Antidepressants and antihistamines are among the most common types of medications people take, and they belong to a class of drugs known as anticholinergics. These drugs can treat a variety of health problems, including COPD, asthma, depression, dizziness, gastrointestinal problems, overactive bladder, and the symptoms of Parkinson’s. Although they can be effective, a large new study has shown that if you take them, you might just be trading one problem for another, possibly bigger one: dementia.
Although people who suffer from depression may be desperate to get relief from this illness that can have such a negative impact on daily life, tricyclic antidepressants fall into this category, so it’s important to pay attention the concerning new findings if you take medications like Elavil, Deptran, Sinequan, or Silenor. The same can be said for antihistamines like Benadryl, among other drugs.
The study, which was published in BMJ, involved more than 40,000 dementia patients and more than 283,000 people who don’t have dementia and followed them from 2006 to 2015. They found that people who had dementia had a greater likelihood of having taken class 3 anticholinergic drugs prior to developing the illness.
These medications block the actions of acetylcholine in the brain, which can prevent it from causing involuntary movements in the muscles in the lungs, urinary tract, gastrointestinal tract, and other parts of the body.
Although the higher risk varied depending on the drugs, some of them raised the risk by 30 percent. Not every anticholinergic drug had the effect, but using some of them even as far back as 20 years raised a person’s risk of dementia later on. Generally speaking, they believe that a person aged 65 to 70 sees their risk of dementia increase by 19 percent if they’ve used anticholinergic antidepressants. The association with dementia goes up with greater levels of exposure to the meds.
The study was praised by experts for its strength and using U.K. healthcare databases rather than relying on patient recall, which isn’t always dependable.
The drugs are believed to have this effect because anticholinergic medications lower the levels of a chemical called acetylcholine in the brain, which is a crucial messenger in memory pathways. This is a known effect that already stops some doctors from prescribing such drugs to older and more frail patients.
Other studies have reached a similar conclusion about anticholinergic drugs
In a different study involving nearly 3,500 people, researchers reached a similar conclusion, finding that those who used anticholinergic drugs had a greater likelihood of developing dementia, and their risk increased according to their cumulative dose. For example, taking such meds for three years or longer was linked to a 54 percent rise in dementia risk compared to taking the same dose for less than three months.
Experts say such findings are a good reminder that people should evaluate all the medications they’re taking from time to time to see if they are really working for you. For example, if you’re taking antidepressants and are still depressed, the medications may not be helping. Many of these drugs have safer alternatives, including non-medication approaches that could make a difference safely and effectively.
With the number of people suffering from Alzheimer’s expected to triple by 2050, it’s important to do all you can to minimize your risk – and that includes staying away from anticholinergic drugs if possible.
Your gastrointestinal tract is now considered one of the most complex microbial ecosystems on earth, and its influence is such that it’s frequently referred to as your “second brain.”
Nearly 100 trillion bacteria, fungi, viruses and other microorganisms compose your gut microbiome, and advancing science has made it quite clear that these organisms play a major role in your health, both mental and physical. Your body is in fact composed of more bacteria and other microorganisms than actual cells, and you have more bacterial DNA than human DNA.
In the interview above, originally aired in 2015, Dr. David Perlmutter discusses the importance of gut health, the connections between your gut and brain, and the role your gut plays in your health, and in the development of autoimmune diseases and neurological disorders.
According to an article published in the June 2013 issue of Biological Psychiatry,1 the authors suggest that even severe and chronic mental health problems, including post-traumatic stress disorder, might be eliminated through the use of certain probiotics.
Two strains shown to have a calming influence, in part by dampening stress hormones, are Lactobacillus helveticus and Bifdobacterium longum. Others may have similar effects, although more research is needed to identify them.
Using MRI scans, Dr. Emeran Mayer, a professor of medicine and psychiatry at the University of California, is also comparing the physical brain structure of thousands of volunteers, looking for connections between brain structure and the types of bacteria found in their guts.
So far, he has found differences in how certain brain regions are connected, depending on the dominant species of bacteria. As reported by NPR:2 “That suggests that the specific mix of microbes in our guts might help determine what kinds of brains we have — how our brain circuits develop and how they’re wired.”
Your Second Brain
The human gut has 200 million neurons — the equivalent of a cat’s or dog’s brain. And, if an animal is considered intelligent, your gut is equally smart. Your gut also houses nearly 100 trillion microorganisms, which influence everything from biological to emotional functioning.
Your upper brain is home to your central nervous system while your gut houses the enteric nervous system. The two nervous systems, the central nervous system in your brain and the enteric nervous system in your gut, are in constant communication, connected as they are via the vagus nerve.
Your vagal nerve is the 10th cranial nerve and the longest nerve in your body, extending through your neck into your abdomen.3 It has the widest distribution of both sensory and motor fibers.
Your brain and gut also use the same neurotransmitters for communication, one of which is serotonin — a neurochemical associated with mood control. However, the message sent by serotonin changes based on the context of its environment.
In your brain, serotonin signals and produces a state of well-being. In your gut — where 95 percent of your serotonin is produced — it sets the pace for digestive transit and acts as an immune system regulator.
Interestingly, gut serotonin not only acts on the digestive tract but is also released into your bloodstream, and acts on your brain, particularly your hypothalamus, which is involved in the regulation of emotions.
While we’ve known that the gut and brain communicate via the vagus nerve, researchers have only recently come to realize that gut serotonin regulates emotions in a much more complex way than previously thought. Not only can your emotions influence your gut, but the reverse is also true.
When Things Go Wrong in the Gut-Brain Axis
Researchers have been able to better examine the gut’s influence on emotions by studying people with irritable bowel syndrome (IBS), which affects 1 in 10 people, and is characterized by digestive difficulties and severe abdominal pain. This, despite the fact that no organic malfunction in the digestive system can be found.
One theory posits that IBS is rooted in dysfunctional information flow between the gastrointestinal tract and the brain. But what could be causing these communication problems? One theory is that the problem originates in the intestinal wall, and that IBS is the result of faulty communication between the mucosal surface of your intestines and the nerves.”
Research shows that in patients with IBS, the nerves in the gut are far more active than in healthy people, which has led researchers to speculate that the pain IBS patients suffer is the result of a hypersensitive nervous system.
Others have noted that IBS is frequently brought on by stress or emotional trauma. To dampen hypervigilance in the nervous system, some researchers are using hypnosis to help ease IBS patients’ pain.
While the brain is still receiving the same kind of pain signals from the gut, hypnosis can make your brain less sensitive to them. So, pain that was previously intolerable is now perceived as tolerable. The effectiveness of hypnosis has been confirmed using brain imaging, showing hypnosis in fact downregulates activation of pain centers in the brain.
Similarly, Dr. Zhi-yun Bo, a doctor of traditional Chinese medicine who specializes in abdominal acupuncture,4 has been able to treat a wide variety of health conditions, both physical and mental, from acute pain to chronic illness and depression, by needling certain areas of the belly.
The Gut as the Seat of the Subconscious
Another intriguing idea is that your gut may in fact be the root of, or at the very least a part of, your subconscious mind. Your gut can send signals, to which your brain responds, even though those signals never reach conscious awareness.
Your ability to think positive thoughts and feel emotionally uplifted is actually strongly associated with the chemical messages broadcast by your gut. Serotonin released during sleep has also been shown to influence your dreams.
The striking similarities between the gut and brain, both structurally and functionally, have also led scientists to consider the possibility that the two organs may share diseases as well. For example, Parkinson’s disease,5 a degenerative neurological disease, may actually originate in the gut.
Parkinson’s Disease — A Gut Disorder?
Parkinson’s affects nearly a half-million people in the U.S.6 According to recent research7 published in the journal Neurology, Parkinson’s disease may start in the gut and travel to the brain via the vagus nerve.
The study participants previously had a resection of their vagus nerve, often performed in people who suffer from ulcers to reduce the amount of acid secretion and reduce the potential for peptic ulcers.8
Using the national registry in Sweden, researchers compared nearly 10,000 people who had a vagotomy against the records of over 375,000 who had not undergone the surgery. Although the researchers did not find a difference in the gross number of people who developed Parkinson’s between the groups, after delving further they discovered something interesting.
People who had a truncal vagotomy, in which the trunk of the nerve is fully resected, as opposed to a selective vagotomy, had a 40 percent lower risk of developing Parkinson’s disease. The scientists adjusted for external factors, such as diabetes, arthritis, obstructive pulmonary disease and other health conditions. According to study author Bojing Liu, of Karolinska Institutet in Sweden:9
“These results provide preliminary evidence that Parkinson’s disease may start in the gut. Other evidence for this hypothesis is that people with Parkinson’s disease often have gastrointestinal problems such as constipation that can start decades before they develop the disease.
In addition, other studies have shown that people who will later develop Parkinson’s disease have a protein believed to play a key role in Parkinson’s disease in their gut.”
Protein Clumps Implicated in Parkinson’s Originate in the Gut
Indeed, mounting research suggests we may have had the wrong idea about Parkinson’s all along. As mentioned by Liu, there’s other compelling evidence suggesting this disease may have its origins in the gut. Research published in 2016 actually found a functional link between specific gut bacteria and the onset of Parkinson’s disease.10,11,12
In short, specific chemicals produced by certain gut bacteria worsen the accumulation of proteins in the brain associated with the disease. What’s more, the actual proteins implicated in the disease actually appear to travel from the gut up to and into the brain.
Once clumped together in the brain, these proteins, called alpha-synuclein, form fibers that damage the nerves in your brain, resulting in the telltale tremors and movement problems exhibited by Parkinson’s patients. In fact, the researchers believe alpha-synuclein producing gut bacteria not only regulate, but are actually required in order for Parkinson’s symptoms to occur.
The link is so intriguing they suggest the best treatment strategy may be to address the gut rather than the brain using specific probiotics rather than drugs. In this study, synthetic alpha-synuclein was injected into the stomach and intestines of mice.
After seven days, clumps of alpha-synuclein were observed in the animals’ guts. Clumping peaked after 21 days. By then, clumps of alpha-synuclein were also observed in the vagus nerve, which connects the gut and brain. As noted by Science News:13
“Sixty days after the injections, alpha-synuclein had accumulated in the midbrain, a region packed with nerve cells that make the chemical messenger dopamine. These are the nerve cells that die in people with Parkinson’s, a progressive brain disorder that affects movement.
After reaching the brain, alpha-synuclein spreads thanks in part to brain cells called astrocytes, a second study suggests. Experiments with cells in dishes showed that astrocytes can store up and spread alpha-synuclein among cells …”
Over time, as these clumps of alpha-synuclein started migrating toward the brain, the animals began exhibiting movement problems resembling those in Parkinson’s patients. Findings such as these suggest that, at least in some patients, the disease may actually originate in the gut, and chronic constipation could be an important early warning sign.
The same kinds of lesions found in Parkinson’s patients’ brains have also been found in their guts, leading to the idea that a simple biopsy of your intestinal wall may in fact be a good way to diagnose the disease. In other words, by looking at the intestinal tissue, scientists can get a pretty clear picture of what’s going on inside your brain.
These findings are now steering researchers toward looking at the potential role the gut might play in other neurological diseases, such as Alzheimer’s and autism, as well as behavioral disorders.
The Immune System in Your Gut
In addition to digesting food and allowing your body to extract energy from foods that would otherwise be indigestible, your gut bacteria also help determine what’s poisonous and what’s healthy, and play a crucial role in your immune system. Your immune system is to a great extent educated based on the information received from your gut bacteria.
So, exposure to a wide variety of bacteria helps your immune system stay alert and actually optimizes its function. Bacterial colonization begins at birth, and things like antibiotic use by the mother or child, birth by cesarean section, bottle feeding instead of breastfeeding and excessive hygiene can all impair a child’s immune function by limiting exposure to beneficial bacteria.
Researchers have also discovered that humans can be divided into three enterotypes14 — three distinct groupings based on the makeup of our gut microbiomes, and the difference between them lies in our capacity to convert food into energy. All three groups produce vitamins, but to varying degrees.
Curiously, these enterotypes do not appear to be related to geographical location, nationality, race, gender or age, and the precise reason for the development of these enterotypes is still unknown. Diet is one possible, and likely probable, factor.
In the future, researchers hope to be able to determine how various bacteria influence health and the onset of diseases. Already, scientists have identified bacteria that appear to predispose people to conditions such as obesity, Type 2 diabetes, liver disease and cardiovascular disease.
Experimental data also show different gut microbiota can have a determining effect on behavior, for better or worse, and probiotics have been shown to dampen emotional reactivity, reducing the effects of stress.
The endocannabinoid system and digestive imbalance play major roles in Parkinson’s disease. Research has demonstrated that cannabis medicine may help.
Researchers use brain patterns to measure placebo effects in Parkinson’s disease patients
Photo Credit: PsyPost/Creative Commons
The endocannabinoid system plays a major role in Parkinson’s Disease (PD).
PD is associated with impairment of motor control after the loss of 60-80% of dopamine-producing neurons in a critical brain region.
Digestive imbalance may play a role in the advancement of PD & the severity of symptoms.
Cannabinoids have neuroprotectant, anti-oxidant and anti-inflammatory properties which can be beneficial for managing PD.
Various combinations of CBD, THC, and THCV may provide relief for Parkinson’s symptoms.
Scientists at the University of Louisville School of Medicine in Kentucky have identified a previously unknown molecular target of cannabidiol (CBD), which may have significant therapeutic implications for Parkinson’s Disease (PD).
A poster by Zhao-Hui Song and Alyssa S. Laun at the 2017 meeting of the International Cannabinoid Research Society in Montreal disclosed that CBD activates a G-coupled protein receptor called “GPR6” that is highly expressed in the basal ganglia region of the brain. GPR6 is considered an “orphan receptor” because researchers have yet to find the primary endogenous compound that binds to this receptor.(1)
It has been shown that a depletion of GPR6 causes an increase of dopamine, a critical neurotransmitter, in the brain. This finding suggests GPR6 could have a role in the treatment of Parkinson’s, a chronic, neurodegenerative disease that entails the progressive loss of dopaminergic (dopamine-producing) neurons and consequent impairment of motor control. By acting as an “inverse agonist” at the GPR6receptor, CBD boosts dopamine levels in preclinical studies.
Parkinson’s affects an estimated 10 million people worldwide, including one million Americans. It is the second most common neurological disorder (after Alzheimer’s Disease). Over 96 percent of those diagnosed with PD are over 50 years old with men being one-and-a-half times more likely to have PD than women. Uncontrolled PD significantly reduces the patient’s quality of life and can render a person unable to care for themselves, trapped in a body they cannot control.
Parkinson’s Disease is most associated with compromised motor function after the loss of 60-80% of dopamine-producing neurons. As dopaminergic neurons become damaged or die and the brain is less able to produce adequate amounts of dopamine, patients may experience any one or combination of these classic PD motor symptoms: tremor of the hands, arms, legs or jaw; muscle rigidity or stiffness of the limbs and trunk; slowness of movement (bradykinesia); and /or impaired balance and coordination (postural instability).
Additional symptoms include decreased facial expressions, dementia or confusion, fatigue, sleep disturbances, depression, constipation, cognitive changes, fear, anxiety, and urinary problems. Pesticide exposure and traumatic brain injury are linked to increased risk for PD. Paraquat, an herbicide sprayed by the DEA in anti-marijuana defoliant operations in the United States and other countries, resembles a toxicant MPTP [methyl-phenyl-tetrahydropyridien], which is used to simulate animal models of Parkinson’s for research purposes.(2)
Within the PD brain there are an inordinate number of Lewy bodies – intracellular aggregates of difficult to break down protein clusters – that cause dysfunction and demise of neurons.(3) This pathological process results in difficulties with thinking, movement, mood and behavior. The excessive presence of Lewy bodies, coupled with the deterioration of dopaminergic neurons, are considered to be hallmarks of Parkinson’s. But mounting evidence suggests that these aberrations are actually advanced-stage manifestations of a slowly evolving pathology.
It appears that non-motor symptoms occur for years before the disease progresses to the brain, and that PD is actually a multi-system disorder, not just a neurological ailment, which develops over a long period of time. According to the National Parkinson’s Foundation, motor symptoms of PD only begin to manifest when most of the brain’s dopamine-producing cells are already damaged.
Patients whose PD is diagnosed at an early stage have a better chance of slowing disease progression. The most common approach to treating PD is with oral intake of L-dopa, the chemical precursor to dopamine. But in some patients, long-term use of L-dopa will exacerbate PD symptoms. Unfortunately, there is no cure – yet.
What causes Parkinson’s? One theory that is gaining favor among medical scientists traces the earliest signs of PD to the enteric nervous system (the gut), the medulla (the brainstem), and the olfactory bulb in the brain, which controls one’s sense of smell. New research shows that the quality of bacteria in the gut – the microbiome – is strongly implicated in the advancement of Parkinson’s, the severity of symptoms, and related mitochondrial dysfunction.
Defined as “the collection of all the microorganisms living in association with the human body,” the microbiome consists of “a variety of microorganisms including eukaryotes, archaea, bacteria and viruses.” Bacteria, both good and bad, influence mood, gut motility, and brain health. There is a strong connection between the microbiome and the endocannabinoid system: Gut microbiota modulate intestinal endocannabinoid tone, and endocannabinoid signaling mediates communication between the central and the enteric nervous systems, which comprise the gut-brain axis.
Viewed as “the second brain,” the enteric nervous system consists of a mesh-like web of neurons that covers the lining of the digestive tract – from mouth to anus and everything in between. The enteric nervous system generates neurotransmitters and nutrients, sends signals to the brain, and regulates gastrointestinal activity. It also plays a major role in inflammation.
The mix of microorganisms that inhabit the gut and the integrity of the gut lining are fundamental to overall health and the ability of the gut-brain axis to function properly. If the lining of the gut is weak or unhealthy, it becomes more permeable and allows things to get into the blood supply that should not be there, negatively impacting the immune system. This is referred to as “leaky gut.” Factor in an overgrowth of harmful bacteria and a paucity of beneficial bacteria and you have a recipe for a health disaster.
The importance of a beneficial bacteria in the gut and a well-balanced microbiome cannot be overstated. Bacterial overgrowth in the small intestine, for example, has been associated with worsening PD motor function. In a 2017 article in the European Journal of Pharmacology, titled “The gut-brain axis in Parkinson’s disease: Possibilities for food-based therapies,” Peres-Pardo et al examine the interplay between gut dysbiosis and Parkinson’s. The authors note that “PD pathogenesis may be caused or exacerbated by dysbiotic microbiota-induced inflammatory responses … in the intestine and the brain.”(4)
Mitochondria, microbiota and marijuana
The microbiome also plays an important role in the health of our mitochondria, which are present in every cell in the brain and body (except red blood cells). Mitochondria function not only as the cell’s power plant; they also are involved in regulating cell repair and cell death. Dysfunction of the mitochondria, resulting in high levels of oxidative stress, is intrinsic to PD neurodegeneration. Microbes produce inflammatory chemicals in the gut that seep into the bloodstream and damage mitochondria, contributing to disease pathogenesis not only in PD but many neurological and metabolic disorders, including obesity, type-2 diabetes, and Alzheimer’s.
The evidence that gut dysbiosis can foster the development of PD raises the possibility that those with the disease could benefit by manipulating their intestinal bacteria and improving their microbiome. Enhancing one’s diet with fermented foods and probiotic supplements may improve gut health and relieve constipation, while also reducing anxiety, depression and memory problems that afflict PD patients.
Cannabis therapeutics may also help to manage PD symptoms and slow the progression of the disease. Acclaimed neurologist Sir William Gowers was the first to mention cannabis as a treatment for tremors in 1888. In his Manual of Diseases of the Nervous System, Grower noted that oral consumption of an “Indian hemp” extract quieted tremors temporarily, and after a year of chronic use the patient’s tremors nearly ceased.
Modern scientific research supports the notion that cannabis could be beneficial in reducing inflammation and assuaging symptoms of PD, as well as mitigating disease progression to a degree. Federally-funded preclinical probes have documented the robust antioxidant and neuroprotective properties of CBD and THC with “particular application … in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia.” Published in 1998, these findings formed the basis of a U.S. government patent on cannabinoids as antioxidants and neuroprotectants.
Pot for Parkinson’s
Although clinical studies focusing specifically on the use of plant cannabinoids to treat PD are limited (because of marijuana prohibition) and convey conflicting results, in aggregate they provide insight into how cannabis may aid those with Parkinson’s. Cannabidiol, THC, and especially THCV all showed sufficient therapeutic promise for PD in preclinical studies to warrant further investigation. Additional research might shed light on which plant cannabinoids, or combination thereof, is most appropriate for different stages of Parkinson’s.
Anecdotal accounts from PD patients using artisanal cannabis preparations indicate that cannabinoid acids (present in unheated whole plant cannabis products) may reduce PD tremor and other motor symptoms. Raw cannabinoid acids (such as CBDA and THCA) are the chemical precursors to neutral, “activated” cannabinoids (CBD, THC). Cannabinoid acids become neutral cannabinoid compounds through a process called decarboxylation, where they lose their carboxyl group through aging or heat. Minimal research has focused on cannabinoid acids, but the evidence thus far suggests that THCA and CBDA have powerful therapeutic attributes, including anti-inflammatory, anti-nausea, anti-cancer, and anti-seizure properties. In a 2004 survey of cannabis use among patients at the Prague Movement Disorder Centre in the Czech Republic, 45 percent of respondents reported improvement in PD motor symptoms.
Cannabis clinicians are finding that dosage regimens for medical marijuana patients with PD don’t conform to a one-size-fits-all approach. In her book Cannabis Revealed (2016), Dr. Bonni Goldstein discussed how varied a PD patient’s response to cannabis and cannabis therapeutics can be:
“A number of my patients with PD have reported the benefits of using different methods of delivery and different cannabinoid profiles. Some patients have found relief of tremors with inhaled THC and other have not. A few patients have found relief with high doses of CBD-rich cannabis taken sublingually. Some patients are using a combination of CBD and THC … Trial and error is needed to find what cannabinoid profile and method will work best. Starting a low-dose and titrating up is recommended, particularly with THC-rich cannabis. Unfortunately, THCV-rich varieties are not readily available.”
Juan Sanchez-Ramos M.D., PhD, a leader in the field of movement disorders and the Medical Director for the Parkinson Research Foundation, told Project CBD that he encourages his patients to begin with a 1:1 THC:CBD ratio product if they can get it. In a book chapter on “Cannabinoids for the Treatment of Movement Disorders,” he and coauthor Briony Catlow, PhD, describe the dosage protocol used for various research studies that provided statistically positive results and a dosing baseline for PD. This data was included in a summary of dosing regimens from various studies compiled by Dr. Ethan Russo:
300 mg/day of CBD significantly improved quality of life but had no positive effect on the Unified Parkinson Disease Rating Scale. (Lotan I, 2014)
0.5 g of smoked cannabis resulted in significant improvement in tremor and bradykinesia as well as sleep. (Venderová K, 2004)
150 mg of CBD oil titrated up over four weeks resulted in decreased psychotic symptoms. (Chagas MH, 2014)
Of course, each patient is different, and cannabis therapeutics is personalized medicine. Generally speaking, an optimal therapeutic combination will include a synergistic mix of varying amounts of CBDand THC – although PD patients with sleep disturbances may benefit from a higher THC ratio at night.
Dr. Russo offers cogent advice for patients with PD and other chronic conditions who are considering cannabis therapy. “In general,” he suggests, “2.5 mg of THC is a threshold dose for most patients without prior tolerance to its effects, while 5 mg is a dose that may be clinically effective at a single administration and is generally acceptable, and 10 mg is a prominent dose, that may be too high for naïve and even some experienced subjects. These figures may be revised upward slightly if the preparation contains significant CBD content … It is always advisable to start at a very low dose and titrate upwards slowly.”
For information about nutritional supplementation to help manage PD, visit the Life Extension Foundation Parkinson’s page.
Lifestyle Modifications for PD Patients
It is important to treat the patient as a whole – mind, body and soul. The following are a few lifestyle modifications that may provide relief from PD symptoms and improve quality of life.
Do cardio aerobic exercise: This benefits the body in so many ways, including stimulating the production of one’s endocannabinoids, increasing oxygen in the blood supply, mitigating the negative impact of oxidative stress, and boosting the production of BDNF, a brain-protecting chemical found to be low in PD patients.
Eat more fruits and vegetables: The old saying “garbage in, garbage out” is so true. The majority of PD patients suffer from chronic constipation. A high fiber diet can be helpful in improving gut motility and facilitating daily bowel movements.
Get restful sleep: Not getting good sleep can undermine one’s immune function, cognition and quality of life. The importance of adequate restful sleep cannot be over emphasized.
Reduce protein intake – This may help reduce the accumulation of protein bodies that result in Lewy bodies that appear in the enteric nervous system and the central nervous system and increase the uptake of L-dopa.
Practice meditation, yoga or Tai Chi: The focus on the integration of movement and breath not only improve mobility but it also improves cognition and immunity. One study showed an increase in grey matter density in the areas of the brain associated with PD. Another showed that yoga improved balance, flexibility, posture and gait in PD patients. Research shows that tai chi can improve balance, gait, functional mobility, and overall well being.
Consume probiotic food and supplements: Probiotic foods — raw garlic, raw onions, bananas, asparagus, yams, sauerkraut, etc.— are a great source for the good bacteria in your large intestine. Augmenting your diet with probiotic supplements, especially after taking antibiotics, can support the immune system by helping to repopulate the upper digestive tract with beneficial bacteria. Consult your doctor regarding a recommendation for a quality probiotic.
Drink coffee: The risk of PD is considerably lower for men who consume coffee daily.
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(1) An inverse agonist binds directly to a receptor and modifies it in a way that causes the receptor to have the opposite effects of activating it normally.
(2) MPTP was found in an underground meperidine (Demerol) synthesis that caused a small epidemic of Parkinson syndrome in i.v. drug abusers in the San Francisco area in the mid-1980s.
The presence of Lewy bodies (a-synuclein protein clusters) in other parts of the body could potentially serve as an early detection marker for PD, especially in the olfactory bulb and the enteric nervous system.
(4) Peres-Prado et al analyzed gut microbiota in PD patients compared to controls and found the following:
Prevotellaceae, a bacterium which supports the production of health-promoting short chain fatty acids (SCFA), biosynthesis of thiamine and folate, and is thought to be associated with increased gut permeability, was 78% lower in the feces of PD patients versus that of their sex-matched and age-matched controls.
Biopsies of colonic tissue retrieved from PD patients indicate high levels of tumor necrosis factor-alpha and other inflammatory agents.
A lower abundance of SCFA-producing and anti-inflammatory bacteria from the class of Blautia, Coprococcus, and Roseburia were found in fecal samples of PD patients. (Paula Perez-Pardo, 2017)
Gastric abnormalities may increase small intestinal bacterial overgrowth (SIBO). SIBO is prevalent in PD patients and correlates directly to worse motor dysfunction.
Gut-derived lipopolysaccharide (LPS – an inflammatory toxin produce by bacteria) promotes the disruption of the blood-brain barrier.
Impaired gherlin, a gut hormone known as the hunger hormone, is thought to be associated with maintenance and protection of dopamine function in the nigrostriatal pathway which is one of four major dopamine pathways and is particularly involved in movement. Impaired gherlin has been reported in PD patients.
Nishi Whiteley, a Project CBD research associate and contributing writer, is the author of Chronic Relief: A Guide to Cannabis for the Terminally and Chronically Ill (2016). Special thanks to Juan Sanchez-Ramos for reviewing this article, Ethan B. Russo, M.D. for providing a summary of Parkinson’s research for inclusion in this article, and to Adrian Devitt-Lee for his research support.
Summary: A new study reports Parkinson’s disease and some of the medications used to treat the condition have distinct effects on the bacteria that make up the gut microbiome.
Source: University of Alabama at Birmingham.
There is growing evidence showing a connection between Parkinson’s disease — a neurodegenerative condition — and the composition of the microbiome of the gut. A new study from researchers at the University of Alabama at Birmingham shows that Parkinson’s disease, and medications to treat Parkinson’s, have distinct effects on the composition of the trillions of bacteria that make up the gut microbiome.
The findings were published in February in Movement Disorders, the journal of the International Parkinson and Movement Disorder Society.
“Our study showed major disruption of the normal microbiome ¬ — the organisms in the gut — in individuals with Parkinson’s,” said Haydeh Payami, Ph.D., professor in the Department of Neurology, in the UAB School of Medicine.
Payami says, at this point, researchers do not know which comes first. Does having Parkinson’s cause changes in an individual’s gut microbiome, or are changes in the microbiome a predictor or early warning sign of Parkinson’s? What is known is that the first signs of Parkinson’s often arise as gastrointestinal symptoms such as inflammation or constipation.
“The human gut hosts tens of trillions of microorganisms, including more than 1,000 species of bacteria,” she said. “The collective genomes of the microorganisms in the gut is more than 100 times larger than the number of genes in the human genome. We know that a well-balanced gut microbiota is critical for maintaining general health, and alterations in the composition of gut microbiota have been linked to a range of disorders.”
Payami’s team studied 197 patients with Parkinson’s and 130 controls. Subjects came from Seattle, New York and Atlanta.
The study indicated that Parkinson’s is accompanied by imbalance in the gut microbiome. Some species of bacteria were present in larger numbers than in healthy individuals; other species were diminished. Different medications used to treat Parkinson’s also appear to affect the composition of the microbiome in different ways.
“It could be that, in some people, a drug alters the microbiome so that it causes additional health problems in the form of side effects,” Payami said. “Another consideration is that the natural variability in the microbiome could be a reason some people benefit from a given drug and others are unresponsive. The growing field of pharmacogenomics — tailoring drugs based on an individual’s genetic makeup — may need to take the microbiome into consideration.”
The study subjects came from three regions, the Northeast, Northwest and South. Payami says the research team detected an unexpected difference in gut imbalance as a function of geographic site, which may reflect the environmental, lifestyle and diet differences between the three regions.
Another function of the microbiome is to help the body rid itself of xenobiotics — chemicals not naturally found in the body often arising from environmental pollutants. The study found evidence that the composition of bacteria responsible for removing those chemicals was different in individuals with Parkinson’s. This may be relevant because exposure to pesticides and herbicides in agricultural settings is known to increase the risk of developing Parkinson’s.
Payami says the study of the microbiome is a relatively new field, and a better understanding of macrobiotics may provide unexpected answers for Parkinson’s disease and potentially other disorders.
A better understanding of macrobiotics may provide unexpected answers for Parkinson’s disease and potentially other disorders. NeuroscienceNews.com image is adapted from the UAB press release.
“This opens up new horizons, a totally new frontier,” she said. “There are implications here for both research and treatment of Parkinson’s disease. Therapies that regulate the imbalance in the microbiome may prove to be helpful in treating or preventing the disease before it affects neurologic function.” However, Payami cautions against grand conclusions until more data are available.
Payami says another study is underway at UAB with individuals with Parkinson’s and healthy individuals in Alabama in an effort to replicate and confirm the results.
“The present findings lend support to the notion that the composition of the gut microbiome may hold new information for assessing efficacy and toxicity of Parkinson’s medications,” Payami said. “Additional studies are needed to assess the effects of those drugs, with larger numbers of treated and untreated patients as well as individuals who do not have Parkinson’s.”
About this Parkinson’s disease research article
Funding: Funding support for the study was provided by National Institutes of Health.
Source: Brian Mullen – University of Alabama at Birmingham Image Source: NeuroscienceNews.com image is adapted from the UAB press release. Original Research:Abstract for “Parkinson’s disease and Parkinson’s disease medications have distinct signatures of the gut microbiome” by Erin M. Hill-Burns PhD, Justine W. Debelius PhD, James T. Morton BS, William T. Wissemann BA, Matthew R. Lewis MS, Zachary D. Wallen MS, Shyamal D. Peddada PhD, Stewart A. Factor DO, Eric Molho MD, Cyrus P. Zabetian MD, MS, Rob Knight PhD, and Haydeh Payami PhD in Movement Disorders. Published online February 14 2017 doi:10.1002/mds.26942
In Parkinson’s disease – which affects about eight million people worldwide – vital nerve cells (neurons) in the brain malfunction or die.
Researchers from UQ’s Institute for Molecular Bioscience examined a genetic mutation that interrupts the traffic of materials within neurons and allows waste products to accumulate, causing Parkinson’s disease.
Associate Professor Rohan Teasdale said previous studies showed that dysfunctions in retromer (a protein machine responsible for transporting biological material within a cell) were linked to Parkinson’s disease, but the biological reasons behind this were unclear until now.
“It has been identified that one of these proteins (Vps35) is mutated in some Parkinson’s patients, which creates congestion in the transport network inside cells,” Associate Professor Teasdale said.
“As a result, it appears that the workers responsible for recycling material within these neurons are not getting to their correct work place and without their assistance the cells within the brain cannot rid themselves of waste materials, which increases the likelihood of cell death.
“It’s this cell death that then causes the symptoms of Parkinson’s disease, such as tremors and muscle stiffness,” he said.
I have to admit that even if Hilarious ‘Windbag’ Clinton’s health is fine, this psychological warfare against her has been more than excellent and efficient. Watch the heads roll now. The idea of her suffering from mental disease has been planted in the collective consciousness of the American citizenry. And Jon wrote this before the release of this report:
Major media are rushing to do damage control on Hillary’s health. They’re trying to lay down the concrete of a fake consensus that she’s fine, because her doctor issued a positive report in 2015. (See here).
But one of the bottom lines is: she’s suffered from dangerous blood clots. And the treatment is blood-thinners, which are given to reduce the possibility of a fatal clot.
It’s a rat poison. It kills rats by causing them to bleed out internally. This is a fact.
Therefore, the prescribing doctor and the patient walk a tightrope. How much Coumadin is too much? How little is too little? Too much, and life-threatening bleeding can occur. Too little and fatal blood clots can occur.
Therefore, Hillary is being monitored VERY closely, on a weekly basis, with tests. But the tests aren’t mathematically precise. The monitoring isn’t ironclad science.
And since Coumadin is highly toxic, serious liver damage is a consequence, especially when the drug is given long-term, which is the case here.
Media outlets are going with, “Well, her doctors know what they’re doing. They’re issuing positive reports. They’re giving her a clean bill of health.”
You put someone on Coumadin, long-term, and you’re rolling the dice. In her case, this treatment is back-against-the-wall, last-line-of-defense.
If her past blood clots were somehow interpreted as minor or incidental, long-term Coumadin would never be the treatment of choice.
This patient, Hillary Clinton, is very high-risk.
The last thing you would want this patient to do is engage in day-to-day, high-stress activity. You would definitely not want the patient to fly in airplanes, because that activity can exacerbate her condition. Lethally.
Her major media allies (and they are, of course, many) have no genuine interest in her health risks. They would be able to handle her as President, even if she turned out to be dead on arrival.
Her closest aides, and her husband, are aware of all these facts. They’re shrugging them off and pressing for a victory in the election this fall. That’s the game plan, come hell or high water.
But the blood clot problem and rat poison problem aren’t going to go away.
Any honest doctor will tell you that.
Whether Hillary has Parkinson’s, whether she has trouble maintaining her balance, whether she has “brain-freezes”…yes, these are all subjects for discussion. But either way, the blood clots and the Coumadin are putting her on a cliff’s edge.
Politics aside, the refusal of major media to bring this into the light on a serious basis is insane.
The author of three explosive collections, THE MATRIX REVEALED, EXIT FROM THE MATRIX, and POWER OUTSIDE THE MATRIX, Jon was a candidate for a US Congressional seat in the 29th District of California. He maintains a consulting practice for private clients, the purpose of which is the expansion of personal creative power. Nominated for a Pulitzer Prize, he has worked as an investigative reporter for 30 years, writing articles on politics, medicine, and health for CBS Healthwatch, LA Weekly, Spin Magazine, Stern, and other newspapers and magazines in the US and Europe. Jon has delivered lectures and seminars on global politics, health, logic, and creative power to audiences around the world. You can sign up for his free NoMoreFakeNews emails here or his free OutsideTheRealityMachine emails here.
Could the very plant that for decades was accused of “frying” users’ brains be far superior to pharmaceuticals in treating the “incurable” neurodegenerative condition known as Parkinson’s disease?
Despite the political controversy surrounding medical marijuana use in the country, research has begun to emerge showing that a component of this plant known as cannabidiol (CBD), and which does not have the controversial psychoactive properties associated with tetrahydrocannabinol (THC), may have a wide range of therapeutic applications, including treating conditions that are refractory to conventional drug-based approaches.
One such condition is Parkinson’s disease, to which there is, at present, no effective conventional treatment. In fact, the primary treatment involves dopamine increasing drugs that also increase a neurotoxic metabolite known as with 6-hydroxy-dopamine, and which therefore can actually accelerate the progression of the disease. This is why natural alternatives that are safe, effective, and backed up by scientific evidence, are so needed today. Thankfully, preclinical research on cannabidiol has already revealed some promising results, including two studies in animal models of Parkinson’s disease (PD) assessing its neuroprotective properties:
“In the first one, Lastres-Becker et al. (2005) showed that the administration of CBD counteracted neurodegeneration caused by the injection of 6-hydroxy-dopamine in the medial prosencephalic bundle, an effect that could be related to the modulation of glial cells and to antioxidant effects (Lastres- Becker et al., 2005). In the next year, Garcia-Arencibia et al. (2007) tested many cannabinoid compounds following the lesion of dopaminergic neurons in the substantia nigra with 6-hydroxy-dopamine and found that the acute administration of CBD seemed to have a neuroprotective action; nonetheless, the administration of CBD one week after the lesion had no significant effects (Garcia-Arencibia et al., 2007). This study also pointed to a possible antioxidant effect with the upregulation of mRNA of the enzyme Cu-Zn-superoxide dismutase following the administration of CBD.” 
In addition to these animal studies, the following three human clinical trials have been conducted to evaluate cannabidiol’s neuroprotective effects.
A 2006 study published in Biological Psychology titled, “Dorsolateral Prefrontal Cortex N-Acetylaspartate/Total Creatine (NAA/tCr) Loss in Male Recreational Cannabis Users,” investigated the N-acetylaspartate to creatine ratios (NAA/Cr) in the brain of regular cannabis users through magnetic resonance spectroscopy (H1-MRS) to assess the neurotoxic and neuroprotective effects of cannabinoids present in the drug and found a strong positive correlation between CBD and NAA/Cr in the globus pallidus and putamen. According to the study, “the globus pallidum is the region with the highest amount of CB1-receptors in the brain and the target of neurostimulation in patients with Parkinson’s disease, who developed a strong tremor. Our MRSI results support a positive effect of CBD on the putamen/globus pallidum region in cannabis use. Therefore, it may be promising to test a possible influence of the nonpsychotropic CBD in the onset of Parkinson’s disease.”
A 2009 study published in the Journal of Psychopharmacology titled, “Cannabidiol for the treatment of psychosis in Parkinson’s disease,” assessed the therapeutic use and neuroprotective effect of CBD in PD patients. The open label study was conducted with six patients with PD-related psychosis. They were administered CBD at doses ranging from 150 mg in the first week to 400 mg in the fourth and last week of treatment (doses were adjusted to optimize the clinical response). The study reported significant improvements in psychosis as well as in the total scores of a scale that measures general symptoms of PD (Unified Parkinson’s disease rating scale – UPDRS)
A 2014 study published in the Journal of Psychopharmacology titled, “Effects of cannabidiol in the treatment of patients with Parkinson’s disease: an exploratory double-blind trial,” evaluated the effects of cannabidiol in Parkinson’s disease patients, dividing 21 patients into 3 groups of 7 receiving either placebo, cannabidiol (CBD) 75 mg/day or CBD 300 mg/day. Increases in well-being and quality of life were observed in the 300 mg/day groups versus the placebo groups. The researchers hypothesized that these improvements may have been due to cannabidiol’s “anxiolytic,” “antidepressant,” “anti-psychotic,” and “sedative” properties.
The study found that cannabidiol protects against the neurotoxin known as MPP(+), which is widely believed to be responsible for the damage to the dopamine-producing cells in the substania nigra of Parkison’s patients, by preventing neuronal cell death and inducing neuritogenesis (a neuro-regenerative process for repairing damaged neurons). This mechanism was found to be independent of the neural growth factor (NGF) pathway, even though it involves NGF receptors. Cannabidiol was also found to increase the expression of axonal and synaptic proteins. The study concluded that CBD’s neuroprotective properties might be of benefit to Parkinson’s disease patients.
“Our citizens should know the urgent facts…but they don’t because our media serves imperial, not popular interests. They lie, deceive, connive and suppress what everyone needs to know, substituting managed news misinformation and rubbish for hard truths…”—Oliver Stone