Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective 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.

Showing posts with label no medical training. Show all posts
Showing posts with label no medical training. Show all posts

Thursday, August 15, 2019

Neural Correlates of Passive Position Finger Sense After Stroke

Useless, measurement only. NO SOLUTION.  I'd suggest reading the Margaret Yekutiel  book about this from 2001, 'Sensory Re-Education of the Hand After Stroke'. But I'm not medically trained so I know 'nuthin'.  If your therapists and doctors don't know of this book, fire them for incompetency.  They are responsible for knowing how to treat stroke and should have already written protocols for this based on this book.

Neural Correlates of Passive Position Finger Sense After Stroke 

First Published July 18, 2019 Research Article
Background. Proprioception of fingers is essential for motor control. Reduced proprioception is common after stroke and is associated with longer hospitalization and reduced quality of life. Neural correlates of proprioception deficits after stroke remain incompletely understood, partly because of weaknesses of clinical proprioception assessments.  
Objective. To examine the neural basis of finger proprioception deficits after stroke. We hypothesized that a model incorporating both neural injury and neural function of the somatosensory system is necessary for delineating proprioception deficits poststroke.
Methods. Finger proprioception was measured using a robot in 27 individuals with chronic unilateral stroke; measures of neural injury (damage to gray and white matter, including corticospinal and thalamocortical sensory tracts), neural function (activation of and connectivity of cortical sensorimotor areas), and clinical status (demographics and behavioral measures) were also assessed. Results. Impairment in finger proprioception was present contralesionally in 67% and bilaterally in 56%. Robotic measures of proprioception deficits were more sensitive than standard scales and were specific to proprioception. Multivariable modeling found that contralesional proprioception deficits were best explained (r2 = 0.63; P = .0006) by a combination of neural function (connectivity between ipsilesional secondary somatosensory cortex and ipsilesional primary motor cortex) and neural injury (total sensory system injury).  
Conclusions. Impairment of finger proprioception occurs frequently after stroke and is best measured using a quantitative device such as a robot. A model containing a measure of neural function plus a measure of neural injury best explained proprioception performance. These measurements might be useful in the development of novel neurorehabilitation therapies.

 

Thursday, September 20, 2018

Dementia Risk Doubled in Patients Following Stroke

What is your doctors EXACT PROTOCOL to prevent such dementia? They have known this for at least 6 years.  I'm doing Alcohol for these 12 reasons, social connections and coffee. Don't follow me, I'm not medically trained.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.

3. A 20% chance in this research.   July 2013.

Dementia Risk Doubled in Patients Following Stroke 

People who have had a stroke are around twice as likely to develop dementia, according to a study published in Alzheimer’s and Dementia.
The study analysed data on stroke and dementia risk from 3.2 million people across the world. The link between stroke and dementia persisted even after taking into account other dementia risk factors such as blood pressure, diabetes and cardiovascular disease. Their findings give the strongest evidence to date that having a stroke significantly increases the risk of dementia.
The study builds on previous research which had established the link between stroke and dementia, though had not quantified the degree to which stroke actually increased dementia risk. To better understand the link between the 2, researchers analysed 36 studies where participants had a history of stroke, totalling data from 1.9 million people. In addition, they analysed a further 12 studies that looked at whether participants had a recent stroke over the study period, adding a further 1.3 million people.
Ilianna Lourida, PhD, University of Exeter Medical School, Exeter, United Kingdom, said: “We found that a history of stroke increases dementia risk by around 70%, and recent strokes more than doubled the risk. Given how common both stroke and dementia are, this strong link is an important finding. Improvements in stroke prevention and post-stroke care may therefore play a key role in dementia prevention.”
According to the World Health Organization, 15 million people have a stroke each year. Meanwhile, around 50 million people globally have dementia - a number expected to almost double ever 20 years, reaching 131 million by 2050.
Stroke characteristics such as the location and extent of brain damage may help to explain variation in dementia risk observed between studies, and there was some suggestion that dementia risk may be higher for men following stroke.
Further research is required to clarify whether factors such as ethnicity and education modify dementia risk following stroke. Most people who have a stroke do not go on to develop dementia, so further research is also needed to establish whether differences in post-stroke care and lifestyle can reduce the risk of dementia further.
David Llewellyn, PhD, University of Exeter Medical School, concluded: “Around a third of dementia cases are thought to be potentially preventable, though this estimate does not take into account the risk associated with stroke. Our findings indicate that this figure could be even higher, and reinforce the importance of protecting the blood supply to the brain when attempting to reduce the global burden of dementia.”
Reference: https://doi.org/10.1016/j.jalz.2018.06.3061
SOURCE: University of Exeter

Monday, August 6, 2018

Teetotalism in midlife makes you more likely to develop dementia? What the research actually says

Your doctor will never tell you of any benefits of alcohol. You can't listen to me since I have no medical training. You are on your own for your health, better start studying up.

Don't do this, I am a complete outlier and should never be followed.

My listing of positives; don't follow me. 

I actually consider alcohol to be the great social engagement lubricant, and stroke survivors needs lots of social interaction to prevent dementia. 


Alcohol for these 12 reasons.



A little daily alcohol may cut stroke risk




Six healthy reasons to drink more beer   Red wine benefits are in this one also.



10 Health Benefits of Whiskey

Study: For those over 90, alcohol better than exercise for longevity

 

NIH withdrawal from controversial trial leaves the question: Does alcohol prevent CVD?

You are completely on your own figuring out what to do about alcohol.

Your choice on what to do with this, your doctor will disapprove. 

The Common Drink Linked To High Intelligence

The latest here:

Teetotalism in midlife makes you more likely to develop dementia? What the research actually says

Imagine if someone told you that not drinking alcohol makes you more likely to develop dementia. That's certainly a bold statement to make, but it is one that some media reports have put forward, leaving the public wondering whether taking up drinking alcohol will somehow be better for their brains.


A recent article in the British Medical Journal has rekindled the scientific argument over the relationship between abstaining from and developing dementia. The study involved 9,000 civil servants working in London, all of whom were aged between 35 and 55 when the study began between 1985 and 1988. When the study ended in 1993, their average age was 50. The participants' medical records were analysed to identify diagnoses of dementia—more than 23 years, on average, after the study had finished. The results found that abstinence in was associated with a 45% higher risk of developing dementia, compared with people who consumed between one and 14 units of alcohol per week.

The findings for those who drank above the recommended 14 units a week were perhaps less surprising. For every seven unit per week increase above 14 units there was a significant 17% increase in the risk of dementia. The study concluded: "These results suggest that abstention and are associated with an increased risk of dementia, although the underlying mechanisms are likely to be different in the two groups."

A confounded nuisance

So what are we to make of this research? In studies such as this, one of the many pitfalls of exploring the association between an exposure variable (alcohol) and the outcome variable (dementia) is the presence of confounders. Confounders are a statistician's worse nightmare – they are variables that may justifiably be associated with both the exposure and outcome variable.

In this study, abstainers with higher levels of illnesses such as heart disease, diabetes and obesity were those at highest risk of dementia. It may be that having a physical illness is the reason that these people abstained from alcohol. These same physical illnesses may also be the reason for developing dementia. In this way, physical illness unrelated to alcohol consumption could be a confounder for both abstinence and dementia. Drinking may just be a red herring.

The other big problem with studies that explore how teetotalism and dementia are connected is the age range covered. The study started looking at habits at a minimum age of 35 and finished when the average age was 50. But what about people who drank heavily in their younger years or above the age of 55? This is particularly important, as it is likely that a large proportion of the study group will have been part of the "baby boomer" generation. This generation has seen the highest rise in rates of alcohol misuse over the past 15 years – a period of time which is well outside the study's range.

We should also be aware that between one-quarter and two-thirds of older people start drinking more than the recommended 14 unit limit for the first time after the age of 60. These drinking patterns at ages before and after the study period could well have influenced the results. Those identified as teetotal during the study period may well have started drinking later in life

Another spirit level

More than 50 years ago, the late Griffiths Edwards, a professor of addictions psychiatry stated: "It would be too optimistic to suppose that the relative under-representation of subjects in the older age groups … is just explained by older people having generally got the treatment they required or having reverted to normal drinking … it seems likely that this finding is in part a hint of the diminished life expectancy of the alcoholic."

Humans have a longer lifespan these days, so there are more people living into their 70s and beyond – which has also provided the opportunity to look at alcohol and dementia in more detail. By examining the differences between alcohol-related dementia and more common forms, such as Alzheimer's Disease, we begin to see that they are different in many ways. For example, the problems with word-finding seen in Alzheimer's Disease is rarely seen in alcohol-related dementia, which also presents much earlier with changes in behaviour.

Researchers need to be sure that they are defining alcohol-related dementia more accurately for these kinds of studies to be definitive. If not, it is highly likely that they are looking at other dementias with other risk factors, such as high blood pressure or diabetes.

Alcohol is a drug that harms increasing numbers of – and we need to get the facts right about how it affects the brain. Maybe we can't handle the truth about drinking. All it takes is the mere flicker of hope as to the benefits of being teetotal to fan the flames of misinformation.

For those that do drink alcohol, people drinking above lower risk limits has, once again, been given a salutary warning. It is one that we should continue to heed – but we also need to get the message out there that alcohol-related needs to be rediscovered and investigated again.


Tuesday, July 10, 2018

Psilocybin and Mental Health–Don't Lose Control

Don't worry, your doctor will never prescribe psilocybin. We can't even get marijuana off of Schedule I. You can read my 5 posts on the subject and see the possibilities there for rehab which will never be followed up. Don't listen to me I have no medical training.

Psilocybin and Mental Health–Don't Lose Control

Monday, June 4, 2018

The lucid dreaming playbook: how to take charge of your dreams

Your doctor should be instructing you in this. In lucid dreaming you could have yourself correctly moving your affected muscles and observe them. Similar to mirror therapy and action observation. If your doctor can't put these three concepts together for your recovery you have to find someone who can.  Our fucking failures of stroke associations don't have enough functioning brain cells to even understand the concept, don't bother their poor brain cells. But don't listen to me, I have no medical training.
https://ideapod.com/the-lucid-dreaming-playbook-how-to-take-charge-of-your-dreams/

In the study I published with colleagues at the University of Adelaide, the best technique turned out to be something called Mnemonic Induction of Lucid Dreams (MILD), originally developed in the 1970s by the American psychophysiologist Stephen LaBerge. It involves the following steps:

1. Set an alarm for five hours after you go to bed.

2. When the alarm sounds, try to remember a dream from just before you woke up. If you can’t, just recall any dream you had recently.

3. Lie in a comfortable position with the lights off and repeat the phrase: ‘Next time I’m dreaming, I will remember I’m dreaming.’ Do this silently in your mind. You need to put real meaning into the words and focus on your intention to remember.

4. Every time you repeat the phrase at step 3, imagine yourself back in the dream you recalled at step 2, and visualise yourself remembering that you are dreaming.

5. Repeat steps 3 and 4 until you either fall asleep or are sure that your intention to remember is set. This should be the last thing in your mind before falling asleep. If you find yourself repeatedly coming back to your intention to remember that you’re dreaming, that’s a good sign it’s firm in your mind.

We relied on data from 169 people from all over Australia, who kept a dream journal so we could measure the effect of induction techniques against their ‘baseline’ tendency. More than half the people who used MILD ended up having at least one lucid dream in the week they started practising; they also went from experiencing these dreams about one night out of 11 to about one night in six. These findings are very exciting, and are some of the highest success rates reported in the scientific literature.

Surprisingly, the number of times that people repeated the mantra about remembering that they’re dreaming, or even the amount of time spent on MILD overall, did not predict success. Instead, the most important factor was being able to complete the technique and then go back to sleep quickly. In fact, it proved almost twice as effective when people fell asleep within five minutes after setting their intention. If you want to try this for yourself, you’ll need to experiment in order to get the right level of wakefulness when the alarm goes off – enough to allow you to complete the steps, but not so much that you’ll struggle to doze off again. Doing the technique after five or so hours of sleep is important, too: most of our dreams occur in the last two to three hours before waking, and you want to minimise the time between finishing the technique and entering REM sleep.

It takes a bit of practice, but if you’re lucky you might even have a lucid dream using MILD on your first night. If you do become aware that you’re dreaming, it’s important to stay calm, since intense emotions can trigger a premature awakening. And if the dream starts to fade or seems unstable, you can try rubbing your hands together vigorously from within the dream. It sounds strange, but this strategy works by flooding the brain with sensations from within the dream, which decreases the chance of becoming aware of your sleeping physical body, and waking up.

Aside from the sheer joy of being able to bend an imaginary world to your will, there’s a range of additional psychological benefits to lucid dreaming. For one, it can help with nightmares: simply knowing that you’re dreaming often brings relief during a nasty episode. You might also be able to use dreams to process trauma: confronting what’s haunting you, making peace with an attacker, escaping the situation by flying away, or even just waking up. Other potential applications include practising sporting skills by night, having more ‘active’ participants for studies about sleep and dreaming, and the pursuit of creative inspiration. With practice, our dream state can feel almost as vivid to us as the world itself – and leaves you wondering, perhaps, where fantasy ends and reality begins.Aeon counter – do not remove

By Denholm Aspy. This article was originally published at Aeon and has been republished under Creative Commons.

Monday, May 28, 2018

NeuCogni is pioneering wearable devices to improve well-being, and relieve pain and symptoms of neuro-disorders.

Maybe you want to read this before starting any brain wave training;

Brainwave woo - RationalWiki

 I tune my neurons with red wine, helps with my needed social connections, although sake and white wine work just as well. Don't follow me, I have no medical training.

NeuCogni is pioneering wearable devices to improve well-being, and relieve pain and symptoms of neuro-disorders

NeuCogni is pioneering wearable devices to improve well-being, and relieve pain and symptoms of neuro-disorders.
Our innovations at the intersection of neuroscience, artificial intelligence and functional psychology can transform existing approaches to overall well-being and mental health treatment.
Our technology lies in fine-tuning brainwave frequencies for the optimal operation of neurons.

Monday, September 11, 2017

E-cigarettes associated with increased blood pressure, heart rate, and arterial stiffness, study reveals

You may not want to get your nicotine this way for your post-stroke recovery. 33 posts on nicotine which your doctor will know zilch about. Time for you to train your doctor again. I'm going to do the nicotine patches for my next stroke even though I have no clue on dosage.  Don't listen to me with no medical knowledge.
https://www.news-medical.net/news/20170911/E-cigarettes-associated-with-increased-blood-pressure-heart-rate-and-arterial-stiffness-in-humans-study-reveals.aspx
A new study, presented at the European Respiratory Society International Congress, suggests that use of e-cigarettes with nicotine causes arterial stiffness in humans, and has significant consequences leading to risk of heart disease and stroke later in life.

Dr Magnus Lundbäck, research leader and clinical registrar at the Danderyd University Hospital, Stockholm, Sweden conducted a study in which he stated that there has been a dramatic increase in the number of e-cigarette smokers. E-cigarettes are often considered harmless by society.
E-cigarette companies promote their product as an approach to help people to quit smoking tobacco and to reduce harm. Nevertheless, the safety of e-cigarettes is disputed, and increasing evidence indicates numerous adverse health effects.
Dr. Lundbäck further stated: "The results are preliminary, but in this study we found there was a significant increase in heart rate and blood pressure in the volunteers who were exposed to e-cigarettes containing nicotine. Arterial stiffness increased around three-fold in those who were exposed to nicotine containing e-cigarettes compared to the nicotine-free group."
The study was performed on 15, healthy, young participants, who were occasional smokers (maximum of ten cigarettes per month) and had not smoked e-cigarettes before conducting this study. Average age of the participants was 26, of which 41% were male and 59% female.
The participants were randomly assigned e-cigarettes with or without nicotine, which the participants smoked for half an hour before coming back another day to smoke the other type of e-cigarette. Their heart rate, blood pressure, and arterial stiffness were measured immediately after smoking the e-cigarettes, and then 2 and 4 hours later.
A significant increase in the arterial stiffness, blood pressure, and heart rate were observed in the first half hour after smoking e-cigarettes containing nicotine, while no such effect was observed on arterial stiffness and heart rate in participants who had used non-nicotine e-cigarettes.
According to Dr Lundbäck, the immediate rise observed in arterial stiffness is mostly associated to nicotine, and it was temporary. Nevertheless, the same short-term effects on arterial stiffness were also observed after smoking normal tobacco cigarettes.
Therefore, it is speculated that the long-term use of e-cigarettes with nicotine may result in chronic and permanent effects on arterial stiffness. So far, there are no studies on the chronic effects on arterial stiffness after the long-term use of e-cigarettes.
Dr Lundbäck further added that it is essential that the conclusions of this and other studies reach healthcare professionals providing preventive health care and the general public. The results of the study emphasize the need for maintaining a cautious and critical attitude toward e-cigarettes, especially by healthcare service providers.
Based on scientific facts, e-cigarette smokers must be aware of their possible health effects, so that they can decide on whether to continue or quit smoking them.
He further remarked that the e-cigarette marketing campaigns target conventional tobacco smokers and offer an alternate product. Nevertheless, numerous studies question the e-cigarette as an approach to quit smoking, and there is a high-risk of double use, where people smoke both conventional cigarettes and e-cigarettes.
Dr Lundbäck and his group of researchers are continuing to examine the effects of e-cigarettes on lung functions and blood vessels in humans and in cell cultures.


Saturday, August 26, 2017

Coffee consumption after myocardial infarction and risk of cardiovascular mortality: A prospective analysis in the Alpha Omega Cohort

Now we just need to know about coffee post-stroke. I however have already made up my mind. Coffee as much as possible and as often as possible. But since I have no medical training, don't listen to me. You can have your doctor summarize the pros and cons of coffee in these 142 posts on coffee.
https://www.mdlinx.com/internal-medicine/medical-news-article/2017/08/25/coffee-myocardial-infarction-patients-cardiovascular-disease/7383175/?

American Journal of Clinical Nutrition
van Dongen LH, et al. – This prospective investigation assessed the link between coffee consumption (caffeinated and decaffeinated) and cardiovascular disease (CVD) mortality, ischemic heart disease (IHD) mortality, and all–cause mortality, respectively, in patients with a previous experience of myocardial infarction (MI). Researchers concluded drinking coffee, either caffeinated or decaffeinated, may lower the risk of CVD and IHD mortality in patients with a prior MI.

Methods

  • This study included 4365 Dutch patients from the Alpha Omega Cohort who were aged 60–80 y (21% female) and had experienced an MI <10 y before study enrollment.
  • Using a 203-item validated food-frequency questionnaire, dietary data including coffee consumption over the past month was collected, at baseline (2002–2006).
  • Until 1 January 2013, researchers monitored causes of death.
  • They obtained HRs for mortality in categories of coffee consumption from multivariable Cox proportional hazard models, adjusting for lifestyle and dietary factors.

Results

  • Findings revealed that most patients (96%) drank coffee, and the median total coffee intake was 375 mL/d (~3 cups/d).
  • Data reported that during a median follow-up of 7.1 y, a total of 945 deaths occurred, including 396 CVD-related and 266 IHD-related deaths.
  • Researchers observed that coffee consumption was inversely associated with CVD mortality, with HRs of 0.69 (95% CI: 0.54, 0.89) for >2–4 cups/d and 0.72 (0.55, 0.95) for >4 cups/d, compared with 0–2 cups/d.
  • In addition, results highlighted that corresponding HRs were 0.77 (95% CI: 0.57, 1.05) and 0.68 (95% CI: 0.48, 0.95) for IHD mortality and 0.84 (95% CI: 0.71, 1.00) and 0.82 (95% CI: 0.68, 0.98) for all-cause mortality, respectively.
  • They also found similar associations for decaffeinated coffee and for coffee with additives.

Friday, August 18, 2017

Cholesterol crystals are sure sign a heart attack may loom

You'll have to ask your doctor how this can be prevented. I'm using the following.

Watermelon juice reverses hardening of the arteries Nov. 2011 

New study shows aged garlic extract can reduce dangerous plaque buildup in arteries  Jan. 2016 

Pomegranate juice consumption for 3 years by patients with carotid artery stenosis reduces common carotid intima-media thickness, blood pressure and LDL oxidation  June 2004 

Regular coffee drinkers have 'cleaner' arteries March 2015 

I'm not medically trained so don't follow me.

Cholesterol crystals are sure sign a heart attack may loom 

A new Michigan State University study on 240 emergency room patients shows just how much of a role a person's cholesterol plays, when in a crystallized state, during a heart attack.
George Abela, lead author and chief cardiologist at MSU, analyzed the material that was obstructing the coronary arteries of patients who had suffered a and found that 89 percent of them had an excessive amount of these crystallized structures, referred to as .
The research is now published online in the American Journal of Cardiology.
These crystals are released from plaque that can build up in the heart and is often made up of fat, calcium and other substances as well. When this material hardens over time in the arteries, it's known as atherosclerosis.
"In previous studies, we showed that when cholesterol goes from a liquid to a solid, or crystal state, it expands in volume like ice and water," Abela said. "This expansion inside the wall of the artery can tear it and block causing a heart attack or stroke."
After entered the , Abela and his team suctioned out this plaque. They were able to see that clusters of large crystals had formed and were able to break through the plaque and walls of the arteries and then released into the heart. This caused damage by blocking blood flow.
"We now know to what great extent these crystals are contributing to a heart attack," Abela said.
This latest research also reconfirms what Abela discovered in an earlier study that cholesterol crystals activated the production of inflammation molecules, known as Interleukin-1 beta, which aggravate, or inflame, coronary arteries.
"Now that we've shown how extensive cholesterol crystals are irritating and blocking off these , treatments that dissolve these crystals may be used to reduce heart damage," Abela said.
Some of these treatments can include the use of statin drugs - often used to lower one's cholesterol - aspirin and solvents such as alcohol that can be injected in low doses into a vein during a heart attack. Using these options could allow doctors to improve patient outcomes and save more lives.
A recent clinical trial using an already FDA-approved antibody, known as canakinumab, has also shown to block the Interleukin-1 beta inflammation molecule and reduce the chances of a cardiac event.
"Saving heart muscle is the most important aspect of treating a heart attack," Abela said. "So, if we are able to provide patients with better, more targeted treatments, then this could help open up and calm down the aggravated artery and protect the muscle from injury."
Abela also added that by simply controlling one's cholesterol by eating a healthy diet, exercising and taking statin medications as needed, could be the best way to prevent these crystals from forming.
More information: Frequency of Cholesterol Crystals in Culprit Coronary Artery Aspirate during Acute Myocardial Infarction and Their Relation to Inflammation and Myocardial Injury , American Journal of Cardiology (2017). DOI: dx.doi.org/10.1016/j.amjcard.2017.07.075
Provided by Michigan State University


Wednesday, August 16, 2017

Little evidence shows cannabis helps chronic pain or PTSD

You can't expect positive evidence on this because of the extreme difficulty of doing research with marijuana.

Does your doctor even know about the 23% chance of stroke survivors getting PTSD? And what is s/he doing about it?

 I will use marijuana post-stroke for these reasons;

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training,


Little evidence shows cannabis helps chronic pain or PTSD

Monday, August 14, 2017

Study Connects Chronic Cannabis Use to Oxygen Changes in Brain

Higher cerebral blood flow and better oxygen uptake sounds like it would be good for our damaged brains. But we will never know since no research will ever be done on this.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training,


http://neurosciencenews.com/oxygen-cannabis-brain-7296/
Summary: According to UT Dallas researchers, chronic cannabis users extract more oxygen from brain blood flow and have higher cerebral blood flow than nonusers.
Source: UT Dallas.
New research from the Center for BrainHealth at The University of Texas at Dallas reveals that levels of THC, the psychoactive ingredient in cannabis that leaves a euphoric feeling, directly correlate to changes in how the brain utilizes oxygen.
Dr. Francesca Filbey, director of Cognitive Neuroscience Research in Addictive Disorders at the Center for BrainHealth, led the team that found chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers. The rate at which oxygen is metabolized in the brain was found to be higher in users as well.
While THC is known to relax blood vessels and alter blood flow in the brain, the study focused on how prolonged THC use might affect the brain by analyzing the differences in regional brain blood oxygenation and metabolism in chronic cannabis users.
Due to the prospective nature of the study, published in the journal Neuropsychopharmacology, researchers cannot say whether cannabis use directly causes the observed changes, or whether other underlying conditions also may be at play.
While the reason for the brain changes related to chronic marijuana use is unclear, Filbey said that these changes may reflect underlying differences in brain tissue metabolic rate.
“Past marijuana research has shown changes in cognitive functions such as memory and executive functioning. Our study seeks to understand the possible neurophysiological mechanisms that may drive these cognitive changes,” said Filbey, who is also Bert Moore Chair in BrainHealth and head of the cognitive neuroscience program in the School of Behavioral and Brain Sciences.
The study consisted of 74 cannabis users and 101 nonusers matched for age and IQ. All users reported at least 5,000 usages over their lifetime and daily use for 60 days leading up to the study. Participants were required to refrain from cannabis for 72 hours before the study to eliminate acute effects of the drug. Participants underwent magnetic resonance imaging, and THC metabolite levels were measured using urinalysis.
Image shows a person smoking.
Increased blood flow in the putamen may either reflect the capacity of THC to dilate blood vessels or the development of additional circulatory pathways. NeuroscienceNews.com image is in the public domain.
Filbey and her team found that cannabis users showed higher global oxygen extraction fraction and cerebral metabolic rate of oxygen compared to nonusers. Also, blood flow in the putamen — an area of the brain associated with reward learning and habit formation — was found to be greater in users than nonusers.
Increased blood flow in the putamen may either reflect the capacity of THC to dilate blood vessels or the development of additional circulatory pathways.
“Currently, cannabis is the most widely used illicit drug. As it becomes more widely legalized, understanding neurophysiological alterations and its effects on the brain’s health and performance are becoming increasingly relevant,” Filbey said.
About this neuroscience research article
Source: Emily Bywaters – UT Dallas
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study will appear in Neuropsychopharmacology.
Cite This NeuroscienceNews.com Article
UT Dallas “Study Connects Chronic Cannabis Use to Oxygen Changes in Brain.” NeuroscienceNews. NeuroscienceNews, 14 August 2017.
.

Wednesday, August 9, 2017

Marijuana use holds three-fold blood pressure death risk: study

Other research showed that if you adjust for those that are smoking also the risk from marijuana disappears. I'd say this was bad research.

So fucking what? The uses for stroke rehabilitation would likely be short-term. But our stupid federal legislators will glom onto anything negative about marijuana and not even approve research proving the positives. With this mindset aspirin, alcohol and warfarin would have never been approved.  I would suggest moving to one of the legal states or countries.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training, you don't need medical training to read and understand research or its' good points on your own.


http://www.reuters.com/article/us-health-marijuana-hypertension-idUSKBN1AP0JS
LONDON (Reuters) - People who smoke marijuana have a three times greater risk of dying from hypertension, or high blood pressure, than those who have never used the drug, scientists said on Wednesday.(This doesn't correspond to the bolded line below that states that CVD risk/death is not linked to marijuana use.)
The risk grows with every year of use, they said.
The findings, from a study of some 1,200 people, could have implications in the United States among other countries. Several states have legalized marijuana and others are moving toward it. It is decriminalized in a number of other countries.
"Support for liberal marijuana use is partly due to claims that it is beneficial and possibly not harmful to health," said Barbara Yankey, who co-led the research at the school of public health at Georgia State University in the United States.
"It is important to establish whether any health benefits outweigh the potential health, social and economic risks. If marijuana use is implicated in cardiovascular diseases and deaths, then it rests on the health community and policy makers to protect the public."
Marijuana is also sometimes used for medicinal purposes, such as for glaucoma.
The study, published in the European Journal of Preventive Cardiology, was a retrospective follow-up study of 1,213 people aged 20 or above who had been involved in a large and ongoing National Health and Nutrition Examination Survey. In 2005–2006, they were asked if they had ever used marijuana.
For Yankey's study, information on marijuana use was merged with mortality data in 2011 from the U.S. National Center for Health Statistics, and adjusted for confounding factors such as tobacco smoking and variables including sex, age and ethnicity.
The average duration of use among users of marijuana, or cannabis, was 11.5 years.
The results showed marijuana users had a 3.42-times higher risk of death from hypertension than non-users, and a 1.04 greater risk for each year of use.
There was no link between marijuana use and dying from heart or cerebrovascular diseases such as strokes.
Yankey said were limitations in the way marijuana use was assessed -- including that researchers could not be sure whether people had used the drug continuously since they first tried it.
But she said the results chimed with plausible risks, since marijuana is known to affect the cardiovascular system.
"Marijuana stimulates the sympathetic nervous system, leading to increases in heart rate, blood pressure and oxygen demand," she said.
Experts not directly involved in the study said its findings would need to be replicated, but already raised concerns.
"Despite the widely held view that cannabis is benign, this research adds to previous work suggesting otherwise," said Ian Hamilton, a lecturer in mental health at Britain's York University.
Reporting by Kate Kelland, editing by Jeremy Gaunt

Tuesday, May 23, 2017

Effect of a Coconut Oil Supplement (2g/d) on Total Cholesterol to HDL Cholesterol Ratio in Healthy Adults

Oh well, I'm still doing coconut oil for reasons in these 38 posts. Don't listen to me I have no medical training. 
http://search.proquest.com/openview/4172252bc6194b82998c2b1f4fe55da4/1?pq-origsite=gscholar&cbl=18750&diss=y
ABSTRACT
There are limited studies exploring the direct relationship between coconut oil and cholesterol concentrations. Research in animals and a few intervention trials suggest that coconut oil increases the good cholesterol (high density lipoprotein, HDL) and thus reduces the risk of cardiovascular disease. Preliminary research at Arizona State University(ASU) has found similar results using coconut oil as a placebo, positive changes in HDL cholesterol
concentrations were observed.
The goal of this randomized, double blind, parallel two arm study, was to further examine the beneficial effects of a 2g supplement of coconut oil taken each day for 8 weeks on cholesterol concentrations, specifically the total cholesterol to HDL cholesterol ratio, compared to placebo.
Forty-two healthy adults between 18-40 years of age, exercising less than 150
minutes each week, non smoking, BMI between 22-35 and not taking any medications that could effect blood lipids were recruited from the ListServs at ASU. Participants were randomized to receive either a placebo capsule of flour or a coconut oil capsule (Puritan’s Pride brand, coconut oil softgels, 2g each) and instructed to take the capsules for 8 weeks.
Results indicated no significant change in total cholesterol to HDL ratio between baseline and 8 weeks in the coconut oil and placebo groups (p=0.369), no significant change in HDL (p=0.648), no change in LDL (p=0.247), no change in total cholesterol (p=0.216), and no change in triglycerides (p=0.369). Blood lipid concentrations were not significantly altered by a 2g/day dosage of coconut oil over the course of 8 weeks in healthy adults, and specifically the total cholesterol to HDL ratio did not change or improve.

Forgot aspirin, replaced with Guinness on this trip.

I managed to not pack my aspirin bottle for this week. So rather than walk one block to Walgreens I am using the Guinness replacement. Don't do this or listen to me, I have no medical training. And since I'm on the 325 one rather than low-dose I assume I need 2-3 pints a day.

Guinness could really be good for you

A pint of the black stuff a day may work as well as a low dose aspirin to prevent heart clots that raise the risk of heart attacks.

Monday, April 10, 2017

Marijuana & Vascular Dementia

So rather than demonizing marijuana like this our researchers should come up with a solution to this  vascular squeezing ability. I bet the stroke and heart attack risk are from the smoking part rather than marijuana itself and people with these other health problems are using marijuana to self-treat themselves.   I plan on using marijuana short term after my next stroke.

My 13 reasons for marijuana use post-stroke.  

But don't listen to me, I have absolutely no medical training.



http://www.alzheimersweekly.com/2017/04/marijuana-vascular-dementia.html
As marijuana legalization spreads, new research is improving our understanding of side effects. Heart cells have cannabis receptors relevant to vascular squeezing ability. Learn about marijuana's link to vascular dementia.




WASHINGTON - Using marijuana raises the vascular risks of stroke and heart failure, major risk factors leading to vascular dementia. Even after accounting for demographic factors, other health conditions and lifestyle risk factors such as smoking and alcohol use, the data is compelling, according to research being presented at the American College of Cardiology’s 66th Annual Scientific Session.

Vascular Health

Coming at a time when marijuana, medically known as cannabis, is on track to become legal for medical or recreational use in more than half of U.S. states, this study sheds new light on how the drug affects vascular health. While previous marijuana research has focused mostly on pulmonary and psychiatric complications, the new study is one of only a handful to investigate cardiovascular outcomes.

“Like all other drugs, whether they’re prescribed or not prescribed, we want to know the effects and side effects of this drug,” said Aditi Kalla, MD, Cardiology Fellow at the Einstein Medical Center in Philadelphia and the study’s lead author. “It’s important for physicians to know these effects so we can better educate patients, such as those who are inquiring about the safety of cannabis or even asking for a prescription for cannabis.”

Nationwide Inpatient Sample

The study drew data from the Nationwide Inpatient Sample, which includes the health records of patients admitted at more than 1,000 hospitals comprising about 20 percent of U.S. medical centers. Researchers extracted records from young and middle-aged patients—age 18-55 years—who were discharged from hospitals in 2009 and 2010, when marijuana use was illegal in most states.

Marijuana use was diagnosed in about 1.5 percent (316,000) of more than 20 million health records included in the analysis. Comparing cardiovascular disease rates in these patients to disease rates in patients not reporting marijuana use, researchers found marijuana use was associated with a significantly increased risk for cardiovascular events such as stroke, heart failure, coronary artery disease and sudden cardiac death.

Marijuana - Independent Association

Marijuana use was also linked with a variety of factors known to increase cardiovascular risk, such as obesity, high blood pressure, smoking and alcohol use. After researchers adjusted the analysis to account for these factors, marijuana use was independently associated with a 26 percent increase in the risk of stroke and a 10 percent increase in the risk of developing heart failure. (Really?)

“Even when we corrected for known risk factors, we still found a higher rate of both stroke and heart failure in these patients, so that leads us to believe that there is something else going on besides just obesity or diet-related cardiovascular side effects,” Kalla said. “More research will be needed to understand the pathophysiology behind this effect.”

Heart Cells Have Canabis Receptors

Research in cell cultures shows that heart muscle cells have cannabis receptors relevant to contractility, or squeezing ability, suggesting that those receptors might be one mechanism through which marijuana use could affect the cardiovascular system. It is possible that other compounds could be developed to counteract that mechanism and reduce cardiovascular risk, Kalla said.

Because the study was based on hospital discharge records, the findings may not be reflective of the general population. The study was also limited by the researchers’ inability to account for quantity or frequency of marijuana use, purpose of use (recreational or medical), or delivery mechanism (smoking or ingestion).

Further Insights

Kalla suggested that the growing trend toward legalization of marijuana could mean that patients and doctors will become more comfortable speaking openly about marijuana use, which could allow for better data collection and further insights into the drug’s effects and side effects.


SOURCE:
  • The American College of Cardiology
    The American College of Cardiology is a 52,000-member medical society that is the professional home for the entire cardiovascular care team. The mission of the College is to transform cardiovascular care and to improve heart health. The ACC leads in the formation of health policy, standards and guidelines. The College operates national registries to measure and improve care, offers cardiovascular accreditation to hospitals and institutions, provides professional medical education, disseminates cardiovascular research and bestows credentials upon cardiovascular specialists who meet stringent qualifications.