Lorazepam for Parkinsons, breathing issues and anxiety

We want to relieve the anxiety among clients with Parkinsons with Lorazepam. Listening to their breathing at night and addiction to the med, makes us change our mind about daily use of Lorazepam. Per our experience, the client had difficulty breathing at 68 with Parkinsons. It also produces more thigh muscle cramps instead of relieving the cramps. Is there a better way?

Most neuro meds are addicting and results in the same health issues it is suppose to relieve.

Combine this med on as needed basis, not used daily with holistic home care with caring caregivers providing massage, extra care and compassion, healthy meals and lorazepam can only be used few times a week instead of daily.

Sometimes, the presence of caregivers relieve their anxiety without the need for medications. A full stomach also helps them sleep well and a regular massage before bedtime, legs and feet massage.

Call or text Motherhealth caregivers , 408-854-1883 , for bay area seniors with Parkinsons or other health issues for holistic home care.

Massage for seniors with cancer and Parkinsons

Many scientific studies have shown that oncology massage is effective in reducing symptoms such as stress, pain, anxiety, depression, nausea and fatigue in people who have had chemotherapy or surgery for cancer.


Most of our senior clients especially those with Parkinsons and Lung cancer love the massages given by their caregivers. Massage helps our cells grow. Even during chronic illness, massage provide relief, calms the mind and help clients feel good.
They are always looking forward to the massage. As if, their life here on earth is worth living for with loving massages.

Call or text 408-854-1883 for caregivers from Motherhealth in the greater bay area who incorporate massage in their caregiving tasks of assistance in daily living. Live-in care starts at $340 depending on level of care. Motherhealth@gmail.com is another way to contact us.

Trained and monitored caring caregivers are important in home care

  • Empowered staff with their customer experience successes
  • Informed teams of areas for improvement as patient experiences unfold
  • Enabled management, with actionable insights, to drive operational changes

Motherhealth trains and monitors its bayarea caregivers to have consistent care matching the home care needs of clients. This is very important for Alzheimer’s and Parkinson’s clients.

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Do Parkinson’s Medications Affect Sleep?

Do Parkinson’s Medications Affect Sleep?
Some PD meds, like MAO-B inhibitors (selegiline, rasagiline, safanimide) and amantadine (a medication used to treat dyskinesia), have alerting properties and may make insomnia worse. These medications are usually taken earlier in the day, so they do not impact sleep. Sinemet does not usually have a big impact on sleep compared to dopamine agonists.

However, nighttime hallucinations can emerge with increased intake of dopaminergic drugs, especially in people with more advanced Parkinson’s.
There are other possible causes of hallucinations, so if you begin to experience this, talk to your doctor right away. For more information, get your free copy of the Parkinson’s Foundation book Psychosis by calling Helpline at 1-800-4PD-INFO (473-4636) or online at Parkinson.org/books.

Sleep hygiene refers to the behaviors and habits that we can control that affect our bodies day-night cycling and readiness to go to sleep or be alert at a given time of day. Follow these tips for better sleeping habits:

  1. It is especially important for individuals with sleep difficulties to set and follow regular bed/sleep and wake times with a goal of spending at least 7 but not much more than 8 hours in bed each night. Bedtimes should be chosen based on a target waking time (i.e. don’t go to bed at 8 pm if you don’t want to be up at 4 am!).
  2. The bed should be used only as a place of sleeping, reading and watching television should be done elsewhere.
  3. Daytime napping should be limited to one nap of no greater than 30 minutes, as longer naps do not seem to provide any greater benefit to daytime fatigue but do disrupt sleep drive for the coming night.
  4. Lastly it is vital that persons with these sleep disorders are exposed to as much light (preferably real daylight) and physical/mental stimulation during the day as possible. Light is an important synchronizer of the sleep-wake cycle and many elderly individuals and individuals with chronic illness have reduced exposure to bright light.

Physical and mental activity stimulates the alerting and wakefulness centers in the brain and increase blood and oxygen flow to the brain. Most importantly, maintaining good sleep and wake habits can improve many sleep issues without the need of medications.

Gut-Dwelling Bacterium Consumes Parkinson’s Drug

Gut-Dwelling Bacterium Consumes Parkinson’s Drug
Posted on June 25th, 2019 by Dr. Francis Collins

Gut bacteria eating a pill

Scientists continue to uncover the many fascinating ways in which the trillions of microbes that inhabit the human body influence our health. Now comes yet another surprising discovery: a medicine-eating bacterium residing in the human gut that may affect how well someone responds to the most commonly prescribed drug for Parkinson’s disease.

There have been previous hints that gut microbes might influence the effectiveness of levodopa (L-dopa), which helps to ease the stiffness, rigidity, and slowness of movement associated with Parkinson’s disease. Now, in findings published in Science, an NIH-funded team has identified a specific, gut-dwelling bacterium that consumes L-dopa [1]. The scientists have also identified the bacterial genes and enzymes involved in the process.

Parkinson’s disease is a progressive neurodegenerative condition in which the dopamine-producing cells in a portion of the brain called the substantia nigra begin to sicken and die. Because these cells and their dopamine are critical for controlling movement, their death leads to the familiar tremor, difficulty moving, and the characteristic slow gait. As the disease progresses, cognitive and behavioral problems can take hold, including depression, personality shifts, and sleep disturbances.

For the 10 million people in the world now living with this neurodegenerative disorder, and for those who’ve gone before them, L-dopa has been for the last 50 years the mainstay of treatment to help alleviate those motor symptoms. The drug is a precursor of dopamine, and, unlike dopamine, it has the advantage of crossing the blood-brain barrier. Once inside the brain, an enzyme called DOPA decarboxylase converts L-dopa to dopamine.

Unfortunately, only a small fraction of L-dopa ever reaches the brain, contributing to big differences in the drug’s efficacy from person to person. Since the 1970s, researchers have suspected that these differences could be traced, in part, to microbes in the gut breaking down L-dopa before it gets to the brain.

To take a closer look in the new study, Vayu Maini Rekdal and Emily Balskus, Harvard University, Cambridge, MA, turned to data from the NIH-supported Human Microbiome Project (HMP). The project used DNA sequencing to identify and characterize the diverse collection of microbes that populate the healthy human body.

The researchers sifted through the HMP database for bacterial DNA sequences that appeared to encode an enzyme capable of converting L-dopa to dopamine. They found what they were looking for in a bacterial group known as Enterococcus, which often inhabits the human gastrointestinal tract.

Next, they tested the ability of seven representative Enterococcus strains to transform L-dopa. Only one fit the bill: a bacterium called Enterococcus faecalis, which commonly resides in a healthy gut microbiome. In their tests, this bacterium avidly consumed all the L-dopa, using its own version of a decarboxylase enzyme. When a specific gene in its genome was inactivated, E. faecalis stopped breaking down L-dopa.

These studies also revealed variability among human microbiome samples. In seven stool samples, the microbes tested didn’t consume L-dopa at all. But in 12 other samples, microbes consumed 25 to 98 percent of the L-dopa!

The researchers went on to find a strong association between the degree of L-dopa consumption and the abundance of E. faecalis in a particular microbiome sample. They also showed that adding E. faecalis to a sample that couldn’t consume L-dopa transformed it into one that could.

So how can this information be used to help people with Parkinson’s disease? Answers are already appearing. The researchers have found a small molecule that prevents the E. faecalis decarboxylase from modifying L-dopa—without harming the microbe and possibly destabilizing an otherwise healthy gut microbiome.

The finding suggests that the human gut microbiome might hold a key to predicting how well people with Parkinson’s disease will respond to L-dopa, and ultimately improving treatment outcomes. The finding also serves to remind us just how much the microbiome still has to tell us about human health and well-being.

Reference:

[1] Discovery and inhibition of an interspecies gut bacterial pathway for Levodopa metabolism. Maini Rekdal V, Bess EN, Bisanz JE, Turnbaugh PJ, Balskus EP. Science. 2019 Jun 14;364(6445).

Links:

Parkinson’s Disease Information Page (National Institute of Neurological Disorders and Stroke/NIH)

Gut microbes eat our medication for Parkinson

Pills illustration (stock image).
Credit: © georgejmclittle / Adobe Stock
Researchers have discovered one of the first concrete examples of how the microbiome can interfere with a drug’s intended path through the body. Focusing on levodopa (L-dopa), the primary treatment for Parkinson’s disease, they identified which bacteria out of the trillions of species is responsible for degrading the drug and how to stop this microbial interference.

The first time Vayu Maini Rekdal manipulated microbes, he made a decent sourdough bread. At the time, young Maini Rekdal, and most people who head to the kitchen to whip up a salad dressing, pop popcorn, ferment vegetables, or caramelize onions, did not consider the crucial chemical reactions behind these concoctions.

Even more crucial are the reactions that happen after the plates are clean. When a slice of sourdough travels through the digestive system, the trillions of microbes that live in our gut help the body break down that bread to absorb the nutrients. Since the human body cannot digest certain substances — all-important fiber, for example — microbes step up to perform chemistry no human can.

“But this kind of microbial metabolism can also be detrimental,” said Maini Rekdal, a graduate student in the lab of Professor Emily Balskus and first-author on their new study published in Science. According to Maini Rekdal, gut microbes can chew up medications, too, often with hazardous side effects. “Maybe the drug is not going to reach its target in the body, maybe it’s going to be toxic all of a sudden, maybe it’s going to be less helpful,” Maini Rekdal said.

In their study, Balskus, Maini Rekdal, and their collaborators at the University of California San Francisco, describe one of the first concrete examples of how the microbiome can interfere with a drug’s intended path through the body. Focusing on levodopa (L-dopa), the primary treatment for Parkinson’s disease, they identified which bacteria are responsible for degrading the drug and how to stop this microbial interference.

Parkinson’s disease attacks nerve cells in the brain that produce dopamine, without which the body can suffer tremors, muscle rigidity, and problems with balance and coordination. L-dopa delivers dopamine to the brain to relieve symptoms. But only about 1 to 5% of the drug actually reaches the brain.

This number — and the drug’s efficacy — varies widely from patient to patient. Since the introduction of L-dopa in the late 1960s, researchers have known that the body’s enzymes (tools that perform necessary chemistry) can break down L-dopa in the gut, preventing the drug from reaching the brain. So, the pharmaceutical industry introduced a new drug, carbidopa, to block unwanted L-dopa metabolism. Taken together, the treatment seemed to work.

“Even so,” Maini Rekdal said, “there’s a lot of metabolism that’s unexplained, and it’s very variable between people.” That variance is a problem: Not only is the drug less effective for some patients, but when L-dopa is transformed into dopamine outside the brain, the compound can cause side effects, including severe gastrointestinal distress and cardiac arrhythmias. If less of the drug reaches the brain, patients are often given more to manage their symptoms, potentially exacerbating these side effects.

Maini Rekdal suspected microbes might be behind the L-dopa disappearance. Since previous research showed that antibiotics improve a patient’s response to L-dopa, scientists speculated that bacteria might be to blame. Still, no one identified which bacterial species might be culpable or how and why they eat the drug.

So, the Balskus team launched an investigation. The unusual chemistry — L-dopa to dopamine — was their first clue.

Few bacterial enzymes can perform this conversion. But, a good number bind to tyrosine — an amino acid similar to L-dopa. And one, from a food microbe often found in milk and pickles (Lactobacillus brevis), can accept both tyrosine and L-dopa.

Using the Human Microbiome Project as a reference, Maini Rekdal and his team hunted through bacterial DNA to identify which gut microbes had genes to encode a similar enzyme. Several fit their criteria; but only one strain, Enterococcus faecalis (E. faecalis), ate all the L-dopa, every time.

With this discovery, the team provided the first strong evidence connecting E. faecalis and the bacteria’s enzyme (PLP-dependent tyrosine decarboxylase or TyrDC) to L-dopa metabolism.

And yet, a human enzyme can and does convert L-dopa to dopamine in the gut, the same reaction carbidopa is designed to stop. Then why, the team wondered, does the E. faecalis enzyme escape carbidopa’s reach?

Even though the human and bacterial enzymes perform the exact same chemical reaction, the bacterial one looks just a little different. Maini Rekdal speculated that carbidopa may not be able to penetrate the microbial cells or the slight structural variance could prevent the drug from interacting with the bacterial enzyme. If true, other host-targeted treatments may be just as ineffective as carbidopa against similar microbial machinations.

But the cause may not matter. Balskus and her team already discovered a molecule capable of inhibiting the bacterial enzyme.

“The molecule turns off this unwanted bacterial metabolism without killing the bacteria; it’s just targeting a non-essential enzyme,” Maini Rekdal said. This and similar compounds could provide a starting place for the development of new drugs to improve L-dopa therapy for Parkinson’s patients.

The team might have stopped there. But instead, they pushed further to unravel a second step in the microbial metabolism of L-dopa. After E. faecalis converts the drug into dopamine, a second organism converts dopamine into another compound, meta-tyramine.

To find this second organism, Maini Rekdal left behind his mother dough’s microbial masses to experiment with a fecal sample. He subjected its diverse microbial community to a Darwinian game, feeding dopamine to hordes of microbes to see which prospered.

Eggerthella lenta won. These bacteria consume dopamine, producing meta-tyramine as a by-product. This kind of reaction is challenging, even for chemists. “There’s no way to do it on the bench top,” Maini Rekdal said, “and previously no enzymes were known that did this exact reaction.”

The meta-tyramine by-product may contribute to some of the noxious L-dopa side effects; more research needs to be done. But, apart from the implications for Parkinson’s patients, E. lenta’s novel chemistry raises more questions: Why would bacteria adapt to use dopamine, which is typically associated with the brain? What else can gut microbes do? And does this chemistry impact our health?

“All of this suggests that gut microbes may contribute to the dramatic variability that is observed in side effects and efficacy between different patients taking L-dopa,” Balskus said.

But this microbial interference may not be limited to L-dopa and Parkinson’s disease. Their study could shepherd additional work to discover exactly who is in our gut, what they can do, and how they can impact our health, for better or worse.

Story Source:

Materials provided by Harvard University. Original written by Caitlin McDermott-Murphy. Note: Content may be edited for style and length.