Archive for the ‘Inflammation’ Category

Depression Not Caused by Chemical Imbalance

https://articles.mercola.com/sites/articles/archive/2018/01/18/chemical-imbalance-theory-for-depression.aspx?

Depression Not Caused by Chemical Imbalance  

depression

January 18, 2018

Story at-a-glance

  • Many people believe depression is caused by a chemical imbalance in the brain; this chemical imbalance theory has been widely promoted by drug companies and psychiatrists alike — without evidence to back it up
  • Pharmaceutical companies were instrumental in bringing the chemical imbalance theory to the mainstream, heavily promoting it as a marketing gimmick to sell antidepressant drugs
  • Studies have repeatedly shown antidepressants work no better than placebo for mild to moderate depression, yet carry a significant risk of side effects
  • Depression is likely the result of multiple environmental and biological factors, including faulty mood regulation by the brain, genetic vulnerability, stressful life events, nutrition, medications and medical problems, among others

By Dr. Mercola

Do you know what causes depression? Many people would respond that it’s due to a chemical imbalance in the brain. This chemical imbalance theory has been widely promoted by drug companies and psychiatrists alike, to the extent that it’s accepted as fact. The glaring problem is that the chemical imbalance theory is just that — a theory — and worse still, it’s a theory that has been largely discredited.

The theory was first proposed by scientists in the 1960s after it appeared certain antidepressant drugs worked by altering brain chemicals, but it was stated that “the findings are inconclusive.”1 Yet, the theory was proposed at a time when treating mental illness via psychoanalysis was falling out of favor while viewing it as tied to a physical or biological mechanism was in vogue.

The idea quickly spread, becoming the medical dogma for depression, despite concrete evidence proving its worth. “The fact that practicing physicians and leaders of science bought that idea, to me, is so disturbing,” Steve Hyman, director of the Stanley Center for Psychiatric Research at the Broad Institute of MIT and Harvard, told Quartz.2 The news outlet continued:

“It’s not hard to see why the theory caught on: It suited psychiatrists’ newfound attempt to create a system of mental health that mirrored diagnostic models used in other fields of medicine. The focus on a clear biological cause for depression gave practicing physicians an easily understandable theory to tell patients about how their disease was being treated.”3

Prozac, Zoloft Bring Chemical Imbalance Theory for Depression to the Mainstream

The release of the antidepressant Prozac (fluoxetine) in the late 1980s was a game changer for depression treatment in that the drug’s maker, Eli Lilly, heavily promoted the chemical balance theory as a marketing gimmick to sell the drug. With fewer side effects than some of the earlier antidepressants, Prozac became a blockbuster drug and the poster child for the selective serotonin reuptake inhibitor (SSRI) class of antidepressants, which target the neurotransmitter serotonin.

“There was, of course, no demonstrable evidence showing that depressed patients had any imbalance, but Lilly ran with it,” Psychology Today noted. “Before long, psychiatrists and psychiatric patients alike came to identify with the idea that mental disorders are caused by chemical imbalances in the brain.”4

Zoloft (sertraline), another SSRI, was another major player in spreading and perpetuating the chemical balance theory, with their television ads going so far as to say, “While the causes are unknown, depression may be related to an imbalance of natural chemicals between nerve cells in the brain. Prescription Zoloft works to correct this imbalance.”5

It’s important to note that in the time since Prozac flooded the market, depression still remains poorly treated, despite a plethora of new antidepressant options to choose from. SSRIs work by preventing the reuptake (movement back into the nerve endings) of the neurotransmitter serotonin.

This makes more serotonin available for use in your brain, which is thought to improve your mood since low serotonin levels are said to lead to depression. Yet, as written in the Handbook of Experimental Pharmacology, it’s a largely disproven theory:6

“Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed their supposed effectiveness is the primary evidence for the chemical imbalance theory. But analyses of the published data and the unpublished data that were hidden by the drug companies reveal that most (if not all) of the benefits are due to the placebo effect.

Some antidepressants increase serotonin levels, some decrease it, and some have no effect at all on serotonin … The serotonin theory is as close to any theory in the history of science having been proved wrong.”

Harvard: Depression ‘More Complex’ Than a Brain Chemical Imbalance

It’s quite possible that people who are depressed may have an imbalance of certain chemicals in their brain. But to speculate that that imbalance is the cause of their symptoms is overly simplistic. For instance, it’s known that psychological stress can cause biological changes in the brain, including a reduction in the size of the hippocampus, which is used for learning and memory.7 In turn, it’s known that some people with depression have a smaller-than-average hippocampus.8

“Evidence of biological changes correlating with environmental stressors is vastly different from evidence that mental illnesses are ‘caused’ by biological deficits,” scientists wrote in a 2008 report on the chemical imbalance theory,9 and this is an important point. Even Harvard Medical School acknowledges that while brain chemicals may play a role in your mood, it is not accurate to suggest that one being too high or too low is at the root of depression. They state:10

“Research suggests that depression doesn’t spring from simply having too much or too little of certain brain chemicals. Rather, there are many possible causes of depression, including faulty mood regulation by the brain, genetic vulnerability, stressful life events, medications, and medical problems.

It’s believed that several of these forces interact to bring on depression … There are millions, even billions, of chemical reactions that make up the dynamic system that is responsible for your mood, perceptions, and how you experience life.”

One theory posits, for instance, that stress could be a major contributor to depression because it suppresses the production of new neurons in the hippocampus. In order to feel better, people with depression may need to increase neurogenesis (the generation of new neurons), which takes weeks.

This would explain why many people who take antidepressants don’t notice any improvement for several weeks.11 If the action was really on neurotransmitters, the patient should feel better right away when levels increase. Instead, triggering the growth of neurons could be the secret, which is a process that can be triggered naturally via exercise.

Believing Depression Is Caused by Chemical Imbalance Worsens Outcomes

Aside from the serious implications of prescribing drugs under a false premise, the chemical balance theory is also dangerous in that it takes away ownership from the patient. If a person feels a chemical imbalance in their brain is to blame for their depression, they may believe taking medications is the only option to feel better. According to Todd Kashdan, professor of psychology at George Mason University in Virginia, upon “buying into a biomedical explanation for their depression:”12

“They become pessimistic that recovery is possible. They become less confident that they can manage and regulate negative moods that arise (and they always do). The notion that depression is their brain’s fault does not lessen the stigma or self-blame one bit.

And they no longer believe that psychotherapy is a credible or useful strategy for treating their depression and instead, are ready to be dispensed a pill cure. Essentially, they become less flexible in their options for treating depression and less confident that they will escape its clutches.”

Indeed, a 2014 study published in Behavior Research and Therapy revealed just that — attributing depressive symptoms to a chemical imbalance made people more pessimistic about their prognosis and led them to believe that drugs would be more effective than psychotherapy.13 At the same time, they still felt the same amount of self-blame. It’s important to note that –

feeling depressed is not anyone’s fault, nor should they feel blamed for or ashamed of their feelings.

However, pinning its cause on a chemical imbalance is likely to worsen outcomes rather than improve them. It’s a vicious cycle as well, because the chemical imbalance theory makes people assume that medications are the best course of treatment. But here again research has shown that people with depression who are treated with medication have poorer long-term outcomes compared to those who are not.14

Antidepressants Work No Better Than Placebo

Nearly 7 percent of U.S adults suffered from a depressive episode in the past year15 while, worldwide, 350 million people suffer from depression, making it a leading cause of disability.16 Despite this, only about one-third of Americans with depression get treated,17 which puts the remaining two-thirds left untreated at increased risk of suicide and with a lower quality of life.

That said, the antidepressant drugs that are supposed to work by fixing a chemical imbalance in the brain are largely ineffective, which means that even when some people attempt to get treatment, they’re left suffering. Studies have repeatedly shown antidepressants work no better than placebo for mild to moderate depression.18

Irving Kirsch, associate director of the Program in Placebo Studies at Harvard Medical School, has conducted meta-analyses of antidepressants in comparison to placebo and has concluded that there’s virtually no difference in their effectiveness, noting, “The difference is so small, it’s not of any clinical importance.”19 What is different, however, is the potential for side effects, which is far greater among antidepressants than placebos.

For instance, antidepressant users have an increased risk of developing Type 2 diabetes,20 even after adjusting for other risk factors, like body mass index (BMI).21 Antidepressant use has also been linked to thicker arteries, which could contribute to the risk of heart disease and stroke.

The results of a study of 513 twin veterans, presented at the American College of Cardiology meeting in New Orleans in 2011, found that antidepressant use resulted in greater carotid intima-media thickness (the lining of the main arteries in your neck that feed blood to your brain).22

This was true both for SSRIs and antidepressants that affect other brain chemicals. Further, the use of antidepressants is also associated with an increased risk of heart attack, specifically for users of tricyclic antidepressants, who have a 36 percent increased risk of heart attack.23

Meanwhile, the drugs are also linked to dementia, with researchers noting “treatment with SSRIs, MAOIs, heterocyclic antidepressants, and other antidepressants was associated with an increased risk of dementia,” and as the dose increased, so too did the risk.24

The drugs are also known to deplete various nutrients from your body, including coenzyme Q10 and vitamin B12 — in the case of tricyclic antidepressants — which are needed for proper mitochondrial function. SSRIs may deplete iodine and folate,25 and you’re even more likely to relapse if you’re treated with antidepressants than if you’re treated via other methods, including placebo or exercise.26,27Given the lack of effectiveness and the risks involved, Kirsch and colleagues concluded:28

“When different treatments are equally effective, choice should be based on risk and harm, and of all of these treatments, antidepressant drugs are the riskiest and most harmful. If they are to be used at all, it should be as a last resort, when depression is extremely severe and all other treatment alternatives have been tried and failed.”

Alternative Treatments for Depression

If the chemical imbalance theory is false, the case for choosing antidepressants as a first-line treatment for depression is incredibly weak. Fortunately, there are many alternatives to drugs for treating depression, including nutritional interventions, light therapy, exercise and more. If you’re struggling with depression, you needn’t suffer in silence. Seek help, from a counselor, a holistic psychiatrist or another natural health practitioner to start the journey toward healing.

That said, if you are feeling desperate or have any thoughts of suicide, please call the National Suicide Prevention Lifeline, a toll-free number: 1-800-273-TALK (8255), call 911, or simply go to your nearest hospital emergency department. You cannot make long-term plans for lifestyle changes when you are in the middle of a crisis. If you’re in a place where you feel you can begin to make positive changes, here are some of the top alternative treatments for depression to consider:

Exercise. Those who didn’t exercise were 44 percent more likely to become depressed compared to those who did so for at least one to two hours a week.29
Light therapy. Light therapy alone and placebo were both more effective than Prozac for the treatment of moderate to severe depression in an eight-week-long study.30
Omega-3 fats, which have been shown to lead to improvements in major depressive disorder.31 Make sure you’re getting enough omega-3s in your diet, either from wild Alaskan salmon, sardines, herring, mackerel and anchovies, or a high-quality animal-based omega-3 supplement.
Optimize your vitamin D levels, another factor linked to depression32
Magnesium. Magnesium supplements led to improvements in mild-to-moderate depression in adults, with beneficial effects occurring within two weeks of treatment.33
B vitamins. Low levels of B vitamins are common in patients with depression, while vitamin B supplements have been shown to improve symptoms.34
Mindfulness meditation35 and the Emotional Freedom Techniques (EFT). In a study of 30 moderately to severely depressed college students, the depressed students were given four 90-minute EFT sessions. Students who received EFT showed significantly less depression than the control group when evaluated three weeks later.36
Cognitive behavioral therapy, which works as well as antidepressants and may reduce your risk of relapse even after it’s stopped.37
Limit sugar. Men consuming more than 67 grams of sugar per day were 23 percent more likely to develop anxiety or depression over the course of five years than those whose sugar consumption was less than 40 grams per day.38
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**Comment**
A very helpful article for Lyme/MSIDS patients as we nearly always at some point suffer with depression.  
Some of you might be on antidepressants and this article has left you floundering.  Take a deep breath and decide you are going to take this information, study it, and talk to your practitioner before deciding upon any course of action.
Please seek help if you need it.  If possible find at least a “Lyme friendly” practitioner as the last thing you need is to be abused by another health professional when you are at your lowest.  Hopefully the word is getting out on the psychiatric manifestations of Lyme/MSIDS.  Start by going to your local Lyme support group and ask around for a good, reputable, understanding, and hopefully experienced practitioner.
For those of you in the trenches, I want to encourage you that this too shall pass.  I found my depression while in treatment for Lyme/MSIDS was directly aligned to how I felt physically.  The worse I felt physically the worse I felt emotionally.  I’ve said this before, but the best advice I ever received from someone who made it to the other side of health was, “Don’t get depressed about feeling depressed.”  Give yourself permission to feel lousy.  Your body is in a battle of epic proportions – you’re bound to feel like crap.
Treating for Lyme/MSIDS is unlike most other treatments that have linear improvement.  You are going to have starts and stops, good days and bad, and down right horribly miserable days.  You are going to have days where you beg to have it all end.
Persevere.  Don’t quit.  Better days are coming.  Do not give in to the moment.  
When I got really low I read books where others had it worse than me.  I watched cartoons, anything to get my mind off the pain and hopelessness.  For a long time I didn’t read anything about treatment outcomes, because frankly I couldn’t have handled the truth.  That’s OK.  You don’t need to know how the watch works when you are at your lowest.  There will come a day when you can handle all that information, but for today, take a nice bath.  Listen to your favorite music.  Read your favorite books.  Call an understanding friend.  Whatever it takes to get through this day, minute, and second.

There has been researching showing that probiotics help with depression as well:  http://www.spring.org.uk/2017/03/probiotics-depression.phpThe scientists found that when mice in the study were put under stress, they developed a reduction in Lactobacillus through the metabolite kynurenine, which is somehow involved with inflammation and was linked to depressed behavior.  Feeding them Lactobacillus almost completely stopped their depressive behaviors.  

All Lyme/MSIDS patients should be on good pro and prebiotics and doing all they can to lower inflammation.  Read here about the microbiome and MSM’s ability to lower inflammation & help heal the gut:  https://madisonarealymesupportgroup.com/2018/01/03/the-invisible-universe-of-the-human-microbiome-msm/

If the depression hangs on, seek help.  Also, if you need to take medication short-term – so be it.  No judgement here.  We are all different and take different things to make it to the other side of health.  But, I encourage you to get to the bottom of things rather than mask it with a pill.  

My experience has shown me that treatment for pathogens is just one prong of our healing journey, and while important, isn’t the end-all.  We must detox.  We must address diet and sleep.  We must learn everything we can about our personal imbalances and weaknesses and seriously address them.  We must address our mental health and all that entails – from lowering our stress to ditching harmful relationships.
Thank you to all the mental health practitioners and patients out there writing about your experiences with Lyme/MSIDS psychiatric issues.  We need to hear what you have to say!

The Invisible Universe Of The Human Microbiome & MSM

 NPR 2013

The next time you look in a mirror, think about this: In many ways you’re more microbe than human. There are 10 times more cells from microorganisms like bacteria and fungi in and on our bodies than there are human cells. But these tiny compatriots are invisible to the naked eye. Artist Ben Arthur gives us a guided tour of the rich universe of the human microbiome.

https://articles.mercola.com/sites/articles/archive/2018/01/03/gut-microbiome-probiotics.aspx?  Dr. Mercola Jan., 2018

Story at-a-glance

  • Because 70 to 80 percent of your immune system resides within your gastrointestinal tract, optimizing your gut microbiome is a worthwhile pursuit that will have far-reaching effects on your physical health and emotional well-being
  • A vital first step toward balancing your gut flora is to eliminate sugar from your diet, especially sugars found in processed foods
  • Eating fermented foods such as kefir, kimchi and sauerkraut, as well as consuming prebiotic foods like garlic, leeks and onions, can help create an optimal environment for beneficial gut bacteria, while decreasing disease-causing bacteria, fungi and yeast
  • Taking a probiotic or sporebiotic supplement can also be beneficial, especially during and following antibiotic treatment, because it helps restore and promote healthy gut flora
  • Your gut bacteria can influence your behavior and gene expression, and has also been shown to play a role with respect to autism, diabetes and obesity

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All Lyme/MSIDS patients should be on a good pro and prebiotic as well as lowering or avoiding sugars, eating a whole-food based diet, and avoiding processed food.  Some will do well eliminating gluten and/or dairy.  We are all so different – what works for one may not work for another, but all are worth trying.

In my quest, I’ve been studying DMSO and MSM.  For that information:  https://madisonarealymesupportgroup.com/2018/03/02/dmso-msm-for-lyme-msids/

Briefly, MSM stands for Methylsulfonylmethane and is 34% sulfur by weight.  Sulfur plays a crucial role in detoxification and is an important antioxidant for producing glutathione.  If you aren’t getting enough sulfur, glutathione can not work.  Even if you have a diet rich in sulfur (think cabbage, onions, garlic, broccoli, etc – essentially the stinky veggies – and many other food items as well) your body still could use supplementation.

For me it was a game-changer.

https://lyngenet.com/msm-wonder-supplement-sinus-digestive-lung-esophageal-health/ By Lyn-Genet Recitas, NMT, Sports Nutritionist, Holistic Health Pracitioner, RYT

Recitas, author of “The Plan,” calls MSM the wonder supplement for your gut.  It can alleviate allergy symptoms, helps with detoxification, eliminates free radicals, and improves cell permeability.  She states that with given time, MSM will start to actually repair damage caused by leaky gut – a common problem with Lyme/MSIDS patients.  It can also help the body’s ability to absorb nutrients from food.  Many Lyme patients struggle with paralysis of the gut where the muscles of the stomach and intestines stop being efficient.  MSM helps this muscle tone as well.

My personal observation after starting MSM

I started out with 1/4 tsp of distilled crystals in about 2 oz of water, since it has a bitter taste.  After studying it, I learned the distillation process is the best one and if you want to find sources easily go here:  http://www.optimsm.com/brands/ You should see the OptiMSM patent on the product.  I happened to get the 16 oz tub of crystals at the Vitamin Shoppe but as you can see there are many brands available. (As always, I don’t make a dime on any of this and have no connection what so ever to any product line)

Within three days I noticed my nails growing faster.  Within a week, about 50% of my pain was gone.  Now this is a big deal as this pain has been resistant to nearly everything I’ve tried over the years.

After this reduction in pain, I increased the dose to 1/4 tsp twice a day and then ultimately to my final dose of 1/2 tsp twice a day in 2 oz of water.

**update** I had to pull back on amount for a few weeks as my body was detoxing and I broke out like a teenager on my face, back, and chest.  All I can say is it does help detoxify as clearly seen on my skin.  After reducing the dose for a month or so I easily went back to my full dose of 1/2 tsp once a day.  Everyone’s different and requires different doses.  Take the lowest amount to achieve desired results.

I have to report that my pain is completely gone on some days with a fraction returning on other days.

For a great MSM guide:  http://msmguide.com/

http://www.nutraceuticalsworld.com/contents/view_breaking-news/2017-04-25/decades-of-discovery-summarized-in-new-msm-review/  This article gives a current 2017 review of MSM as well as studies and 195 references.

MSM has been studied for decades.

It is recommended to start at a low initial dose and allow the body to acclimate.  You can slowly increase the dose after a week.  It is also stated that those with chronic conditions may take up to 6 or more months to notice a difference.

You can also get MSM in creams, gels, and lotions for topical application – as well as pills.  Make sure you read about the other ingredients and if the MSM is made from distillation.  Like any other supplement, the devil’s in the details.

I’ve had patients report back to me that MSM has been a game-changer for them too.  Considering the fact it’s cheap, helps with pain and inflammation, helps with detoxification and helping the gut, it is one item I can suggest to anyone to try.

MSM is derived from DMSO and has many similar properties plus DMSO has many all of its own worth investigating.  DMSO takes more knowledge to use so please read that article above in detail as it’s a penetrating agent and will drive anything and everything into your body.  If using topically you want it to completely dry before anything touches it and your hands, utensils and everything it’s stored in must be clean and preferably glass.  DMSO should never be stored in plastic.

 

 

 

 

Joint Swelling & Inflammation Found in Bb Infected Mice After Treatment with Ceftriaxone

Targeting of vascular adhesion protein-1 by positron emission tomography visualizes sites of inflammation in Borrelia burgdorferi-infected mice

Siitonen R, Pietikäinen A, Liljenbäck H, Käkelä M, Söderström M, Jalkanen S, Hytönen J, Roivainen A.
Arthritis Research & Therapy, online first Nov 22, 2017.

https://doi.org/10.1186/s13075-017-1460-4

Abstract

Background
In the present study, we sought to evaluate the feasibility of targeting vascular adhesion protein-1 (VAP-1) by positron emission tomography (PET) for the longitudinal quantitative assessment of Borrelia burgdorferi infection-induced inflammation in mice.

Methods
Mice with B. burgdorferi infection-induced arthritis were studied. During a 7-week follow-up period, the progression of arthritis was monitored weekly with 68Ga-DOTA-Siglec-9 PET/computed tomography (CT) and measurement of tibiotarsal joint swellings. A subgroup of infected mice was treated with ceftriaxone. Finally, histopathological assessment of joint inflammation was performed and VAP-1 expression in joints were determined.

Results
Explicit joint swelling and 68Ga-DOTA-Siglec-9 uptake could be demonstrated in the affected joints from B. burgdorferi-infected mice. By contrast, no obvious accumulation of 68Ga-DOTA-Siglec-9 was detected in joints of uninfected mice. The maximum swelling and highest uptake in the affected joints were observed 4 weeks after the infection. 68Ga-DOTA-Siglec-9 uptake in joints correlated with joint swelling (P < 0.0001) and histopathological scoring of inflammation (P = 0.020). Despite short-term antibiotic treatment, the arthritis persisted, and the PET signal remained as high as in nontreated mice. Immunohistochemistry revealed strong-to-moderate expression of VAP-1 in the synovium of B. burgdorferi-infected mice, while only weak expression of VAP-1 was detected in uninfected mice.

Conclusions
The present study showed that 68Ga-DOTA-Siglec-9 can detect B. burgdorferi infection-induced arthritis in mice. Furthermore, longitudinal PET/CT imaging allowed monitoring of arthritis development over time.

Free, full text:
https://doi.org/10.1186/s13075-017-1460-4

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For more:  https://madisonarealymesupportgroup.com/2015/09/19/proof-of-borrelia-persistence/

https://madisonarealymesupportgroup.com/2017/08/18/drexel-prof-lyme-persists/

https://madisonarealymesupportgroup.com/2016/12/21/dr-zhang-on-persisters/

https://madisonarealymesupportgroup.com/2017/11/03/lyme-bug-stronger-than-antibiotics-in-animals-and-test-tubes-now-study-people/

Bartonella: Endocarditis, Opportunistic Infection in Cancer Patients, and Eye Inflammation

https://www.ncbi.nlm.nih.gov/m/pubmed/28490579/  Bartonella Species, an Emerging Cause of Blood-Culture-Negative Endocarditis.

Okaro U1, Addisu A2, Casanas B2, Anderson B3. Clin Microbiol Rev. 2017.

Abstract
Since the reclassification of the genus Bartonella in 1993, the number of species has grown from 1 to 45 currently designated members. Likewise, the association of different Bartonella species with human disease continues to grow, as does the range of clinical presentations associated with these bacteria. Among these, blood-culture-negative endocarditis stands out as a common, often undiagnosed, clinical presentation of infection with several different Bartonella species. The limitations of laboratory tests resulting in this underdiagnosis of Bartonella endocarditis are discussed. The varied clinical picture of Bartonella infection and a review of clinical aspects of endocarditis caused by Bartonella are presented. We also summarize the current knowledge of the molecular basis of Bartonella pathogenesis, focusing on surface adhesins in the two Bartonella species that most commonly cause endocarditis, B. henselae and B. quintana. We discuss evidence that surface adhesins are important factors for autoaggregation and biofilm formation by Bartonella species. Finally, we propose that biofilm formation is a critical step in the formation of vegetative masses during Bartonella-mediated endocarditis and represents a potential reservoir for persistence by these bacteria.

https://www.ncbi.nlm.nih.gov/m/pubmed/28328183/  Seroprevalence of Bartonella species, Coxiella burnetii and Toxoplasma gondii among patients with hematological malignancies: A pilot study in Romania.

Messinger CJ1, Gurzau ES2,3, Breitschwerdt EB4,5, Tomuleasa CI6,7, Trufan SJ8, Flonta MM9, Maggi RG4,5, Berindan-Neagoe I6,10,11, Rabinowitz PM8. Zoonoses Public Health. 2017.

Abstract
Patients receiving immunosuppressive cancer treatments in settings where there is a high degree of human-animal interaction may be at increased risk for opportunistic zoonotic infections or reactivation of latent infections. We sought to determine the seroprevalence of selected zoonotic pathogens among patients diagnosed with haematologic malignancies and undergoing chemotherapeutic treatments in Romania, where much of the general population lives and/or works in contact with livestock. A convenience sample of 51 patients with haematologic cancer undergoing chemotherapy at a referral clinic in Cluj-Napoca, Romania, was surveyed regarding animal exposures. Blood samples were obtained and tested for evidence of infection with Bartonella species, Coxiella burnetii and Toxoplasma gondii, which are important opportunistic zoonotic agents in immunocompromised individuals. 58.8% of participants reported living or working on a farm, and living or working on a farm was associated with contact with livestock and other animals. 37.5% of participants were IgG seroreactive against one or more of five Bartonella antigens, and seroreactivity was statistically associated with living on farms. Farm dwellers were 3.6 times more likely to test IgG seroreactive to Bartonella antibodies than non-farm dwellers. 47.1% of the participants tested T. gondii IgG positive and 13.7% tested C. burnetii IgG positive, indicating past or latent infection. C. burnetii IgM antibodies were detected in four participants (7.8%), indicating possible recent infection. These results indicate that a large proportion of patients with haematologic cancer in Romania may be at risk for zoonotic infections or for reactivation of latent zoonotic infections, particularly with respect to Bartonella species. Special attention should be paid to cancer patients’ exposure to livestock and companion animals in areas where much of the population lives in rural settings.

https://www.ncbi.nlm.nih.gov/m/pubmed/28405890/  Seroprevalence of Bartonella Species in Patients with Ocular Inflammation.

Brydak-Godowska J1, Kopacz D1, Borkowski PK2, Fiecek B3, Hevelke A4, Rabczenko D5, Tylewska-Wierzbanowska S3, Kęcik D1, Chmielewski T3. Adv Exp Med Biol. 2017.

Abstract
Bartonella species, vector-borne etiologic agents of many systemic or self-limited infections, are responsible for a widening spectrum of diseases in humans, including inflammatory conditions of the eye. The aim of this study was to determine whether there is any relationship between uveitis and the evidence of Bartonella spp. infection in the serum, ocular fluid, and cataract mass in patients with intraocular inflammation. Polymerase chain reaction (PCR)-based tests and DNA sequencing were performed on surgery-extracted specimens of intraocular fluid and lens mass of 33 patients. Sera from 51 patients and 101 control subjects were tested for the presence of specific antibodies against Bartonella spp. Neither IgM-class antibodies against Bartonella spp. nor Bartonella spp. DNA were detected. A specific IgG-class antibody was found in 33.3% of the patients with uveitis. The rate of positive Bartonella serology was higher among the uveitis patients than that in control subjects. This high rate may in part result from unrecognized indirect mechanisms rather than the immediate presence and multiplication of Bartonella spp. in the eyeball. Nonetheless we believe that screening for Bartonella spp. should become part of the diagnostic workup in uveitis.

Another ocular study:  https://madisonarealymesupportgroup.com/2017/04/06/ocular-bartonellosis/

Proof of Borrelia Persistence

The following work by microbiologist Thomas Grier and pathologist Alan MacDonald should prove to the CDC that Borrelia can undoubtably persist inside the human body.

http://whatislyme.com/lyme-a-beautiful-killer-by-thomas-grier/

“For years pathologists stained for amyloid to make the diagnosis, but when the same plaques in a serial sectioning were stained for B burgdorferi or B miyamotoi, individual classical spirochetes could be seen, but more commonly a biofilm of Borrelia could be seen in the same plaques. Borrelia is a brain-pathogen.”

grier

Above:  “Borrelia miyamotoi using Alan MacDonald’s FISH stain. This is the first documented case of Bm in Minnesota.”

tom2

Above and below:  “Since Fluorescence FISH stain target species specific nucleotide sequences, it is species specific. Spirochetes are excellent subjects because the Borrelia DNA is associated with the cell wall and membrane. Another probe can isolate cytoplasmic DNA thus giving a 3-D look to it. What a beautiful killer.”

spiro

Below:  “This patient was told for 22 years that she had MS, our work on MS allowed us to determine that this brain MRI was probably a result of Lyme. Do you see the markers? This Philadelphia woman made a very good recovery from her disability and went back to work.”

Below:  “This is Borrelia burgdorferi in the brain of a man sick for two decades. The others in red were Borrelia miyamotoi. Another finding was even after treatment he had neutrophils in the brain, and indication of a breakdown of the BBB and inflammation. He was sicker than doctors realized!”

ms-lyme

“The last photo taken of Grier’s friend Scott from Twig MN.  His deathbed video is all about helping other Lyme victims.”  Scotty was a 57 year old Lumberman who lived his whole life in the forest.  Scotty was seronegative for Lyme but was bedridden with pain and neurolyme and was treated for 7+ years with aggressive antibiotics.  His brain autopsy revealed several surprises and live active Borrelia burgdorferi.”  

scott

Contact Thomas Grier M.S. at donatebrain@gmail.com to ask him about helping fund his research.

For more:  https://madisonarealymesupportgroup.com/2018/04/17/persistent-borrelia-infection-in-patients-with-ongoing-symptoms-of-lyme-disease/  Conclusions: Using multiple corroborative detection methods, we showed that patients with persistent Lyme disease symptoms may have ongoing spirochetal infection despite antibiotic treatment, similar to findings in non-human primates. The optimal treatment for persistent Borrelia infection remains to be determined.

https://madisonarealymesupportgroup.com/2019/01/16/study-shows-diminished-pathogen-specific-antibody-production-in-coinfected-mice-contributing-to-persistent-infection/

https://madisonarealymesupportgroup.com/2018/10/30/study-shows-lyme-msids-patients-infected-with-many-pathogens-and-explains-why-we-are-so-sick/  For the first time, Garg et al. show a 85% probability for multiple infectionsincluding not only tick-borne pathogens but also opportunistic microbes such as EBV and other viruses….In addition to tick-borne co-infections and non-tick-borne opportunistic infections, pleomorphic Borrelia persistent forms may induce distinct immune responses in patients by having different antigenic properties compared to typical spirochetes32,33,34,35. Nonetheless, current LD diagnostic tools do not include Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic infections.

http://norvect.no/230-peer-reviewed-studies-show-evidence-of-persistent-lyme-disease/

http://lymerick.net/persistent-borreliosis.htm  Microscopy, Culture or PCR-verified cases of persistent [seronegative] Lyme Borreliosis

https://madisonarealymesupportgroup.com/2018/04/13/chronic-lyme-post-mortem-study-needed-to-end-the-lyme-wars/

https://madisonarealymesupportgroup.com/2018/07/23/exploring-the-controversial-concept-of-chronic-lyme-disease/