteins whereas its antagonists, anti-TNF-?, can ameliorate intestinal permeability. However, TNF-? may contribute to altered intestinal permeability as well, inducing apoptosis of enterocytes, increasing their rate of shedding and preventing the redistribution of TJs which should seal the remaining gaps.

 

Goblet cells are specialized in the secretion of mucus that covers the surface of the intestinal epithelium. Mucus is made up of carbohydrates, proteins, lipids, and a high amount of water while it also has antimicrobial properties because of antimicrobial peptides, mainly defensins produced by Paneth cells, and secretory IgA. Individuals with ulcerative colitis demonstrate a lesser variety of goblet cells, a reduced thickness of the mucus layer, and an altered mucus composition regarding mucins, phosphatidylcholine, and glycosylation. Moreover, modified Paneth cell distribution and function has been reported in IBD: these cells are typically limited to the small intestines, within the crypts of Lieberk�hn, but in IBD, metaplastic Paneth cells may be found in colonic mucosa, together with subsequent secretion of defensins also from the large intestine. The role of Paneth cells may differ in the two disease phenotypes because the expression of defensins is caused by colonic inflammation in UC but is reduced in patients with colonic Crohn’s disease, or CD. The decreased Paneth cell antimicrobial function might be a main pathogenic component in Crohn’s disease, or CD, particularly ileal CD, although the greater secretion of defensins in UC could be a physiological response to mucosal damage.

 

Etiology of Intestinal Permeability in Inflammatory Bowel Disease

 

Whether mucosal barrier dysfunction is a result of the inflammatory response or a primary defect that prompts mucosal inflammation, still remains under debate. However, several research studies suggest that altered intestinal permeability may be an early event in Crohn’s disease pathogenesis. Increased paracellular permeability was found in patients with quiescent IBD and was connected to intestinal symptoms even when endoscopic activity was absent. Furthermore, an ex vivo study with Ussing chambers on colonic biopsies from CD patients revealed a spatially uniform increase in transepithelial conductivity regardless of the presence of minimal mucosal erosions. This finding was attributed to the downregulation of TJ proteins. Lastly, animal models of CD, particularly, IL-10 knockout mice and SAMP1/YitFc mice, also declared that increased permeability can be determined before the onset of mucosal inflammation.

 

Genes involved in intestinal barrier homeostasis have also been associated with IBD susceptibility, demonstrating a genetic predisposition that’s further supported by the observation that up to 40 percent of first-degree relatives of CD patients have altered small intestinal permeability, with a significant connection to familial CD and NOD2/CARD15 variations. This gene, which is involved in bacterial recognition, regulates both innate and adaptive immune responses and is the main susceptibility locus for the development of Crohn’s disease. Other research studies have not found a correlation between permeability and hereditary polymorphisms but it’s noteworthy they’ve mostly involved sporadic CD instances. However, environmental factors are also principal contributors in determining mucosal permeability because permeability is raised even in a percentage of CD spouses. Additionally, a recent research highlighted the value of age and smoking status rather than genotype in family. There is only one reported instance of CD development predicted by an abnormal permeability test in a healthy relative.

 

Independently from being genetically determined or caused by environmental factors, intestinal permeability leads to the disruption of the physiological equilibrium between mucosal barrier and luminal challenge which cannot be properly counteracted by inherent resistance of IBD patients, which on the opposite reacts with an underactive immune trigger. As a matter of fact, many defects in bacterial recognition and processing have been documented in CD patients taking certain genetic polymorphisms, mainly of pattern-recognition receptors, such as NOD2/CARD15 and genes involved in autophagy, like ATG16L1 and IRGM. In intestinal mucosa, the absence of feedback between mutated NOD2/CARD15 expression and gut luminal microbiota may result in the breakdown of tolerance. Interestingly, a recent research study by Nighot et al. revealed that autophagy is also involved with the regulation of the TJs by degradation of a pore-forming claudin, connecting autophagy with permeability.

 

Finally, intestinal microbiota may become altered in IBD, especially in its relative diversity and composition. This could represent a consequence of chronic mucosal inflammation however, the influence of host genotype in shaping microbial community cannot be missed in CD and NOD2/CARD15 genotype has been shown to influence the composition of gut microbiota in humans. This dysbiosis can further exacerbate permeability dysfunction from the reduction of the symbiotic connection between the microbiota and the mucosal barrier integrity. Information referenced from the National Center for Biotechnology Information (NCBI) and the National University of Health Sciences. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

By Dr. Alex Jimenez

 

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Clinical Application of Neuromuscular Techniques: Assessment and Treatment of Hip Flexors � Rectus Femoris, Iliopsoas

 

Patient lies supine with buttocks (coccyx) as close to end of table as possible, non-tested leg in flexion at hip and knee, held by patient or by having sole of foot of non-tested side placed against the lateral chest wall of the practitioner. Full flexion of the hip helps to maintain the pelvis in full rotation with the lumbar spine flat, which is essential if the test is to be meaningful and stress on the spine is to be avoided.

 

Notes on Psoas

 

  • Lewit (1985b) mentions that in many ways the psoas behaves as if it were an internal organ. Tension in the psoas may be secondary to kidney disease, and one of its frequent clinical manifestations, when in spasm, is that it reproduces the pain of gall-bladder disease (often after the organ has been removed).
  • The definitive signs of psoas problems are not difficult to note, according to Harrison Fryette (1954). He maintains that the distortions produced in inflammation and/or spasm in the psoas are characteristic and cannot be produced by other dysfunction. The origin of the psoas is from 12th thoracic to (and including) the 4th lumbar, but not the 5th lumbar. The insertion is into the lesser trochanter of the femur, and thus, when psoas spasm exists unilaterally, the patient is drawn forwards and sidebent to the involved side. The ilium on the side will rotate backwards on the sacrum, and the thigh will be everted. When both muscles are involved the patient is drawn forward, with the lumbar curve locked in flexion. This is the characteristic reversed lumbar spine. Chronic bilateral psoas contraction creates either a reversed lumbar curve if the erector spinae of the low back are weak, or an increased lordosis if they are hypertonic.
  • Lewit says, �Psoas spasm causes abdominal pain, flexion of the hip and typical antalgesic (stooped) posture. Problems in psoas can profoundly influence thoraco-lumbar stability.�
  • The 5th lumbar is not involved directly with psoas, but great mechanical stress is placed upon it when the other lumbar vertebrae are fixed in either a kyphotic or an increased lordotic state. In unilateral psoas spasms, a rotary stress is noted at the level of 5th lumbar. The main mechanical involvement is, however, usually at the lumbodorsal junction. Attempts to treat the resulting pain (frequently located in the region of the 5th lumbar and sacroiliac) by attention to these areas will be of little use. Attention to the muscular component should be a primary focus, ideally using MET.
  • Bogduk (Bogduk et al 1992, Bogduk 1997) provides evidence that psoas plays only a small role in the action of the spine, and states that it �uses the lumbar spine as a base from which to act on the hip�. He goes on to discuss just how much pressure derives from psoas compression on discs: �Psoas potentially exerts massive compression loads on the lower lumbar discs � upon maximum contraction, in an activity such as sit-ups, the two psoas muscles can be expected to exert a compression on the L5�S1 disc equal to about 100 kg of weight.�
  • There exists in all muscles a vital reciprocal agonist�antagonist relationship which is of primary importance in determining their tone and healthy function. Psoas�rectus abdominis have such a relationship and this has important postural implications (see notes on lower crossed syndrome in Ch. 2).
  • Observation of the abdomen �falling back� rather than mounding when the patient flexes indicates normal psoas function. Similarly, if the patient, when lying supine, flexes knees and �drags� the heels towards the buttocks (keeping them together), the abdomen should remain flat or fall back. If the abdomen mounds or the small of the back arches, psoas is incompetent.
  • If the supine patient raises both legs into the air and the belly mounds it shows that the recti and psoas are out of balance. Psoas should be able to raise the legs to at least 30� without any help from the abdominal muscles.
  • Psoas fibres merge with (become �consolidated� with) the diaphragm and it therefore influences respiratory function directly (as does quadratus lumborum).
  • Basmajian (1974) informs us that the psoas is the most important of all postural muscles. If it is hypertonic and the abdominals are weak and exercise is prescribed to tone these weak abdominals (such as curl-ups with the dorsum of the foot stabilised), then a disastrous negative effect will ensue in which, far from toning the abdominals, increase of tone in psoas will result, due to the sequence created by the dorsum of the foot being used as a point of support. When this occurs (dorsiflexion), the gait cycle is mimicked and there is a sequence of activation of tibialis anticus, rectus femoris and psoas. If, on the other hand, the feet could be plantarflexed during curl-up exercises, then the opposite chain is activated (triceps surae, hamstrings and gluteals) inhibiting psoas and allowing toning of the abdominals.
  • When treating, it is sometimes useful to assess changes in psoas length by periodic comparison of apparent arm length. Patient lies supine, arms extended above head, palms together so that length can be compared. A shortness will commonly be observed in the arm on the side of the shortened psoas, and this should normalise after successful treatment (there may of course be other reasons for apparent difference in arm length, and this method provides an indication only of changes in psoas length).

 

If the thigh of the tested leg fails to lie in a horizontal position in which it is parallel to the floor/table, then the indication is that iliopsoas is short. If the lower leg of the tested side fails to achieve an almost 90� angle with the thigh, vertical to the floor, then shortness of the rectus femoris muscle is indicated (Fig. 4.6B). If this is not clearly noted, application of light pressure towards the floor on the lower third of the thigh will produce a compensatory extension of the lower leg only when rectus femoris is short. A slight degree (10�15�) of hip extension should be possible in this position, by pushing downwards on the thigh, without knee extension occurring. This can subsequently be checked by seeing whether or not the heel on that side can easily flex to touch the buttock of the prone patient (if rectus is short heel will not easily reach the buttock). If effort is required to achieve 10� of hip extension, this confirms iliopsoas shortening on that side. If both psoas and rectus are short, rectus should be treated first. If the thigh hangs down below a parallel position, this indicates a degree of laxity in iliopsoas (Fig. 4.6C). A further cause of failure of the thigh to rest parallel to the floor can be due to shortness of tensor fascia lata. If this structure is short (a further test proves it, see later in this chapter) then there should be an obvious groove apparent on the lateral thigh and the patella, and sometimes the whole lower leg will deviate laterally. A further indication of short psoas is seen if the prone patient�s hip is observed to remain in flexion. In this position passive flexion of the knee will result in compensatory lumbar lordosis and increased hip flexion if rectus femoris is also short. (See also functional assessment method for psoas in Ch. 5 and notes on psoas in Box 4.4.)

 

Figure 4.6A

 

Figure 4.6A Test position for shortness of hip flexors. Note that the hip on the non-tested side must be fully flexed to produce full pelvic rotation. The position shown is normal.

 

Figure 4.6B

 

Figure 4.6B In the test position, if the thigh is elevated (i.e. not parallel with the table) probable psoas shortness is indicated. The inability of the lower leg to hang more or less vertically towards the floor indicates probable rectus femoris shortness (TFL shortness can produce a similar effect).

 

Figure 4.6C

 

Figure 4.6C The fall of the thigh below the horizontal indicates hypotonic psoas status. Rectus femoris is once again seen to be short, while the relative external rotation of the lower leg (see angle of foot) hints at probable shortened TFL involvement.

 

Mitchell�s Strength Test

 

Before using MET methods to normalise a short psoas, Mitchell recommends that you have the patient at the end of the table, both legs hanging down and feet turned in so that they can rest on your lateral calf areas as you stand facing the patient. The patient should press firmly against your calves with her feet as you rest your hands on her thighs and she attempts to lift you from the floor. In this way you assess the relative strength of one leg�s effort, as against the other. Judge which psoas is weaker or stronger than the other. If a psoas has tested short (as in the test described earlier in this chapter) and also tests strong in this test, then it is suitable for MET treatment, according to Mitchell. If it tests short and weak, then other factors such as tight erector spinae muscles should be treated first until psoas tests strong and short, at which time MET should be applied to start the lengthening process. It is worth recalling Norris�s (1999) advice that a slowly performed isotonic eccentric exercise will normally strengthen a weak postural muscle. (Psoas is classified as postural, and a mobiliser, depending on the model being used. Richardson et al (1999) describe psoas as �an exception� to their deep/superficial rule since, �it is designed to act exclusively on the hip�. There is therefore universal agreement that psoas will shorten in response to stress.) NOTE: It has been found to be clinically useful to suggest that before treating a shortened psoas, any shortness in rectus femoris on that side should first be treated.

 

MET Treatment for Shortness of Rectus Femoris

 

Patient lies prone, ideally with a cushion under the abdomen to help avoid hyperlordosis. The practitioner stands on the side of the table of the affected leg so that he can stabilise the patient�s pelvis (hand covering sacral area) during the treatment, using the cephalad hand. The affected leg is flexed at hip and knee. The practitioner can either hold the lower leg at the ankle (as in Fig. 4.7), or the upper leg can be cradled so that the hand curls under the lower thigh and is able to palpate for bind, just above the knee, with the practitioner�s upper arm offering resistance to the lower leg. Either of these holds allows flexion of the knee to the barrier, perceived either as increasing effort, or as palpated bind. If rectus femoris is short, then the patient�s heel will not easily be able to touch the buttock (Fig. 4.7).

 

Figure 4.7

 

Figure 4.7 MET treatment of left rectus femoris muscle. Note the practitioner�s right hand stabilises the sacrum and pelvis to prevent undue stress during the stretching phase of the treatment. Once the restriction barrier has been established (how close can the heel get to the buttock before the barrier is noted?) the decision will have been made as to whether to treat this as an acute problem (from the barrier), or as a chronic problem (short of the barrier). Appropriate degrees of resisted isometric effort are then introduced. For an acute problem a mild 15% of MVC (maximum voluntary contraction), or a longer, stronger (up to 25% of MVC) effort for a chronic problem, is used as the patient tries to both straighten the leg and take the thigh towards the table (this activates both ends of rectus). Appropriate breathing instructions should be given (see notes on breathing earlier in this chapter, Box 4.2).

 

The contraction is followed, on an exhalation, by taking of the muscle to, or stretching through, the new barrier, by taking the heel towards the buttock with the patient�s help. Remember to increase slight hip extension before the next contraction (using a cushion to support the thigh) as this removes slack from the cephalad end of rectus femoris. Repeat once or twice using agonists or antagonists. Once a reasonable degree of increased range has been gained in rectus femoris it is appropriate to treat psoas, if this has tested as short.

 

MET Treatment of Psoas

 

Method (a) (Fig. 4.8) Psoas can be treated in the prone position described for rectus above, in which case the stretch following the patient�s isometric effort to bring the thigh to the table against resistance would be concentrated on extension of the thigh, either to the new barrier of resistance if acute or past the barrier, placing stretch on psoas, if chronic.

 

Figure 4.8

 

Figure 4.8 MET treatment of psoas with stabilising contact on ischial tuberosity as described by Greenman (1996). The patient is prone with a pillow under the abdomen to reduce the lumbar curve. The practitioner stands on the side opposite the side of psoas to be treated, with the table-side hand supporting the thigh. The non-table-side hand is placed so that the heel of that hand is on the sacrum, applying pressure towards the floor, to maintain pelvic stability (see also Fig. 4.11A). The fingers of that hand are placed so that the middle, ring and small fingers are on one side of L2/3 segment and the index finger on the other. This allows these fingers to sense a forwards (anteriorly directed) �tug� of the vertebrae when psoas is stretched past its barrier. (An alternative hand position is offered by Greenman (1996) who suggests that the stabilising contact on the pelvis should apply pressure towards the table, on the ischial tuberosity, as thigh extension is introduced.

 

The author agrees that this is a more comfortable contact than the sacrum. However, it fails to allow access to palpation of the lumbar spine during the procedure.) The practitioner eases the thigh (knee is flexed) off the table surface and senses for ease of movement into extension of the hip. If there is a strong sense of resistance there should be an almost simultaneous awareness of the palpated vertebral segment moving anteriorly. It should � if psoas is normal � be possible to achieve approximately 10� of hip extension before that barrier is reached, without force. Greenman (1996) suggests that �Normally the knee can be lifted 6 inches [15 cm] off the table. If less, tightness and shortness of psoas is present.� Having identified the barrier, the practitioner either works from this (in an acute setting) or short of it (in a chronic setting) as the patient is asked to bring the thigh towards the table against resistance, using 15�25% of their maximal voluntary contraction potential, for 7�10 seconds. Following release of the effort (with appropriate breathing assistance if warranted), the thigh is eased to its new barrier if acute, or past that barrier, into stretch (with patient�s assistance, �gently push your foot towards the ceiling�). If stretch is introduced, this is held for not less than 10 seconds and ideally up to 30 seconds. It is important that as stretch is introduced no hyperextension occurs of the lumbar spine. Pressure from the heel of hand on the sacrum can usually ensure that spinal stability is maintained. The process is then repeated.

 

Method (b) (Fig. 4.9A) Grieve�s method involves using the supine test position, in which the patient lies with the buttocks at the very end of the table, non-treated leg fully flexed at hip and knee and either held in that state by the patient, or by placement of the patient�s foot against the practitioner�s lateral chest wall. The leg on the affected side is allowed to hang freely with the medioplantar aspect resting on the practitioner�s far knee or shin.

 

Figure 4.9A

 

Figure 4.9A MET treatment of psoas using Grieve�s method, in which there is placement of the patient�s foot, inverted, against the practitioner�s thigh. This allows a more precise focus of contraction into psoas when the hip is flexed against resistance.

 

Figure 4.9B

 

Figure 4.9B Psoas treatment variation, with the leg held straight and the pelvis stabilised. The practitioner stands sideways on to the patient, at the foot of the table, with both hands holding the thigh of the extended leg. The practitioner�s far leg should be flexed slightly at the knee so that the patient�s foot can rest as described. This is used as a contact which, with the hands, resists the attempt of the patient to externally rotate the leg and, at the same time, flex the hip. The practitioner resists both efforts, and an isometric contraction of the psoas and associated muscles therefore takes place. This combination of forces focuses the contraction effort into psoas very precisely. Appropriate breathing instructions should be given (see notes on breathing, Box 4.2). If the condition is acute, the treatment of the patient�s leg commences from the restriction barrier, whereas if the condition is chronic, the leg is elevated into a somewhat more flexed position. After the isometric contraction, using an appropriate degree of effort (i.e. is this acute or chronic?), the thigh should, on an exhalation, either be taken to the new restriction barrier, without force (acute), or through that barrier with slight, painless pressure towards the floor on the anterior aspect of the thigh (chronic), and held there for 10�30 seconds (see Fig 4.10B; see also variation Fig. 4.9B). Repeat until no further gain is achieved.

 

Method (c) (Figs. 4.10A, B) This method is appropriate for chronic psoas problems only. The supine test position is used in which the patient lies with the buttocks at the very end of the table, nontreated leg fully flexed at hip and knee and either held in that state by the patient (Fig 4.10A), or by the practitioner�s hand (Fig 4.7B), or by placement of the patient�s foot against the practitioner�s lateral chest wall. The leg on the affected side is allowed to hang freely. The practitioner resists (for 7�10 seconds) a light attempt of the patient to flex the hip. Appropriate breathing instructions should be given (see notes on breathing, Box 4.2). After the isometric contraction, using an appropriate degree of effort, the thigh should, on an exhalation, be taken very slightly beyond the restriction barrier, with a light degree of painless pressure towards the floor, and held there for 10�30 seconds (Fig. 4.10B). Repeat until no further gain is achieved.

 

Figure 4.10A

 

Figure 4.10A MET treatment involves the patient�s effort to flex the hip against resistance.

 

 

Figure 4.10B Stretch of psoas, which follows the isometric contraction (Fig. 4.10A) and is achieved by means of gravity plus additional practitioner effort.

 

Self-Treatment of Psoas

 

Method (a) Lewit suggests self-treatment in a position as above in which the patient lies close to the end of a bed (Fig 4.10A without the practitioner) with one leg fully flexed at the hip and knee and held in this position throughout, while the other leg is allowed to reach the limit of its stretch, as gravity pulls it towards the floor. The patient then lifts this leg slightly (say 2 cm) to contract psoas, holding this for 7�10 seconds, before slowly allowing the leg to ease towards the floor. This stretch position is held for a further 30 seconds, and the process is repeated three to five times. The counterpressure in this effort is achieved by gravity.

 

Method (b) Patient kneels on leg on side to be self-stretched so that the knee is behind the trunk, which remains vertical throughout. The non-treated side leg is placed anteriorly, knee flexed to 90�, foot flat on floor. The patient maintains a slight lumbar lordosis throughout the procedure as she lightly contracts psoas by drawing the treated side knee anteriorly (i.e. flexing the hip) without actually moving it. Resistance to this isometric movement is provided by the knee contact with the (carpeted) floor. After 7�10 seconds the patient releases this effort, and while maintaining a lumbar lordosis and vertical trunk, eases her pelvis and trunk anteriorly to initiate a sense of stretch on the anterior thigh and hip area. This is maintained for not less than 30 seconds before a further movement anteriorly of the pelvis and trunk introduces additional psoas stretch (see also Fig. 4.11B).

 

Figure 4.11A

 

Figure 4.11A Alternative prone treatment position, not described in text (see also Fig. 4.8). B Psoas self-stretch, not described in text.

 

Dr. Alex Jimenez offers an additional assessment and treatment of the hip flexors as a part of a referenced clinical application of neuromuscular techniques by Leon Chaitow and Judith Walker DeLany.

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

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ADDITIONAL TOPIC: EXTRA EXTRA: Treating Back Pain