Donnerstag, 19. Dezember 2013

Sinnstiftendes Weihnachten

Jörg Linder wünscht wunderbar sinnvolle und sinnstiftende Begegnungen an und um Weihnachten.



JÖRG LINDER AKTIV-TRAINING
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76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Aktiv-Trainings-Weblog:  http://www.aktiv-training.de/blog/

Montag, 9. Dezember 2013

Der Darm und die Emotoinen

"......Eigene Rezeptoren (Anm: des Darms) registrieren sogar Geschmacksrichtungen wie bitter oder süß, oder sie erkennen bestimmte Nährstoffe.......Signale empfängt das Gehirn über das Nervensystem und über den Blutkreislauf, Botenstoffe wie Hormone oder Neurotransmitter und Immunmediatoren spielen dabei eine Rolle. Ein Großteil der Kommunikation gelangt über den Vagusnerv ins Gehirn und wird dort in Regionen verarbeitet, die für Emotionen zuständig sind, dem sogenannten limbischen System. Diese enge Verbindung zwischen Bauch und Gefühlen hat sich irgendwann in der Evolution entwickelt. Forscher diskutieren, ob das Nervensystem im Darm ein Satellit des limbischen Systems ist - oder ob Letzteres sogar aus dem Nervensystem im Bauch entstanden ist,..... "

Quelle und vollständiger Artikel: http://www.spiegel.de/spiegelwissen/neue-forschung-wie-der-darm-das-wohlbefinden-beeinflusst-a-934518.html

 


JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Gesundheitsmanagement: www.gesundheitsmanager-24.de
Aktiv-Trainings-Weblog:  http://www.aktiv-training.de/blog/





Dienstag, 12. November 2013

High-intensity aquatic exercises (HydrOS)......

........improve physical function and reduce falls among postmenopausal women.

"OBJECTIVE:

This study aims to investigate the effects of an aquatic exercise program (HydrOS) on neuromuscular function and falls among postmenopausal women......

CONCLUSIONS:

The aquatic exercise program HydrOS is a safe and efficient way to improve physical function and to reduce falls among postmenopausal women."

Quelle: http://www.ncbi.nlm.nih.gov/pubmed/23531689


Sturzprävention durch hochintensives Aqua-Fitnesstraining!!

  

 Jörg Linder / Master of Arts in Gesundheitsmanagement und Prävention / Dipl.-Sozialarbeiter / Sozialtherapeut / Personal Fitness Trainer
 
JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Gesundheitsmanagement: www.gesundheitsmanager-24.de
Aktiv-Trainings-Weblog:  http://www.aktiv-training.de/blog/

Samstag, 9. November 2013

Dietary Sodium Restriction / Salz ist gesund

Take It with a Grain of Salt:
"However, low sodium diets have not been shown to reduce cardiovascular events in normotensive individuals or in individuals with pre-hypertension or hypertension. Moreover, there is evidence that a low sodium diet may lead to a worse cardiovascular prognosis in patients with cardiometabolic risk and established cardiovascular disease......" 
Quelle:http://www.amjmed.com/article/S0002-9343%2813%2900594-9/abstract
 
Jörg Linder – Master of Arts in Gesundheitsmanagement und Prävention
 
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JÖRG LINDER AKTIV-TRAINING 
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Aktiv-Training: www.aktiv-training.de
Sturzprävention: www.sturztraining.de
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Mittwoch, 6. November 2013

Neues Band im Knie entdeckt......

.........bzw. ein Band, dass in 97 Prozent aller menschlichen Knie vorhanden ist, wurde beschrieben und hat einen Namen erhalten.

Für  Patienten mit Kreuzbandriss – und nicht nur solche –  könnte das durchaus interessant sein, denn bei einer Kreuzbandrissverletzung ist häufig das "neue Band" - anterolateral ligament (ALL) - mitbetroffen, wird aber nicht mitbehandelt.

…   Wenn das alles keine “Ente” ist, spielt das durchaus eine Rolle für die Kniestabilität.


…… Their research shows that the ligament, which was given the name anterolateral ligament (ALL), is present in 97 per cent of all human knees. Subsequent research shows that pivot shift, the giving way of the knee in patients with an ACL tear, is caused by an injury in the ALL ligament…..”

Quelle und vollständiger Artikelhttp://www.sciencedaily.com/releases/2013/11/131105081352.htm


Jörg Linder – Master of Arts in Gesundheitsmanagement und Prävention - Ihr Personal Trainer für Baden-Baden, Karlsruhe, Pforzheim, Ortenau, Nordschwarzwald.

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JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Ich bin dann mal fit: www.ich-bin-dann-mal-fit.com
Facebook: https://www.facebook.com/joerglinderaktivtraining
Aktiv-Training: www.aktiv-training.de
—————————————————–

Dienstag, 5. November 2013

Review / Metananlyse zu Kompressionsbekleidung im Sport / Englisch


 Br J Sports Med doi:10.1136/bjsports-2013-092456

Compression garments and recovery from exercise-induced muscle damage: a meta-analysis

Abstract

"The purpose of the study was to determine the effects of compression garments on recovery following damaging exercise. ....... Studies were extracted from a literature search of online databases. Data were extracted from 12 studies,...... ........These results indicate that compression garments are effective in enhancing recovery from muscle damage." 

 

Gesichtet wurden tausende von Studien; in das Review aufgenommen wurden 12 Studien. Es gibt Hinweise, dass Kompressionsbekleidung die muskuläre Erholung verbessern kann. 





Jörg Linder / Master of Arts in Gesundheitsmanagement und Prävention / Dipl.-Sozialarbeiter / Sozialtherapeut / Personal Fitness Trainer
 

JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Gesundheitsmanagement: www.gesundheitsmanager-24.de
Personal Training: www.personal-training-baden-baden.blogspot.com
Wordpress: www.aktivtraining.wordpress.com



Montag, 28. Oktober 2013

Freitag, 25. Oktober 2013

Warum Erfolg wenig mit IQ zu tun hat und andere Ergebnisse der Gehirnforschung

".......Obwohl manche Resilienz-Aspekte von Anfang an in unserem Gehirn fest verschaltet sind, sagt die Wissenschaft uns heute, dass sie auch entwickelt werden können. Der Kampf gegen Widrigkeiten aller Art ist etwas, dass Sie bewusst üben - und besser hinkriegen können......Der anteriorore zinguläre Kortex ist eine entscheidende Region im Stirnlappen. Er ist ein wichtiger Akteur bei vielen Gewinnergehirn-Eigenschaften. Im Hinblick auf die Resilienz hat er die Aufgabe, Fehler und Konflikte sofort zu erkennen und anderen Hirnregionen zu helfen, ihre emotionale Reaktion auf sie zu regulieren.

Wenn das Gehirn bemerkt, das die Dinge nicht besonders gut laufen, rasen die elektrischen Impulse in diese drei Areale. Bei kürzlichen fMRT-Experimenten konnte beobachtet werden, wie dieses Phänomen sich ausbreitet, und deshalb wissen wir, wie praktisch jedes normal funktionierende Gehirn auf einen Misserfolg reagiert. Was Gewinnergehirne von Durchschnittsgehirnen unterscheidet, ist das, was als Nächstes passiert....Die sehr resilienten Personen konnten die emotionalen Zentren abkoppeln, insbesondere die Inselrinden, während wenig resiliente Personen angespannt blieben und diese Regionen auch noch einige Zeit danach aktiv waren. Wenig resiliente Gehirne konnten ihre Aktivität - vor allem in der reaktionshemmenden Inselrinde - nichtzurückdrehen, wenn sich die Bedrohung nicht konkretisierte......."

Aus:  BROWN / FENSKE - So denken Gewinner -Warum Erfolg wenig mit IQ zu tun hat und andere Ergebnisse der Gehirnforschung - Goldmann 2011 - S. 186 / 187 / 188




Jörg Linder / Master of Arts in Gesundheitsmanagement und Prävention / Dipl.-Sozialarbeiter / Sozialtherapeut / Personal Fitness Trainer
 

JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Gesundheitsmanagement: www.gesundheitsmanager-24.de
Personal Training: www.personal-training-baden-baden.blogspot.com
Wordpress: www.aktivtraining.wordpress.com


Donnerstag, 24. Oktober 2013

Gute Lehrer

"Was ich sagen möchte ist, vergesst die Zuhörer nicht. Strebt nicht danach zu zeigen wie intelligent ihr seid, sondern strengt euch an und zeigt welch gute Lehrer ihr seid."  Michael Boyle 


Samstag, 19. Oktober 2013

THE SACCHARINE DISEASE


Man beachte vor allem das Datum der Veröffentlichung - 1974!! - von THE SACCHARINE DISEASE.

Es dreht sich hier um die (verheerenden gesundheitlichen) Auswirkungen von raffiniertem Zucker und raffiniertem Mehl.

Hier der Direktlink zum pdf-Download:


http://www.hcvsociety.org/files/Diet/The-Saccharine-Disease.pdf



Jörg Linder – Master of Arts in Gesundheitsmanagement und Prävention


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JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Aktiv-Training: www.aktiv-training.de
Sturzprävention: www.sturztraining.de

Donnerstag, 17. Oktober 2013

Neurodegenerative Erkrankungen


Neurodegenerative Erkrankungen wie Alzheimer, Parkinson, ALS, CJK oder Demenz haben oft Gemeinsamkeiten und können sich gegenseitig begünstigen.  

"Gibt es einen gemeinsamen Mechanismus bei der Entstehung neurodegenerativer Erkrankungen? Offenbar schon.
Bei den meisten dieser Krankheiten finden sich fehlgefaltete Proteine, die im Gehirn verklumpen, wobei diese Aggregate zunächst in einer begrenzten Hirnregion auftreten, von der aus sie sich sukzessive auf das restliche Gehirn ausbreiten......." (Thomas Müller / aerztezeitung.de)

Quelle und vollständiger Artikel:   http://www.aerztezeitung.de/medizin/krankheiten/neuro-psychiatrische_krankheiten/morbus_parkinson/default.aspx?sid=847094&cm_mmc=Newsletter-_-Newsletter-C-_-20131017-_-Morbus+Parkinson






Jörg Linder – Master of Arts in Gesundheitsmanagement und Prävention


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JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Aktiv-Training: www.aktiv-training.de
Sturzprävention: www.sturztraining.de
———————————————————

Donnerstag, 3. Oktober 2013

BGM-Projektmanagement: Agile Methoden

BGM-Projektmanagement: Agile Methoden: "Agile Entwicklung verzichtet auf die methodische Strenge der klassischen Phasenabläufe und strebt einen iterativen Teamdialog mit dem...

Mittwoch, 18. September 2013

Synaptisches Feuern und Neurochemie

"Neuronen, die Nervenzellen des Gehirns, sind nicht direkt miteinander verbunden. Zwischen ihnen befindet sich ein schmaler Spalt, die Synapse. Ein elektrischer Impuls, der durch den Nervenstrang geleitet wird, wird an der Synapse in ein chemisches Signal verwandelt. Auf beiden Seiten der Synapse befinden sich Rezeptoren, die Botschaften aus derlei chemischen Signalen aufnehmen.  Synapsen senden und empfangen eines von zwei Signalen: entweder einen exzitatorischen Inpuls, der das Neuron aktiviert, oder ein inhibitorisches Signal, welches das Neuron an weiterer Tätigkeit hindert Dieses elektrische-zu-chemische-zu-elektrische Kommuniaktionssystem über die Synapsen wird manchmal als synaptisches Feuern bezeichnet. Billionen von sich ständig verändernden Neuronen sind durch Muster neuronalen Feuerns zu Netzwerken verbunden. Diese Netzwerke sind die mentalen Karten......

........dass eine Synapse im präfrontalen Kortex nur dann konkret feuert, wenn das richtige Maß an zwei neurochemischen Stoffen präsent ist. Diese chemischen Stoffe heißen Dopamin und Noradrenalin (auch Norepinephrin)."

Quelle: David Rock - Brain at work - Campus-Verlag - 2011 - S.94 "Auf der Suche nach optimaler Leistungsfähigkeit"

Kursiv: im Original


Jörg Linder – Master of Arts in Gesundheitsmanagement und Prävention


 ————————————————————————–

JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Aktiv-Training: www.aktiv-training.de
Sturzprävention: www.sturztraining.de
———————————————————

Donnerstag, 12. September 2013

Treatment of myotendinous achilles ruptures

Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, and fair, respectively. None of the patients they treated have developed recurrent myotendinous Achilles ruptures to date.

They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief.
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, and fair, respectively. None of the patients they treated have developed recurrent myotendinous Achilles ruptures to date.

They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief.
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, and fair, respectively. None of the patients they treated have developed recurrent myotendinous Achilles ruptures to date.

They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief.
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, and fair, respectively. None of the patients they treated have developed recurrent myotendinous Achilles ruptures to date.

They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief.
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, and fair, respectively. None of the patients they treated have developed recurrent myotendinous Achilles ruptures to date.

They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief.
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, and fair, respectively. None of the patients they treated have developed recurrent myotendinous Achilles ruptures to date.

They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief.
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, and fair, respectively. None of the patients they treated have developed recurrent myotendinous Achilles ruptures to date.

They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief.
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, and fair, respectively. None of the patients they treated have developed recurrent myotendinous Achilles ruptures to date.

They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief.
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpu
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. - See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients - See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf
They concluded that a nonsurgical approach to the treatment of myotendinous Achilles ruptures results in a high rate of myotendinous healing with improved patient function and pain relief. - See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf

Hier finden Sie eine Studie zu Achillessehnenrisse (Englisch; Kurzversion):
Treatment of myotendinous achilles ruptures.Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients experienced improved function and less pain at their latest follow-up. Mean Foot and Ankle Ability Measure-Sports (FAAM-Sports) increased from 20.2% at the time of initial presentation to 95.2% at the latest follow-up (P < .05). Mean Visual Analog Scores (VAS) of pain decreased from 8.2 at the time of initial presentation to 1.3 at latest follow-up (P < .01). In all, 23 (76.7%), 6 (20%), and 1 (3.3%) patients rated their satisfaction as excellent, good, an
- See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf

http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/



Not much literature exists regarding the treatment of myotendinous Achilles ruptures. The authors conducted this study in order to retrospectively examine clinical outcomes from uniform nonsurgical treatment of these injuries. Between November 2005 and May 2011, 30 patients presented with an acute, complete myotendinous Achilles rupture. The location of the Achilles injury was confirmed on magnetic resonance imaging (MRI) for all patients. All patients were treated nonsurgically, with a system including 3 weeks of non-weight-bearing and then 3 weeks of progressive to full weight-bearing in an Achilles boot. Physical therapy was provided for 4 to 6 weeks after this period of immobilization. 21 males and 9 females participated. The patients had a mean age of 40.8 years (range, 24-54). Patients were followed an average of 40.5 months (range, 23-81). They achieved full healing of the Achilles myotendinous junction  clinically in all 30 patients . All patients - See more at: http://www.physiospot.com/research/treatment-of-myotendinous-achilles-ruptures/#sthash.xbNFyzNu.dpuf

Jörg Linder – Master of Arts in Gesundheitsmanagement und Prävention


————————————————————————–

JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Aktiv-Training: www.aktiv-training.de
Sturzprävention: www.sturztraining.de

———————————————————-

Montag, 26. August 2013

Wie gut altern wir? - Über die Qualität des Alterns

Aus: John Medina – Gehirn und Erfolg – Spektrum Akademischer Verlag – 2013:

“…….Gibt es einen Faktor, der bestimmt, wie gut wir altern?…..Zu den wichtigsten Faktoren, die über die Qualität des Alterns entscheiden, gehört offenbar der Grad der körperlichen Betätigung…….

Der wichtigste Grund für diesen Unterschied (Anm: zwischen einem aktiven und passiven Lebensstil) liegt allem Anschein nach darin, das sich durch körperliches Training die Leistungsfähigkeit von Herz und Kreislauf verbessert, und das wiederum vermindert das Risiko für Erkrankungen wie Herzinfarkt und Schlaganfall.

Die Wissenschaftler überlegten nun weiter, warum Menscheen, die “erfolgreich” alt werden, offenbar auch geistig beweglicher sind……..Sportliche Menschen übertreffen die Stubenhocker in Langzeitgedächtnis, logischem Denken, Aufmerksamkeit und Problemlösungsverhalten, ja sogar bei der sogenannten fluiden Intelligenz, der Fähigkeit schnell zu überlegen und abstrakt zu denken, auf grund früher erlernter Dinge zu improvisieren und so ein neues Problem zu lösen.”

Aus: John Medina – Gehirn und Erfolg – Spektrum Akademischer Verlag – 2013 – 6-7 und
Kursiv: im Original


Jörg Linder – Master of Arts in Gesundheitsmanagement und Prävention


————————————————————————–
JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
Aktiv-Training: www.aktiv-training.de
Sturzprävention: www.sturztraining.de

———————————————————-

Montag, 12. August 2013

Improvements in balance.......

........in older adults engaged in a specialized home care falls prevention program

 Whitney SL, et al

J Geriatr Phys Ther. 2013 Jan-Mar;36(1):3-12. doi: 10.1519/JPT.0b013e3182550ea5.

Abstract

"BACKGROUND AND PURPOSE: To determine if persons older than 65 years receiving a combination of physical therapy, occupational therapy, speech, or nursing interventions in their home demonstrated changes in gait/balance function after an episode of home care services.......

.......RESULTS: The gait/balance measures demonstrated MDCs ranging between 68% and 91% for the study sample........
 
......CONCLUSION: On the basis of established criteria, participants seemed to make clinically meaningful gains after the home care episode of care."



 
JÖRG LINDER AKTIV-TRAINING
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Mail: info@aktiv-training.de
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Donnerstag, 18. Juli 2013

Vibrationstraining im Vergleich zum Exzentrischen Krafttraining

In der Pilotstudie von Holger Matthias  Vibrationstraining vs. Exzentrisches Training zur Behandlung von chronischen Achillessehnenbeschwerden bei Freizeitsportlern  (2009) wurde das Vibrationstraining im Vergleich zum Exzentrischen Training untersucht.

Ergebnis:  Durch das Vibrationstraining  konnten Schmerzen in der Sehnenmitte, ähnlich dem Exzentrischen Training, deutlich reduziert werden. Vibrationstraining steht in Zukunft somit auch als Therapieoption der  zur Achillestendinopathie Wahl.


Link zur Studie: 

http://nbn-resolving.de/urn:nbn:de:bsz:21-opus-42345




Jörg Linder - Master of Arts in Gesundheitsmanagement und Prävention
 


JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271 
 
 

Montag, 1. Juli 2013

Training und Gymnastik bei Rheuma und Bechterew

Körperliche Bewegung hält Patienten mit rheumatischen Erkrankungen fit. Das gilt auch für Morbus Bechterew, rheumatoide Arthritis und für Arthrose.


"Patienten mit Morbus Bechterew wird von den meisten Rheumatologen heute eine gewisse sportliche Betätigung empfohlen. Es gibt sogar Sportgruppen speziell für diese Patienten, nicht selten Volleyballgruppen. " 

Quelle: Philipp Grätzel von Grätz / http://www.aerztezeitung.de/medizin/krankheiten/skelett_und_weichteilkrankheiten/rheuma/article/841079/kraefte-sammeln-training-gymnastikball-hilft-rheuma.html?sh=22&h=-1905100477

Im weiteren wird eine RCT-Studie zum Training mit Gymnastikball vorgestellt.  (siehe o.g. Link)





JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
 

Freitag, 21. Juni 2013

Diabetes Typ 1 kündigt sich durch Antikörper an - Bluttest ermöglicht vorbeugende Behandlung

Pressemitteilung Deutsche Diabetes Gesellschaft:

".......Diabetes mellitus Typ 1 ist eine Autoimmunerkrankung und bricht meist im Kindes- und Jugendalter aus: Die körpereigene Abwehr zerstört Zellen in der Bauchspeicheldrüse, die das blutzuckersenkende Hormon Insulin produzieren. Dadurch kann der Körper den Blutzucker nicht mehr regulieren und die Betroffenen müssen lebenslang Insulin spritzen. Indikatoren des Angriffs auf die Bauchspeicheldrüse sind Abwehrstoffe,........"

Quelle und vollständiger Artikel: http://www.deutsche-diabetes-gesellschaft.de/presse/pressemeldungen/meldungen-detailansicht/article/diabetes-typ-1-kuendigt-sich-durch-antikoerper-an-bluttest-ermoeglicht-vorbeugende-behandlung-1.html?cHash=9328b696abc423143ff74a90d8d482ab




JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271
 
 

Samstag, 11. Mai 2013

Recherche statt googeln - Erste Schritte

Die einfache Internetsuche (googeln) für wissenschaftliche Inhalte liefert selten hohe inhaltliche Qualität und ist auch selten von hoher Relevanz.

Googeln genügt nicht wissenschaftlichen Standards - aber es kann sein, dass googeln einen Überblick verschafft.

Es kann auch sein - wenn genügend spezifische Key-Words vorhanden sind - sich ein Text über google (oder jede andere kommerzielle Suchmaschine) wiederfinden lässt.

Suchmaschinen erfassen grrundsätzlich nur einen kleinen Teil vorhandener Inhalte.

Für wissenschaftliche Arbeiten ist daher Recherche statt googeln das Thema.

Sinn und Zweck einer solchen Recherche ist die Informationsbeschaffung.

Nötig ist dazu zunächst:

- Der Recherchierende muss seinen Informationsbedarf definieren

- Er muss geeignete Systeme und Recherchemethoden auswählen

- eine effektive Suchstrategie (hängt ab von der Frage- und Problemstellung der Arbeit)

- die Qualität der Informationen muss durch ihn beurteilt werden (hierfür sind entsprechende Kriterien notwendig)

- ggf. muss der Rechercheprozess modifiziert werden

- die gewonnen Informationen müssen verwaltet werden

- die gewonnen Informationen müssen zusammengefasst werden


 
 Jörg Linder - Master of Arts in Gesundheitsmanagement und Prävention



JÖRG LINDER AKTIV-TRAINING
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271 
Gesundheitsmaangement: www.gesundheitsmanager-24.de
 
 
 
 
 
 
 
 
 
 

Montag, 29. April 2013

Stürze im Alter


 Zuammenfassender Artikel von Springerlink und der Studie von T:S Kaeding "Stürze im Alter" (März 2009 / Sportwissenschaft):

Stürze im Alter  "...... verringern die Lebensqualität der Betroffenen und können einen negativen Einfluss auf das Selbstwertgefühl die Eigenaktivität und die Anzahl sozialer Kontakte haben. Die jährliche Sturzquote bei über 65-Jährigen liegt bei etwa 30%.


Dieser Anteil steigt bis zum Alter von 80 Jahren auf etwa 50%, wobei fast die Hälfte davon öfter als einmal im Jahr einen Sturz erleidet. Mehr als 90% aller Stürze ereignen sich in alltäglichen Situationen, zumeist als Folge eines Fehlers in der Fortbewegung......"

Quelle und vollständiger Artikel: http://link.springer.com/article/10.1007%2Fs12662-009-0006-6?LI=true


 
 
JÖRG LINDER AKTIV-TRAINING-
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271 
 
 
 

Montag, 11. März 2013

Understanding Our Adrenal System: Norepinephrine

Author:   Vanessa Bennington

Quelle:  http://breakingmuscle.com/health-medicine/understanding-our-adrenal-system-norepinephrine
 
There is a lot of talk about adrenal health lately, particularly adrenal fatigue.

Most of us get the gist of it. If you stress your body out too much, for too long your adrenals just up and quit on you. Most of us also understand that when our adrenals are not functioning properly our energy levels and moods suffer, as well as our mental and physical performance. But how many of us really understand the chemicals and hormones made by the adrenals?

I am going to explain these adrenal chemicals one by one, so we can all better understand the complex mechanisms of adrenal function and how to maintain or regain healthy adrenal function to maximize our athletic performance. The first chemical up is norepinephrine.

Norepinephrine, also referred to as noradrenaline, along with epinephrine is what most of us think of as the “fight-or-flight” hormones.

It’s technically a catecholamine, but it functions as a hormone and neurotransmitter and is produced by the adrenal gland, postganglionic neurons of the sympathetic nervous system, and part of the brain called the locus coerules. From the locus coerules, noradrenergic neurons branch out and form a system that enables norepinephrine to be delivered to different parts of the brain. In a similar fashion, the postganglionic neurons enable norepinephrine to be delivered directly to target organs and cells in the body. The adrenal glands dump norepinephrine directly into the blood. These mechanisms usually come into play when we are under stress.

That release of norepinephrine (as well as epinephrine) is what gets your blood pumping and heart pounding, giving you the shakes when you’re put in a stressful situation. It triggers the release of glucose into the blood stream  and increases blood pressure, heart rate, mental alertness, and respiratory rate. When released from the locus coerules, it has an anti-inflammatory effect on the brain. It also shunts blood away from the skin and to the heart, brain, muscles, and kidneys. (Ever wonder why you have to urinate constantly right before a super tough workout?)

In other words, norepinephrine gets you ready to respond physically to a perceived stressor. It is also used as a drug to maintain blood pressure and treat bradycardia (slow heartbeat), among other things.

Norepinephrine is synthesized by tyrosine, an amino acid, through a series of steps in the adrenal medulla and part of the sympathetic nervous system. L-tyrosine is converted to L-DOPA, L-DOPA to dopamine, and dopamine to norepinephrine. Norepinephrine is then stored in synaptic vesicles where it stays until something stimulates the release. Once released norepinephrine can bind with adrenergic receptor sites that enable it to carry out its actions (increasing heart rate, respirations, releasing glucose, etc.).

Norepinephrine’s effects are then terminated by either the degradation of norepinephrine or its reuptake. However, there are many substances that either cause norepinephrine to be released or inhibit that release. There are also substances that influence the termination of norepinephrine’s effect on the cell.

Since, we know that norepinephrine, in the right amounts and at the right time, is essential for optimal mental and physical health, it warrants a brief overview of some of the ways its production and actions may be altered. I won’t get into the specifics of disease processes and treatments.

Just be aware that depression, anxiety, blood pressure problems, heart rate issues, and many other illness can be attributed, at least partially, to the deregulation of norepinephrine production and function in the body. 

 We’ll address the specifics of disease processes and treatments related to adrenal function in another article in the future, but I want you to have a basic understanding of how norepinephrine production and function might be changed.

First we need tyrosine available to make dopamine and eventually norepinephrine. If we don’t have enough of the raw materials we can’t make the hormone.

Tyrosine is considered a conditionally essential amino acid. Most of the time, we do not need to actually ingest foods high in tyrosine. We can use phenylalanine, another amino acid that must be ingested, to make tyrosine.  

However, if the diet is lacking in phenylalanine then tyrosine is considered essential and we will need either supplementation or diet to be changed to include foods higher in phenylalanine and tyrosine. Foods high in phenylalanine include meat, fish, and some dairy like cottage cheese.

Foods high in tyrosine include meat and dairy as well as bananas and seaweed.

I mentioned above there are substances that can influence or inhibit the release of norepinephrine from the synaptic vesicle. These are called release modulators and can be broken down into inhibitory and stimulatory modulators. 

Substances like dopamine, acetylcholine, norepinephrine itself, epinephrine, 5-HT, adenosine, histamine, ATP, and enkaphalin cause the body to reduce the release of norepinephrine.

This might seem weird since some of these are stress hormones and why would norepinephrine itself decrease its on release.

To put it simply, once the body has enough of these hormones circulating, it will down regulate the release of more in order to maintain or return to homeostasis. Epinephrine (tricky devil, playing both sides) and angiotensin II both increase norepinephrine release.

There are also substances that can alter the way norepinephrine’s actions are terminated, either by changing how norepinephrine binds with receptors or how it is taken up and out of the system.

The results can either be an increase or decrease of its actions causing increased or decreased circulating norepinephrine or an increase or decrease in its ability to bind to receptors an initiate its effects.

Drugs like cocaine, amphetamines, and antidepressants alter the reuptake of norepinephrine. Alpha and beta blockers (also drugs) alter how norepinephrine binds with receptors.

So, there’s a lot that can go wrong when you look at all the things that can interfere with proper production and function of norepinephrine.

We know that we want our norepinephrine production to be on point. Not too much. Not too little.
Without that balance we develop problems involving our moods, energy levels (adrenal fatigue), blood pressure, and more. All of which can negatively affect your fitness, ability to reach your goals, and ability to enjoy your workouts.


Quelle:  http://breakingmuscle.com/health-medicine/understanding-our-adrenal-system-norepinephrine
 



JÖRG LINDER AKTIV-TRAINING - www.aktiv-training.de
Mauerbergstraße 110
76534 Baden-Baden
Tel.: 07223 / 8004699
Mobil: 0177 / 4977232
Mail: info@aktiv-training.de
Fax: 07223 / 8005271 
Mobility-Walking: http://mobility-walking.blogspot.com
Personal Fitness: www.personal-fitness-4u.de

Glutens and Lectins: A Dangerous Dietary Duo

Artikel von:  Carolyn Pierini

Quelle: http://www.cpmedical.net/articles/glutens-and-lectins-a-dangerous-dietary-duo

Healthcare practitioners and patients alike are familiar with the increasing incidence and widening spectrum of gluten-related disorders. Although celiac disease is the national icon of gluten sensitivity, “atypical” presentations of the disease are rapidly becoming more common, as is the concept of non-celiac gluten sensitivity.

Presently, gluten sensitivity or intolerance might best be defined as a state of heightened immunological responsiveness in genetically susceptible people. Gluten-related issues represent another star in a constellation of growing public health concerns plaguing the U.S. population.

Gluten Sensitivity on the Rise

On the surface, celiac disease offers an easy model of epigenetic interplay—genetic predisposition (as HLA-DQ 2 or HLA-DQ 8) meets dietary trigger as wheat gluten. In reality, gluten sensitivity is more complex and better understood through the influence of diet and environment on epigenetic factors responsible for amplifying or silencing multiple genes.

Celiac disease represents one of at least 200 medical conditions, involving nearly every organ of the body, which are now being linked to gluten sensitivity.1 In people with celiac disease, however, the overall clinical picture is more severe and is accompanied by the concurrence of tissue transglutaminase autoantibodies.2 Transglutaminase enzymes are comprised of a family of eight enzymes found throughout the body, including prostate, skin, lungs, testicles and elsewhere. Because gluten triggers reactivity of this enzyme, all of these tissues can be potentially affected.
Moreover, newly published research, sometimes inconsistent, is unveiling the health effects of not only gluten, but other components of wheat and non-wheat grains. The fact is, modern-day grain science is in its infancy with regard to its impact on human health.

Given this, you, as clinicians, should understand why grain—and, in particular, wheat-related gastrointestinal and related disorders—may be increasing in your patient population.

Gluten Primer

The term “gluten” actually refers to a mixture of proteins found in many grains including wheat, spelt, rye and barley. Lectins, often included in this group, are technically not glutens, but are equally important proteins found in several food groups, including grains. Gluten literally means glue in Latin and is primarily composed of “storage” proteins called glutelins (glutenins) and prolamines (named for the high proline and glutamine content).

Gliadin is a type of prolamine and therefore a type of protein found in gluten. Gliadins constitute the majority of protein found in wheat and are thus far the most well-studied components of celiac disease.3 Different types of glutens and lectins can be found in grain.

Many people are also sensitive to glutens and lectins found in other non-wheat grain, particularly corn. Corn antibodies have been found in patients with celiac disease, Crohn’s disease and ulcerative colitis.4 Each seed or grain is composed of an outer bran layer, an endosperm that houses 90 percent of these prolamines, and the germ nucleus, which contains the developing plant embryo that will use the storage protein as a nitrogen source during germination.

The Wheat Has Changed

The rise of wheat sensitivity in general may reflect the convergence of many phenomena. The first point to consider is that modern commercial wheat bears little resemblance to the wheat that sustained our ancestors, which remained largely the same for 10,000 years... until recent years.
In the past few decades, agricultural science has and continues to use extensive hybridization, introgression and crossbreeding, making “synthetic” wheat plants that are more resistant to drought and pathogens. This has greatly increased dough properties but, more importantly, yield and profit.

Seeds are equipped with anti-nutrients such as lectin, gluten, phytates and enzymes to ensure protection from predation and resist digestion long enough to be spread across the land through excretion. Genetically selecting for anti-nutrients in an attempt to make the plant more resistant and less costly to grow appears to have added an increased threat to the gut immune system. New strains of wheat have undergone innumerable, drastic transformations in their genetic code yet, incredibly, no human or animal safety studies were performed to gauge their suitability for human or animal consumption.5

The hybridization process increases the quantity of genes for gluten proteins in modern wheat, including uniquely new gluten proteins not found in the parent plants. This process is likely contributing to gluten-related disease.6-8 Perhaps it should not be surprising that there is a naturally protective immune response to ingesting more of something that is specifically designed to resist digestion.5 To quote one gluten researcher, “If we view celiac disease not as an unhealthy response to a healthy food but a healthy response to an unhealthy food, classical celiac symptoms like diarrhea may make more sense.”9

A Hidden Culprit

Also, beware of assuming that the primary causes of wheat intolerance are directly attributable to gluten alone. In previous articles, we’ve exposed wheat lectin for the serious problem it is. The wheat seed embryo contains a tiny lectin called wheat germ agglutinin (WGA). It is largely responsible for many pervasive ill-effects of wheat consumption. WGA is inflammatory and capable of inflicting direct damage to the majority of tissues in the body. It may help explain why degenerative conditions are associated with heavy wheat-consuming populations, even when wheat sensitivities appear uncommon.

By nature, lectins are resilient and resist degradation. Thus soaking, sprouting, cooking and fermenting were historically implemented in an effort to make grains such as wheat more digestible. Being a powerful insecticide for the germinating seed, WGA has not escaped the attention of biotech firms, which create genetically modified plants with built-in WGA pest control.

As with gluten, selective breeding for particular proteins has unfortunately led to proportionate increases in the WGA content of modern-day wheat. The list of WGA-induced disruptions to health is extensive and a reminder of how important the understanding of lectins is.
Eating wheat delivers WGA to the gastrointestinal tract, where it can cause mucosal injury and initiate inflammatory imbalance. WGA is small enough to gain even greater access systemically through a leaky gut. Anything that increases intestinal permeability, such as gluten or NSAIDs, increases the likelihood of systemic inflammatory imbalance created by WGA.

Although currently under-appreciated, WGA will eventually get its share of the spotlight. In fact, some studies propose that WGA may contribute in the pathogenesis of celiac disease. For example, one of the hallmarks of celiac disease (crypt hyperplasia) appears to be due to WGA’s ability to mimic the growth-promoting effects of epidermal growth factor.10 While serological antibody testing for WGA is currently not performed, in one test study, antibodies to WGA were demonstrated in the serum of celiac patients.11

Our Love for Grains is Harming Us

A second point to consider is the sheer volume of ingested grain. In 2007, researchers in the United States, Italy and Great Britain hypothesized that the incidence of celiac disease was on the rise worldwide because wheat had become so prevalent in the Western diet that humans are actually overdosing on it.

It is true. Modern-day wheat is found in nearly everything we consume: cereal and flour-containing items, food and drink additives, grain-derived alcoholic beverages and even medications and cosmetics. This is exemplified by a 2005 study, which revealed that an unprecedented epidemic of symptomatic celiac disease in Sweden was at least half explained by an increase in infant exposure to comparatively large amounts of gluten as a result of national dietary recommendations and infant food content.12

Foundationally, microbial interactions in the gastrointestinal tract provide the cues for the development of regulated pro- and anti-inflammatory signals that promotes immunological tolerance.13 Doctors report that it is not uncommon to see patients with a conglomeration of gastrointestinal symptoms due to exposure to gluten and lectin of wheat and other grains.
The gliadin protein of gluten in all forms of wheat is capable of increasing intestinal permeability by triggering the release of zonulin, a protein that disassembles tight junctions between intestinal cells.14 Small intestine bacterial overgrowth (SIBO),15 gastroesophageal reflux disease16 and intestinal Candidiasis17-18 are all associated with gluten intolerance. Additionally, a 2009 research review in the Journal of Gastroenterology suggests that patients with irritable bowel syndrome (IBS) be genetically tested for gluten sensitivity, as symptom resolution was observed with wheat elimination.

The health consequences of consuming wheat extend beyond the immune system, making diagnosis complicated for physicians. For example, wheat exorphins exhibit addictive effects on the brain and nervous system, and wheat’s high glucose-insulin effects contribute to cardiovascular disorders, diabesity, hormone imbalance and acne.19-20 Complete removal of wheat or other grains is often necessary to deconstruct the clinical picture.

Gluten-Free Foods—Not Always the Perfect Answer

It is helpful to caution patients using “gluten-free” alternatives to replace the wheat proteins. In addition to being a source of insulin-provoking carbohydrate, alternatives such as sorghum, millet, corn, barley, oats or other grains and starches contain their own gluten/lectin proteins, which may cause problems in gluten-sensitive people.21-23

The majority of the population is not aware that their present health and weight problems have anything to do with environmental factors, and certainly not the iconic “healthy” whole grains. After all, Americans are encouraged by government and private groups, advertising and elements of the healthcare community to eat them at every sitting.

There is a looming public perception that if you don’t have celiac disease, you don’t have a wheat problem. However, the belief that modern grain is a healthy food is just not sufficiently supported by facts. Grain education to change deeply held convictions about food will be a formidable challenge, but a worthy one.

Resources
1. http://theglutensyndrome.net/primer.pdf.
2. Sapone A, et al. BMC Medicine. 2011;9:23.
3. www.glutenfreesociety.org.
4. Davidson IW, et al. Clin Exp Immunol. 1979 Jan;35(1):147-8.
5. Davis W. Wheat Belly. New York: Rodale. 2011 pg 14-30.
6. Song X, et al. Theor Appl Genet. 2009;118(2):213-25.
7. Gao X, et al. Planta. 2010;23(2):245-50.
8. Van den Broeck HC, et al. Theor Appl Genet. 2010;121(8):1527-39.
9. http://www.greenmedinfo.com/page/dark-side-wheat-new-perspectives-celiac-disease-wheat-intolerance-sayer-ji.
10. http://www.glutenfreesociety.org/gluten-free-society-blog/wheat-germ-agglutinin-wga/.
11. Sollid LM, et al. Clin. Exp. Immunol. 1986;63(1):95-100.
12. Ivarsson A, et al. Best Pract Res Clin Gastroenterol. 2005;19(3):425-40.
13. Vitetta L, et al. Inflammopharmacology. 2012 Mar 18.[Epub ahead of print].
14. Drago S, et al. Scand J Gastroenterol. 2006;41:408-19.
15. Rubio-Tapia A, et al. J Clin Gastroenterol. 2009;43(2):157-61.
16. Levine A, et al. Scand J Gastroenterol.2009;44(12):1424-8.
17. Nieuwenhuizen WF, et al. Lancet. 2003;361(9375):2152-4.
18. Staab JF, et al. Science. 1999;283(5407):1535-8.
19. Rudman SM, et al. J Invest Dermatol. 1997;109(6):770-7.
20. Cordain L, et al. Arch Dermatol. 2002;138:1584-90.
21. Kristjansson G, et al. Gut. 2005;54:769-74.
22. Sandhu JS, et al. Gut. 1983;24:825-30.
23. Troncone R, et al. J Pediatr Gastroenterol Nutr. 1987;6(3):346-50.
 
Quelle: http://www.cpmedical.net/articles/glutens-and-lectins-a-dangerous-dietary-duo





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