**********************************************************************
E stim for incontinenc e
**********************************************************************
Here are the abstracts for two articles about estim and leaky
bladders.
The bottom line is that a rectal probe or a vaginal probe to deliver
electrical stimulation to help strengthen pelvic floor muscles works.
It is like an electrified kegel exercise. It is uncomfortable, but
one controls how much electricity is delivered. I have used it, and
am using it now each day and have found it to be quite helpful.
A second method uses electrical stimulation to skin over the posterior
tibiliais nerve (by the ankle). That has been quite helpful as well,
but I have not personallly tried that version. I've pasted copies of
the abstracts from two articles talking about estim and incontinence.
You could take the abstracts to your physician and discuss possible
treatments with estim for your leaky bladdder if that is an issue for
you.
Although it is not yet approved for strengthening muscles to walk,
electrical stimulation of muscles is approved for strengthening
muscles to control one’s bladder. Treating a leaky bladder with
electrical stimulation works using a vaginal or rectal probe to
increase the strength of pelvic muscle works. Multiple studies have
shown this to be effective. The FDA has approved the use of such
devices. Minnova, manufactured by EMPI is one such device. If you
want to learn more – go to the EMPI web page.
Below is an abstract which one could take their physician or physical
therapist for more information to support the request to try e-stim
for incontence.
Treatment of urinary stress incontinence by intravaginal electrical
stimulation and pelvic floor physiotherapy
Amaro,J.L.
Int.Urogynecol.J.Pelvic.Floor.Dysfunct.
.Treatment of urinary stress incontinence (USI) by intravaginal
electrical stimulation (IES) and pelvic floor physiotherapy represents
an alternative to other therapies. The purpose of this work was to
evaluate the effectiveness of this treatment inpatients with urinary
incontinence. From January 1998 to May 2000, 30 women (mean age 54
years) were studied. All patients had USI and 70% urge incontinence;
average follow-up was 7 months. Selection criteria were based on
clinical history, objective evaluation of perineal musculature by
perineometry, and urodynamics. The treatment protocol consisted of
three sessions of IES per week for 14 weeks using INNOVA equipment.
Physiotherapy was initiated in the fifth week of IES. A significant
decrease in the number of micturitions and urgency was observed after
treatment ( P<0.01). The pad test showed a reduction in urinary
leakage from 13.9 to 5.9 g after treatment ( P<0.01). Objective
evaluation of perineal muscle strength showed a significant
improvement in all patients after treatment ( P<0.01). A positive
correlation was observed between maximum flow rate (Qmax) and all
three variables: urethral pressure profile at rest and on straining
(stop test), and abdominal leak-point pressure (ALPP). A positive
correlation was also observed between ALPP and the stop test. Over 100
different surgical and conservative treatments have been tried to
manage USI. The majority of these procedures reveal that despite
progress already made in this area, there is no ideal treatment.
Satisfactory results can be achieved with this method, especially with
patients who are reluctant to undergo surgery because of personal or
clinical problems.
Urodynamic effect of acute transcutaneous posterior tibial nerve
stimulation in overactive bladder
J.Urol. Amarenco,G 2003
PURPOSE: Of the various treatments proposed for urge incontinence,
frequency and urgency electrostimulation has been widely tested.
Different techniques have been used with the necessity of surgical
implantation (S3 neuromodulation or sacral root stimulation) or
without requiring surgery (perineal transcutaneous
electrostimulation). Recently peripheral electrical stimulation of the
posterior tibial nerve was proposed for irritative symptoms in first
intention or for intractable incontinence. Clinical studies have
demonstrated good results and urodynamic parameters were improved
after chronic treatment. However, to our knowledge no data concerning
acute stimulation and immediate cystometry modifications have been
reported. We verified urodynamic changes during acute posterior tibial
nerve stimulation. MATERIALS AND METHODS: A total of 44 consecutive
patients with urge incontinence, frequency and urgency secondary to
overactive bladder were studied. There were 29 women and 15 men with a
mean age +/-SD of 53.3 +/- 18.2 years. Of the patients 37 had detrusor
hyperreflexia due to multiple sclerosis (13), spinal cord injury (15)
or Parkinson's disease (9), and 7 had idiopathic detrusor instability.
Routine cystometry at 50 ml. per minute was done to select the
patients with involuntary detrusor contractions appearing before 400
ml. maximum filling volume. Repeat cystometry was performed
immediately after the first study during left posterior tibial nerve
stimulation using a surface self-adhesive electrode on the ankle skin
behind the internal malleolus with shocks in continuous mode at 10 Hz.
frequency and 200 milliseconds wide. Volume comparison was done at the
first involuntary detrusor contraction and at maximum cystometric
capacity. The test was considered positive if volume at the first
involuntary detrusor contraction and/or at maximum cystometric
capacity increased 100 ml. or 50% during stimulation in compared with
standard cystometry volumes. RESULTS: Mean first involuntary detrusor
contraction volume on standard cystometry was 162.9 +/- 96.4 ml. and
it was 232.1 +/- 115.3 ml. during posterior tibial nerve stimulation.
Mean maximum cystometric capacity on standard cystometry was 221 +/-
129.5 ml. and it was 277.4 +/- 117.9 ml. during stimulation. Posterior
tibial nerve stimulation was associated with significant improvement
in first involuntary detrusor contraction volume (p <0.0001) and
significant improvement in maximum cystometric capacity (p
<0.0001). The test was considered positive in 22 of the 44
patients. CONCLUSIONS: These results suggest an objective acute effect
of posterior tibial nerve stimulation on urodynamic parameters.
Improved bladder overactivity is an encouraging argument to propose
posterior tibial nerve stimulation as a noninvasive treatment modality
in clinical practice
Wednesday, September 9, 2009
Acrylamide - kills brain cells
We are getting too many toxins in our food.
I thought you would want to hear about Acrylamide.
Acrylamide - kills brain cells
Acrylamide is a potent neurotoxin. It is used experimentally to induce damage to brain and spinal cord in animal models of brain disorders. It is also present in our food. See the links to the National Cancer Institute.
It is used primarily in industrial process – especially making plastics. Most important to recognize is that it is also in our food, especially foods that are cooked at high temperature – such as fried foods. French fries, potato chips and other fried foods are at particular risk. This adds to the growing list of toxins in our food which are capable of damaging brain tissues.
Eating organic, and NOT frying one’s food is a good thing to do for your brain. Eating for your mitochondria will make it easier to for your body to excrete the toxins which show up in your food.
I thought you would want to hear about Acrylamide.
Acrylamide - kills brain cells
Acrylamide is a potent neurotoxin. It is used experimentally to induce damage to brain and spinal cord in animal models of brain disorders. It is also present in our food. See the links to the National Cancer Institute.
It is used primarily in industrial process – especially making plastics. Most important to recognize is that it is also in our food, especially foods that are cooked at high temperature – such as fried foods. French fries, potato chips and other fried foods are at particular risk. This adds to the growing list of toxins in our food which are capable of damaging brain tissues.
Eating organic, and NOT frying one’s food is a good thing to do for your brain. Eating for your mitochondria will make it easier to for your body to excrete the toxins which show up in your food.
Venous Insufficiency and MS
This a copy of press release on a meeting convened this week about the dramatic improvement in MS patients treated for venous sufficiency. The results suggest that venous blockages occur prior to the onset of symptoms and the severity of the blockages are strongly associated with the severity of the MS symptoms and rate of decline.
I knew you would want to know about this exciting news.
Venous blockages and MS
This is long - but it is a copy of the press release from a scientific meeting convened to discuss venous blockages in the setting of MS.
The bottom line is that maybe having procedures to evaluate for the presence of blockages in the blood vessels and repairing those blockages will someday soon replace taking immune modulating drugs like Tysabri. I still think nutrition will be very important. Although we may be born with the predisposition to develop blockages -- our diets, and our mother's diet coupled with the toxins in our environment may play a strong role in turning on the genes that cause blood vessels to be twisty and at risk of blockages. This is breaking news. Yet - genetics take hundreds of thousands of years to shift how our bodies are made. Shifts in diet and toxins can shift which genes are on and how our bodies are made in one generation. As dramatic as this news is, it does not change the critical role of feeding one's mitochondria and our brain cells with all the nutrients they need.
PRESS RELEASE
Bologna, Tuesday Sept. 8, 2009
FONDAZIONE HILARESCERE
Venous Function And Multiple Sclerosis
International Coterie
Four main points concerning the relationship between CCSVI and
MULTIPLE SCLEROSIS were covered by several experts at a Meeting in
Bologna. All the investigations that gave an answer to these 4
fundamental points were coordinated by Prof Paolo Zamboni who discovered CCSVI and its association with Multiple Sclerosis; in some other cases, research was carried out in cooperation between Prof Zamboni and major foreign Universities.
1) What is the origin of the extracranial cerebral vein stenoses which
characterize CCSVI?
2) Are there advanced diagnostic systems capable of identifying which
changes are caused by CCSVI in the central nervous system?
3) Can CCSVI be treated and how?
4) Can CCSVI therapy improve the clinical outcomes of MS and affect its
prognosis?
Venous Function And Multiple Sclerosis is an international coterie of
experts who met in Bologna on September 8 to discuss these issues from the
perspective of neurologists – who have developed the scientific body of
knowledge on MS – and the vascular and neurological surgeons who have
further investigated these topics following the discovery of CCSVI. All
investigations were coordinated by Professor Paolo Zamboni who discovered CCSVI and its association with multiple sclerosis.
This first study was conducted by an Italian research team composed of the
vascular surgeons’ group headed by Professor Paolo Zamboni from the
University of Ferrara and the neurologists’ group from the Department of
Neurosciences of the Bellaria Hospital in Bologna headed by Dr. Fabrizio
Salvi.
Fondazione Hilarescere is a foundation specially set up to provide adequate
means and resources for research into medical and scientific insights aimed at
fully understanding and curing diseases which are still partly unknown.
Fondazione HILARESCERE, chaired by Professor Fabio Roversi-Monaco, was
set up on an initiative of Fondazione Cassa di Risparmio in Bologna.
THE MOST IMPORTANT ANSWER OF ALL:
endovascular therapy has led to a decrease in the number of disease
relapses, a marked reduction in the number of active brain and spinal
lesions and also a clear-cut improvement in the patients’ quality of life.
Prof. Paolo Zamboni headed a study where, together with Dr. Fabrizio Salvi,
he was able to show that in patients with the clinical form of Relapsing-
Remitting MS – which is the most common – there is a drop in the number of
active lesions which persists up to 18 months after surgery. The percentage of
active lesions falls from 50% to 12%, thus showing that the additional
treatment of CCSVI reduces the aggressiveness of the disease. This finding is
further confirmed by the number of patients who showed no relapses after
endovascular surgery. In the 2 years before surgery, acute multiple sclerosis
attacks were found in 50% of the recruited patients, while in the 2 years
following surgery 73% of the patients had no more attacks, with a change in
the clinical course of the disease. In all these patients also cognitive and motor
activities – assessed by means of an outcome measure called MSFC - are
significantly and persistently improved while the same is not true for patients
with the progressive forms of the disease. In the latter, however, progression
was stopped and the patients’ quality of life improved.
________________
The experts discussed, provided data and gave an answer to all 4
fundamental questions:
1) What is the origin of the extracranial cerebral vein stenoses which
characterize CCSVI?
3 scientists answered this question from different perspectives: Professor
Byung B. Lee, Georgetown University School of Medicine di Washington DC,
showed that the malformations found in CCSVI are congenital truncular
malformations which therefore certainly precede the development of Multiple
Sclerosis. For this reason they cannot be regarded as a consequence of
Multiple Sclerosis. Prof. Lee showed in which phases of the venous system
development the malformations observed in CCSVI may appear. Byung B. Lee
is the Chairman of the World Consensus Conference which gathers vascular
experts from 47 countries and recently approved a scientific update on venous
malformations in Montecarlo. (1)Professor Giulio Gabbiani, Centre Médical Universitaire di Ginevra,demonstrated that there are no auto-immune phenomena in diseased veins thus excluding that the malformations found in CCSVI result from Multiple Sclerosis. He showed the results of a study which provides a histologic
comparison between the walls of the veins affected by CCSVI-MS and those of
normal subjects. Furthermore, at molecular level, CCSVI veins are structurally
different from those of the control subjects, thus confirming the approach of the
Montecarlo Consensus Conference. Prof. Gabbiani is one of the most important
world experts in microscopic vessel wall morphology. (2)
The third presentation was about whether – genetically speaking – these
malformations have any correlation with the findings so far obtained from the
genetic study of MS. Prof. Alessandra Ferlini, Director of the Institute of
Genetics at the University of Ferrara, discussed this point by presenting the
promising results of a pilot study. (3)2) Are there advanced diagnostic systems capable of identifying which changes are caused by CCSVI in the central nervous system? This is the second question addressed at the Meeting. Professor Mark Haacke,
Director of the MRI Istitute for Biomedical Research in Detroit (4,5,6) and
Professor Bianca Weinstock-Guttman, Neurologist at the Jacobs Neurological
Institute (7) showed new magnetic resonance (MRI) parameters linked to CCSVI which might in the future bring about a true revolution in the way of diagnosing MS. These new parameters include: quantification of iron deposits and volume assessment of intracranial veins and CSF. 3) The third question that was answered at the Meeting was: Can CCSVI be treated and how? Innovative minimally-invasive endovascular repair
techniques were discussed on account of the findings obtained by Dr. Roberto
Galeotti (8), Head of the Interventional Radiology Section at the University
Hospital of Ferrara who was the first in the world to perform this type of surgery,
and Dr. Michael Dake, Chief of Cardiovascular and Interventional Radiology at
Stanford University School of Medicine (California), who was the first to treat
CCSVI outside Italy. The most important finding is safety. At 2-year follow-up no major complications were observed. All surgical procedures were performed on a day hospital basis. Statistically, this treatment decreases pressure in the cerebral veins in a highly significant way, thus showing its enormous anti-inflammatory potential.(8)The risk of re-stenosis is 16 times higher in the jugular veins than in the azygos vein, thus pointing to the need for more sophisticated and efficient tools
to approach the former. Research will make such tools available during 2010.
4) The fourth and fundamental point is whether CCSVI therapy can improve
the clinical conditions of MS and affect its prognosis.
Dr. Fabrizio Salvi from the Bellaria Hospital in Bologna was the first
Neurologist who studied the clinical correlations of CCSVI treatment in
MS patients together with Prof. Paolo Zamboni. The patients enrolled in this
study were 120 from all clinical classes, but only the results of the 65 subjects
who are over 18 months from surgery will be reported in order to describe the
outcome with the greatest possible accuracy. Generally speaking, patients
treated with endovascular therapy showed a decrease in the number of
disease relapses, a marked reduction in the number of active brain and
spinal lesions and also a clear-cut improvement in the patients’ quality of
life. The findings of this investigations will soon be published in detail on the
Journal of Vascular Surgery (8).
Finally, Dr. Robert Zivadinov, Jacobs Neurogical Institute di Buffalo, discussed
the results of a revolutionary pilot study performed last year where both
American and Italian patients were blindly assessed in the USA by means of
advanced MRI technology, then submitted to vascular surgery in Italy and
followed up during the following year (9). This study was defined by the patients
who volunteered to participate as the study of the 50,000 miles for treatment,
because of the many trips they had to take overseas. This study was sponsored
by Fondazione Hilarescere.
References
(1) World Consensus Conference on Venous Malformations, Montecarlo
September 4th 2009. This document was approved by experts from 47 different
countries and will be published on all most important vascular surgery journals.
(2) G. Gabbiani, M. Coen, F. Mascoli, P. Zamboni. Manuscript in
preparation.
(3) A. Ferlini, M. Bovolenta, M. Neri, F. Gualandi, A.Yuryev, F. Salvi, A.
Liboni and P. Zamboni. Manuscript in preparation.
(4) Haacke EM, Makki M, Ge Y, Maheshwari M, Sehgal V, Hu J, Selvan M,
Wu Z, Latif Z, Xuan Y, Khan O, Garbern J, Grossman RI. Characterizing iron
deposition in multiple sclerosis lesions using susceptibility weighted imaging. J
Magn Reson Imaging. 2009;29:537-44.
(5) A. V. Singh and P. Zamboni Anomalous venous blood flow and iron
deposition in multiple sclerosis. J Cereb Blood Flow Metab. 2009 Sep 2. [Epub
ahead of print]
(6) P. Zamboni, E. Menegatti, B. Weinstock-Guttman, C. Schirda, J. L. Cox,
A. M. Malagoni, D. Hojnacki, C. Kennedy, E. Carl, M. G. Dwyer, N. Bergsland,
R. Galeotti, Sara Hussein, I. Bartolomei, F. Salvi, R. Zivadinov. The severity of
altered venous haemodynamics is related to CSF dynamics in chronic
cerebrospinal venous insufficiency Submitted To Current Neurovascular
Research
(7) P. Zamboni, E. Menegatti, B. Weinstock-Guttman, C. Schirda, J. L. Cox,
A. M Malagoni, D. Hojnacki, C. Kennedy, M. G. Dwyer, N. Bergsland, R.
Galeotti, I. Bartolomei, F. Salvi, M. Ramanathan, R. Zivadinov. Csf flow and
brain volume in multiple sclerosis are associated with altered cerebral venous
doppler haemodynamics. Study presented at the European Multiple Sclerosis
Congress ECTRIMS Düsseldorf, 9-12 September 2009
(8) P. Zamboni, R. Galeotti; E. Menegatti; A. M. Malagoni, S. Gianesini, I.
Bartolomei, F. Mascoli, F. Salvi Endovascular treatment of chronic
cerebrospinal venous insufficency. A prospective opern-label study. Journal of
Vascular Surgery, 2009, in press.
(9) P. Zamboni, R. Galeotti, B. Weinstock-Guttman, G. Cutter, E. Menegatti,
A. M. Malagoni, D. Hojnacki, J. L. Cox, C. Kennedy, I. Bartolomei, F. Salvi, R.
Zivadinov Endovascular Treatment for Chronic Cerebrospinal Venous
Insufficiency in Multiple Sclerosis . A longitudinal pilot study. Study presented at
the European Multiple Sclerosis Congress ECTRIMS Düsseldorf, 9-12
September 2009
Bologna, 8 September 2009
Press Office: Laboratorio delle idee – Francesca Rossini –
www.terrywahls.com
Although this is dramatic news, there are also press releases that indicate foods from the cabbage family influence how our blood vessels are shaped. That tells me that our nutrients influence how likely we are to develop chronic blockages which may lead to more aggressive MS. Once again, I think it is very important to have 3 cups of greens, cabbage family and onion family vegetables each day. To learn more about nutrition for mitochondria and brain check out my web site.
I knew you would want to know about this exciting news.
Venous blockages and MS
This is long - but it is a copy of the press release from a scientific meeting convened to discuss venous blockages in the setting of MS.
The bottom line is that maybe having procedures to evaluate for the presence of blockages in the blood vessels and repairing those blockages will someday soon replace taking immune modulating drugs like Tysabri. I still think nutrition will be very important. Although we may be born with the predisposition to develop blockages -- our diets, and our mother's diet coupled with the toxins in our environment may play a strong role in turning on the genes that cause blood vessels to be twisty and at risk of blockages. This is breaking news. Yet - genetics take hundreds of thousands of years to shift how our bodies are made. Shifts in diet and toxins can shift which genes are on and how our bodies are made in one generation. As dramatic as this news is, it does not change the critical role of feeding one's mitochondria and our brain cells with all the nutrients they need.
PRESS RELEASE
Bologna, Tuesday Sept. 8, 2009
FONDAZIONE HILARESCERE
Venous Function And Multiple Sclerosis
International Coterie
Four main points concerning the relationship between CCSVI and
MULTIPLE SCLEROSIS were covered by several experts at a Meeting in
Bologna. All the investigations that gave an answer to these 4
fundamental points were coordinated by Prof Paolo Zamboni who discovered CCSVI and its association with Multiple Sclerosis; in some other cases, research was carried out in cooperation between Prof Zamboni and major foreign Universities.
1) What is the origin of the extracranial cerebral vein stenoses which
characterize CCSVI?
2) Are there advanced diagnostic systems capable of identifying which
changes are caused by CCSVI in the central nervous system?
3) Can CCSVI be treated and how?
4) Can CCSVI therapy improve the clinical outcomes of MS and affect its
prognosis?
Venous Function And Multiple Sclerosis is an international coterie of
experts who met in Bologna on September 8 to discuss these issues from the
perspective of neurologists – who have developed the scientific body of
knowledge on MS – and the vascular and neurological surgeons who have
further investigated these topics following the discovery of CCSVI. All
investigations were coordinated by Professor Paolo Zamboni who discovered CCSVI and its association with multiple sclerosis.
This first study was conducted by an Italian research team composed of the
vascular surgeons’ group headed by Professor Paolo Zamboni from the
University of Ferrara and the neurologists’ group from the Department of
Neurosciences of the Bellaria Hospital in Bologna headed by Dr. Fabrizio
Salvi.
Fondazione Hilarescere is a foundation specially set up to provide adequate
means and resources for research into medical and scientific insights aimed at
fully understanding and curing diseases which are still partly unknown.
Fondazione HILARESCERE, chaired by Professor Fabio Roversi-Monaco, was
set up on an initiative of Fondazione Cassa di Risparmio in Bologna.
THE MOST IMPORTANT ANSWER OF ALL:
endovascular therapy has led to a decrease in the number of disease
relapses, a marked reduction in the number of active brain and spinal
lesions and also a clear-cut improvement in the patients’ quality of life.
Prof. Paolo Zamboni headed a study where, together with Dr. Fabrizio Salvi,
he was able to show that in patients with the clinical form of Relapsing-
Remitting MS – which is the most common – there is a drop in the number of
active lesions which persists up to 18 months after surgery. The percentage of
active lesions falls from 50% to 12%, thus showing that the additional
treatment of CCSVI reduces the aggressiveness of the disease. This finding is
further confirmed by the number of patients who showed no relapses after
endovascular surgery. In the 2 years before surgery, acute multiple sclerosis
attacks were found in 50% of the recruited patients, while in the 2 years
following surgery 73% of the patients had no more attacks, with a change in
the clinical course of the disease. In all these patients also cognitive and motor
activities – assessed by means of an outcome measure called MSFC - are
significantly and persistently improved while the same is not true for patients
with the progressive forms of the disease. In the latter, however, progression
was stopped and the patients’ quality of life improved.
________________
The experts discussed, provided data and gave an answer to all 4
fundamental questions:
1) What is the origin of the extracranial cerebral vein stenoses which
characterize CCSVI?
3 scientists answered this question from different perspectives: Professor
Byung B. Lee, Georgetown University School of Medicine di Washington DC,
showed that the malformations found in CCSVI are congenital truncular
malformations which therefore certainly precede the development of Multiple
Sclerosis. For this reason they cannot be regarded as a consequence of
Multiple Sclerosis. Prof. Lee showed in which phases of the venous system
development the malformations observed in CCSVI may appear. Byung B. Lee
is the Chairman of the World Consensus Conference which gathers vascular
experts from 47 countries and recently approved a scientific update on venous
malformations in Montecarlo. (1)Professor Giulio Gabbiani, Centre Médical Universitaire di Ginevra,demonstrated that there are no auto-immune phenomena in diseased veins thus excluding that the malformations found in CCSVI result from Multiple Sclerosis. He showed the results of a study which provides a histologic
comparison between the walls of the veins affected by CCSVI-MS and those of
normal subjects. Furthermore, at molecular level, CCSVI veins are structurally
different from those of the control subjects, thus confirming the approach of the
Montecarlo Consensus Conference. Prof. Gabbiani is one of the most important
world experts in microscopic vessel wall morphology. (2)
The third presentation was about whether – genetically speaking – these
malformations have any correlation with the findings so far obtained from the
genetic study of MS. Prof. Alessandra Ferlini, Director of the Institute of
Genetics at the University of Ferrara, discussed this point by presenting the
promising results of a pilot study. (3)2) Are there advanced diagnostic systems capable of identifying which changes are caused by CCSVI in the central nervous system? This is the second question addressed at the Meeting. Professor Mark Haacke,
Director of the MRI Istitute for Biomedical Research in Detroit (4,5,6) and
Professor Bianca Weinstock-Guttman, Neurologist at the Jacobs Neurological
Institute (7) showed new magnetic resonance (MRI) parameters linked to CCSVI which might in the future bring about a true revolution in the way of diagnosing MS. These new parameters include: quantification of iron deposits and volume assessment of intracranial veins and CSF. 3) The third question that was answered at the Meeting was: Can CCSVI be treated and how? Innovative minimally-invasive endovascular repair
techniques were discussed on account of the findings obtained by Dr. Roberto
Galeotti (8), Head of the Interventional Radiology Section at the University
Hospital of Ferrara who was the first in the world to perform this type of surgery,
and Dr. Michael Dake, Chief of Cardiovascular and Interventional Radiology at
Stanford University School of Medicine (California), who was the first to treat
CCSVI outside Italy. The most important finding is safety. At 2-year follow-up no major complications were observed. All surgical procedures were performed on a day hospital basis. Statistically, this treatment decreases pressure in the cerebral veins in a highly significant way, thus showing its enormous anti-inflammatory potential.(8)The risk of re-stenosis is 16 times higher in the jugular veins than in the azygos vein, thus pointing to the need for more sophisticated and efficient tools
to approach the former. Research will make such tools available during 2010.
4) The fourth and fundamental point is whether CCSVI therapy can improve
the clinical conditions of MS and affect its prognosis.
Dr. Fabrizio Salvi from the Bellaria Hospital in Bologna was the first
Neurologist who studied the clinical correlations of CCSVI treatment in
MS patients together with Prof. Paolo Zamboni. The patients enrolled in this
study were 120 from all clinical classes, but only the results of the 65 subjects
who are over 18 months from surgery will be reported in order to describe the
outcome with the greatest possible accuracy. Generally speaking, patients
treated with endovascular therapy showed a decrease in the number of
disease relapses, a marked reduction in the number of active brain and
spinal lesions and also a clear-cut improvement in the patients’ quality of
life. The findings of this investigations will soon be published in detail on the
Journal of Vascular Surgery (8).
Finally, Dr. Robert Zivadinov, Jacobs Neurogical Institute di Buffalo, discussed
the results of a revolutionary pilot study performed last year where both
American and Italian patients were blindly assessed in the USA by means of
advanced MRI technology, then submitted to vascular surgery in Italy and
followed up during the following year (9). This study was defined by the patients
who volunteered to participate as the study of the 50,000 miles for treatment,
because of the many trips they had to take overseas. This study was sponsored
by Fondazione Hilarescere.
References
(1) World Consensus Conference on Venous Malformations, Montecarlo
September 4th 2009. This document was approved by experts from 47 different
countries and will be published on all most important vascular surgery journals.
(2) G. Gabbiani, M. Coen, F. Mascoli, P. Zamboni. Manuscript in
preparation.
(3) A. Ferlini, M. Bovolenta, M. Neri, F. Gualandi, A.Yuryev, F. Salvi, A.
Liboni and P. Zamboni. Manuscript in preparation.
(4) Haacke EM, Makki M, Ge Y, Maheshwari M, Sehgal V, Hu J, Selvan M,
Wu Z, Latif Z, Xuan Y, Khan O, Garbern J, Grossman RI. Characterizing iron
deposition in multiple sclerosis lesions using susceptibility weighted imaging. J
Magn Reson Imaging. 2009;29:537-44.
(5) A. V. Singh and P. Zamboni Anomalous venous blood flow and iron
deposition in multiple sclerosis. J Cereb Blood Flow Metab. 2009 Sep 2. [Epub
ahead of print]
(6) P. Zamboni, E. Menegatti, B. Weinstock-Guttman, C. Schirda, J. L. Cox,
A. M. Malagoni, D. Hojnacki, C. Kennedy, E. Carl, M. G. Dwyer, N. Bergsland,
R. Galeotti, Sara Hussein, I. Bartolomei, F. Salvi, R. Zivadinov. The severity of
altered venous haemodynamics is related to CSF dynamics in chronic
cerebrospinal venous insufficiency Submitted To Current Neurovascular
Research
(7) P. Zamboni, E. Menegatti, B. Weinstock-Guttman, C. Schirda, J. L. Cox,
A. M Malagoni, D. Hojnacki, C. Kennedy, M. G. Dwyer, N. Bergsland, R.
Galeotti, I. Bartolomei, F. Salvi, M. Ramanathan, R. Zivadinov. Csf flow and
brain volume in multiple sclerosis are associated with altered cerebral venous
doppler haemodynamics. Study presented at the European Multiple Sclerosis
Congress ECTRIMS Düsseldorf, 9-12 September 2009
(8) P. Zamboni, R. Galeotti; E. Menegatti; A. M. Malagoni, S. Gianesini, I.
Bartolomei, F. Mascoli, F. Salvi Endovascular treatment of chronic
cerebrospinal venous insufficency. A prospective opern-label study. Journal of
Vascular Surgery, 2009, in press.
(9) P. Zamboni, R. Galeotti, B. Weinstock-Guttman, G. Cutter, E. Menegatti,
A. M. Malagoni, D. Hojnacki, J. L. Cox, C. Kennedy, I. Bartolomei, F. Salvi, R.
Zivadinov Endovascular Treatment for Chronic Cerebrospinal Venous
Insufficiency in Multiple Sclerosis . A longitudinal pilot study. Study presented at
the European Multiple Sclerosis Congress ECTRIMS Düsseldorf, 9-12
September 2009
Bologna, 8 September 2009
Press Office: Laboratorio delle idee – Francesca Rossini –
www.terrywahls.com
Although this is dramatic news, there are also press releases that indicate foods from the cabbage family influence how our blood vessels are shaped. That tells me that our nutrients influence how likely we are to develop chronic blockages which may lead to more aggressive MS. Once again, I think it is very important to have 3 cups of greens, cabbage family and onion family vegetables each day. To learn more about nutrition for mitochondria and brain check out my web site.
School lunch changes to make it healthier
This is from the Slow Foods movement --
While not directly related to MS -- the issue of how we feed our children has direct impact on their future risk of MS.
See the notes below.
Dear members, supporters and friends,
On Labor Day, more than 20,000 people came together in all 50 states to tell Congress it's time to give kids real food at school. If you went to an Eat-In, we'd like to say thank you. And if you're one of the Slow Food Chapter Leaders and Eat-In Organizers who put incredible time and energy into the 300 Eat-Ins that took place nationwide, we'd like to shout thank you -- you made the day possible.
Check out some of the incredible photos: http://www.flickr.com/photos/ tags/timeforlunch/.
The momentum helped us surpass our Labor Day petition goal - there are more than 20,000 signatures online, another 10,000 on paper, and many more still coming in. That's a huge show of support. When Congress starts debating the Child Nutrition Act this fall, we'll be able to take those signatures to legislators and make a strong case for reform.
In the meantime, please take a moment to share some of the photos and stories of the Eat-Ins with your friends, and invite them to get involved. This movement is growing stronger by the day, and there will be plenty to do in the next phase of the Time for Lunch campaign.
P.S. The Day of Action is over, but the "Give More If You Can, Less If You Can't"membership offer lasts through the month of September. Make sure to tell your friends why it's a good time to be joining our movement for change.
Thank you,
Josh, Brian, Jerusha, Gordon, Deena, Emily
The Time for Lunch Team
timeforlunch@slowfoodusa.org
While not directly related to MS -- the issue of how we feed our children has direct impact on their future risk of MS.
See the notes below.
Dear members, supporters and friends,
On Labor Day, more than 20,000 people came together in all 50 states to tell Congress it's time to give kids real food at school. If you went to an Eat-In, we'd like to say thank you. And if you're one of the Slow Food Chapter Leaders and Eat-In Organizers who put incredible time and energy into the 300 Eat-Ins that took place nationwide, we'd like to shout thank you -- you made the day possible.
Check out some of the incredible photos: http://www.flickr.com/photos/ tags/timeforlunch/.
The momentum helped us surpass our Labor Day petition goal - there are more than 20,000 signatures online, another 10,000 on paper, and many more still coming in. That's a huge show of support. When Congress starts debating the Child Nutrition Act this fall, we'll be able to take those signatures to legislators and make a strong case for reform.
In the meantime, please take a moment to share some of the photos and stories of the Eat-Ins with your friends, and invite them to get involved. This movement is growing stronger by the day, and there will be plenty to do in the next phase of the Time for Lunch campaign.
P.S. The Day of Action is over, but the "Give More If You Can, Less If You Can't"membership offer lasts through the month of September. Make sure to tell your friends why it's a good time to be joining our movement for change.
Thank you,
Josh, Brian, Jerusha, Gordon, Deena, Emily
The Time for Lunch Team
timeforlunch@slowfoodusa.org
Monday, September 7, 2009
MInding My Mitochondria
Minding My Mitochondria
By Dr. Terry L. Wahls
Dr. Wahls is an academic general internal medicine physician who has secondary progressive multiple sclerosis. Her MS confined her to a life of dependence on a tilt-recline wheelchair for four years. Eighteen months after starting her intensive, focused nutrition and electrical therapy to strengthen her muscles, Dr. Wahls now commutes to work five miles each day on her bicycle.
Minding My Mitochondria is a clear and concise explanation of the biochemistry that drives our brains and how the food we eat is linked to the health we do or do not have. Dr. Wahls teaches us how our brain cells work, the building blocks our cells need to do the work of living, and how to eat to ensure you have enough of them.
If you have a neurological or a psychological problem improving the health of your mitochondria will help your brain. If you have a chronic medical problem, improving the health of your mitochondria will help your body.
This book reveals the interventions, and the science behind them, that Dr. Wahls has used to restore her own health and the physical and mental health of her patients. Over 40 brain health recipes are included!
I.S.B.N. 13: 978-0-9821750-9-5
I.S.B.N. 10: 0-9821750-9-4
Publisher: TZ Press
119 pages
CONTENTS
Chapter 1. The Beginning
Chapter 2. Mitochondria
Chapter 3. Cellular Function and Brain Health
Chapter 4. Micronutrients, Supplements, and Food sources
Chapter 5. Neuro-protection
Chapter 6. Food Matters and MS
Chapter 7. Recipes
Chapter 8. The Synergy between Neuromuscular Electrical Stimulation and Nutrition
Chapter 9. Frequently Asked Questions--and Answers
Chapter 10. Conclusion
Photographs
Nutrient and Function Chart
Abbreviations
Glossary
References
Excerpt
Chapter 1. The Beginning
Rising costs of health care is crushing us. It’s not just old people getting diabetes, heart disease, arthritis, and cancers that are adding the cost of healthcare. Nearly a third of our children have serious medical problems like autism, depression, learning disabilities, obesity, or pre-diabetes. In addition to the exploding costs of health care, productivity of the American worker is falling because of declining worker health. Despite all the money spent on health care, we, and our children, are progressively less well.
Why is this happening to us? Have our genes gone bad? After all scientists are identifying more genes associated with chronic disease each day. Are mutations transforming our strong, lean bodies into obese, chronically diseased ones, or is there something else going on that is causing this change in the health our country?
I think the explanation for what has happening can be found in the corn fields of Iowa. When you buy seed corn, all the kernels have essentially the same DNA. The way farmers know what kind of crop to expect in the fall. Say the farmer plants half of the bag of seed corn in black Iowa soil and the other half in a trash heap filled with clay, plastic debris, and rock. Return in the fall to harvest the corn. The corn planted in the black dirt will be tall with three ears of corn on every plant. But the corn in the trash heap will look diseased. Instead of being dark green, the corn stalks will yellowed, stunted and barely three feet tall. Very few will have an ear of corn. If they do, only a few kernels will be present on tiny nubbins. It was the same DNA in both fields. But the black Iowa dirt was filled with the nutrients the corn’s DNA needed. The trash heap lacked nutrients, and you saw the results.
All moving things, including our bodies, break down with time. Fortunately, our bodies have tiny little maintenance workers who are busy repairing all the little wear-and-tear damage that occurs each day. Our DNA provides the blueprint for all the proteins and other stuff that needs to be replaced. If those little maintenance workers don’t have the all the building blocks, that is, the correct minerals, amino acids, and fatty acids, then trouble happens. They can’t make things according to the DNA blueprints. Those replacement molecules and structures get made not at all, or incorrectly, and we begin to deteriorate.
By Dr. Terry L. Wahls
Dr. Wahls is an academic general internal medicine physician who has secondary progressive multiple sclerosis. Her MS confined her to a life of dependence on a tilt-recline wheelchair for four years. Eighteen months after starting her intensive, focused nutrition and electrical therapy to strengthen her muscles, Dr. Wahls now commutes to work five miles each day on her bicycle.
Minding My Mitochondria is a clear and concise explanation of the biochemistry that drives our brains and how the food we eat is linked to the health we do or do not have. Dr. Wahls teaches us how our brain cells work, the building blocks our cells need to do the work of living, and how to eat to ensure you have enough of them.
If you have a neurological or a psychological problem improving the health of your mitochondria will help your brain. If you have a chronic medical problem, improving the health of your mitochondria will help your body.
This book reveals the interventions, and the science behind them, that Dr. Wahls has used to restore her own health and the physical and mental health of her patients. Over 40 brain health recipes are included!
I.S.B.N. 13: 978-0-9821750-9-5
I.S.B.N. 10: 0-9821750-9-4
Publisher: TZ Press
119 pages
CONTENTS
Chapter 1. The Beginning
Chapter 2. Mitochondria
Chapter 3. Cellular Function and Brain Health
Chapter 4. Micronutrients, Supplements, and Food sources
Chapter 5. Neuro-protection
Chapter 6. Food Matters and MS
Chapter 7. Recipes
Chapter 8. The Synergy between Neuromuscular Electrical Stimulation and Nutrition
Chapter 9. Frequently Asked Questions--and Answers
Chapter 10. Conclusion
Photographs
Nutrient and Function Chart
Abbreviations
Glossary
References
Excerpt
Chapter 1. The Beginning
Rising costs of health care is crushing us. It’s not just old people getting diabetes, heart disease, arthritis, and cancers that are adding the cost of healthcare. Nearly a third of our children have serious medical problems like autism, depression, learning disabilities, obesity, or pre-diabetes. In addition to the exploding costs of health care, productivity of the American worker is falling because of declining worker health. Despite all the money spent on health care, we, and our children, are progressively less well.
Why is this happening to us? Have our genes gone bad? After all scientists are identifying more genes associated with chronic disease each day. Are mutations transforming our strong, lean bodies into obese, chronically diseased ones, or is there something else going on that is causing this change in the health our country?
I think the explanation for what has happening can be found in the corn fields of Iowa. When you buy seed corn, all the kernels have essentially the same DNA. The way farmers know what kind of crop to expect in the fall. Say the farmer plants half of the bag of seed corn in black Iowa soil and the other half in a trash heap filled with clay, plastic debris, and rock. Return in the fall to harvest the corn. The corn planted in the black dirt will be tall with three ears of corn on every plant. But the corn in the trash heap will look diseased. Instead of being dark green, the corn stalks will yellowed, stunted and barely three feet tall. Very few will have an ear of corn. If they do, only a few kernels will be present on tiny nubbins. It was the same DNA in both fields. But the black Iowa dirt was filled with the nutrients the corn’s DNA needed. The trash heap lacked nutrients, and you saw the results.
All moving things, including our bodies, break down with time. Fortunately, our bodies have tiny little maintenance workers who are busy repairing all the little wear-and-tear damage that occurs each day. Our DNA provides the blueprint for all the proteins and other stuff that needs to be replaced. If those little maintenance workers don’t have the all the building blocks, that is, the correct minerals, amino acids, and fatty acids, then trouble happens. They can’t make things according to the DNA blueprints. Those replacement molecules and structures get made not at all, or incorrectly, and we begin to deteriorate.
Tuesday, September 1, 2009
Glutathione reduced in brains of MS patients
More articles are confirming my theory that oxidative stress, a marker for sick mitochondria, are an important driver in progressive or worsening MS. A recent article was published in "Science Direct" which found that glutathione is present in statistically smaller amounts in the brains of people with MS than age matched controls. That is consistent with my theory that oxidative stress is a problem for many with MS.
The abstact is posted below.
Detection of glutathione (GSH) is technically challenging at clinical field strengths of 1.5 or 3 T due to its low concentration in the human brain coupled with the fact that conventional single-echo acquisitions, typically used for magnetic resonance (MR) spectroscopy acquisitions, cannot be used to resolve GSH given its overlap with other resonances. In this study, an MR spectral editing scheme was used to generate an unobstructed detection of GSH at 7 T. This technique was used to obtain normative white (WM) and gray matter (GM) GSH concentrations over a two-dimensional region. Results indicated that GSH was significantly higher (P<.001) in GM relative to WM in normal subjects. This finding is consistent with previous radionuclide experiments and histochemical staining and validates this 7 T MR spectroscopy technique. To our knowledge, this is the first study to report normative differences in WM and GM glutathione concentrations in the human brain. Glutathione is a biomarker for oxidative status and this non-invasive in vivo measurement of GSH was used to explore its sensitivity to oxidative state in multiple sclerosis (MS) patients. There was a significant reduction (P<.001) of GSH between the GM in MS patients and normal controls. No statistically significant GSH differences were found between the WM in controls and MS patients. Reduced GSH was also observed in a MS WM lesion. This preliminary investigation demonstrates the potential of this marker to probe oxidative state in MS.
How does one reduce oxidative stress? Eat 9 cups of vegetables and fruit. Three cups of cruciferous vegetables (especially kale or collards), 1 to 2 cups of onion, garlic and or mushrooms and 3 cups of brightly colored vegetables and fruit.
More details on how to improve one's oxidative status and health of one's mitochondria can be found in my book, Minding My Mitochondria. I've have just gotten it back from the printers and so it is now available on my web site www.terrywahls.com. The book reviews how the mitochondria support brain health, remove toxins and the key nutrients needed for optimal mitochondrial health. It also has 40 plus recipes which are mitochondria and brain healthy.
The abstact is posted below.
Detection of glutathione (GSH) is technically challenging at clinical field strengths of 1.5 or 3 T due to its low concentration in the human brain coupled with the fact that conventional single-echo acquisitions, typically used for magnetic resonance (MR) spectroscopy acquisitions, cannot be used to resolve GSH given its overlap with other resonances. In this study, an MR spectral editing scheme was used to generate an unobstructed detection of GSH at 7 T. This technique was used to obtain normative white (WM) and gray matter (GM) GSH concentrations over a two-dimensional region. Results indicated that GSH was significantly higher (P<.001) in GM relative to WM in normal subjects. This finding is consistent with previous radionuclide experiments and histochemical staining and validates this 7 T MR spectroscopy technique. To our knowledge, this is the first study to report normative differences in WM and GM glutathione concentrations in the human brain. Glutathione is a biomarker for oxidative status and this non-invasive in vivo measurement of GSH was used to explore its sensitivity to oxidative state in multiple sclerosis (MS) patients. There was a significant reduction (P<.001) of GSH between the GM in MS patients and normal controls. No statistically significant GSH differences were found between the WM in controls and MS patients. Reduced GSH was also observed in a MS WM lesion. This preliminary investigation demonstrates the potential of this marker to probe oxidative state in MS.
How does one reduce oxidative stress? Eat 9 cups of vegetables and fruit. Three cups of cruciferous vegetables (especially kale or collards), 1 to 2 cups of onion, garlic and or mushrooms and 3 cups of brightly colored vegetables and fruit.
More details on how to improve one's oxidative status and health of one's mitochondria can be found in my book, Minding My Mitochondria. I've have just gotten it back from the printers and so it is now available on my web site www.terrywahls.com. The book reviews how the mitochondria support brain health, remove toxins and the key nutrients needed for optimal mitochondrial health. It also has 40 plus recipes which are mitochondria and brain healthy.
Subscribe to:
Posts (Atom)