Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,991 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
I don't necessarily trust this since it involves Shai Efrati. Shai Efrati has a bias, he is the director of the Sagol Center for Hyperbaric Medicine and Research at the Yitzhak Shamir Medical Center in Israel. Since this is available in few places and is expensive, I have no desire to try this.
Hard HBOT in a hyperbaric clinic typically costs $250 per session, or $10,000 for 40 sessions. Thus, the standard HBOT protocol costs $20,000 for 80 sessions.
And you don't want to smoke in one of these. Google this for risks: hyperbaric oxygen therapy deaths.
Shai Efrati is a physician from Israel and an associate
professor at the Sackler Faculty of Medicine and the Sagol School of
Neuroscience at Tel Aviv University as well as director of the Sagol
Center for Hyperbaric Medicine and Research at the Yitzhak Shamir
Medical Center in Israel.
Stroke remains a leading cause of long-term disability, with limited recovery potential during the chronic phase. Hyperbaric oxygen therapy has shown promise in promoting neuroplasticity and functional recovery through mechanisms such as the hyperoxic-hypoxic paradox.
Case presentation
We report the case of a 45-year-old Arabic male who experienced a left-sided hemorrhagic stroke and presented with persistent neurological deficits 15 months post-event. He exhibited right hemiparesis, impaired gait requiring a wheelchair, and cognitive dysfunction. The patient underwent 83 sessions of hyperbaric oxygen therapy over 16 weeks (2.0 ATA, 90 minutes with air breaks). Pre- and postintervention assessments included neurological and cognitive evaluations alongside advanced imaging: diffusion tensor imaging and Single photon emission computed tomography. Clinically, the patient showed marked improvements in muscle strength, spasticity, balance, and walking—progressing from wheelchair dependence to ambulation with a quadruped cane. Cognitive testing demonstrated improved attention, verbal memory, and processing speed. Imaging findings supported these changes: diffusion tensor imaging showed increased fractional anisotropy in major white matter tracts, and single photon emission computed tomography demonstrated significant perfusion increases in the right motor cortex (+ 15.83%) and right frontal lobe (+ 15.92%).
Conclusion
This case highlights hyperbaric oxygen therapy’s potential to facilitate recovery in chronic post-stroke stages by enhancing neuroplasticity and neurovascular function in nonnecrotic brain regions. Advanced imaging techniques, such as diffusion tensor imaging and single photon emission computed tomography, provide valuable insights into treatment efficacy and may support personalized therapeutic protocols in the future.
I don't necessarily trust this since it involves Shai Efrati. Shai Efrati has conflicts, he is the director
of the Hyperbaric Oxygen Institute at the Assaf Harofeh Medical Center.
Since this is available in few places and is expensive I'll have to wait
for something simpler.
Hard HBOT in a hyperbaric clinic typically costs $250 per session, or $10,000 for 40 sessions. Thus, the standard HBOT protocol costs $20,000 for 80 sessions.
Dr.Efrati
is Founder and Director of the world-leading Sagol Center for
Hyperbaric Medicine and Research at Shamir Medical Center, where he also
serves as Director of Research and Development and Head of Nephrology.
The
case report evaluated the patient’s hand motor function and functional
MRI after HBOT, and analysis revealed improvements in motor function,
brain activation and inter-hemispheric connectivity
ORLANDO, Fla., Oct. 02, 2023 (GLOBE NEWSWIRE) -- Aviv Clinics,
one of the world’s most advanced brain clinics, shares the results of a
new case report showing a unique hyperbaric oxygen therapy (HBOT)
protocol was effective for improving hand motor function in a chronic
post-stroke patient.
The
case report evaluated the effect of a unique HBOT protocol to induce
motor rehabilitation in a chronic post-stroke patient with severe
upper-limb motor impairment. The patient was a 61-year-old right-handed
male patient who was suffering with right hemiparesis (physical weakness
or the inability to move one side of the body) two years after his
stroke. The case report analyzed the patient’s functional MRI (fMRI) to
evaluate the neural response mechanisms and functional reorganization of
the patient’s brain following HBOT. The fMRIs were evaluated pre- and
post-HBOT treatment, which included 60 daily sessions over 12 weeks. The
patient’s motor function was assessed at baseline and after treatment
using the Fugl–Meyer assessment (FMA), a validated post-stroke
assessment, and the handgrip maximum voluntary contraction (MVC).
Results
of the case report showed that following the HBOT protocol, the
patient’s FMA score improved from 17 (severe impairment) to 31 (moderate
impairment), and there was an increase in fMRI activation in both the
supplementary motor cortex (SMA) and the premotor cortex (PMA),
bilaterally. Additionally, analysis showed increased connectivity
between the two hemispheres and between specific regions in the
hemisphere which was not injured.
“In our
current healthcare system, the focus is on teaching chronic stroke
patients how to compensate and live with their post-stroke symptoms
rather than stimulating neuroplasticity to recover and heal those
symptoms,” said Dr. Amir Hadanny, Chief Medical Officer at Aviv
Scientific and Chief Medical Research Officer at the Sagol Center. “With
the specific HBOT protocol that we’re using, we see evidence that we
can repair brain connectivity and see real improvements in post-stroke
symptoms. Stroke patients shouldn’t have to settle for coping with their
symptoms; there may be hope and a true possibility for recovery and
improvement.”
HBOT is a medical treatment in
which 100% oxygen is administered at an increased environmental
pressure. Aviv’s unique HBOT protocol, the hyperoxic-hypoxic paradox,
fluctuates oxygen levels during treatment and is being used to repair
and regenerate damaged brain tissue in several types of brain injuries
including stroke, traumatic brain injury, PTSD, long COVID and
age-related cognitive decline, among others. A previous study from the
research team at the Sagol Center for Hyperbaric Medicine and Research
has demonstrated the efficacy of HBOT for improving neurocognitive function in post-stroke patients. Another randomized prospective study from this group reported significant neurological function and quality of life changes compared to the control group.
Aviv
Clinics offers an advanced treatment program with a multidisciplinary
team of medical experts providing patients with top-line care with the
goal of improving their quality of life. The Aviv Medical Program
includes an in-depth assessment of the patient’s physical and
neurological condition to assess their overall health. For patients that
meet the criteria, the Aviv team prepares a comprehensive, personalized
treatment schedule combining HBOT with cognitive and physical training
and dietary coaching, for a holistic approach to patient health. The
HBOT sessions are conducted in state-of-the-art multiplace chambers that
are comfortable, safe and allow for medical staff to accompany patients
during the treatment. The elevated pressure in the HBOT chamber creates
an optimal oxygenation condition, ultimately providing damaged brain
and body tissues the environment necessary to heal.
The full study is available here. For more on Aviv Clinics, visit aviv-clinics.com.
About Aviv Clinics Aviv Clinics
is the leader in the research and treatment of age-related cognitive
and functional decline and novel applications of hyperbaric oxygen
therapy (HBOT) to maximize human performance. Based on an exclusive
partnership with the world’s largest hyperbaric medicine and research
facility, the Sagol Center at Shamir Medical Center in Israel, Aviv is
introducing a global network of clinics delivering the most effective
evidence-based treatment of age-related decline—the Aviv Medical
Program. The three-month regimen was developed based on over a decade of
research and thousands of patients treated worldwide under the
scientific leadership of Shai Efrati, M.D., chair of Aviv Scientific’s
Medical Advisory Board and director of the Sagol Center.
I don't necessarily trust this since it
was done by Shai Efrati. Shai Efrati has conflicts, he is the director
of the Hyperbaric Oxygen Institute at the Assaf Harofeh Medical Center. Since this is available in few places and is expensive I'll have to wait for something simpler.
Hard HBOT in a hyperbaric clinic typically costs $250 per session, or $10,000 for 40 sessions. Thus, the standard HBOT protocol costs $20,000 for 80 sessions.
Alzheimer’s disease could be delayed or even reversed by giving oxygen therapy to patients in pressurised chambers, a new study suggests.
In
a world first, Israeli researchers found that elderly patients with
Mild Cognitive Impairment – a forerunner to dementia – had improved
memory and brain functioning following regular 90-minute sessions in a hyperbaric chamber.
The
pressure change allows more oxygen to be dissolved into the tissues and
mimics a state of "hypoxia", or oxygen shortage, which is known to have
regenerating effects.
In separate animal studies, the researchers also showed that the therapy can help clear away sticky amyloid plaques in the brain which stop cells from communicating, and are a major sign of Alzheimer’s disease.
The team believes that the treatment works by changing the structure of vessels in the brain so that more blood can get through.
Prof
Uri Ashery, of the Sackler School of Medicine, at Tel Aviv University,
said: “We have discovered for the first time that hyperbaric oxygen
therapy induces degradation and clearance of pre-existing amyloid
plaques, and the appearance of newly formed plaques.
“Elderly
patients suffering from significant memory loss at baseline revealed an
increase in brain blood flow and improvement in cognitive performance,
demonstrating hyperbaric oxygen therapy's potency to reverse core
elements responsible for the development of Alzheimer’s disease.”
Although
experts said the findings needed to be replicated in a larger trial and
that such therapy may be difficult to offer at scale, they said it
could open new doors in using oxygen therapy for the treatment of
dementia.
“The paper presents an interesting approach, in
particular reminding us of the importance of vascular factors in the
development not only of vascular dementia but Alzheimer’s disease too,”
said Tom Dening, professor of dementia research at University of
Nottingham.
Dr Richard Oakley, the head of research at the Alzheimer’s Society added: “Dementia is now the UK’s biggest killer, with someone developing it every three minutes.
“Research
is essential to improve care and find new treatments for the 850,000
people in the UK with dementia, set to reach 1.6 million by 2040.”
Cure for dementia could lie in the air we breathe
For
decades, scientists across the globe have struggled to find a drug that
could prevent or reverse dementia, coming up with ever-more complex
molecules to try to dampen the devastating impacts.
Yet the answer may be simpler than anyone thought: oxygen.
A
study from Tel Aviv University has shown that placing patients with
Mild Cognitive Impairment (MCI) in a hyperbaric chamber boosts blood
flow in the brain, flooding vessels with oxygen and improving memory,
attention and processing speed.
Many people diagnosed with MCI go on to develop Alzheimer’s, so it may be the first treatment that could prevent such a decline.
Finding
a therapy which could stop the disease in its tracks has never been
more needed, as there are currently 850,000 people living with dementia
in Britain, and the figure is expected to rise to one million by 2025.
Although the first drug for Alzheimer’s – Aducanumab – was approved by the US earlier this year, there are fears it will not live up to expectations outside of clinical trials.
Hyperbaric therapy
In
contrast to a drug, hyperbaric therapy works by giving patients pure
oxygen through a mask while inside a pressurised chamber. It is a
similar high pressure environment used to help divers to recover from the bends.
The
pressure change allows more oxygen to be dissolved into the tissues and
mimics a state of "hypoxia", or oxygen shortage, which is known to have
regenerating effects.
Reduced blood flow to the brain, and the
decrease in oxygen that it brings, is known to precede the onset of
dementia and the level of flow directly correlates with the degree of
cognitive impairment in Alzheimer’s. So, it makes sense to think that
improving blood flow might also improve the condition.
Improved memory and attention
In
the new study, six elderly patients were given oxygen inside a chamber
for 90 minutes, five days a week over the course of three months. The
results showed that the blood flow in the brain had increased by 16 to
23 per cent.
At the same time, memory test scores improved by 16.5
per cent, attention by six per cent, and information processing speed
was boosted by 10.3 per cent.
Researchers believe that treatment
not only improves levels of oxygen in the brain, but actually changes
the structure of blood vessels, increasing their width and reducing wall
thickness. It suggests that the beneficial effects may last for some
time after the treatment.
Testing on mice
Although the
therapy has not yet been tested on patients with Alzheimer’s disease,
when scientists tried it on mice with Alzheimer’s they found it reduced
the number of amyloid plaques by up to 30 per cent, shrank remaining
plaques by 18 per cent, and prevented the reemergence of new ones.
The
sticky plaques are believed to prevent brain cells from communicating,
and are one of the major targets in drugs for Alzheimer's.
The mice even started building better nests after the treatment, and navigated mazes more proficiently.
Prof
Uri Ashery, of the Sackler School of Medicine, at Tel Aviv University,
said: “Elderly patients suffering from significant memory loss at
baseline revealed an increase in brain blood flow and improvement in
cognitive performance, demonstrating hyperbaric oxygen therapy's potency
to reverse core elements responsible for the development of Alzheimer’s
disease.”
In 2020, the same team showed that hyperbaric therapy
can reverse the ageing process, lengthening telomeres (the protective
carps at the end of chromosomes) by 20 per cent.
It also reduced senescent, or dormant, cells by up to 37 per cent, making way for new healthy cells to regrow.
As
well as cognitive improvements, patients undergoing therapy have also
reported improved physical abilities such as increased energy, stamina
and even sexual performance, in men.
Few hospitals can offer hyperbaric treatment
However,
there is a drawback. Few hospitals are able to offer hyperbaric
treatment and the current therapy comes with a gruelling timetable of
sessions.
“Presumably to be useful, the treatment would have to be
continued indefinitely, so any patients would have to be very highly
motivated and have good transport links to the treatment facility,” said
Tom Dening, professor of Dementia Research, University of Nottingham.
“If
we consider that the number of people with dementia in the UK is
approaching one million, it is hard to see how hyperbaric oxygen could
ever be available on this scale.
“In short, it’s an interesting idea but a long way off meeting the usual criteria to become a standard treatment.”
But
it does open a new avenue for treating the disease. Oxygen delivering
drugs are already in development for heart conditions and may also be
useful for dementia.
“The paper presents an interesting approach,
in particular reminding us of the importance of vascular factors in the
development not only of vascular dementia but Alzheimer’s disease too,”
added Prof Dening.
Clinical trials needed
Alzheimer’s
charities said that further larger trials were needed to really know if
the treatment is effective but that therapies which prevent dementia in
the first place may end up being the most useful.
Dr Susan
Kohlhaas, the director of research, Alzheimer’s Research UK, said: “Many
of the Alzheimer’s treatments that are currently being tested are drugs
that target the hallmark disease proteins directly, but it’s important
we maintain a broad spectrum of potential approaches.
“Larger
scale clinical trials with many more people are needed to ascertain
whether this treatment is effective, particularly when measuring longer
term benefits to memory and thinking.
“We know the diseases that
cause dementia begin in the brain many years before symptoms like memory
loss show and it’s likely for treatments to be effective at slowing
down the diseases that cause dementia, they need to be given earlier
rather than later.”
The Israeli study is part of a larger research
program looking to reverse ageing and its accompanying ailments and the
team say that further trials will take place shortly.
For now,
the research is a tantalising glimpse that hope may be on the horizon
for the treatment of Alzheimer’s and that it may come from the most
unlikely source. The air that we breathe.
I don't necessarily trust this since it was done by Shai Efrati. Shai Efrati has conflicts, he is the director of the Hyperbaric Oxygen Institute at the Assaf Harofeh Medical Center.
Aging is characterized by the progressive
loss of physiological capacity. At the cellular level, two key
hallmarks of the aging process include telomere length (TL) shortening
and cellular senescence. Repeated intermittent hyperoxic exposures,
using certain hyperbaric oxygen therapy (HBOT) protocols, can induce
regenerative effects which normally occur during hypoxia. The aim of the
current study was to evaluate whether HBOT affects TL and senescent
cell concentrations in a normal, non-pathological, aging adult
population.
Methods:
Thirty-five healthy independently living adults, aged 64 and
older, were enrolled to receive 60 daily HBOT exposures. Whole blood
samples were collected at baseline, at the 30th and 60th
session, and 1-2 weeks following the last HBOT session. Peripheral
blood mononuclear cells (PBMCs) telomeres length and senescence were
assessed.
Results:
Telomeres length of T helper, T cytotoxic, natural killer
and B cells increased significantly by over 20% following HBOT. The most
significant change was noticed in B cells which increased at the 30th session, 60th session and post HBOT by 25.68%±40.42 (p=0.007), 29.39%±23.39 (p=0.0001) and 37.63%±52.73 (p=0.007), respectively.
There was a significant decrease in the number of senescent T helpers
by -37.30%±33.04 post-HBOT (P<0.0001). T-cytotoxic senescent cell
percentages decreased significantly by -10.96%±12.59 (p=0.0004)
post-HBOT.
In conclusion, the study indicates that HBOT may induce significant
senolytic effects including significantly increasing telomere length and
clearance of senescent cells in the aging populations.
Introduction
Aging can be characterized by the progressive loss of
physiological integrity, resulting in impaired functions and
susceptibility for diseases and death. This biological deterioration is
considered a major risk factor for cancer, cardiovascular diseases,
diabetes and Alzheimer’s disease among others. At the cellular level,
there are two key hallmarks of the aging process: shortening of telomere
length and cellular senescence [1].
Telomeres are tandem nucleotide repeats located at the
end of the chromosomes which maintain genomic stability. Telomeres
shorten during replication (mitosis) due to the inherent inability to
fully replicate the end part of the lagging DNA strand [2].
Telomere length (TL), measuring between 4 to 15 kilobases, gradually
shorten by ~20-40 bases per year and is associated with different
diseases, low physical performance and cortical thinning of the brain [3–5]. When TL reaches a critical length, cells cannot replicate and progress to senescence or programmed cell death [6]. Goglin et al. demonstrated that adults with shorter TLs have increased mortality rates [7].
Shortened TLs can be a direct inherited trait, but several
environmental factors have also been associated with shortening TL
including stress, lack of physical endurance activity, excess body mass
index, smoking, chronic inflammation, vitamins deficiency and oxidative
stress [2, 8, 9].
Cellular senescence is an arrest of the cell cycle which can be caused by telomere shortening [10], as well as other aging associated stimuli independent of TL such as non-telomeric DNA damage [1].
The primary purpose of senescence is to prevent propagation of damaged
cells by triggering their elimination via the immune system. The
accumulation of senescent cells with aging reflects either an increase
in the generation of these cells and/or a decrease in their clearance,
which in turn aggravates the damage and contributes to aging [1].
A growing body of research has found several pharmacological agents that can reduce the telomere shortening rate [11, 12].
Several lifestyle interventions including endurance training, diets and
supplements targeting cell metabolism and oxidative stress have
reported relatively small effects (2-5%) on TL3, [2, 8, 9].
Hyperbaric oxygen therapy (HBOT) utilizes 100% oxygen in
an environmental pressure higher than one absolute atmospheres (ATA) to
enhance the amount of oxygen dissolved in body’s tissues. Repeated
intermittent hyperoxic exposures, using certain HBOT protocols, can
induce physiological effects which normally occur during hypoxia in a
hyperoxic environment, the so called hyperoxic-hypoxic paradox [13–16].
In addition, it was recently demonstrated that HBOT can induce
cognitive enhancements in healthy aging adults via mechanisms involving
regional changes in cerebral blood flow [17].
On the cellular level, it was demonstrated that HBOT can induce the
expression of hypoxia induced factor (HIF), vascular endothelial growth
factor (VEGF) and sirtuin (SIRT), stem cell proliferation, mitochondrial
biogenesis, angiogenesis and neurogenesis [18]. However, no study to date has examined HBOT’s effects on TL and senescent cell accumulation.
The aim of the current study was to evaluate whether HBOT affects TL and senescence-like T-cells population in aging adults.
Results
Thirty-five individuals were assigned to HBOT. Five
patients did not complete baseline assessments and were excluded. All 30
patients who completed baseline evaluations completed the
interventions. Due to the low quality of blood samples (low number of
cells or technician error), four patients were excluded from the
telomere analysis and 10 patients from senescent cell analysis (Figure 1). The baseline characteristics and comparison of the cohorts following exclusion of the patients are provided in Table 1. There were no significant differences between the three groups (Table 1).
Figure 1.Patient flowchart.
Table 1. Baseline characteristics.
HBOT
Telomere analysis
Senescent analysis
P-value
N
30
25 (83.3%)
20 (66.6%)
Age (years)
68.41±13.2
67.56±14.35
66.70±16.00
0.917
BMI
26.77±3.20
26.89±3.34
27.14±3.81
0.946
Males
16 (53.3%)
13 (52.0%)
10 (50.0%)
0.987
Females
14 (47.7%)
12 (48.0%)
10 (50.0%)
0.987
Complete blood count
Hemoglobin
6.33±1.25
6.57±1.15
6.58±1.29
0.707
White blood cells
14.02±1.40
13.92±1.35
13.97±1.49
0.969
%PBMC
39.96±6.75
39.25±6.64
38.59±6.63
0.774
Platelets
239.87±1.39
244.08±43.0
254.05±41.4
0.559
Chronic medical conditions
Atrial fibrillation
4 (13.3%)
4 (16.0%)
2 (10.0%)
0.841
Hypothyroidism
4 (13.3%)
4 (16.0%)
3 (15.8%)
0.956
Obstructive sleep apnea
4 (13.3%)
4 (16.0%)
3 (15.0%)
0.961
Asthma
1 (3.3%)
1 (4.0%)
0
0.680
BPH
7 (23.3%)
5 (20.0%)
6 (30.0%)
0.733
GERD
3 (10%)
2 (8.0%)
2 (10.0%)
0.961
Osteoporosis
5 (16.7%)
5 (20.0%)
4 (20.0%)
0.936
Rheumatic arthritis
1 (3.3%)
0
1 (5.0%)
0.561
Osteoarthritis
7 (23.3%)
4 (16.0%)
5 (25.0%)
0.755
Diabetes mellitus
3 (10%)
3 (12.0%)
2 (10.0%)
0.966
Hypertension
7 (23.3%)
5 (20.0%)
5 (25.0%)
0.918
Dyslipidemia
16 (53.3%)
14 (56.0%)
12 (60.0%)
0.897
Ischemic heart disease
2 (6.7%)
1 (4.0%)
2 (10.0%)
0.725
History of smoking
10 (33.3%)
8 (32.0%)
7 (35.0%)
0.978
Chronic medications
Anti-aggregation
8 (26.7%)
6 (24.0%)
5 (25.0%)
0.974
ACE-Inhibitors/ARB blockers
6 (20%)
6 (24.0%)
6 (30.0%)
0.720
Beta blockers
5 (16.7%)
5 (20.0%)
3 (15.0%)
0.901
Calcium blockers
3 (10%)
3 (12.0%)
2 (10.0%)
0.966
Alpha blockers
7 (23.3%)
5 (20.0%)
6 (30.0%)
0.733
Diuretics
2 (6.7%)
1 (4.0%)
1 (5.0%)
0.906
Statins
10 (33.3%)
9 (36.0%)
7 (35.0%)
0.978
Oral hypoglycemic
1 (3.3%)
1 (4.0%)
1 (5.0%)
0.958
Bisphosphonates
1 (3.3%)
1 (4.0%)
1 (5.0%)
0.958
Proton pump inhibitors
3 (10%)
3 (12.0%)
3 (15.0%)
0.726
Hormones
3 (10%)
3 (12.0%)
2 (10.0%)
0.966
Benzodiazepines
3 (10%)
2 (8.0%)
1 (5.0%)
0.816
SSRI
5 (16.7%)
5 (20.0%)
3 (15.0%)
0.990
Telomere length
Compared to the baseline, the T-helper telomere lengths were significantly increased at the 30th session and post-HBOT by 21.70±40.05 (p=0.042), 23.69%±39.54 (p=0.012) and 29.30±38.51 (p=0.005), respectively (Figure 2). However, repeated measures analysis shows a non-significant trend (F=4.663, p=0.06, Table 2 and Figure 2).
Figure 2.Telomere length changes with HBOT. Mean+SEM *p<0.05, **p<0.01, ***p<0.001.
Table 2. Telomere length and senescent cell changes post-HBOT.
Absolute changes
Relative changes (%)
Repeated measures F (p)
PBMC
Baseline
30th Session
60th Session
Post HBOT
30th session
60th session
Post-HBOT
PBMC ((N=25)
2.55±0.53
-0.15±0.40
-4.91±16.70
1.987 (t) 0.09
PBMC (N=20)
2.50±0.53
-0.13±0.31
-4.21±11.99
1.810 (t) 0.07
Relative telomeres length (N=25)
Natural killer
9.27±1.91
11.77±5.14 (0.045)
10.73±2.73 (0.013)
11.75±4.22 (0.06)
25.02±51.42
20.56±33.35
22.16±44.81
0.812 (0.391)
B-cells
8.36±2.02
10.22±3.04 (0.007)
11.23±3.58 (0.0001)
11.17±2.98 (0.007)
25.68±40.42
29.39±23.39
37.63±52.73
7.390 (0.017)
T Helper
8.04±1.82
9.92±3.68 (0.042)
9.63±2.17 (0.012)
10.20±2.77 (0.005)
21.70±40.05
23.69±39.54
29.30±38.51
4.663 (0.063)
T Cytotoxic
8.26±1.54
9.83±4.08 (0.11)
10.08±3.33 (0.019)
10.15±2.74 (0.023)
18.29±45.62
24.13±40.88
19.59±33.98
1.159 (0.310)
Senescent cells (% of T cells) (N=20)
T Helper
10.29±5.42
7.84±7.09 (0.09)
8.51±7.45 (0.20)
6.22±4.88 (<0.0001)
-19.66±80.03
-11.67±94.30
-37.30±33.04
8.548 (0.01)
T Cytotoxic
52.19±21.07
45.53±19.91 (<0.0001)
45.45±18.81 (0.002)
46.59±21.91 (0.0004)
-12.21±8.74
-9.81±9.50
-10.96±12.59
6.916 (0.018)
P-values shown in () compared to baseline.
P-values in bold <0.05.
Compared to baseline, telomere lengths of B cells increased significantly at the 30th session, 60th session and post-HBOT by 25.68%±40.42 (p=0.007), 29.39%±23.39 (p=0.0001) and 37.63%±52.73 (p=0.007), respectively (Figure 2). Repeated measures analysis shows a significant within-group effect (F=0.390, p=0.017, Table 2 and Figure 2).
Compared to baseline, natural killer cells telomer lengths significantly increased at the 30th session (p=0.045) and at the 60th session by 20.56% ±33.35 (p=0.013). Post-HBOT, telomere lengths increased by 22.16%±44.81 post-HBOT (p=0.06, Table 2 and Figure 2). Repeated measures analysis indicates that there was no additional significant effect after the 30th session (F=0.812, p=0.391).
Compared to baseline, cytotoxic T-cells had a non-significant increase at the 30th session by 18.29%±45.62 (p=0.11), followed by a significant increase of 24.13%±40.88 at the 60th
session (p=0.0019) and 19.59%±33.98 post-HBOT (p=0.023). Repeated
measures analysis indicates that there was no additional significant
effect after the 30th session (F=1.159, p=0.310, Table 2 and Figure 2).
Senescent cells
There was a non-significant decrease in the number of senescent T-helpers at the 30th session and 60th
session by -19.66%±80.03 (p=0.09) and -11.67%±94.30 (p=0.20)
respectively. However, there was a significant drop in the number of
senescent T helpers by -37.30%±33.04 post-HBOT (P<0.0001, Figure 3). Repeated measures analysis showed a significant continuous effect even after the 30th session, with a within-group effect (F=8.547, p=0.01, Table 2 and Figure 3).
I would trust this piece from Dana before the puff piece from HBOT pushers(Efrati). Your doctor can decipher the competing claims. http://dana.org/news/features/detail.aspx?id=41174 While many agree that
Efrati’s data are promising, a prior study run by the U.S. Air Force
found no significant differences between hyperbaric oxygen treatment and
a sham treatment on patients with mild traumatic brain injury (TBI).Both groups showed significant improvement over the course of the trial. Those results were published in the November 2012 issue of the Journal of Neurotrauma.
Researchers have revisited hyperbaric oxygen sessions as a possible
treatment for brain damage sustained after a concussion. According to a
report compiled for Congress by the Centers for Disease Control
(CDC), in a single year, approximately 2.2 million emergency room
visits were for traumatic brain injuries (TBI). The majority of these
injuries are considered mild and are commonly called concussions. These
injuries are common in contact sports and in soldiers.
Most individuals who suffer a concussion are able to heal back to
normal brain activity, yet up to five percent of sufferers can
experience long-term symptoms. This is called post-concussion syndrome
and it can manifest with headaches, mood changes, and other cognitive
problems. The symptoms are caused by damage to blood vessels in the
brain, making it more difficult for the organ to receive adequate
oxygen.
A study published in 2013
showed that treating post-concussion syndrome patients with pure oxygen
significantly improved cognitive function and quality of life for
participants. Research conducted by a team at Tel-Aviv University in
Israel, which was published in the journal Frontiers in Human Neuroscience,shows
exactly how this treatment heals the brain. Shai Efrati, the lead
researcher explained that “Once the extra oxygen diffuses into damaged
areas, it supplies energy and the regenerative process can happen.” The
extra oxygen helped to regrow blood vessels and nerve fibers.
Athletes in contact sports are at a high-risk of suffering concussions. Image Credit: West Point
The “Sham” Was a Sham
This treatment was previously tested in 2015 by researchers at the
University of Utah. They concluded that the treatment was not effective.
However, their conclusions were based on a faulty interpretation of
their supposed “sham” treatment. The researchers subjected a group of
participants to a pressurized chamber with normal levels of oxygen.
These patients also showed improved cognitive function, so the
researchers concluded that the treatment was no more effective than
breathing normally.
However, the researchers did not account for the higher pressure
actually allowing more oxygen to enter the brain, thus performing along
the same lines as the patients who were actually receiving the active
treatment. “It was meant to be a sham treatment, but it was actually an
active treatment,” says Efrati.
Using hyperbaric oxygen treatments for post-concussion syndrome still
needs to be approved by the FDA. More research is needed to confirm its
safety and efficacy. However, should the treatment prevail, it will be
the first to tackle the underlying causes of the syndrome, as opposed to
treating individual symptoms.
I'm not sure I trust this. At least one of the authors, Dr. Shai Efrati, is directly associated with Head of the Hyperbaric Unit at Assaf Harofeh Medical Center. Using SPECT scan to prove anything may be worthless.
You will notice it doesn't say anything about recovery, only 'increased neuronal activity'. That is a huge red flag stating that this hasn't proven anything.
While many agree that
Efrati’s data are promising, a prior study run by the U.S. Air Force
found no significant differences between hyperbaric oxygen treatment and
a sham treatment on patients with mild traumatic brain injury (TBI).Both groups showed significant improvement over the course of the trial.
Shai Efrati has conflicts, he is the director of the Hyperbaric Oxygen Institute at the Assaf Harofeh Medical Center. Without reading the complete article I wouldn't trust this because 6 of them work for the
Hyperbaric Oxygen Institute. They believe because they have to believe.
Traumatic
brain injury (TBI) is the leading cause of death and disability in the
US. Approximately 70-90% of the TBI cases are classified as mild, and up
to 25% of them will not recover and suffer chronic neurocognitive
impairments. The main pathology in these cases involves diffuse brain
injuries, which are hard to detect by anatomical imaging yet noticeable
in metabolic imaging. The current study tested the effectiveness of
Hyperbaric Oxygen Therapy (HBOT) in improving brain function and quality
of life in mTBI patients suffering chronic neurocognitive impairments.
Methods and Findings
The
trial population included 56 mTBI patients 1–5 years after injury with
prolonged post-concussion syndrome (PCS). The HBOT effect was evaluated
by means of prospective, randomized, crossover controlled trial: the
patients were randomly assigned to treated or crossover groups. Patients
in the treated group were evaluated at baseline and following 40 HBOT
sessions; patients in the crossover group were evaluated three times: at
baseline, following a 2-month control period of no treatment, and
following subsequent 2-months of 40 HBOT sessions. The HBOT protocol
included 40 treatment sessions (5 days/week), 60 minutes each, with 100%
oxygen at 1.5 ATA. “Mindstreams” was used for cognitive evaluations,
quality of life (QOL) was evaluated by the EQ-5D, and changes in brain
activity were assessed by SPECT imaging. Significant improvements were
demonstrated in cognitive function and QOL in both groups following HBOT
but no significant improvement was observed following the control
period. SPECT imaging revealed elevated brain activity in good agreement
with the cognitive improvements.
Conclusions
HBOT
can induce neuroplasticity leading to repair of chronically impaired
brain functions and improved quality of life in mTBI patients with
prolonged PCS at late chronic stage.
You will notice it doesn't say anything about recovery, only 'increased neuronal activity'. That is a huge red flag stating that this hasn't proven anything. http://www.jewishvoiceny.com/index.php?option=com_content&view=article&id=3022:tau-research-team-discovers-new-treatment-for-stroke&catid=114:parsha&Itemid=297
A doctor at Tel Aviv University has come up with a new treatment for
stroke and other issues that can restore significant neurological
function even years after the initial event.
Dr. Shai Efrati, a member of TAU’s Sackler Faculty of Medicine,
theorized that high levels of oxygen could reinvigorate dormant neurons
in brain tissue chronically damaged by stroke, traumatic brain injury
and metabolic disorder.
The conditions are major causes of brain damage and permanent
disabilities such as motor dysfunction, psychological problems, memory
loss, outright dementia and more. Current treatments and rehabilitation
programs can help patients to heal, but with limited success.
He and colleagues Prof. Eshel Ben-Jacob of TAU’s School of Physics
and Astronomy and the Sagol School of Neuroscience recruited 74
post-stroke patients, 6 to 36 months after the injury, whose condition
had stopped improving, for hyperbaric oxygen therapy (HBOT).
The treatment involved 40 two-hour sessions five times a week in a
high pressure chamber that contains oxygen-rich air which increases
oxygen levels in the body ten-fold.
The findings of Efrati’s study, published in PloS ONE, showed
significantly increased neuronal activity after a group of affected
patients received two months of hyperbaric treatment, compared to a
group that received none, he said.
The study “opens the gate into a new territory of treatment,” said
Efrati. “It is now understood that many brain disorders are related to
inefficient energy supply to the brain. HBOT treatment could right such
metabolic abnormalities before the onset of full dementia, where there
is still potential for recovery.”
Shai Efrati has conflicts, he is the director of the Hyperbaric Oxygen Institute at the Assaf Harofeh Medical Center.
Without reading the complete article I wouldn't trust this because 6 of them work for the
Hyperbaric Oxygen Institute. They believe because they have to believe.
The way to objectively prove this would be fMRIs before and after. You would be able to see lit up areas that were formerly dark. So simple to do but why isn't it done? http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0053716#abstract0
Abstract
Background
Recovery
after stroke correlates with non-active (stunned) brain regions, which
may persist for years. The current study aimed to evaluate whether
increasing the level of dissolved oxygen by Hyperbaric Oxygen Therapy
(HBOT) could activate neuroplasticity in patients with chronic
neurologic deficiencies due to stroke.
Methods and Findings
A
prospective, randomized, controlled trial including 74 patients (15
were excluded). All participants suffered a stroke 6–36 months prior to
inclusion and had at least one motor dysfunction. After inclusion,
patients were randomly assigned to "treated" or "cross" groups. Brain
activity was assessed by SPECT imaging; neurologic functions were
evaluated by NIHSS, ADL, and life quality. Patients in the treated group
were evaluated twice: at baseline and after 40 HBOT sessions. Patients
in the cross group were evaluated three times: at baseline, after a
2-month control period of no treatment, and after subsequent 2-months of
40 HBOT sessions. HBOT protocol: Two months of 40 sessions (5
days/week), 90 minutes each, 100% oxygen at 2 ATA. We found that the
neurological functions and life quality of all patients in both groups
were significantly improved following the HBOT sessions while no
improvement was found during the control period of the patients in the
cross group. Results of SPECT imaging were well correlated with clinical
improvement. Elevated brain activity was detected mostly in regions of
live cells (as confirmed by CT) with low activity (based on SPECT) –
regions of noticeable discrepancy between anatomy and physiology.
Conclusions
The
results indicate that HBOT can lead to significant neurological
improvements in post stroke patients even at chronic late stages. The
observed clinical improvements imply that neuroplasticity can still be
activated long after damage onset in regions where there is a brain
SPECT/CT (anatomy/physiology) mismatch.
