H Pylori And Parkinson’s

Can Altering The Microbiome Improve Parkinsons Symptoms

With the awareness that the microbiome may play a role in PD, came the idea that altering the microbiome may help with PD symptoms. While there is still a lot of research to be done, there have been some small, but promising findings so far.

Probiotics, or particular strains of bacteria that are ingested in order to alter the gut microbiome, have been studied to help PD symptoms. A number of small studies suggest that probiotics may improve constipation in people with PD, which is a common problem for many people with the disease.

As mentioned above, treatment of Helicobacter pylori and SIBO typically requires antibiotics, which are drugs designed to kill particular bacteria. Antibiotics can be helpful, but are only considered if a particular gut organism is being targeted. Otherwise, antibiotics can kill both good and bad bacteria, and potentially be detrimental to the overall health of the gut microbiome.

Another idea that has been considered is fecal transplantation, a technique in which fecal matter from a healthy person is delivered to the gut of a person with PD, with the goal of restoring a less PD-like microbiome. Only case reports and very small studies have been reported so far in the literature, but this may be an area worth exploring. There are a few additional studies underway which you can read about here:

How Is The Microbiome Different In People With Pd

Based on numerous studies comparing the microbiome from the gut of people with PD with the microbiome from the gut of people without PD, there appear to be some differences. The studies are not consistent in their findings, but there are similarities across studies. These include an increase in certain families of bacteria such as Lactobacillaceae and Verrucomicrobiaceae, and a decrease in the family Prevotellaceae.

Cognition And Affect In Relation To H Suis Status

Fourteen of the 59 patients traced developed cognitive impairment whilst attending clinic or were diagnosed as having dementia after last seen there. The observed number of deaths in those with and without incident cognitive impairment was not significantly different from number expected were death and cognitive impairment unrelated . Cognitive impairment occurred in 8/19 H. suis-positive patients and 6/40 H. suis-negative: odds for being H. suis-positive tended to be higher in those who developed cognitive impairment.

The majority of the PD-patients were classified as having at least mild depression at some time during follow-up. There was no evidence of association between mortality and depression score . The odds of being H. suis-positive was weakly related to the worst depression score recorded per individual, 4/5 patients with severe depression being H. suis-positive .

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Differential Effect Of H Suis Status On Blood Profile

Table 5A illustrates the differential effect of H. suis on blood indices. H. suis-positivity was associated with a markedly higher T-cell count, through an effect on both CD4+ and CD8+ subsets. This contrasts with a lower lymphocyte count with H. pylori , and a lower neutrophil count but numerically much higher natural killer cell count with SIBO.

Table 5. Independent associations of two Helicobacter species and SIBO with total white cell and subset counts and cardiovascular measures.

Mean hemoglobin concentration and red cell and platelet counts were not associated with Helicobacter species or SIBO status. Mean platelet volume was toward the upper end of the reference range, larger with H. pylori-positivity . Serum folate was lower with H. pylori-positivity. No other association with haematinics or with serum homocysteine was identified. Helicobacter-positivity, in general, was associated with anti-intrinsic factor gastric autoantibody, both H. pylori– and H. suis-positivity contributing to the effect , only H. suis-positivity tending to be associated with parietal cell antibody .

Helicobacter Pylori Bacteria In The Gut And Parkinson’s Disease

I am currently researching the links between gut bacteria/micro-organisms and the symptoms of Parkinson’s Disease, due to the extremely strong evidence now that many instances of PD begin in the gut. Based on this, we can therefore assume that if, indeed many forms of PD begin in the gut, and only later migrate to brain, the initiating and causal gut problems will still remain too after the brain damage has occured. We will certainly need to address these digestive tract issues, therefore, if we are ever to fully heal. In my view, even if we could correct the resulting brain problems tomorrow, if we do not also attend to the original causes which reside in gut then we will not be “fixed” for very long.

One of the problem bacteria that I’ve been researching is Helicobacter Pylori , which has previously been linked with stomach ulcers, but is also now very directly implicated in Parkinson’s too, as this abstract from a 2016 science article highlights:

I first came across the relationship between HP with PD myself when I was contacted on twitter by , who alerted me to the Parkinson’s Improvement Programme Project website, where Andrew JC Carmichael, the Project’s founder, writes:

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Parkinsons Disease From Helicobacter Pylori

Infection with the stomach bacteria Helicobacter pylori is the most common cause of stomach inflammation . Yet, these widespread bacteria can also cause many other diseasespossibly even Parkinsons disease.

Several clinical studies suggest that these bacteria, with which more than half of the worlds population is infected, can promote the nervous system disorder Parkinsons disease. For example, Professor Dr. David J. McGees team at LSU Health Sciences Center in Shreveport identified four links between Helicobacter infections and Parkinsons disease :

• Parkinsons patients have a one- to three-fold elevated risk of having a H. pylori infection compared to healthy comparators.
• Parkinsons patients who are infected with H. pylori have worse motor functions than non-infected Parkinsons patients.
• Eradication of H. pylori improves the motor skills in Parkinsons patients.
• Eradication of H. pylori improves the absorption of the Parkinsons medication levodopa.

In Parkinsons patients who respond poorly to levodopa therapy, it is, therefore, recommended to test for a possible Helicobacter infection and to eradicate the bacteria, if found.

The Link Between H Pylori Infection And Constipation

In a 2018 study, treatment of h. pylori in patients with constipation resulted in some improvement in constipation .

Also, H. pylori is linked to Parkinsons disease in the research . Parkinsons disease is known to cause severe chronic constipation.

These pieces of evidence may indicate that h. pylori may play a role in constipation. However, the evidence is still weak, and constipation with H. pylori is not a frequent complaint.

If you have constipation with H. pylori, consult your doctor about the possible causes and best treatment.

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A Causative Role Of Helicobacter Pylori In Parkinsons Disease

There is today epidemiological data to suggest an increased prevalence of HP infection in PD patients . As compared to healthy controls, one case-control study has shown HP antibodies to be 5-fold more common in PD patients over 80 years of age another study found HP to be 3-fold more common .

Table 1

Prevalence of Helicobacter pylori in Parkinsons disease patients

Helicobacter pylori prevalence in PD	Helicobacter pylori prevalence in background population
Dobbs et al.	48
Pierantozzi et al.	36
Lee et al.	53
Dobbs et al.	70
Tan et al.	32
Mridula et al.	50	50 69

Background population Helicobacter pylori prevalence according to .

A concluding meta-analysis of eight eligible studies comprising 33,125 patients showed the pooled odds ratio of PD in HP-infected persons to be 1.59 . In subgroup analyses, the combined odds ratios of PD in HP-infected subjects were 1.96 in Asia, 1.55 in Europe, 1.59 in case-control studies, 1.56 in cross-sectional studies, 1.56 in studies with confounders adjusted, and 1.71 in studies with no confounder adjusted. Hence, HP infection might be associated with an increased risk of PD .

Bacteria ‘linked’ To Parkinson’s Disease

The bacteria responsible for stomach ulcers have been linked to Parkinson’s disease, according to researchers in the US.

Mice infected with Helicobacter pylori went onto develop Parkinson’s like symptoms.

The study, presented at a meeting of the American Society for Microbiology, argues that infection could play “a significant role”.

The charity Parkinson’s UK said the results should be treated with caution.

Parkinson’s disease affects the brain and results in slow movements and a tremor.

Middle-aged mice, the equivalent of being between 55 and 65 in humans, were infected. Six months later they showed symptoms related to Parkinson’s, such as reduced movement and decreased levels of a chemical, dopamine, in the brain.

These changes were not noticed in younger mice.

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Can H Pylori Cause Black Or Coffee Ground Stool

Black, coffee ground, or tar-like poop may indicate bleeding from the upper part of your digestive tract (the esophagus, stomach, duodenum, and the early part of your small intestines.

H. pylori-infected individuals have a 10-20% lifetime risk of peptic ulcer disease . but bleeding from such ulcers is infrequent

So, the incidence of h. pylori-induced black stool is rare but dangerous. The presence of black tarry stool can be a symptom of bleeding H. pylori-induced ulcers.

This is a medical emergency please call your doctor now or head to the ER t get medical help.

What Is The Microbiome

The human gut harbors trillions of micro-organisms referred to collectively as the microbiome. Current understanding is that the microbiome provides a number of benefits to the human including help with digestion of food, help with warding off harmful microorganisms, aid in the absorption of particular nutrients, and creation of needed vitamins. These functions can influence the nervous system of the gut, called the enteric nervous system . In addition, the gut microbiome releases byproducts and metabolites that have effects on nerves. The microbiome varies from person to person and is influenced by many factors including diet, environment, and genetics. Although no two microbiomes are identical, people with certain diseases may share similarities in their microbiomes.

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Histopathology Immunohistochemistry And Molecular Microbiology In Pigs

Table 6A shows detection and density of immuno-stained corkscrew organisms, by gastric region sampled, in the 10 initial pig stomachs. Antrum was evidently the optimal sampling site. Enlarged lymph-nodes, found along the lesser curvature of stomach in 5 pigs, were immuno-stain-negative, despite 4 of them having obvious gastric Helicobacter. Table 6B compares frequency of detection and density of HLOs in antra from the 91 subsequent pigs and from 10 adult sows . Immunostained corkscrew organisms were seen in 47% of pig antra. There was no difference in detection frequency between pigs and adult sows.

Table 6. Presence and density of Helicobacter on immunostaining in 111 UK pigs at slaughter, by gastric region and in any enlarged lymph-nodes in initial pigs , and in antra of pigs , and adult sows .

In the 101 subsequent pigs, chronic inflammation was ubiquitous and more severe in presence of HLOs. Active inflammation was associated with eosinophils in 99%, with neutrophils in only 10%. Neutrophil infiltration was associated with cryptitis , but not with HLOs. Lymphoid aggregates were found in 41% . Lymphoid follicles were found in 73%, in medium or high density in two-thirds, and more evident in presence of HLOs. Erosive changes were present in two cases, both without HLOs. Mucosal morphology was confirmed as antral in type in 88 of the 91 subsequent pigs, being body-type in one, mixed body/antral in 2.

Can An Altered Microbiome Contribute To A Diagnosis Of Pd

Research studies in animals have shown that an altered microbiome might contribute to PD pathology. For example, one study showed that in a mouse model of PD that overexpressed alpha-synuclein, there was more alpha-synuclein accumulation in the brain of the mice with an intact microbiome as compared to the same mice who were raised in a germ-free environment with no bacteria in their gut. This supports the theory that abnormal alpha-synuclein accumulation in the brain is enhanced by a particular microbiome in the gut.

Other studies showed that transplantation of fecal material from PD mice to normal mice, thereby introducing a PD microbiome into mice without PD pathology their brain, led to impairment of motor function and a decline in brain dopamine. These studies also support the theory that a particular microbiome might be integral in causing PD pathology in the brain.

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Differential Effect Of H Suis Status On Cardiovascular Measures

Table 5B illustrates differential effect of H. suis on mean arterial pressure and pulse rate. With H. suis-positivity, only, mean arterial pressure was lower, and this by a clinically-relevant amount , for all standing measurement times. Lying and post-exercise values were numerically lower by a similar amount. With SIBO, only, lying and standing pulse rates were lower , an effect lost on exercise.

Data Acquisition And Assessment

Standardized techniques were adapted for assessing risk factors along with socioeconomic strata.10 Data were collected using face-to-face interviews and in physical and neurological examinations. The Hoehn and Yahr stage11 and motor subset of the Unified Parkinson’s Disease Rating Scale -III12 were used to assess the motor severity of PD. Motor examinations were performed both at the practically defined off state and on state . The time from consuming levodopa to the onset of the on time was noted. After the levodopa challenge, the duration of the on time was noted. The individual levodopa daily dosage was noted and was not changed throughout the study period. The total on time over 24 hours was calculated by the patient from home diaries filled on the day prior to the visit, because this method has been generally employed in previous studies of motor fluctuations in PD.12

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Histopathology And Immunohistochemistry In Patients

Presence of Helicobacter was confirmed in immuno-stained sections from H. pylori positive control patients, absence confirmed in negative controls. No Helicobacter staining was seen in sections from 4 of the 6 patients with the highest abundance of H. suis DNA. However, in the 2 others, who had evidence of both Helicobacter species, irregularly-shaped immuno-stained Helicobacter-like organisms were attached to the mucosal surface. In one of these, most HLOs were thicker than usual for H. pylori and tended to bank-up in irregular bundles, the rest being of typical H. pylori morphology. In the other, the HLOs also tended to bank-up, but were smaller, more homogenous.

What Do H Pylori Look Like In Stool

H. pylori are microscopic organisms it is impossible to see them in the stool with your naked eyes. However, H. pylori pass in the stool, and your doctor may order a stool test to diagnose H. pylori infection.

H. pylori stool antigen is widely used to detect active infection. And it is the only way we use a stool to find H. pylori.

Under the electron microscope, H. pylori look like a rod with multiple tails that helps the organism move. Moreover, conventional stool anallysis and light microscopy examination cannot detect H. pylori in your stool.

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Effects Of Helicobacter Pylori On Levodopa Pharmacokinetics

Article type: Review Article

Authors: Nyholm, Dag * | Hellström, Per M.

Affiliations: Department of Neuroscience, Neurology and Department of Medical Sciences, Gastroenterology, Uppsala University, Sweden

Correspondence: Correspondence to: Assoc Prof Dag Nyholm, MD, PhD, Department of Neuroscience, Uppsala University, Uppsala University Hospital, bldg. 85, SE-75185 UPPSALA, Sweden. E-mail: .

Keywords: Parkinsons disease, inflammation, microbiome, levodopa, pharmacodynamics

DOI: 10.3233/JPD-202298

Journal: Journal of Parkinson’s Disease, vol. 11, no. 1, pp. 61-69, 2021

Abstract

The Gastrointestinal Tract And Parkinsons

As promised in a previous blog, I now return to the topic of the gastrointestinal tract and Parkinsons disease . As most of you know, GI symptoms are very common in PD. We will discuss what those symptoms are, why they occur, and the current research that links what is happening in the gut to theories as to why PD occurs at all. Many of you have suggested gut-related topics for this blog including a discussion of symptoms such as bloating and constipation, and a discussion of the use of probiotics in PD. I will address these issues as well. Submit additional topics that you would like to read about here.

GI symptoms can be among the most bothersome of the non-motor symptoms of PD. Constipation is the most common of these symptoms, affecting 80-90% of people with PD. APDA has a helpful brochure with practical tips to prevent and treat constipation in PD.

GI pathology in Parkinsons disease however, can involve the entire GI tract and includes sialorrhea and dysphagia . In addition, delayed gastric emptying, in which the digestive contents are held up in the stomach and do not move normally into the small intestine, can cause sensations of nausea and bloating.

The gut has its own nervous system

The gut as a biomarker

Entry to the brain

How do Lewy bodies propagate?

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Selection And Characteristics Of The Included Studies

The initial PubMed database search and examination of the references of the retrieved publications yielded 85 studies published between 1 November 1996 and 13 November 2017 . After reviewing titles and abstracts, articles not eligible for the meta-analysis were excluded, resulting in 28 potentially eligible studies. A case-control study was written in Polish and was therefore excluded from the meta-analysis . Furthermore, the following studies were excluded: a)

Eradicating Helicobacter Pylori Infections May Be A Key Treatment For Parkinson’s Disease

Date:

IOS Press

Summary:

While human genetic mutations are involved in a small number of Parkinson’s disease cases, the vast majority of cases are of unknown environmental causes, prompting enormous interest in identifying environmental risk factors involved.

While human genetic mutations are involved in a small number of Parkinson’s disease cases, the vast majority of cases are of unknown environmental causes, prompting enormous interest in identifying environmental risk factors involved. The link between Helicobacter pylori and gastric ulcers has been known for several decades, but new evidence suggests that this harmful bacterium may play a role in PD as well. A new review in the Journal of Parkinson’s Disease summarizes the current literature regarding the link between H. pylori and PD and explores the possible mechanisms behind the association.

In a comprehensive review of prior studies, investigators uncovered four key findings:

• People with PD are 1.5-3-fold more likely to be infected with H. pylori than people without PD.
• H. pylori-infected PD patients display worse motor functions than H. pylori-negative PD patients.
• Eradication of H. pylori improved motor function in PD patients over PD patients whose H. pylori was not eradicated.
• Eradication of H. pylori improved levodopa absorption in PD patients compared to PD patients whose H. pylori was not eradicated.

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