Proximal humeral Fx account for 4-6% of all Fxs. Osteoporotic (OSP) Fx in >60 y.o associated with minimal trauma with F: M 2:1 ratio. In young patients, acute high energy trauma predominates.
Complications: AVN humeral head, Axillary N paralysis.
Neer Classification: considers fractures along 4-anatomical lines with or w/o displacement >1-cm & 45-degree angulation
One part Neer Fx- no displacement or very minimal <1-cm/45-degree. Can affect 1-4 lines and M/C at greater tuberosity. 80% of proximal humeral Fx are one-part Neer.
Two-part Fx: 1-part is displaced >1-cm/45-degrees. m/c involves the surgical neck
Three-part Fx: 2-parts are displaced >1-cm/45-degrees.
Four-part Fx: all 4-parts can be displaced. Uncommon <1%
Imaging: 1st step-radiography, CT may be used in more complex cases. Orthopedic referral
Management: Neer one-part Fx is treated with Sling Immobilisation and progressive rehab
The vast majority of Fx in the elderly are treated non-operatively
Younger patients (40-65) may occasionally require hemiarthroplasty if 3 or 4-part Neer Fx present. Greater risk of AVN
Proximal Humerus Fractures
Note: Left image: Fx involving the anatomical neck and the greater tuberosity with minimal displacement <1-cm/45-degree thus Dx as one-part Fx. Right image: Small avulsion Fx of the greater tuberosity with significant displacement (>45-degrees & 1-cm) thus Dx as two-part Fx
Note: three-part Neer Fx (left) and four-part Neer Fx (right)> Management: operative in most cases in younger (40-65) patients
Refers to complete separation of the humerus from scapula glenoid. In 20-40s M: F 9:1 ratio, in60-80S M: F 3:1
Anatomy: Shoulder stability is sacrificed for mobility, and overall GHJD is the m/c among large joints in the body
Protective falls (e.g., FOOSH) and MVA are m/c causes. GHJ is most vulnerable in abduction, extension and external rotation. Anatomical factors: shallow glenoid, laxed ant-inferior capsule and GH ligaments. GHJD will induce severe tearing of major GHJ restraints. Associated osseous and labral injuries are common and may lead to chronic instability, DJD,�and functional changes
3-types: Anterior GHJD (95%)
Posterior GHJD (4%) especially associated with epileptic seizures, electrocution and can occur b/l
Inferior GHJD aka Laxatio Erecta (<1%) associated with severe trauma
Clinically: AGHJD presents with severe pain, the arm is externally rotated and adducted, severe limitation of movement. GHJD may persist as chronic dislocation.
Management: prompt reduction in ED under anesthesia or heavy sedation with Kocher technique top image (not used), External rotation method (middle) or Milch technique (can be used w/o anesthesia) and a few other methods. Delay in reduction correlates with greater risk of immediate and long-term�complications
Diagnostic Imaging Approach
Shoulder series x-radiography is sufficient. Additional Imaging with CT scanning and MRI may be helpful to Dx osseous, cartilage, labral/ligaments pathology
Anterior GHJD (95%). Subcoracoid position(top right) of the humerus is the m/c
Anterior GHJD may also occur as subglenoid(bottom left)and infrequently as subclavicular
Key to radiographic search is to evaluate associated Bankart and Hill-Sachs injuries
Bankart Lesion
Occurs during anterior GHJD d/t impaction of the head into anterior-inferior glenoid. Variations exist (see next slide). BonyBankart can be seen on x-rays. So-called soft tissue Bankart requires MRI. Cartilage (soft)Bankart is the m/c.
Hill-Sachs aka Hatchet deformity (arrow postreduction)occurs during the same mechanism as Bankart, i.e., compression and impaction of posterolateral aspect of the head against the glenoid producing wedge-shape Fx. Hill-Sachs lesion may predispose to recurrent/chronic GHJD.
Bankart lesion may heal, but operative suture anchors are needed sometimes
CT arthrogram and MRI may be helpful
Types of Bankart Lesion
Note different types of Bankart lesion. Onlyosseous Bankart can be seen radiographically. Soft tissue Bankart requires MRI with and without intra-articular gadolinium(arthrogram).
Posterior Dislocation
Note: posterior GHJD with its characteristic signs:
Trough sign aka reverse Hill-Sachs. Occurs d/t anterolateral head impaction Fx
Rim sign: only occurs in the PGHJD d/t posterior position of the head and anterior glenoid-to humeral head distance 6-mm or greater
Light-bulb sign: d/t acute internal rotation of the humerus (head)
Inferior GHJD
Inferior GHJD aka Laxatio Erecta
Severe hyperabduction and inferior displacement of the humerus. Greater chances of severe neurovascular injury and acromial Fx
The dislocated arm is hyperabducted and fixed with the elbow flexed and the arm above the head
ACJ Dislocation (ACJD)
ACJD: common injury, 9% of shoulder girdle injuries esp. in male athletes by a direct blow
Rockwood classification (left) evaluates tearing of AC and CC ligaments and regional muscles
Type1, 2, 3 among the m/c
Type 1: sprain of ACL w/o tearing
Type 2: tear of ACL and sprain of CCL
Type 3: tear of AC & CCL. The clavicle is elevated above the acromion. If <2-cm good results with conservative Rx.
Imaging: x-radiography with b/l ACJ views with and w/o weights to compare both ACJs. In complex cases CT scanning esp. if Fx is considered
Management: Type 3 (>2-cm) & Types 4-6Operative
Type 3 ACJ Separation
Type 3 ACJ separation (top left)
More significant ACJD (bottom images) with clinical sign of acromion under the skin and resultant ORIF
Rotator Cuff Muscles (RCM) Pathology
RCM tendinopathy: collagenous degeneration of RCM particularly Supraspinatus M. tendon(SSMT) d/t overuse/degeneration-micro tearing with collagenous replacement. Impingement syndrome is a 2nd extrinsic cause. Presented clinically as pain and limited ROM
Imaging Dx: MSK US can be as accurate as MRI and better in some cases d/t dynamic evaluation v. cost effective
Key MRI clue is thickened inhomogeneous SSMTwith increased signal on all pulse sequences d/t fatty degeneration and inflammation (left images: T1 & T2 FS)
MSKUS findings: thickening of the SSMTsubstance with a change�in normal echogenicity.MSKUS is good to DDx with SSMT tears. US advantages are that it allows dynamic evaluation of painful structures
Partial tear of SSMT: partial (incomplete) tear ofSSMT may occur at the bursal and articular surface or interstitial, i.e., intra-substance/noncommunicating. Etiology: sub-acromial impingement, acute strain, and chronic microtrauma tendinosis
Clinically: pain on abd and flexion, impingement tests, Hawkins-Kennedy tests, etc. Pearls: partial tears can be more painful than complete tears
Imaging Dx: MSKUS is as good as MRI (N.B.some studies indicated MSKUS is more superior to MRI). Key MRI findings: gap/incomplete tear of SSMT filled with joint fluid +/- granulation tissue
MSKUS: decreased echogenicity of SSMT, thinning and partial tearing filled with fluid(anechoic areas arrows). Lost convexity of tendon bursal or articular interface.
Full Thickness SSMT (rot cuff) tear: degeneration/tearing of rot cuff. 2nd to impingement by Hooked acromion, overhead overuse or acute trauma. 7-25% of shoulder pain in the general population. Clinically: pain on impingement tests.
Imaging Dx: MSKUS is as good as MRI.Limitations: poor Dx of labral pathology. Key USDx: focal tendon interruption, an anechoic gap (fluid filled), hypoechoic tendon, tendon retraction, uncovered cartilage sign (bottom left, A: US B: MRI)
MRI: key Dx: insertional tear extending through entire SSMT crescent, retraction with fatty degeneration of SSMT and the muscle. If retraction is at 12 o�clock or greater (top images), it may not be anchored operatively
Rotator Cuff (RTC) Calcific Tendinitis: usually d/t calcium HADD crystals. Middle-aged women are most affected. Ranges from asymptomatic imaging finding to severe destructive arthropathy or Milwaukee shoulder(infrequent)
HADD has 3-pathological phases: formation resting-resorption.Mild-to-moderate pain esp. in resting phase.
Imaging: x-radiography: homogenous ovoid mineralization within RTCMT, m/c in SSMT. MRI: ovoid/globular decreased signal on all pulse sequences often with surrounding edema (bottom left)
Rx: self-resolution occurs. Advanced cases: operative aspiration etc.
Superior Labrum Anterior to Posterior (SLAP) Lesions/Tears
SLAP tears: FOOSH and throwing sports or chronic shoulder instability aka Multidirectional shoulder instability (in 20%). Type 1-9 exist but the M/C areType 1-4
In all 4-types superior labrum is affected with or w/oLHBMT anchor tear (see pictures). Clinically: pain, limitation of AROM with active compression tests, typically non-specific findings mimicking RTCpathology
Imaging is crucial: best imaging is MRI arthrography. Key signs: hyperintense linear fluid signal within superior labrum +/- extending along the LHBT on fat-suppressed fluid sensitive imaging and FS T1 arthrogram. Best observed on coronal slices.
Rx: small tears may heal, but unstable tears require operative care.
Key DDx: anatomical variants like Buford complex andSub-labral foramen
SLAP tear with a paralabral cyst (bottom right)
Normal variant DDx: sub labral foramen(bottom left) note: MR arthrography with contrast undercutting the labrum but w/o extending posteriorly to the LHBT
Shoulder Arthritis
GHJ DJD: usually associated with a 2nd cause: trauma, instability, AVN, CPPD, etc. Presented with pain, crepitus and decreased ROM/function. Associated RTC disease may be present. Imaging; x-radiography is sufficient and provides grading/care planning.Major findings: joint narrowing, osteophytosis esp. at the inferior-medial head (orange arrow), subchondral sclerosis/cysts. Often noted superior head migration d/t RTC disease.
ACJ OA: common and typically primary with aging. Presents with ACJ loss and osteophytes. Osteophytes along the undersurface of the ACJ �keel osteophytes�(blue arrow) may lead to RTC muscle tear. Regional bursitis is other clinical feature of ACJ arthrosis.
Management: usually conservative depending on clinical signs/symptoms
Rheumatoid Arthritis GHJ: RA is a multisystem inflammatory disease affecting multiple joints lined by the synovium. GHJ RA is common (m/c large joints in RA knees/shoulders). Clinically: pain, limited ROM and instability, muscle weakness/wasting. Hands, feet,�and wrists are m/c affected. Imaging: x-radiography reveals periarticular erosions, uniform joint space loss, juxta-articular osteoporosis, subluxations,�and soft tissue swelling. MRI can help detect�commonly associated RTC tearing and instability. Early changes can be detected by MSKUS esp. with power Doppler use indicating hyperemia/inflammation.
Note: L shoulder x-ray revealing cartilage destruction and symmetrical joint loss, multiple erosions, and likely loss of RTCM support with superior head migration, ST effusion present.
Note: PDFS coronal and axial MRI slices of GHJ RA indicating marked inflammatory joint effusion, bone erosion/edema, synovial pannus formation and likely tear in RTC m. Management: Rheumatological referral and pharmacotherapy with DMARD. Operative care asRTCM repair. 10% of patients are disabled d/t RA
Neuropathic Osteoarthropathy aka Charcot’s shoulder: d/t neurovascular and neural periarticular damage. Multiple causes exist.M/c develops in diabetics in midfoot. Shoulder Charcot is m/c in Syringomyelia (25%), trauma paralysis, MS, etc. Dx: clinical(50% pain/swelling 50% painless destruction). Imaging is crucial. X-radiography is sufficient in well-established cases, but early Dx is challenging. MRI may help with early Dx and delayed complications. Rad Dx: Shoulder Charcot is m/c presented as atrophic type destructive arthropathy with humeral head appearing as if surgically amputated along with intra-articular debris, density, distention, dislocation, and other key features
Septic Shoulder: shoulder is the 3rd m/c followingknee>hips. Patients at risk: diabetics, RA pts, immunocompromised, I.V. drug users, indwelling catheters, etc. Routes: hematogenous (m/c), direct inoculation (iatrogenic, trauma etc.) adjacent spread(e.g. OM). Staph. Aureus (>50%) m/c.
Clinically: joint pain and dec. ROM, fever 60% only, toxemia, inc. ESR/CRP. Dx: imaging and joint aspiration/culture. RadDx: early x-rays often unremarkable except ST effusion/fat planes obscuration, joint widening. Later7-12 days patchy osteopenia, moth-eaten/permeating bone resorption, articular destruction, joint narrowing. May progress to severe joint destruction and ankyloses. Early Dx & I.V. antibiotics are crucial even before culture. Operative irrigation and joint drainage in some cases. Complications are possible esp. if Rx is delayed. MSKUS with needle aspiration may help. Note: (top image) non-traumatic joint widening with inferolateral head displacement d/t septic A dx: by needle aspiration Staph. Aures.
Ischemic Osteonecrosis
Ischemic Osteonecrosis of the humeral head may occur d/t trauma (Neer four-part Fx), Steroids, Lupus, Sickle cell, Alcoholism, Diabetes,�and many other conditions. Imaging is crucial: MRI detects earliest changes as intraosseous edema. X-ray features are late, presented as a collapse of subchondral bone with sclerosis �snow cap� sign, fragmentation, and progressive severe DJD
Management: orthopedic referral, core decompression in early cases, hemiarthroplasty in moderate and total arthroplasty in severe cases.
Shoulder Neoplasms
In adults >40, bone Mets d/t lung, breast, renal cell, thyroid CA & prostate are the m/c causes. Clinically: may mimic pain resemblingRTC/joint changes. Should be evaluated carefully. Key to Dx: Hx, PE and Imaging esp.in pts with known primary
Imaging: 1st step x-rays, MRI can help, Tc99bone scintigraphy helps to detect regional and distant disease. X-ray features: destructive lytic changes typically in prox humerus(red marrow) with or w/o path Fx. DDx: Mets, MM, lymphoma
Clinically: night pain, pain at rest, etc. Lab tests: unrewarding, in severe cases hypercalcemia may be noted.
Primary Malignant bone neoplasms (shoulder) Adults: M. Myeloma or Solitary plasmacytoma, Chondrosarcoma may transform from an enchondroma and some others. In children/teenagers: OSA vs. Ewing�s
Primary benign bone neoplasms (shoulder). Adults: Enchondroma (patients in their 20-30s)GCT. In children: Simple bone cyst (Unicameral Bone cyst), Osteochondroma, Aneurysmal Bone Cyst, Chondroblastoma (rare)
Imaging: 1st step x-radiography
MRI is essential to Dx. Especially in cases of primary malignant neoplasms Evaluate extent, soft tissue invasion, preoperative planning, staging, etc.
The Texas Board of Chiropractic Examiners (Board) adopts new �78.14 concerning acupuncture.New �78.14 is adopted with changes to the proposed text as published in the July 20, 2018, issue�of the�Texas Register�(43 TexReg 4817).
This new rule with changes is adopted under Texas Occupations Code �201.152, which authorizes the Board to adopt rules necessary to perform the Board’s duties and to regulate the practice of chiropractic.
No other statute, article, or rule is affected by this rule.
Background and Justification
The Board adopts the new �78.14 (with non-substantive changes made to the proposed version)to replace the Board’s previous acupuncture rule in order to promote a clearer understanding of the requirements for the practice of acupuncture as performed by doctors of chiropractic. The rule also delineates the differences between the way chiropractors practice acupuncture and the way that of other Texas health professions do. The new rule clarifies the degree of regulatory oversight the Board exercises over the practice of acupuncture to safeguard the public while not imposing unnecessary economic burdens on either chiropractors who offer the acupuncture modality or on consumers.
Comments
The thirty-day comment period ended on August 20, 2018.
The Board received numerous comments regarding the proposed new rule, including from theTexas Chiropractic Association (TCA), the Texas Medical Association (TMA), the Texas Association of Acupuncture and Oriental Medicine (TAAOM), and eighty-seven individuals.
Comment: TCA urged the adoption of the proposed rule in its current form, but recommended the Board not adopt the proposed 200 hours of training in the use and administration of acupuncture in order for a chiropractor to receive a permit. TCA reiterated its position that increasing the training requirement from the current 100 hours is unnecessary to protect the public. Numerous other commenters also pointedly raised this issue. TCA further noted that it is inconsistent and arbitrary to impose this heightened regulatory burden on chiropractors when medical doctors, dentists, and physical therapists perform acupuncture with far less training.
Response: The Board agrees with TCA and the other commenters that the proposed increase in required training from 100 to 200 hours would impose an unnecessary economic and regulatory burden on chiropractors and students currently enrolled at chiropractic colleges without increasing public safety in any significant way. The Board notes that no evidence has been produced that the currently required 100 hours of training in acupuncture is inadequate to protect the public. The Board acknowledges that the increase in required hours could be seen as an economic barrier to market entry for newly licensed chiropractors, especially in light of the fact that other licensed health professionals are permitted to practice acupuncture with far fewer hours of training. The Board, therefore, has reduced the number of required hours from 200 to the existing 100.
Comment: Two commenters raised concerns about the proposed rule’s permission to use the terms “Board Certified,” “Board Certified in Chiropractic Acupuncture,” and “Board Certified in Acupuncture as an adjunctive modality by the Texas Board of Chiropractic Examiners” in advertising by chiropractors. The concerns were the terms were confusing and too lengthy.
Response: The Board agrees in part and has modified the rule’s language. The Board has kept the language allowing a chiropractor to use the terms “Board Certified” and “Board Certified in Chiropractic Acupuncture” if used in conjunction with the name of the nationally recognized certifying board and the specific credentials granted. The Board concurs that the advertising term “Board Certified in Acupuncture as an adjunctive modality by the Texas Board of Chiropractic Examiners” is too lengthy and may give the impression that the Board is acting as an accredited certifying board. Therefore, the Board has changed the term “certificate” to”permit” throughout the rule to make it clear that the Board is acknowledging a chiropractor’s qualifications.
The Board has also eliminated the provision in the proposed rule that required the Board to issue a separate document to permit a chiropractor to practice acupuncture; the Board will instead include the permitting language on each renewal license issued to chiropractors who meet the rule’s requirements.
Comment: Several individuals submitted comments urging the Board to include the practice of dry needling in this rule.
Response: The Board appreciates the comments but declines to address this issue as it is outside the bounds of this rule.
Comment: The Board received several comments from chiropractors who found the proposed rule’s language confusing regarding the requirements for obtaining a permit to practice acupuncture, especially for those who have been successfully practicing acupuncture in Texas under the Board’s current rule for several years.
Response: The Board agrees with the commenters that the language regarding the requirements for obtaining a permit in the proposed rule was unclear. The Board has changed what is now subsection (e) to be more precise.
The Board removed the requirement to provide patient records as proof of having practiced for at least ten years and substituted it with providing a written statement of having practiced acupuncture in a clinical setting, with the statement subject to Board verification. The Board believes the original requirement of providing redacted patient records, which could go back several years, was too onerous on chiropractors.
Comment: Several individuals said the continuing education provision in the proposed rule that required eight hours of acupuncture education for each two years of licensure was not clear.
Response: The Board agrees and has modified the language in what is now subsection (f) to state that a chiropractor permitted to practice acupuncture must complete a minimum of eight hours in Board-approved acupuncture courses every biennium.
Comment: One individual questioned why the rule’s training requirements for acupuncture only allow for didactic, clinical, and practical training, but exclude online and distance learning options.
Response: The Board appreciates the comment, but declines to include those training methods at this time.
Comment: TMA expressed its strong opposition to the proposed rule on the grounds the Board lacks the legal authority to regulate the practice of acupuncture by chiropractors. TMA made no direct comments on the language of the proposed rule itself.
Response: The Board disagrees with TMA’s position. Acupuncture or filiform needles used in the practice of acupuncture are non-incisive, meaning those needles do not cut or leave a wound when properly used. Texas courts have found that the Board’s position is not unreasonable or inconsistent with Texas Occupations Code Chapter 201. Because the use of acupuncture or filiform needles is non-incisive, their use falls within the chiropractic scope of practice, and thus the Board has statutory authority to enact rules regulating that use.
Comment: Numerous licensed acupuncturists wrote to object to the proposed rule on nearly identical grounds, including objections that the Board lacks the legal authority to promulgate the rule, that the rule potentially endangers the public, and that the rule has the potential to cause economic harm to licensed acupuncturists. These individuals made no direct comments on the language of the proposed rule itself.
Response: Regarding the objections concerning the Board’s legal authority to promulgate the proposed rule, the Board disagrees and notes its response to similar comments by TMA above.
The Board disagrees that the public would somehow be at risk from the continued practice of acupuncture by chiropractors because of a lack of training. The Board again notes there is no empirical evidence that any person in Texas has been harmed by a chiropractor practicing acupuncture under either the Board’s current rule, which requires 100 hours of training in acupuncture beyond the extensive training in physiology and anatomy all chiropractors receive in their four-year chiropractic college degree programs, or in the several decades before the current rule’s adoption. This argument is further undercut by the fact that other Texas health professionals are permitted to practice acupuncture with far fewer hours of additional training or experience.
The Board also disagrees with the argument that allowing chiropractors to practice acupuncture would economically harm acupuncturists. Chiropractors and acupuncturists have both practiced acupuncture, albeit with differing philosophies, for several decades in Texas. the existing were safely practicing acupuncture in Texas long before the enactment of Texas Occupations Code Chapter 205. There is no evidence that acupuncturists have suffered been produced harm up to now, nor is there any to show there will be any future harm. The Board takes seriously its oversight mandate to protect the public health without imposing unnecessary economic costs on either chiropractors or consumers.
Comment: TAAOM submitted lengthy comments to the Board regarding the proposed rule.
Response: The Board disagrees with TAAOM’s assertion that the Board has no authority to define acupuncture or to authorize the practice of acupuncture by its licensees. The Board does have such statutory authority. As noted above in the Board’s response to TMA, acupuncture or filiform needles used in the practice of acupuncture are non-incisive, and thus within the scope of practice under Texas Occupations Code Chapter 201.
The Board declines to respond to TAAOM’s comments concerning dry needling as that is outside the bounds of this rulemaking.
The Board agrees, in part, with TAAOM that the use of the term “board certification” could cause confusion. The rule has been changed to state that a chiropractor who meets the rule’s requirements for the practice of acupuncture will be granted a permit to perform acupuncture as opposed to a certificate, so as not to give the impression that the chiropractor has been credentialed by the Board.
The Board disagrees with TAAOM’s claim that the hours of training in acupuncture chiropractors receive are inadequate to protect the public. Doctors of chiropractic on average receive over 4200 hours of doctoral-level training that focuses on anatomy and physiology, which far exceeds the training an undergraduate-level acupuncturist receives. It is, therefore, incorrect to suggest that a chiropractor trained in acupuncture has a lesser understanding of physiological mechanics than does an acupuncturist.
The Board disagrees with TAAOM’s insistence the Board increase the verification requirements for chiropractors who began practicing acupuncture before 2010 and have always done so safely before the Board may grant them permits. Because it lacks a legitimate public health rationale, TAAOM’s position would only add unnecessary and burdensome economic costs on chiropractors. The Board believes the documentation the new rule requires of chiropractors who began practicing acupuncture before 2010 is more than sufficient to protect the public health.
The Board disagrees with TAAOM’s position that a chiropractor who practices acupuncture should be prevented from advertising that fact. The practice of acupuncture is within a chiropractor’s scope of practice. To deny a chiropractor the ability to advertise without a legitimate public safety rationale, as TAAOM urges the Board to do, is nothing more than the restriction of the economic freedom and commercial free speech rights of one profession for the benefit of another. The Board declines to impose such a limit.
The Board agrees with TAAOM that unnecessary references to other Board rules should be removed. Those references have been removed.
Chiropractic care is an alternative treatment option which utilizes a variety of methods and techniques to treat injuries and/or conditions. As mentioned in the article, when it comes to the use of acupuncture in chiropractic care, the final ruling is that chiropractors, or doctors of chiropractic, are allowed to practice acupuncture. Dr. Alex Jimenez D.C., C.C.S.T. Insight
�78.14. Acupuncture.
(a) Acupuncture, and the related practices of acupressure and meridian therapy, includes methods for diagnosing and treating a patient by stimulating specific points on or within the musculoskeletal system by various means, including manipulation, heat, cold, pressure,vibration, laser, ultrasound, light electro current, and the insertion of acupuncture needles or solid filiform needles for the purpose of obtaining a bio-positive reflex response by nerve stimulation.
(b) A licensee shall practice acupuncture only after obtaining a permit from the Texas Board of Chiropractic Examiners (Board).
(c) The Board shall place on each renewal license to practice chiropractic a statement that a licensee who has met all Board requirements is permitted to practice acupuncture. A licensee whose license does not contain the statement permitting the practice of acupuncture shall not practice or advertise the practice of acupuncture.
(d) A licensee with an acupuncture permit cannot delegate the performance of acupuncture.
(e) Requirements for an acupuncture permit:
(1) On or after the effective date of this rule, a licensee may receive an acupuncture permit from the Board by completing at least one hundred (100) hours of training in acupuncture and passing the National Board of Chiropractic Examiners’ examination. The training must be provided by an accredited chiropractic college, or post-secondary university, or other educational or testing institution approved by the Board. Such training shall include didactic, clinical, and practical training in the practice of acupuncture, clean needle techniques, examination, and protocols that meet the blood-borne pathogen standard established by the Occupational Safety and Health Administration.
(2) A person who became a licensee after January 1, 2010, and before the effective date of this rule, who has been practicing acupuncture in compliance with previous Board rules, shall have until September 1, 2019, to obtain an acupuncture permit from the Board by passing the National Board of Chiropractic Examiners’ standardized certification examination in acupuncture and completing 100 hours of acupuncture training.
(3) A person who became a licensee before January 1, 2010, shall have until September 1, 2019, to obtain an acupuncture permit from the Board by having:
(A) Successfully completed and passed an examination in a one hundred (100) hour training course in acupuncture; or
(B) Successfully completed and passed either the National Board of Chiropractic Examiners’standardized certification examination in acupuncture or the examination offered by the National Certification Commission of Acupuncture before the effective date of this rule; or
(C) Successfully completed formal training along with providing a statement to the Board of having practiced acupuncture in clinical practice for at least ten years before January 1, 2010, and is in good standing with the Board and the regulatory entities of the other jurisdictions in which the licensee is licensed. The Board may audit any statement for accuracy.
(4) Documentation of acupuncture training shall be in the form of signed certificates of attendance or completion, or diplomas from course sponsors or instructors.
(f) A licensee permitted to practice acupuncture must complete a minimum of eight (8) hours in Board-approved acupuncture courses every biennium.
(g) A licensee shall not practice acupuncture until the licensee has submitted proof of compliance with subsection (e) and has received a permit from the Board.
(h) A licensee practicing acupuncture shall not advertise in a manner that suggests the licensee possesses a license to practice acupuncture issued by the Texas State Board of AcupunctureExaminers, including using any of the terms “acupuncturist,” “licensed acupuncturist,” “L.Ac.,” “Traditional Chinese Medicine,” or “degreed in acupuncture.”
(i) A licensee’s advertising may include the terms “Board Certified” or “Board Certified in Chiropractic Acupuncture” if it also clearly identifies the nationally recognized certifying board and credentials.
(j) Approved programs in clinical acupuncture or meridian therapy offered by accredited chiropractic colleges or universities are designed for doctors of chiropractic and other disciplines. These courses are not intended as a substitute for a full curriculum teaching traditional Chinese medicine; rather they focus on the principle, theory, scientific findings, and practical modern application of acupuncture as currently practiced by doctors of chiropractic.
(k) The practice of acupuncture by a licensee who has not complied with the requirements of this section constitutes unprofessional conduct and subjects the licensee to disciplinary action. A licensee who advertises acupuncture without first obtaining a permit also has engaged in unprofessional conduct.
The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topics: Chiropractic for Athletes with Back Pain
Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.
Oxidative stress is described as cell damage caused by free radicals, or unstable molecules, which can ultimately affect healthy function. The human body creates free radicals to neutralize bacteria and viruses, however, external factors, such as oxygen, pollution, and radiation, can often also produce free radicals. Oxidative stress has been associated with numerous health issues.
Oxidative stress and other stressors turn on internal protective mechanisms which can help regulate the human body’s antioxidant response. Nrf2 is a protein which senses levels of oxidative stress and enables the cells to protect themselves from internal and external factors. Nrf2 has also been demonstrated to help regulate genes involved in the production of antioxidant enzymes and stress-response genes. The purpose of the article below is to explain the effects of Nrf2 in cancer.
Abstract
The Keap1-Nrf2 pathway is the major regulator of cytoprotective responses to oxidative and electrophilic stress. Although cell signaling pathways triggered by the transcription factor Nrf2 prevent cancer initiation and progression in normal and premalignant tissues, in fully malignant cells Nrf2 activity provides growth advantage by increasing cancer chemoresistance and enhancing tumor cell growth. In this graphical review, we provide an overview of the Keap1-Nrf2 pathway and its dysregulation in cancer cells. We also briefly summarize the consequences of constitutive Nrf2 activation in cancer cells and how this can be exploited in cancer gene therapy.
The Keap1-Nrf2 pathway is the major regulator of cytoprotective responses to endogenous and exogenous stresses caused by reactive oxygen species (ROS) and electrophiles [1]. The key signaling proteins within the pathway are the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) that binds together with small Maf proteins to the antioxidant response element (ARE) in the regulatory regions of target genes, and Keap1 (Kelch ECH associating protein 1), a repressor protein that binds to Nrf2 and promotes its degradation by the ubiquitin proteasome pathway (Fig. 1). Keap1 is a very cysteine-rich protein, mouse Keap1 having a total of 25 and human 27 cysteine residues, most of which can be modified in vitro by different oxidants and electrophiles [2]. Three of these residues, C151, C273 and C288, have been shown to play a functional role by altering the conformation of Keap1 leading to nuclear translocation of Nrf2 and subsequent target gene expression [3] (Fig. 1). The exact mechanism whereby cysteine modifications in Keap1 lead to Nrf2 activation is not known, but the two prevailing but not mutually exclusive models are (1) the �hinge and latch� model, in which Keap1 modifications in thiol residues residing in the IVR of Keap1 disrupt the interaction with Nrf2 causing a misalignment of the lysine residues within Nrf2 that can no longer be polyubiquitinylated and (2) the model in which thiol modification causes dissociation of Cul3 from Keap1 [3]. In both models, the inducer-modified and Nrf2-bound Keap1 is inactivated and, consequently, newly synthesized Nrf2 proteins bypass Keap1 and translocate into the nucleus, bind to the ARE and drive the expression of Nrf2 target genes such as NAD(P)H quinone oxidoreductase 1 (NQO1), heme oxygenase 1 (HMOX1), glutamate-cysteine ligase (GCL) and glutathione S transferases (GSTs) (Fig. 2). In addition to modifications of Keap1 thiols resulting in Nrf2 target gene induction, proteins such as p21 and p62 can bind to Nrf2 or Keap1 thereby disrupting the interaction between Nrf2 and Keap1 [1], [3] (Fig. 3).
Fig. 1. Structures of Nrf2 and Keap1 and the cysteine code. (A) Nrf2 consists of 589 amino acids and has six evolutionarily highly conserved domains, Neh1-6. Neh1 contains a bZip motif, a basic region � leucine zipper (L-Zip) structure, where the basic region is responsible for DNA recognition and the L-Zip mediates dimerization with small Maf proteins. Neh6 functions as a degron to mediate degradation of Nrf2 in the nucleus. Neh4 and 5 are transactivation domains. Neh2 contains ETGE and DLG motifs, which are required for the interaction with Keap1, and a hydrophilic region of lysine residues (7 K), which are indispensable for the Keap1-dependent polyubiquitination and degradation of Nrf2. (B) Keap1 consists of 624 amino acid residues and has five domains. The two protein�protein interaction motifs, the BTB domain and the Kelch domain, are separated by the intervening region (IVR). The BTB domain together with the N-terminal portion of the IVR mediates homodimerization of Keap1 and binding with Cullin3 (Cul3). The Kelch domain and the C-terminal region mediate the interaction with Neh2. (C) Nrf2 interacts with two molecules of Keap1 through its Neh2 ETGE and DLG motifs. Both ETGE and DLG bind to similar sites on the bottom surface of the Keap1 Kelch motif. (D) Keap1 is rich in cysteine residues, with 27 cysteines in human protein. Some of these cysteines are located near basic residues and are therefore excellent targets of electrophiles and oxidants. The modification pattern of the cysteine residues by electrophiles is known as the cysteine code. The cysteine code hypothesis proposes that structurally different Nrf2 activating agents affect different Keap1 cysteines. The cysteine modifications lead to conformational changes in the Keap1 disrupting the interaction between the Nrf2 DLG and Keap1 Kelch domains, thus inhibiting the polyubiquitination of Nrf2. The functional importance of Cys151, Cys273 and Cys288 has been shown, as Cys273 and Cys288 are required for suppression of Nrf2 and Cys151 for activation of Nrf2 by inducers [1], [3].
Fig. 2. The Nrf2-Keap1 signaling pathway. (A and B) in basal conditions, two Keap1 molecules bind to Nrf2 and Nrf2 is polyubiquitylated by the Cul3-based E3 ligase complex. This polyubiquitilation results in rapid Nrf2 degradation by the proteasome. A small proportion of Nrf2 escapes the inhibitory complex and accumulates in the nucleus to mediate basal ARE-dependent gene expression, thereby maintaining the cellular homeostasis. (C) Under stress conditions, inducers modify the Keap1 cysteines leading to the inhibition of Nrf2 ubiquitylation via dissociation of the inhibitory complex. (D) According to the hinge and latch model, modification of specific Keap1 cysteine residues leads to conformational changes in Keap1 resulting in the detachment of the Nrf2 DLG motif from Keap1. Ubiquitination of Nrf2 is disrupted but the binding with the ETGE motif remains. (E) In the Keap1-Cul3 dissociation model, the binding of Keap1 and Cul3 is disrupted in response to electrophiles, leading to the escape of Nrf2 from the ubiquitination system. In both of the suggested models, the inducer-modified and Nrf2-bound Keap1 is inactivated and, consequently, newly synthesized Nrf2 proteins bypass Keap1 and translocate into the nucleus, bind to the Antioxidant Response Element (ARE) and drive the expression of Nrf2 target genes such as NQO1, HMOX1, GCL and GSTs [1], [3].
Fig. 3. Mechanisms for constitutive nuclear accumulation of Nrf2 in cancer. (A) Somatic mutations in Nrf2 or Keap1 disrupt the interaction of these two proteins. In Nrf2, mutations affect ETGE and DLG motifs, but in Keap1 mutations are more evenly distributed. Furthermore, oncogene activation, such as KrasG12D[5], or disruption of tumor suppressors, such as PTEN [11] can lead to transcriptional induction of Nrf2 and an increase in nuclear Nrf2. (B) Hypermethylation of the Keap1 promoter in lung and prostate cancer leads to reduction of Keap1 mRNA expression, which increases the nuclear accumulation of Nrf2 [6], [7]. (C) In familial papillary renal carcinoma, the loss of fumarate hydratase enzyme activity leads to the accumulation of fumarate and further to succination of Keap1 cysteine residues (2SC). This post-translational modification leads to the disruption of Keap1-Nrf2 interaction and nuclear accumulation of Nrf2 [8], [9]. (D) Accumulation of disruptor proteins such as p62 and p21 can disturb Nrf2-Keap1 binding and results in an increase in nuclear Nrf2. p62 binds to Keap1 overlapping the binding pocket for Nrf2 and p21 directly interacts with the DLG and ETGE motifs of Nrf2, thereby competing with Keap1 [10].
Mechanisms of Activation and Dysregulation of Nrf2 in Cancer
Although cytoprotection provided by Nrf2 activation is important for cancer chemoprevention in normal and premalignant tissues, in fully malignant cells Nrf2 activity provides growth advantage by increasing cancer chemoresistance and enhancing tumor cell growth [4]. Several mechanisms by which Nrf2 signaling pathway is constitutively activated in various cancers have been described: (1) somatic mutations in Keap1 or the Keap1 binding domain of Nrf2 disrupting their interaction; (2) epigenetic silencing of Keap1 expression leading to defective repression of Nrf2; (3) accumulation of disruptor proteins such as p62 leading to dissociation of the Keap1-Nrf2 complex; (4) transcriptional induction of Nrf2 by oncogenic K-Ras, B-Raf and c-Myc; and (5) post-translational modification of Keap1 cysteines by succinylation that occurs in familial papillary renal carcinoma due to the loss of fumarate hydratase enzyme activity [3], [4], [5], [6], [7], [8], [9], [10] (Fig. 3). Constitutively abundant Nrf2 protein causes increased expression of genes involved in drug metabolism thereby increasing the resistance to chemotherapeutic drugs and radiotherapy. In addition, high Nrf2 protein level is associated with poor prognosis in cancer [4]. Overactive Nrf2 also affects cell proliferation by directing glucose and glutamine towards anabolic pathways augmenting purine synthesis and influencing the pentose phosphate pathway to promote cell proliferation [11] (Fig. 4).
Fig. 4. The dual role of Nrf2 in tumorigenesis. Under physiological conditions, low levels of nuclear Nrf2 are sufficient for the maintenance of cellular homeostasis. Nrf2 inhibits tumor initiation and cancer metastasis by eliminating carcinogens, ROS and other DNA-damaging agents. During tumorigenesis, accumulating DNA damage leads to constitutive hyperactivity of Nrf2 which helps the autonomous malignant cells to endure high levels of endogenous ROS and to avoid apoptosis. Persistently elevated nuclear Nrf2 levels activate metabolic genes in addition to the cytoprotective genes contributing to metabolic reprogramming and enhanced cell proliferation. Cancers with high Nrf2 levels are associated with poor prognosis because of radio and chemoresistance and aggressive cancer cell proliferation. Thus, Nrf2 pathway activity is protective in the early stages of tumorigenesis, but detrimental in the later stages. Therefore, for the prevention of cancer, enhancing Nrf2 activity remains an important approach whereas for the treatment of cancer, Nrf2 inhibition is desirable [4], [11].
Given that high Nrf2 activity commonly occurs in cancer cells with adverse outcomes, there is a need for therapies to inhibit Nrf2. Unfortunately, due to structural similarity with some other bZip family members, the development of specific Nrf2 inhibitors is a challenging task and only a few studies of Nrf2 inhibition have been published to date. By screening natural products, Ren et al. [12] identified an antineoplastic compound brusatol as an Nrf2 inhibitor that enhances the chemotherapeutic efficacy of cisplatin. In addition, PI3K inhibitors [11], [13] and Nrf2 siRNA [14] have been used to inhibit Nrf2 in cancer cells. Recently, we have utilized an alternative approach, known as cancer suicide gene therapy, to target cancer cells with high Nrf2 levels. Nrf2-driven lentiviral vectors [15] containing thymidine kinase (TK) are transferred into cancer cells with high ARE activity and the cells are treated with a pro-drug, ganciclovir (GCV). GCV is metabolized to GCV-monophosphate, which is further phosphorylated by cellular kinases into a toxic triphosphate form [16] (Fig. 5). This leads to effective killing of not only TK containing tumor cells, but also the neighboring cells due to the bystander effect [17]. ARE-regulated TK/GCV gene therapy can be further enhanced via combining a cancer chemotherapeutic agent doxorubicin to the treatment [16], supporting the notion that this approach could be useful in conjuction with traditional therapies.
Fig. 5. Suicide gene therapy. Constitutive Nrf2 nuclear accumulation in cancer cells can be exploited by using Nrf2-driven viral vector for cancer suicide gene therapy [16]. In this approach, lentiviral vector (LV) expressing thymidine kinase (TK) under minimal SV40 promoter with four AREs is transduced to lung adenocarcinoma cells. High nuclear Nrf2 levels lead to robust expression of TK through Nrf2 binding. Cells are then treated with a pro-drug, ganciclovir (GCV), which is phosphorylated by TK. Triphosphorylated GCV disrupts DNA synthesis and leads to effective killing of not only TK containing tumor cells, but also the neighboring cells due to the bystander effect.
Nrf2 is a master regulator which triggers the production of powerful antioxidants in the human body which help eliminate oxidative stress. Various antioxidant enzymes, such as superoxide dismutase, or SOD, glutathione, and catalase, are also activated through the Nrf2 pathway. Furthermore, certain phytochemicals like turmeric, ashwagandha, bacopa, green tea, and milk thistle, activate Nrf2. Research studies have found that Nrf2 activation can naturally enhance cellular protection and restore balance to the human body.
Dr. Alex Jimenez D.C., C.C.S.T. Insight
Sulforaphane and Its Effects on Cancer, Mortality, Aging, Brain and Behavior, Heart Disease & More
Isothiocyanates are some of the most important plant compounds you can get in your diet. In this video I make the most comprehensive case for them that has ever been made. Short attention span? Skip to your favorite topic by clicking one of the time points below. Full timeline below.
Key sections:
00:01:14 – Cancer and mortality
00:19:04 – Aging
00:26:30 – Brain and behavior
00:38:06 – Final recap
00:40:27 – Dose
Full timeline:
00:00:34 – Introduction of sulforaphane, a major focus of the video.
00:01:14 – Cruciferous vegetable consumption and reductions in all-cause mortality.
00:02:12 – Prostate cancer risk.
00:02:23 – Bladder cancer risk.
00:02:34 – Lung cancer in smokers risk.
00:02:48 – Breast cancer risk.
00:03:13 – Hypothetical: what if you already have cancer? (interventional)
00:03:35 – Plausible mechanism driving the cancer and mortality associative data.
00:04:38 – Sulforaphane and cancer.
00:05:32 – Animal evidence showing strong effect of broccoli sprout extract on bladder tumor development in rats.
00:06:06 – Effect of direct supplementation of sulforaphane in prostate cancer patients.
00:07:09 – Bioaccumulation of isothiocyanate metabolites in actual breast tissue.
00:08:32 – Inhibition of breast cancer stem cells.
00:08:53 – History lesson: brassicas were established as having health properties even in ancient Rome.
00:09:16 – Sulforaphane’s ability to enhance carcinogen excretion (benzene, acrolein).
00:09:51 – NRF2 as a genetic switch via antioxidant response elements.
00:10:10 – How NRF2 activation enhances carcinogen excretion via glutathione-S-conjugates.
00:10:34 – Brussels sprouts increase glutathione-S-transferase and reduce DNA damage.
00:11:20 – Broccoli sprout drink increases benzene excretion by 61%.
00:13:31 – Broccoli sprout homogenate increases antioxidant enzymes in the upper airway.
00:15:45 – Cruciferous vegetable consumption and heart disease mortality.
00:16:55 – Broccoli sprout powder improves blood lipids and overall heart disease risk in type 2 diabetics.
00:19:04 – Beginning of aging section.
00:19:21 – Sulforaphane-enriched diet enhances lifespan of beetles from 15 to 30% (in certain conditions).
00:20:34 – Importance of low inflammation for longevity.
00:22:05 – Cruciferous vegetables and broccoli sprout powder seem to reduce a wide variety of inflammatory markers in humans.
00:36:32 – Sulforaphane improves learning in model of type II diabetes in mice.
00:37:19 – Sulforaphane and duchenne muscular dystrophy.
00:37:44 – Myostatin inhibition in muscle satellite cells (in vitro).
00:38:06 – Late-video recap: mortality and cancer, DNA damage, oxidative stress and inflammation, benzene excretion, cardiovascular disease, type II diabetes, effects on the brain (depression, autism, schizophrenia, neurodegeneration), NRF2 pathway.
00:40:27 – Thoughts on figuring out a dose of broccoli sprouts or sulforaphane.
00:41:01 – Anecdotes on sprouting at home.
00:43:14 – On cooking temperatures and sulforaphane activity.
00:43:45 – Gut bacteria conversion of sulforaphane from glucoraphanin.
00:44:24 – Supplements work better when combined with active myrosinase from vegetables.
00:44:56 – Cooking techniques and cruciferous vegetables.
00:46:06 – Isothiocyanates as goitrogens.
Acknowledgments
This work was supported by the Academy of Finland, the Sigrid Juselius Foundation and the Finnish Cancer Organisations.
In conclusion, nuclear factor (erythroid-derived 2)-like 2, also known as NFE2L2 or Nrf2, is a protein which increases the production of antioxidants which protect the human body against oxidative stress. As described above, the stimulation of the Nrf2 pathway are being studies for the treatment of diseases caused by oxidative stress, including cancer. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Additional Topic Discussion: Relieving Knee Pain without Surgery
Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
If you are like most people, at some point in your life, you will experience back pain � if you haven�t already. The American Chiropractic Association estimates that around 80% of the population suffers from back pain, has suffered from back pain, or at some point in the future will suffer from back pain. That puts you in good company.
It also means that you have a better than average chance of falling into that 80%, so the smart thing to do is take steps not to prevent it. One powerful preventative measure against back pain is stretching. Try these four stretches to help your back pain.
Forward Bend
Stand with your feet shoulder width apart and your knees soft (not locked). Take a deep breath and as you exhale, bend forward at the waist, hands out as if you are reaching for the floor. When you feel a little stretching in your hamstrings (the backs of your legs), stop and hold that position for two or three breaths. If you can�t reach the floor, that is OK, don�t force it. If you need extra stability, you can use a chair to hold on to for balance. Repeat this movement seven to ten times.
Cat and Camel
This stretch is typically done on the floor, but if you don�t think you can safely get back up, you can stand and hold on to a chair. On the floor, get on your hands and knees with your back straight. If using a chair, stand with your feet shoulder width apart and your knees soft. Bend slowly and place your palms in the seat of the chair so that your back is parallel to the floor. Keep it straight.
Begin by arching your back up as high as you can. Hold for two or three breaths. Return to the starting position, then let it sway down toward the floor and hold for two or three breaths. Return to the starting position. Do this five to seven times.
Back Extension
Lie on your stomach on the floor or bed with your hand’s palm down near your face. Slowly push up with your arms, keeping your head level with your shoulders, until you are on your elbows. Hold for three or four breaths.
If you can push all the way up so that you are on your hands, that will give you a deeper stretch. You can also hold it for a little longer. Just remember to keep the movements slow and gentle to avoid injury.
If you are not able to safely get on the floor, you can stand with your feet several inches from a wall. Place both of your hands on the wall and bring your upper body toward them, letting your pelvis naturally follow. Gently push against the wall with your hands, pushing your upper body away from the wall. You can also do this with a chair if you need extra support. Repeat five to seven times.
Hip Flex and Stretch
Get on your hands and knees on the floor or bed. Slowly move your body back so that your bottom is over your heels. Keep your hips straight as you extend your arms in front of you. Drop your head between your arms and hold the stretch for three to five breaths.
If you can�t get on your hands and knees, sit in a chair with your feet flat on the floor in front of you, hip-width apart. Extend your arms in front of you and reach forward. Lean forward slightly until you feel the stretch.
You can also place your hands on your knees for support while you sit in a chair and bend at the waist, slowly rounding out your back over your thighs. Hold the stretch for three to five breaths then return to your upright position. Do this seven to ten times.
Before you begin any new exercise or stretching regimen, talk to your doctor or chiropractor to make sure you aren�t doing something that could exacerbate your problem. For the most part, stretching is very therapeutic and beneficial, but some injuries and conditions can be made worse.
It is well worth taking the extra time to talk with your doctor and perhaps even show him or her the movements. This will also allow them to correct any form problems you may have or recommend any modifications that will help you get the most out of your stretches.
Chiropractic care is an alternative treatment option which focuses on the diagnosis, treatment, and prevention of a variety of injuries and/or underlying conditions associated with the musculoskeletal and nervous system. Dr. Alex Jimenez, a chiropractor, has helped many patients find relief from their symptoms of neck pain, back pain, and sciatica, among other health issues. Recommended for his outstanding services and ability to provide care and education to his patients, Dr. Alex Jimenez, and his staff make sure to offer the best treatment option for each patient’s specific needs. The patients express how Dr. Alex Jimenez has helped them find pain relief.
Most Recommended Chiropractor
We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.
As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused on treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
If you have enjoyed this video and we have helped you in any way, please feel free to subscribe and recommend�us.
Influenced since a young age to pursue a career in massage therapy, Brittaney always wished to offer relief to people in pain. Along with Dr. Alex Jimenez, doctor of chiropractic, Brittaney cares deeply about the attention and care she provides to every single one of her patients. Brittaney is motivated to know that she can help people find pain relief through the treatment she and Dr. Alex Jimenez give their patients. Brittaney highly recommends Dr. Alex Jimenez as the non-surgical choice for a variety of health issues, including back pain.
Massage Rehabilitation
Massage therapy is the manual manipulation of soft body tissues (muscle, tendons, and ligaments) to enhance an individual’s well-being. There are many different types of massage therapy approaches. Massage techniques are commonly applied with hands, fingers, elbows, knees, forearms, feet, or a device. The objective of massage therapy is to treat pain or body stress, although it may also help in treating injuries and aggravated conditions. Chiropractic care may also involve the use of massage therapy.
We are blessed to present to you�El Paso�s Premier Wellness & Injury Care Clinic.
As El Paso�s Chiropractic Rehabilitation Clinic & Integrated Medicine Center,�we passionately are focused on treating patients after frustrating injuries and chronic pain syndromes. We focus on improving your ability through flexibility, mobility and agility programs tailored for all age groups and disabilities.
If you have enjoyed this video and we have helped you in any way, please feel free to subscribe and recommend�us.
DNA supports approximately 20,000 genes, each holding a program for the creation of a protein or enzyme required for a healthy lifestyle. Every one of these patterns needs to be constantly regulated by a sort of “promoter” which manages exactly how much of each substance and/or chemical is generated and under which conditions these will also develop.
By connecting to a particular kind of the switch-like promoter areas, known as the Antioxidant Response Element, or ARE, the Nrf2 factor�supports the speed of creation for hundreds of distinct genes which enable the cells to survive under stressful circumstances. These genes then generate a selection of antioxidant enzymes which develop a defense network by neutralizing oxidants and by cleaning up the toxic by-products left behind in their�production, in addition to helping restore the�damage they caused.
What is Oxidative Stress?
Several oxidants like the superoxide radical, or O2-., and hydrogen peroxide, or H2O2, have been created through the practice of burning off the substances and/or chemicals which sustain the human body. The human body�possesses antioxidant enzymes which�neutralize and detoxify reactive foods and drinks we consume. The Nrf2 modulates their production to keep equilibrium and underscores the demand for all these enzymes. This balance can be interrupted by a�couple of factors, including age.
As we age,�the human body creates less Nrf2 and this delicate equilibrium can gradually begin to�turn towards the oxidative side, a state referred to as oxidative stress. Disease may also cause the overproduction of oxidants. Infections, allergies, and autoimmune disorders can additionally trigger our immune cells to create reactive oxidants, such as O2-. , H2O2, OH and HOCl, where healthy cells become damaged and respond with inflammation. Diseases associated with aging, including heart attacks, stroke, cancer, and neurodegenerative conditions like Alzheimer’s disease, also increase the development of oxidants, generating stress and an inflammation response.
What are Nrf2 Activators?
The Nrf2 protein, also called a transcription factor due to the way it can support and control enzymes and genes, is the secret element of a sequence of biochemical reactions within the cell which reacts to modifications in cognitive equilibrium as well as oxidative balance. The sensing elements of this pathway modify and discharge Nrf2, triggering it so it might spread into the nucleus of the cell towards the DNA. The Nrf2 may alternatively turn on or switch off the genes and enzymes it supports to protect the cell.
Fortunately, a variety of substances which are Nrf2 activators develop through the consumption of certain plants and extracts utilized centuries ago in Chinese and Native American traditional remedies. These phytochemicals seem to be equally as powerful with fewer side-effects, as the Nrf2-activating pharmaceutical products which are being used today.
Nuclear factor erythroid 2-related factor, more commonly known as Nrf2, is a transcription factor which protects the cell by regulating genes, enzymes and antioxidant responses. Transcription factors are a type of protein which attach to DNA to promote the creation of specific substances and chemicals, including glutathione S-transferases, or GSTs. Nrf2 activation induces the production of active proteins which exhibit a powerful antioxidant capacity to help decrease oxidative stress.
Dr. Alex Jimenez D.C., C.C.S.T. Insight
The Science Behind Nrf2 Activation
Once the initial Nrf2-activating dietary supplement was created in 2004, minimal information was known concerning the function of the Nrf2 pathway. Approximately 200 newspapers in the literature on Nrf2, also known as nuclear factor-like 2 or NFE2L2, existed and researchers were only just starting to discover the antioxidant response of Nrf2 in mammals. As of 2017, however, over 9,300 academic research studies on this “master regulator,” have been printed.
In reality, Nrf2 regulates many antioxidant enzymes which don’t correlate to the genes, instead, they offer protection against a variety of stress-related circumstances which are encountered by cells, organs and ultimately organisms, under healthy and pathological conditions. Based on this new quantity of information from published academic research studies, researchers can now develop better Nrf2 dietary supplements.
As of 2007,�research studies have demonstrated the complex function of the Nrf2 pathway. Nrf2 activators have been found to mimic factors of different structures within the human body. Through these pathways, Nrf2 activators have been equipped to feel changing conditions throughout the cell in order to keep balance and respond to the evolving requirements of the genes.
Why Use Nrf2-Activating Supplements?
As Nrf2-activation abilities diminish with age in organisms, changes may begin to occur. Research studies have demonstrated that the focus of Nrf2 in cells declines with age, showing increased markers of oxidative stress. A variety of age-related diseases like atherosclerosis and cardiovascular disease, arthritis, cancer, obesity, type 2 diabetes, hypertension, cataracts, and Alzheimer’s disease as well as Parkinson’s diseases can develop due to these changes. Oxidative stress has been found with these health issues.
By stimulating the cell’s capacity to increase the production of Nrf2 activators, Nrf2 dietary supplements can help revive the human body’s own ability to counteract the effects of oxidative stress. Polyunsaturated fatty acids, or PUFAs, are one of the most readily oxidized molecules and they’re particularly vulnerable to suffer damage from free radicals. Thiobarbituric acid, or TBARS, production can increase with age, indicating heightened oxidative stress along with a drop in Nrf2-regulated pathways.
Biologically, gene induction is a really slow mechanism, generally requiring hours to transfer through a pathway. As a result,�many enzymes possess their very own on/off switches which could be triggered in minutes by different regulatory enzymes. Researchers have developed proprietary compositions of Nrf2 activators which utilize this knowledge base of activation. Nrf2 activation is composed not just of the Nrf2 transcription factor being discharged from its inhibitor and migrating to the cell nucleus, but also binding to specific DNA sequences to encourage cytoprotective gene expression, regulating the pace at that Nrf2 is taken out of the nucleus.
Understanding the elimination procedure and the activation of Nrf2 in the human body has allowed researchers to build combinations of different Nrf2 activators to accomplish the reflection of genes through its modulation. The combination of the knowledge base, together with the wide variety of other research studies has�helped produce Nrf2 activators for use as dietary supplements. The scope of our information is limited to chiropractic and spinal health issues. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.
Curated by Dr. Alex Jimenez
Additional Topic Discussion: Relieving Knee Pain without Surgery
Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including�sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.
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