Saturday, September 8, 2012
5 Weird Medical Tests You Can Try Right Now and fail at
I failed Romberg's Test at the hospital although I can pass it now.
I can't tell if I failed Finger Measurement Test because I can't get my left hand into that position. Right hand looks ok.
I failed the Nose Test at the hospital with my left hand and still fail it(I must be constantly intoxicated, damn that red wine and dark beer)
I failed the Heel Test at the hospital with my left leg and still fail it today because my leg spasticity doesn't allow me to bend my knee.
I failed The "Prayer Position" Test and the Pinky Tests because I can't even flatten my left hand at all.
http://health.yahoo.net/articles/healthcare/photos/5-weird-medical-tests-you-can-try-right-now#0
I can't tell if I failed Finger Measurement Test because I can't get my left hand into that position. Right hand looks ok.
I failed the Nose Test at the hospital with my left hand and still fail it(I must be constantly intoxicated, damn that red wine and dark beer)
I failed the Heel Test at the hospital with my left leg and still fail it today because my leg spasticity doesn't allow me to bend my knee.
I failed The "Prayer Position" Test and the Pinky Tests because I can't even flatten my left hand at all.
http://health.yahoo.net/articles/healthcare/photos/5-weird-medical-tests-you-can-try-right-now#0
Study looks at rhythms of the brain
May be useful for our visual deficits so ask your researcher what it means for your rehab.
http://therapytoronto.ca/news/?p=5938
http://therapytoronto.ca/news/?p=5938
Combination of blood thinning drugs shown to be ineffective as stroke preventer
You have to read the complete article because they refer to lacunar strokes. This is for your doctor to consider so if they don't ask about it tell them.
http://www.healthcanal.com/brain-nerves/32026-Combination-blood-thinning-drugs-shown-ineffective-stroke-preventer.html
An international team led by a neurologist at the University of British Columbia and Vancouver Coastal Health has shown that a combination of aspirin and clopidogrel, both common blood thinners, does not prevent recurrence of a common type of stroke, and may even pose serious risks.
Combining aspirin and clopidogrel (known commercially as Plavix) was thought to hold promise in preventing recurring lacunar strokes – the death of brain cells caused by a narrowing of small blood vessels – by reducing the formation of clots in arteries supplying the brain.
Dr. Oscar Benavente, a UBC professor of neurology and research director of the Stroke and Cerebrovascular Health Program at Vancouver Coastal Health, sought to determine if a combination of clopidogrel and aspirin –another anti-clotting agent that is used to prevent strokes — would lower the recurrence of lacunar strokes more than aspirin alone. The study involved 3,020 patients from 82 sites in North America, Latin America, and Spain who were followed for several years.
White matter dementia
So make sure your doctors test for this before assuming your cognition problems are a result of the stroke. Then ask for a protocol to correct those problems.
http://tan.sagepub.com/content/5/5/267.abstract?etoc=
http://tan.sagepub.com/content/5/5/267.abstract?etoc=
Abstract
White matter dementia (WMD) is a syndrome
introduced in 1988 to highlight the potential of cerebral white matter disorders to produce cognitive loss of sufficient severity to qualify as dementia. Neurologists have long understood that such a syndrome can occur, but the dominance of gray matter as the
locus of higher function has strongly directed neurobehavioral inquiry to the cerebral cortex while white matter has
received less attention. Contemporary neuroimaging has been crucial in enabling the recognition of white matter abnormalities in a host of disorders, and the correlation of these changes with cognitive performance. Comprising about half the brain, white
matter is prominently or exclusively involved in well over 100 disorders,in each of which white matter dysfunction can
potentially cause or contribute to dementia. Neuropsychological findings from ten categories of white matter disorder lead to a
convergence of findings that document remarkable neurobehavioral commonality among the dementias produced. More recently, the
syndrome of mild cognitive dysfunction (MCD) has been introduced to expand the concept of WMD by proposing a precursor
syndrome related to early white matter neuropathology. WMD and MCD inform the understanding of how white matter contributes to
normal and abnormal cognition, and the specific neuroanatomic focus of these syndromes may enhance the diagnosis and treatment
of many disabling disorders that do not primarily implicate the cerebral cortex. Forming essential connections within widely
distributed neural networks, white matter is critical for rapid and efficient information transfer that complements the
information processing of gray matter. As neuroimaging continues to advance, further information on white matter structure can be
expected, and behavioral neurology will play a central role in elucidating the functional significance of these emerging data. By
emphasizing the contribution of myelinated systems to higher function, the study of white matter and cognition represents
investigation of the basic neuroscience of human behavior.
Cardiac Benefits of Red Wine Not From the Alcohol
Good luck finding dealcoholized red wine, unless you can substitute grape juice.
http://www.medpagetoday.com/Cardiology/Hypertension/34610
Rest at the link, I suppose that they will next test the dark beers and say that the alcohol in them is not needed either. Taking all the fun out of life.
http://www.medpagetoday.com/Cardiology/Hypertension/34610
Action Points
- Explain that a small Spanish open-label, crossover study found that consumption of a moderate amount of dealcoholized red wine over a 4-week period, but not red wine itself or gin, was associated with a modest decrease in both systolic and diastolic blood pressure.
- Note that plasma nitric oxide was also increased when dealcoholized red wine was consumed, leading the authors to speculate that the blood pressure lowering effect might be due to nitric oxide.
Degenerative Diseases Of The Brain – New Therapies
Nothing directly for us here but our researchers should be able to posit some hypotheses about this helping our brain problems.
Degenerative Diseases Of The Brain – New Therapies
Late onset diseases like Alzheimer’s disease (AD), Parkinson’s
disease (PD) and amyotrophic lateral sclerosis (ALS) are degenerative as
well as progressive and thereby diminish the quality of life of
patients significantly. At present, therapies to treat or reverse
degeneration of brain cells are limited and these diseases usually
progress into disabilities. However, recent research seems to indicate
that it may be possible to limit the damage caused by the onset of AD,
PD and ALS by activating innate biological mechanisms.A consequence of the natural respiration process that is always active in our cells is the production of harmful forms of oxygen, which are known as reactive oxygen species (ROS). Reactive oxygen species like hydroxyl ions and hydrogen peroxide are produced in mitochondria. During periods of wakefulness, our brain consumes 20% of the total oxygen used in the body and it therefore follows that the chances of generating reactive oxygen species in brain cells are very high. These highly destructive molecules are neutralized by two enzyme: heme oxidase-1 (HO-1) and superoxide dismutase (SOD). In the early stages of AD and PD, the activity of these enzymes is either normal or reduced. It is surmised that the capability of the brain to increase the activity of these antioxidants is diminished in the stages preceding the onset of these degenerative diseases. In the case of AD, the protein (beta-amyloid peptide) deposited on nerve cells actually causes an increase in the ROS within nerve cells.
Recent research suggests that inhalation of gases like hydrogen, hydrogen sulfide and carbon monoxide, in low and regulated doses, can actually help to reduce oxidative damage caused by ROS. Although hydrogen sulfide is toxic, small quantities of this gas can actually be therapeutic against ROS. A modified form of aspirin which can release hydrogen sulfide, termed as S-aspirin, is able to protect brain cells from damage caused by the beta-amyloid peptide. Similarly, hydrogen, when inhaled, can reach the brain within an hour and can help to reverse nerve cell damage evident in PD. Hydrogen can be also given to patients in the form of hydrogen water and is faster in action than when inhaled in gas form. In experimental animal models for Parkinson’s disease, treatment with hydrogen water helped to rescue neurons which respond to dopamine from damage caused by ROS.
Hydrogen is capable of reacting with hydroxyl radicals to form water. In addition to this short-term chemical neutralization of reactive oxygen species, exposure to low doses of hydrogen also causes enhanced expression of HO-1 and SOD enzymes. Similar effects are also seen when nerve cells are exposed to carbon monoxide and hydrogen sulfide. These medical gases boost innate protective responses against reactive oxygen species and provide long-term protection that goes beyond immediate and local chemistry in the brain. Exposure of brain cells to hydrogen sulfide also reduces the amount of beta-amyloid peptide in nerve cells thereby limiting the damage caused by this protein.
Since administration of medical gases is a pretty standard procedure in hospitals and clinics, these scientific advances may represent a chance of recovery to patients who have been diagnosed with debilitating diseases like AD, Parkinson’s disease and ALS, at least in the early stages. The efficiency of these treatments in patients suffering from advanced stages of these neurodegenerative diseases is not known yet.
AHA Scientific Sessions Offers Outstanding Late-Breaking Science
| From a AHA email I received. You will notice there is not one session on stroke rehabilitation or prevention of neuronal cascade of death. Scientific Sessions will again offer the latest science via its popular Late-Breaking Clinical Trials. Attendees will have the opportunity to hear 28 LBCTs. These presentations are selected based on their unique approach to the topic, their design methods and the overall quality of the statistical plan. In addition, 19 trials will be presented in the format of Clinical Science: Special Report sessions and will focus on registries, updates to existing trials and important clinical science. |
| The following presentations are scheduled, as of Aug. 13, 2012. LBCTs Practice Implications for CAD and VTE
A Population Perspective
|
| Clinical Science: Special Report sessions Prevention and Treatment of Ischemic Heart Disease: Novel Approaches
The AHA will live stream 2012's LBCT Sessions I through VI. View these ground-breaking presentations from the convenience of your personal computer--as if you were with us in Los Angeles. Sessions will be available for purchase beginning Oct. 24.
|
Towards more effective robotic gait training for stroke rehabilitation: a review
This is probably more for your therapists and their management, so hand it to them and ask when it will be implemented. If we as survivors don't push new ideas it will take 30 years to get to clinical practice. So yes, I am blaming survivors for not pushing back on their medical staff for a lack of evidence-based practice for stroke rehab.
http://www.jneuroengrehab.com/content/9/1/65/abstract
http://www.jneuroengrehab.com/content/9/1/65/abstract
Abstract (provisional)
Background
Stroke is the most common cause of disability in the developed world and can severely
degrade walking function. Robot-driven gait therapy can provide assistance to patients
during training and offers a number of advantages over other forms of therapy. These
potential benefits do not, however, seem to have been fully realised as of yet in
clinical practice.
Objectives
This review determines ways in which robot-driven gait technology could be improved
in order to achieve better outcomes in gait rehabilitation.
Methods
The literature on gait impairments caused by stroke is reviewed, followed by research
detailing the different pathways to recovery. The outcomes of clinical trials investigating
robot-driven gait therapy are then examined. Finally, an analysis of the literature
focused on the technical features of the robot-based devices is presented. This review
thus combines both clinical and technical aspects in order to determine the routes
by which robot-driven gait therapy could be further developed.
Conclusions
Active subject participation in robot-driven gait therapy is vital to many of the
potential recovery pathways and is therefore an important feature of gait training.
Higher levels of subject participation and challenge could be promoted through designs
with a high emphasis on robotic transparency and sufficient degrees of freedom to
allow other aspects of gait such as balance to be incorporated.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
Longitudinal Analysis of Balance Confidence in Individuals With Stroke Using a Multilevel Model for Change
I do remember my OT telling me I needed confidence in my bad legs ability to hold myself up. And I bet I would have had a lot more confidence if fall-based therapy had been available.
http://nnr.sagepub.com/content/26/8/999.abstract?etoc
http://nnr.sagepub.com/content/26/8/999.abstract?etoc
Abstract
Background. Confidence about balance may be an important factor affecting self-efficacy for daily activities after stroke. Objective. The authors investigated whether confidence changes and the parameters that may predict changes in self-perceived balance
within the first year of community reintegration. Methods.
In this prospective study, 98 hemiparetic participants who could walk
at least 10 m independently were assessed 1, 3, 6,
and 12 months postdischarge from rehabilitation by
the Berg Balance Scale, Timed Up and Go, 6-minute walking distance, and
depression and anxiety scales. The 98
age-/sex-matched controls were assessed at enrollment and the same
intervals. Multilevel
modeling was used to determine if assessed
covariates predicted changes in balance confidence by the
Activities-Specific Balance
Confidence Scale. Results. Stroke subjects
had lower initial balance confidence than controls and showed a
statistically significant increase in confidence
over 1 year at each assessment. Poor balance and
high state anxiety were associated with lower balance confidence.
Significant
interactions were observed between greater
depression, along with more impaired walking capacity and balance tests,
in predicting
lower change trajectories in confidence. Falls
predicted a reduced rate of improvement. Conclusions. Balance
confidence after stroke remained lower than controls over the first
year. Physical therapies and supportive interventions
designed to treat confidence should be initiated at
discharge from inpatient rehabilitation.
Theta Burst Stimulation in the Rehabilitation of the Upper Limb A Semirandomized, Placebo-Controlled Trial in Chronic Stroke Patients
A cooler name like theta probably makes getting grants for repeating similar research easier.
http://nnr.sagepub.com/content/26/8/976.abstract?etoc
http://nnr.sagepub.com/content/26/8/976.abstract?etoc
Abstract
Background. Noninvasive cortical stimulation could represent an add-on treatment to enhance motor recovery after stroke. However, its
clinical value, including anticipated size and duration of the treatment effects, remains largely unknown. Objective.
The authors designed a small semi-randomized clinical trial to explore
whether long-lasting clinically important gains can
be achieved by adding theta burst stimulation
(TBS), a form of repetitive transcranial magnetic stimulation (TMS), to a
rehabilitation
program for the hand. Methods. A total of
41 chronic stroke patients received excitatory TBS to the ipsilesional
hemisphere or inhibitory TBS to the contralesional
hemisphere in 2 centers; each active group was
compared with a group receiving sham TBS. TBS was followed by physical
therapy
for 10 working days. Patients and therapists were
blinded to the type of TBS. Primary outcome measures (9-hole Peg Test
[9HPT],
Jebsen Taylor Test [JTT], and grip and pinch-grip
dynamometry) were assessed 4, 30, and 90 days post treatment. The
clinically
important difference was defined as 10% of the
maximum score. Results. There were no differences between the
active treatment and sham groups in any of the outcome measures. All
patients achieved
small sustainable improvements—9HPT, 5% of maximum
(confidence interval [CI] = 3%-7%); JTT, 5.7% (CI = 3%-8%); and grip
strength,
6% (CI = 2%-10%)—all below the defined clinically
important level. Conclusions. Cortical stimulation did not augment the gains from a late rehabilitation program. The effect size anticipated by the authors
was overestimated. These results can improve the design of future work on therapeutic uses of TMS.
Effects of Fast Functional Exercise on Muscle Activity After Stroke
If I could do anything fast I would.
http://nnr.sagepub.com/content/26/8/968.abstract?etoc
http://nnr.sagepub.com/content/26/8/968.abstract?etoc
Abstract
Background. In stroke rehabilitation,
considerable emphasis is placed on improving muscle strength with less
focus on the speed of movement.
Muscle power (product of force and velocity) is
essential for balance and mobility but velocity of movement is impaired
after
stroke. Objective. The purpose of this efficacy study is to determine if a single session of fast functional movements can increase muscle
activation and the speed of movement in participants with a subacute stroke. Methods.
In total, 32 individuals poststroke and 32 age- and sex-matched
controls performed a single session of 50 fast squats and
steps. Electromyographic (EMG) activity was
measured bilaterally in the rectus femoris (RF), biceps femoris (BF),
tibialis
anterior (TA), and soleus muscles. The average EMG
area and the movement speed were calculated over 10 trials. The effect
of exercise was determined as the change from the
second set (Start) to the last set (End) of 10 trials. Results.
The stroke group had significant increases in EMG area of the TA, BF,
and RF during the squatting exercise. There was an
increase in EMG area of the RF and BF when the
paretic leg was stepping. Improvements in EMG area of the soleus and RF
when
the paretic leg was in stance accompanied increases
in EMG area when the nonparetic leg was stepping. There was a trend for
improved movement speed for both exercises. Conclusion. A single session of exercises emphasizing speed of movement can be used to improve muscle activation in persons with mild
to moderately severe strokes.
Amount of Exercise in the First Week After Stroke Predicts Walking Speed and Unassisted Walking
I bet with some additional research they could correlate penumbra damage with predictions on walking speed and that would be objective and repeatable.
Amount of Exercise in the First Week After Stroke Predicts Walking Speed and Unassisted Walking
Abstract
Background.
Predicting walking outcomes poststroke is a challenge for clinicians.
Objective.
To identify the extent to which exercise dose (repetitions of leg movements) in the first week of a comprehensive stroke
unit stay predicts discharge mobility.
Methods.
A cohort study was conducted on 200 consecutive people admitted to a comprehensive stroke unit who required physical therapy.
Results.
Discharge and predictor data were
available for 191 survivors (99%). On admission, 86 participants were
able to walk, and
the average walking velocity was 0.42 m/s. On
discharge, the average walking velocity was 0.77 m/s, and 152
participants were
able to walk. A discharge walking velocity of
greater than 0.8 m/s was predicted by the exercise dose achieved in the
first
week after admission. Adding other predictors did
not significantly increase the predictive ability of the model.
Completion
of more than the median number of exercise
repetitions (703) in the first week of admission was associated with a
quicker
recovery of unassisted walking. This effect
persisted after adjustment for walking velocity on admission, cognition,
and comorbidity.
Conclusion.
Exercise dose in the first week after admission for stroke is an important indicator of walking speed at discharge and the
time to achieve unassisted walking.
Getting Neurorehabilitation Right What Can Be Learned From Animal Models?
And Dale Corbett is one of the authors.
Getting Neurorehabilitation Right What Can Be Learned From Animal Models?
Abstract
Animal models suggest that a month of
heightened plasticity occurs in the brain after stroke, accompanied by
most of the recovery
from impairment. This period of peri-infarct and
remote plasticity is associated with changes in excitatory/inhibitory
balance
and the spatial extent and activation of cortical
maps and structural remodeling. The best time for experience and
training
to improve outcome is unclear. In animal models,
very early (<5 and="and" conversely="conversely" damage.="damage." days="days" from="from" histological="histological" increased="increased" intense="intense" late="late" lead="lead" may="may" onset="onset" rehabilitation="rehabilitation" to="to" training="training">30 days) is much less effective both in terms of
outcome and morphological
changes associated with plasticity. In clinical
practice, rehabilitation after disabling stroke involves a relatively
brief
period of inpatient therapy that does not come
close to matching intensity levels investigated in animal models and
includes
the training of compensatory strategies that have
minimal impact on impairment. Current rehabilitation treatments have a
disappointingly
modest effect on impairment early or late after
stroke. Translation from animal models will require the following: (1)
substantial
increases in the intensity and dosage of treatments
offered in the first month after stroke with an emphasis on impairment;
(2) combinational approaches such as noninvasive
brain stimulation with robotics, based on current understanding of motor
learning and brain plasticity; and (3) research
that emphasizes mechanistic phase II studies over premature phase III
clinical
trials.
Friday, September 7, 2012
Symptomatic therapy in multiple sclerosis: the role of cannabinoids in treating spasticity
I don't care if we accept workable clinical trials from Germany, if it works in MS lets test it in stroke survivors and get this done. Then we can get our states to allow medical marijuana. One step at a time but only if we as survivors demand it. Ask your doctor to sponsor such research and legislation. If I didn't have to fight spasticity all the time, recovering movement would be a breeze, contrary to Dr. William Landaus' opinion and research articles.
http://tan.sagepub.com/content/5/5/255.abstract?etoc=
http://tan.sagepub.com/content/5/5/255.abstract?etoc=
Abstract
A large proportion of patients with
multiple sclerosis (MS) have spasticity, which has a marked impact on
their quality of
life. Anecdotal evidence suggests a beneficial
effect of cannabis on spasticity as well as pain. Recently, randomized,
double-blind,
placebo-controlled studies have confirmed the
clinical efficacy of cannabinoids for the treatment of spasticity in
patients
with MS. Based on these data, nabiximols (Sativex),
a 1:1 mix of Δ-9-tetrahydrocannabinol and cannabidiol extracted from
cloned
Cannabis sativa chemovars, received
approval for treating MS-related spasticity in various countries around
the globe. In this article we
review the current understanding of cannabinoid
biology and the value of cannabinoids as a symptomatic treatment option
addressing
spasticity in patients with MS.
Thursday, September 6, 2012
How Does the Brain Recover After Stroke?
You have to read this bloggers description of what happens and then educate your doctor on it.
http://brainblogger.com/2012/09/05/how-does-the-brain-recover-after-stroke/
The last paragraph;
This study demonstrates that the brain is extremely capable at repairing itself, and suggests exciting new possibilities for improving recovery after traumatic brain injury and stroke in humans. Developing treatments that enhance this rewiring, sprouting and branching process may improve the likelihood of recovery for people who have lost cognitive or motor function due to injury.
http://brainblogger.com/2012/09/05/how-does-the-brain-recover-after-stroke/
The last paragraph;
This study demonstrates that the brain is extremely capable at repairing itself, and suggests exciting new possibilities for improving recovery after traumatic brain injury and stroke in humans. Developing treatments that enhance this rewiring, sprouting and branching process may improve the likelihood of recovery for people who have lost cognitive or motor function due to injury.
Vitamin D supplement fails to lower cholesterol in short term
So ask your doctor what you should do.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=123605&CultureCode=en
Taking vitamin D supplements to compensate for vitamin D deficiency didn’t improve cholesterol — at least in the short term, according to new research in Arteriosclerosis, Thrombosis and Vascular Biology, an American Heart Association journal.
Researchers studied 151 people with vitamin D deficiency who received either a mega-dose (50,000 internationals units) of vitamin D3 or placebo weekly for eight weeks. Participants’ cholesterol levels were measured before and after treatment.
Correcting vitamin D deficiencies with high doses of oral vitamin D supplements did not change cholesterol levels, researchers found. This was despite effectively increasing vitamin D to recommended levels. Vitamin D levels nearly tripled in the group that received actual supplements, but were unchanged in the placebo group.
“Our study challenges the notion that vitamin D repletion improves cholesterol levels” said Manish Ponda, M.D., M.S., study lead author and assistant professor of clinical investigation in Dr. Jan Breslow’s laboratory of biochemical genetics and metabolism at The Rockefeller University in New York, N.Y. “These clinical trial results confirm those from a recent data mining study.”
The researchers also tested the effect of vitamin D supplementation on more sophisticated biomarker measures of cholesterol, such as particle size and number. “These measures of cholesterol, which are not used in routine clinical practice, also did not change in response to vitamin D therapy,” Ponda said.
As expected, replenishing subjects with high-dose supplements of oral vitamin D decreased parathyroid hormone levels and increased calcium levels — physical functional changes that were linked to participants’ increase in low-density lipoprotein (LDL, bad cholesterol).
“For example, participants receiving vitamin D who had an increase in calcium levels experienced a 7 percent increase in LDL cholesterol, while those whose calcium levels fell or did not change had a 5 percent decrease in LDL cholesterol,” Ponda said.
The study questions the use of vitamin D supplements to improve cholesterol, Ponda said. While the dose of vitamin D in this study was high, it was appropriate for correcting a vitamin D deficiency over an eight week period.
However, longer-term studies on the impact of the changes in LDL cholesterol as a result of high dose vitamin D supplementation are needed to make stronger recommendations. And questions remain about whether increasing vitamin D levels with exposure to sunlight, the predominant natural source, would have a different effect than with high-dose oral supplements.
To address these issues, Ponda and Breslow will begin another clinical trial this fall, comparing the effect of oral vitamin D to ultraviolet light exposure with a longer follow-up period.
I am however taking this because it might help fatigue.
Or maybe to prevent muscle atrophy.
Or fall prevention.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=123605&CultureCode=en
Taking vitamin D supplements to compensate for vitamin D deficiency didn’t improve cholesterol — at least in the short term, according to new research in Arteriosclerosis, Thrombosis and Vascular Biology, an American Heart Association journal.
Researchers studied 151 people with vitamin D deficiency who received either a mega-dose (50,000 internationals units) of vitamin D3 or placebo weekly for eight weeks. Participants’ cholesterol levels were measured before and after treatment.
Correcting vitamin D deficiencies with high doses of oral vitamin D supplements did not change cholesterol levels, researchers found. This was despite effectively increasing vitamin D to recommended levels. Vitamin D levels nearly tripled in the group that received actual supplements, but were unchanged in the placebo group.
“Our study challenges the notion that vitamin D repletion improves cholesterol levels” said Manish Ponda, M.D., M.S., study lead author and assistant professor of clinical investigation in Dr. Jan Breslow’s laboratory of biochemical genetics and metabolism at The Rockefeller University in New York, N.Y. “These clinical trial results confirm those from a recent data mining study.”
The researchers also tested the effect of vitamin D supplementation on more sophisticated biomarker measures of cholesterol, such as particle size and number. “These measures of cholesterol, which are not used in routine clinical practice, also did not change in response to vitamin D therapy,” Ponda said.
As expected, replenishing subjects with high-dose supplements of oral vitamin D decreased parathyroid hormone levels and increased calcium levels — physical functional changes that were linked to participants’ increase in low-density lipoprotein (LDL, bad cholesterol).
“For example, participants receiving vitamin D who had an increase in calcium levels experienced a 7 percent increase in LDL cholesterol, while those whose calcium levels fell or did not change had a 5 percent decrease in LDL cholesterol,” Ponda said.
The study questions the use of vitamin D supplements to improve cholesterol, Ponda said. While the dose of vitamin D in this study was high, it was appropriate for correcting a vitamin D deficiency over an eight week period.
However, longer-term studies on the impact of the changes in LDL cholesterol as a result of high dose vitamin D supplementation are needed to make stronger recommendations. And questions remain about whether increasing vitamin D levels with exposure to sunlight, the predominant natural source, would have a different effect than with high-dose oral supplements.
To address these issues, Ponda and Breslow will begin another clinical trial this fall, comparing the effect of oral vitamin D to ultraviolet light exposure with a longer follow-up period.
I am however taking this because it might help fatigue.
Or maybe to prevent muscle atrophy.
Or fall prevention.
Statins are killers and cause major artery damage, say researchers
Inflammatory article from WDDTY - What Doctors don't tell you.
http://www.wddty.com/statins-are-killers-and-cause-major-artery-damage-say-researchers.html
The abstract this is based on is here; unless the complete study says something different, I don't see it.
http://www.wddty.com/statins-are-killers-and-cause-major-artery-damage-say-researchers.html
The abstract this is based on is here; unless the complete study says something different, I don't see it.
Progression of Vascular Calcification Is Increased With Statin Use in the Veterans Affairs Diabetes Trial (VADT).
Ask your doctor to clarify.
Exercises to Target Specific Hamstring Muscles
There is no way I can even summarize this so ask your therapist to put it into understandable words if your hamstring needs help.
http://sportsmedresearch.blogspot.com/2012/08/hamstring-exercise-rankings.html
http://sportsmedresearch.blogspot.com/2012/08/hamstring-exercise-rankings.html
Blood Sugar Levels Linked to Brain Loss
We've already had enough brain loss so make sure your doctor doesn't allow any more of your brain to be lost.
http://www.medpagetoday.com/Neurology/GeneralNeurology/34588
Higher blood glucose levels were associated with brain atrophy among healthy individuals in their early 60s, even when levels remained within the official normal range, an Australian study demonstrated.
After adjustment for age, sex, body mass index (BMI), hypertension, alcohol use, smoking, and APOE genotype, the associations between glucose and left and right hippocampal volumes were −131 and −148 (P=0.001 for both), with a positive association reflecting less atrophy, according to Nicolas Cherbuin, PhD, of Australian National University in Canberra, and colleagues.
The rest at the link.
http://www.medpagetoday.com/Neurology/GeneralNeurology/34588
Higher blood glucose levels were associated with brain atrophy among healthy individuals in their early 60s, even when levels remained within the official normal range, an Australian study demonstrated.
After adjustment for age, sex, body mass index (BMI), hypertension, alcohol use, smoking, and APOE genotype, the associations between glucose and left and right hippocampal volumes were −131 and −148 (P=0.001 for both), with a positive association reflecting less atrophy, according to Nicolas Cherbuin, PhD, of Australian National University in Canberra, and colleagues.
The rest at the link.
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