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Saturday, September 22, 2018

Spanish scientists challenge origins of Parkinson's

Sep 22, 2018 news@thinkspain


SCIENTISTS at a Madrid neurobiology laboratory have made a ground-breaking discovery as to the origins of Parkinson's disease, throwing into conjecture previous assumptions about where the condition starts.
The HM CINAC, or Integral Centre for Neurosciences, says the disease may not, in fact, 'spread' to the cerebral cortex as its 'final destination', as has hitherto been believed: it could be that this is where it starts.
This would explain why Parkinson's starts off with motor issues, or problems affecting general movement, speech and the body's outward physical activity.
A neurodegenerative condition characterised by rigidity, slowness and trembling – although the latter may not always be present, especially in young victims – has largely been explained by the death of 'black mater' neurons, or nerve sources in the part of the brain that generates dopamine, a brain chemical associated with the feeling of being 'switched on' and 'positive' and an over-firing of which is thought to be behind delusional disorders such as psychosis and schizophrenia, as well as attention deficit-hyperactivity disorder (ADHD).
The loss of neurons in the dopamine or 'active' and 'feel-good' part of the brain has never yet been explained, but the HM CINAC scientists believe it is not a localised phenomenon: instead, it is a 'stage on a more complex pathological journey which literally progresses in a bottom-up direction'.
Explaining it more in layman's terms, Dr José A Obeso and Dr Guglielmo Foffani compare the brain to a tree.
“The illness starts in the bottom of the trunk, at which point it is asymptomatic, then rises to about halfway up, when early signs start to show,” Foffani and Obeso say.
“It eventually spreads to the leaves – which is the brain cortex – and that's when you see the most advanced cases.”
Symptoms most typical of Parkinson's tend to manifest themselves in a very 'localised' or 'focal' manner, such as a slow-moving leg or a trembling hand, but the disease may have already been present before any of these occur, Dr Foffani and Dr Obeso say.
The motor area and somatosensory area – responsible for voluntary actions, movements and responses – are the parts of the brain containing 'the best and most detailed map of the rest of the body', and these could be the parts which suppress vulnerable dopamine-transmitting neurons and cause them to degenerate.
“This theory is disruptive in terms of existing beliefs about the origin of Parkinson's, but does not necessarily break away from current hypotheses; rather, it could coexist with these and even contribute to developing new and possibly less-invasive forms of treatment,” the research paper says.
Considering the discovery 'very valuable', the HM CINAC team have started a series of experiments to falsify their theories.
https://www.thinkspain.com/news-spain/30981/spanish-scientists-challenge-origins-of-parkinson-s

An Interview with 23andMe’s Parkinson’s disease program Manager Paul Cannon

September 21, 2018

Paul Cannon, Ph.D., 23andMe’s Parkinson’s Research Community manager.


We’re reprinting this interview with Paul Cannon, Ph.D, about treatment for his Parkinson’s as well as updates on 23andMe’s research, that was put together by Tomorrow Edition blogger Benjamin Stecher.

Paul, who took the helm of 23andMe’s research community in 2014, shared with Ben decision to undergo surgery for Deep Brain Stimulation, as a way to treat his Parkinson’s symptoms.  Below is an excerpt from the interview, or see the full article : https://tmrwedition.com/2018/09/15/interview-with-23andmes-dr-paul-cannon/

You very recently underwent Deep Brain Stimulation (DBS) surgery, how did you come to that decision?

So obviously it is not a decision to be made lightly, it is brain surgery. I have always had a good response to Sinemet (the primary drug used for the treatment of Parkinson’s disease), but in the last year or so I had been having more severe fluctuations in my response to the drug. That was what essentially moved me towards going through with DBS. I made the decision earlier this year and scheduled the procedure for the summer when the chances of getting a cold or an infection that might interrupt the procedure were diminished. I had the surgery just over three weeks ago.

What were some of your biggest reservations that went into that decision?

Well it is a fairly invasive and long procedure. I was awake for parts of it, which is an interesting experience. Also I’m very interested in the closed-loop technology that is being developed for DBS, hopefully the equipment that I got could be adapted to that later. The stimulator itself can be changed, but the electrodes you probably get for life.

Was there any hesitancy around the fact that many clinical trials list DBS as one of their exclusion criteria?

That is fairly common, but most disease modifying trials mainly target earlier stage patients. I was diagnosed seven and a half years ago and was symptomatic a good number of years before that, so I would probably be ineligible for many of them anyway.

What was the day of the surgery itself like?

The day before the surgery I had my head shaved and they put five screws into my head followed by a CT scan to help position the brain when I was in the operating theater. The next morning I went in for the first procedure to implant the electrodes. I was awake when they put the electrodes into the brain and they listen to the activity of your brain as an indication that they are in the right region. 

Then they apply a number of stimuli via the electrode and test for impact on motor symptoms (I was off PD medication) as well as speech. They did one side and then the other. I went home the next day with the wires implanted but without the stimulator and battery put in, that was done the following week and was a straight-forward outpatient surgery. I am getting the device turned on and programmed for the first time this week, some 5 weeks after the initial surgery. 

The reason for the delay between the two is that there is a micro-lesion effect where actually having the surgery itself improves the symptoms. Over time that wears off. I am now back to my regular medication.

What is it like to be awake while somebody is fiddling around inside your brain?

It is a little disconcerting I must say, more stressful than I anticipated. The operating staff were great and helped me manage anxiety. They put you to sleep at first and then wake you up once the electrodes are ready to be inserted. I did hear and feel suction at the back of my head, I also had a headache that came up during the procedure. Otherwise it is just lying on your back trying not to think about what is going on behind you. You then go through a simple set of tests as they turn on the stimulation. It takes a couple of hours to do both sides. They then put you back to sleep, sew you up and you wake up a couple hours later.

Was there anything surprising or unexpected about the surgery?

I felt pretty good the next day. Though the surgery was tough, once I was in recovery there was very little pain associated with it and very few side effects from it.

One other thing I would stress is from some of the data that has come in recently. DBS used to be reserved more for people in an advanced state. But we are seeing it being done more in younger people and at an earlier state because when you are younger you are more able to withstand the surgical procedure and the associated stress. There is data that indicates that there is more benefit to having it done earlier and is more cost effective:
https://www.medscape.com/viewarticle/779416

Moving into your day job, could you give a little background about 23andMe’s involvement with Parkinson’s disease?

23andMe is a direct to consumer genetics company with a long standing interest in PD. The PD community project was launched over nine years ago. We have been working closely with The Michael J. Fox Foundation and others to build up a sizeable genotyped and broadly phenotyped cohort of people with self-reported PD. Some of the more interesting data in that cohort comes from the self-reported information that has not traditionally been directly associated with PD.

What have been some of the most surprising findings that have emerged from your time at 23andMe?

It is less the data and more just the engagement of people with the research process. A high percentage of people have been regularly engaged with what we do, especially in the disease cohorts. It has been impressive, inspiring and humbling at the same time. Without them, it would be much more difficult for us to look at how genetics, along with environmental data, can inform disease risk, progression and response to medication.

What can you tell us about 23andMe’s recent partnership with GlaxoSmithKline?

It covers a lot of disease areas to try and identify targets and treatments. In Parkinson’s specifically we are developing a joint program in the LRRK2 inhibitor area. It is very exciting because it brings both of our expertise together to learn from each other and develop better treatments.

What excites you most about the future of genetic research in PD?

I think study of PD genetics can lead us to a better understanding of the molecular underpinnings of this disease as well as the variability in presentation, progression and medication response. The question is how best to use that to inform new targets and predict individual treatment responses. We aren’t as interested in telling people if they are fast or slow progressors, what we want focus on now is can we help doctors decide which treatment regime is best for each individual. This will only become more important when truly disease modifying medications become available.

Could you talk about a paper you authored that was just released looking at combining genetic data with self-reported data?

It was a collaboration with Pfizer looking at people with specific genetic mutations and asking whether they differ in terms of self-reported phenotype data. The lack of objective symptom data was mentioned as a concern by one of the reviewers, however most healthcare data today is still self-reported, i.e. the doctor asks you how you feel and records it. In fact the phenotypes that we found associated with the specific mutations were consistent with those found by others in more traditional research cohorts, suggesting that self-reported data can reliably be used to support PD genetics research. But even when we do have objective biomarkers, the ultimate measures are still whether the patient feels and functions better.

Update from Paul on September 14th: “I went in yesterday to have the device turned on and programmed. Currently set at a low level of stimulation, whilst we taper off the dopamine replacement medication. But even at this level I notice a marked improvement in my ability to walk, especially in terms of arm swing etc. so I am hopeful of a very positive journey”

https://blog.23andme.com/research-communities/an-interview-with-23andmes-parkinsons-disease-program-manager-paul-cannon/

Friday, September 21, 2018

Easy strategies to boost your dopamine levels naturally

September 20, 2018 by: Zoey Sky



(Natural News) Dopamine, a major neurotransmitter, is linked to focus, motivation, and productivity. However, factors such as diet and lifestyle can deplete your dopamine levels. If you feel like you’re not living your life to its fullest, you may be suffering from low dopamine levels. Thankfully, there are natural ways to increase dopamine.

What is dopamine and why is it important?

The human brain has around 86 billion neurons, and they communicate with each other through brain chemicals known as neurotransmitters. Dopamine, one of the most widely studied neurotransmitters, is associated with various aspects of human behavior, including addictions, motivation, and pleasure-seeking. It has crucial roles in anticipatory pleasure, attention, learning, memory, mood, movement, and sleep.

On the other hand, dopamine dysfunction is behind several diseases such as Parkinson’s disease, which is caused by the death of cells that produce dopamine. Only a handful of neurons create dopamine, and these neurons are only found in a few areas of the brain.
The neurotransmitter is also used by several systems outside the central nervous system, like immune cells, the kidneys, and the pancreas. This dopamine is created locally because it’s unable to move across the brain’s protective blood-brain barrier.

Dopamine affects your daily life because it is a “motivation molecule.” This means that the neurotransmitter can boost your concentration, drive, and focus. It also controls the pleasure-reward system. It makes you feel bliss, enjoyment, and euphoria.

If you suffer from dopamine deficiency, you may feel lethargic, unfocused, and unmotivated. It can also leave you feeling depressed. (Related: Dopamine influences your decisions; scientists discover that how long we have to wait for what we want affects its value.)
Common symptoms of dopamine deficiency may include:
  • Engaging in self-destructive behaviors (e.g., addictions)
  • Inability to feel pleasure
  • Lack of motivation
  • Low libido
  • Sleep problems
  • Trouble concentrating
  • Trouble connecting with others
A dopamine deficiency can also manifest as certain psychiatric disorders like addiction, attention deficit disorder (ADD), bipolar disorder, and depression. Dopamine deficiency may have underlying causes like addictions, obesity, a poor diet, nutritional deficiencies, thyroid disorders, and the use of dopamine antagonist drugs.



How can you boost your dopamine levels?

Activities, foods, or supplements don’t always increase your dopamine levels. In some cases, this means your dopamine levels stay the same but it is better utilized through various neurochemical changes.

Dopamine-boosting foods

There are foods that contain dopamine, but their dopamine content can’t cross the blood-brain barrier. You need a workaround for this to happen.
Dopamine is produced from l-tyrosine, an amino acid often found in protein-rich foods. By following a diet high in l-tyrosine, you can have the necessary building blocks for dopamine synthesis.
These are some of the drinks, foods, and spices that either have l-tyrosine or can help increase dopamine directly:
  • All animal products (e.g., dairy, eggs, fish, meat, and poultry)
  • Avocados
  • Bananas
  • Coffee
  • Green leafy vegetables
  • Nuts
  • Oats
  • Peanuts
  • Rosemary
  • Soy products
  • Turmeric
  • Wheat
Broad beans/fava beans contain l-dopa, a direct precursor to dopamine that is used to cure Parkinson’s. Probiotic-rich foods such as kefir, raw sauerkraut, and yogurt can help boost dopamine production.

How can you boost your dopamine levels?

Activities, foods, or supplements don’t always increase your dopamine levels. In some cases, this means your dopamine levels stay the same but it is better utilized through various neurochemical changes.

Dopamine-boosting foods

There are foods that contain dopamine, but their dopamine content can’t cross the blood-brain barrier. You need a workaround for this to happen.
Dopamine is produced from l-tyrosine, an amino acid often found in protein-rich foods. By following a diet high in l-tyrosine, you can have the necessary building blocks for dopamine synthesis.
These are some of the drinks, foods, and spices that either have l-tyrosine or can help increase dopamine directly:
  • All animal products (e.g., dairy, eggs, fish, meat, and poultry)
  • Avocados
  • Bananas
  • Coffee
  • Green leafy vegetables
  • Nuts
  • Oats
  • Peanuts
  • Rosemary
  • Soy products
  • Turmeric
  • Wheat
Broad beans/fava beans contain l-dopa, a direct precursor to dopamine that is used to cure Parkinson’s. Probiotic-rich foods such as kefir, raw sauerkraut, and yogurt can help boost dopamine production.


Dopamine supplements

Here are some supplements that can also naturally increase your dopamine levels.
  • Curcumin – Curcumin, the main active ingredient in turmeric, can cross the blood-brain barrier and boost dopamine levels. Buy curcumin supplements with piperine, a compound found in black pepper that boosts curcumin absorption by a whopping 2,000 percent.
  • Ginkgo Biloba – Ginkgo biloba is traditionally used to treat brain-related conditions such as anxiety, depression, memory problems, and poor concentration.
  • L-theanine – L-theanine is a unique compound found in black, green, and white teas. It can boost dopamine and serotonin levels. Additionally, the compound can increase levels of the relaxing neurotransmitter gamma-aminobutyric acid (GABA). L-theanine can boost your learning and recall, and it can enhance your mood.
  • L-tyrosine – L-tyrosine is an amino acid that’s the precursor to dopamine.
  • Mucuna pruriens – Velvet bean (Mucuna pruriens), a tropical legume, has l-dopa. Anti-aging M. pruriens supplements can boost your libido and enhance your memory, mood, and overall brain health.
  • Phosphatidylserine – Phosphatidylserine is the brain’s “gatekeeper,” meaning it regulates nutrients and waste in and out of the brain.

Lifestyle changes

These lifestyle changes can also boost your dopamine levels:
  • A cold shower – You can either take a cold shower or end a hot shower with a cold blast of water. Taking a shower with 14-degree Celsius (57 degrees Fahrenheit) water can boost dopamine levels by as much as 250 percent.
  • Meditation – Meditating regularly can help you relax, enhance learning ability, and increase creativity. Creative hobbies like drawing, knitting, photography, and woodworking allow the brain to go into a meditative state.
  • Music – Music can help release dopamine. Like eating or making love, listening to music can make the brain’s pleasure center light up.
  • Regular exercise – Physical activity will raise baseline levels of dopamine via the promotion of the growth of new brain cell receptors. Gentle and no-impact exercises like tai chi/qi gong, taking walks, or yoga can also boost dopamine levels. Aim for at least 20 minutes of exercise daily to improve your mood.
  • Sleep – Dopamine helps control the production of melatonin, the sleep hormone.
  • Touch – Different kinds of pleasurable touch, such as a therapeutic massage or petting animals, can increase dopamine.
  • Weight loss – Obese people have fewer dopamine receptors than average and their brains function the same as a drug addict’s brain does. Because dopamine controls the brain’s pleasure center, being obese means you get less pleasure and satisfaction from eating. This makes you want to eat more.
To increase your dopamine levels and stay motivated, follow a healthy diet and make the necessary lifestyle changes.
Learn more about dopamine and how it can boost your mental health at Mind.news.

Sources include:

http://www.topix.com/newsmail/art-iframe?node=health/parkinsons-disease&u=https%3A//www%2Enaturalnews%2Ecom/2018-09-20-easy-strategies-to-boost-your-dopamine-levels-naturally%2Ehtml&z=TM6OKMDI955Q5EJ3

New Videos Answer Basic Alzheimer’s Germ Questions, says Dr. Leslie Norins of Alzheimer’s Germ Quest, Inc.

NAPLES, FL, UNITED STATES, September 20, 2018 


A new video series by Dr. Leslie Norins answers the public's most pressing questions about the possible role germs play in Alzheimer's disease.



Alzheimer’s Germ Quest, Inc., announced it is posting eight one-minute videos—one per week—to answer some of the questions most frequently asked by the public about its proposition that a germ might be the cause of Alzheimer’s disease. The respondent is the Quest’s CEO, Leslie Norins, MD, PhD


The first has been posted on the company’s website and its YouTube channel.

The initial video asks, “Do Normal Brains Contain Any Germs?” Dr. Norins explains that “Brains of perfectly normal people, surprisingly, contain viruses and bacteria. So, any invading Alzheimer’s germ would add to these.”

Also in the queue are questions such as “Could There be an Antibiotic for Alzheimer’s?” and “Could Alzheimer’s be Transmitted to Caretakers?” Simple language is used to aid comprehension of the material presented.

“Almost no research on possible infectious causes of Alzheimer’s is funded by government agencies despite $2 billion in research money given to them by Congress to solve this disease puzzle. Advocacy groups equally ignore funding investigations of infectious agents,” says Dr. Norins.

The short videos were produced in response to many inquiries from the public, which included encouragement of further investigation of the germ possibility.
Dr. Norins, a 44-year medical publisher, in his early career directed a research laboratory at the federal Centers for Disease Control and Prevention. 

Two years ago he became interested in Alzheimer’s disease, and upon reviewing the scientific literature was surprised to find possible infectious triggers had been little explored.

Alzheimer’s Germ Quest, Inc. is a public benefit corporation headquartered in Naples Florida. Its mission is to accelerate and deepen scientific investigations into the possible role of infectious agents as the root cause of Alzheimer’s disease. It is the sponsor of the $1 Million Alzheimer’s Germ Quest Challenge Award for scientists. (ALZgerm.org).

Mollie Page Griffin2397777243
Alzheimer's Germ Quest

Do Normal Brains Contain Any Germs?

Watch Alzheimer’s Germ Quest CEO Dr. Leslie Norins, MD, Ph.D announce the $1 million challenge award for the scientist who provides persuasive 

https://www.einpresswire.com/article/462522034/new-videos-answer-basic-alzheimer-s-germ-questions-says-dr-leslie-norins-of-alzheimer-s-germ-quest-inc?ref=email&code=3WorCQnvElu3nxD6&utm_source=NewsletterPR&utm_medium=email&utm_campaign=Healthcare+%26+Pharmaceuticals+Industry+Press+Releases&utm_content=article

How cannabinoid drugs affect the experience of pain

 Ana Sandoiu    Sept. 21, 2018

Cannabis-derived drugs may help treat pain, but the mechanisms behind their benefits may come as a surprise.


The Centers for Disease Control and Prevention (CDC) suggest that up to 50 million people in the United States have chronic pain.

An increasing amount of people now turn to the medicinal benefits of cannabis for treating and alleviating pain.

As a result, scientists are trying to keep up by studying the effects of cannabinoids on pain.

So far, however, studies have produced mixed results. A recent study that spanned over 4 years found "no evidence" that cannabis alleviates chronic pain that is not associated with cancer.

New research puts forth an interesting explanation for why the current clinical evidence does not fully support the popularity of cannabis as a painkiller and people's subjective accounts of its benefits.

It may be that the "feel-good" factor in the use of cannabis and cannabinoid drugs makes pain "more tolerable" and "less unpleasant," suggests the new study, and that the benefits of cannabinoid drugs may operate more on an affective level rather than a sensory one.

Martin De Vita, a doctoral researcher in the clinical psychology program at Syracuse University in New York, led the new study, which was published in the journal JAMA Psychiatry. 

He explains the motivation for the new research, saying, "Cannabinoid drugs are widely used as analgesics [painkillers], but experimental pain studies have produced mixed findings."

"Pain is a complex phenomenon with multiple dimensions that can be affected separately," adds the researcher. "Patients reliably endorse the belief that cannabis is helpful in alleviating pain; however, its analgesic properties are poorly understood."

Pain feels 'less unpleasant, more tolerable'

To help clarify the analgesic properties, De Vita and colleagues examined over 1,830 experimental studies on the effects of cannabinoids that were carried out over a 40-year period.

Cannabinoids are active chemical substances in the cannabis plant, of which tetrahydrocannabinol (THC) is one. THC binds to pleasure-controlling brain receptors and boosts levels of dopamine, a substance known as the "sex, drugs, and rock 'n' roll" hormone due to its euphoric effects.

After narrowing the initial pool of studies down to 18, the researchers looked at data from over 440 study participants. The data were also separately examined by two independent reviewers.

"The mean quality and validity score across the studies was high," notes De Vita, "and analyses did not suggest publication bias."

The results revealed that cannabinoid drugs correlated with "modest increases in experimental pain threshold and tolerance," and a reduction in the "perceived unpleasantness of painful stimuli."

However, the researchers found no association with a reduction in the intensity of the experimental pain, or in hyperalgesia, which is a heightened sensitivity to pain.

Therefore, the authors conclude, "Cannabinoid drugs may prevent the onset of pain by producing small increases in pain thresholds but may not reduce the intensity of experimental pain already being experienced."

"[I]nstead," they say, "cannabinoids may make experimental pain feel less unpleasant and more tolerable, suggesting an influence on affective processes."

"What this means is that cannabinoid analgesia may be driven by an affective, rather than a sensory component. These findings have implications for understanding the analgesic properties of cannabinoids."
Martin De Vita

"The cumulative research synthesized in our review has helped characterize how cannabis and cannabinoids affect different dimensions of pain reactivity," De Vita adds. "It may underlie the widely held belief that cannabis relieves pain. For now, we still have much to learn."

https://www.medicalnewstoday.com/articles/323125.php?utm_source=newsletter&utm_medium=email&utm_country=US&utm_hcp=no&utm_campaign=MNT%20Daily%20Full%20%28non-HCP%20US%29%20-%20OLD%20STYLE%202018-09-21&utm_term=MNT%20Daily%20News%20%28non-HCP%20US%29

Experience: I will be plastinated when I die

Gunther von Hagens      Fri 21 Sep 2018 

The challenges I face are immense. Suffering from Parkinson’s disease is like practicing dying

Gunther von Hagens: ‘I envisage my plastinated body standing in a welcoming pose at the entrance of an exhibition.’ Photograph: Michele Tantussi/Getty Images


In July 1977, I was working as a research scientist at the University of Heidelberg’s Institute of Pathology and Anatomy. Looking at specimens embedded in plastic – the most advanced preservation technique then available – I wondered why the plastic was poured around bodies rather than into them.

That was when I came up with the idea of vacuum-impregnation, whereby bodily fluids and soluble fat are extracted and replaced with resins, silicon rubbers and epoxies, a process I later named plastination. But it was only after a year of intense research, and hundreds of experiments, that I got some presentable results. By March 1978, I filed the first patent for plastination, a technique now used in 400 medical schools and universities worldwide (although the first whole-body plastinate was still 13 years away).

In the beginning, I thought plastination would mainly contribute to improving medical teaching. But the huge subsequent lay interest inspired me to create public exhibitions – not to shock people, but capture their imaginations. The first Body Worlds exhibition, featuring whole body plastinates, was shown in Japan in 1995; next month, we will open a permanent museum at the London Pavilion. 

Now, at the age of 73, my body is breaking down. I have Parkinson’s disease and the challenges I face are immense. Suffering from Parkinson’s is like practising dying. My hands tremble, my speech is faltering and my movements are uncoordinated. I have lost skills I had, and they will never return. I can’t play my beloved violin any more. The doctors prognosticated that I would end up in a wheelchair, but fortunately I can still walk and move around freely. The biggest obstacle is my speech; I now avoid speaking in public. 

I always wanted to be plastinated. Among the 17,000 who have signed up to donate their bodies for plastination are my wife, Angelina, who has been working with me for more than 30 years, and my son Rurik, who takes care of our finances. After years of physical decline, I feel better having transferred many of my stressful duties to my wife and son. I have started to actively fight the disease, and changed my attitude towards it. My strong will is my most powerful gift. I feed my body well, and give it enough sleep and exercise. I focus on new projects that keep my brain cells alive.

I want to live longer than my father, who just celebrated his 101st birthday. After my death, we have agreed that Angelina will plastinate me. I could envisage my plastinated body standing in a welcoming pose at the entrance of an exhibition, or rendered into slices and distributed across various sites. The ultimate decision rests with her. What can be done with plastination is dependent on many factors; if I were injured in a car accident, for example, slices would be unlikely to be an option.

Although I approach the body as a modernist and a minimalist, I feel that my role is to carry on the tradition of Renaissance anatomists. This is to reject the taboos and convictions people have about death and the dead, our joint and inescapable fate.

I want my work to live on. It gives me great satisfaction to know that I will continue to teach after my death. Sometimes, at this stage of my life and illness, I wish I could suspend my convictions and embrace the idea of a divinity and an afterlife. Kierkegaard said that religion was the great consolation of his life. But I don’t think there is a continuum beyond death. Every deceased body I have seen has shown me the absence of the soul. I don’t believe anything is left of us after we die.

My critics allege that I violate the sanctity of the dead. I say that there is no violation in giving a deceased human a postmortal identity– and decomposition is not sacred, either. The postmortal body is confrontational. It forces us to set aside our unconscious and conscious repudiation of death; all of us die a little every day.

https://www.theguardian.com/lifeandstyle/2018/sep/21/i-want-to-be-plastinated-when-i-die

Always Look on the Bright Side

   By Michael Church · September 20, 2018




When I tell some people that I have Parkinson’s disease (PD), I get a variety of responses. I am sure you do too. Often they involve more questions but the most common reaction is: “Oh, I’m sorry.” Living with PD is different for everyone because each of us is different and experience symptoms, attitudes and personalities. One thing I am sure of is this; no matter what PD deals me, I play those cards to the best outcome possible. That may mean a bit of bluffing and sometimes it is real hard to smile and laugh when you feel like crying. The crying part is real easy for me considering living with a chronic, neurological, progressive illness stacks the deck against me and the odds don’t look good. I suppose our brains are just wired that way. No pun intended for those with deep brain stimulation (DBS). It’s a PD humorthing! So what are we supposed to do to put on a happy face to avoid those long dark periods of life with PD.

Chase the PD blues away

Things to chase the PD blues away first include determination. You must consciously decide that you really want to be happy today. When you wake up, it is important to convince yourself, against the rigidity and pain you might feel, that staying in bed and pulling the covers over your head is not an option. Tell yourself, I am going to be a participant, not just a spectator of life. You can start by putting your feet on the floor. There, that’s a start. You would be surprised what neurons begin firing by this arduous task. If you are like me, your next neuron induced thought is “God, help me make it to the bathroom on time.” This can be a problem especially for people living with PD but I digress. Another thing once you are physically up, before you retreat back to your bed, open the blinds and let the sunshine in or if you are fortunate enough to have a sun porch or sun room. Spend a few minutes soaking up a little vitamin D which a large percentage of those living with PD are depleted of according to medical science. Take advantage of these few minutes of time to set goals for today. These are short term goals that assist in overcoming apathy which runs high among those people living with PD. I actually use a white eraser board and write down the things I want to accomplish that day. Such as:
  • Pick up medication at the pharmacy.
  • Go grocery shopping.
  • Get my hair cut. (actually not on my personal list, see photo)
  • Get a manicure/pedicure
The point is to make these small obtainable goals that you can accomplish successfully without wearing yourself out. Remember, fatigue is one of your symptoms and you only have so much energy.

The power of positive thinking

Ignore the negative, brain draining, stressful and drama filled events that use up all your dopamine. Avoid situations that attack your emotional and mental wellbeing. This won’t be easy. I know from experience that less drama equals less mental stress, which we all know is detrimental to good mental health. Incorporate positive up lifting music into your daily routine. Studies have shown that music and light exercise is important and beneficial in treating PD. Here are some things you can do every day to help:
The emphasis is to explore the available programs for therapy for PD in your area and find one that you enjoy. So the next time you feel down and blue, fight back against the disease with purposeful and positive mental health. Don’t let the PD win. This is a battle of which you are not alone. So put your feet on the floor, throw open those shades and live well with Parkinson’s Disease. As always, I encourage you to add your questionsstories, and comments and keep battling my friends.

Michael Church


https://parkinsonsdisease.net/living/bright-side/