Archive for the ‘research’ Category

Lyme Disease Study Raises Possibility of Mother-to-Baby Transmission

Lyme disease study raises possibility of mother-to-baby transmission

 A female blacklegged tick is embedded in a human arm. A new study says that a developing fetus can be harmed if the mother has Lyme disease. - Public Health Agency of Canada
A female blacklegged tick is embedded in a human arm. A new study says that a developing fetus can be harmed if the mother has Lyme disease. – Public Health Agency of Canada

A scientist who co-authored a recent Public Health Agency of Canada study on the impact of Lyme disease during pregnancy says the illness can have fatal consequences for a developing fetus if the mother goes untreated.

“Miscarriage, newborn death, and newborns with respiratory problems or jaundice have been found to occur,” said American epidemiologist Alison Hinckley.

But the Centers for Disease Control and Prevention scientist says more research is needed to show a definitive link between Lyme disease and pregnancy complications, including whether the tick-borne illness can be passed from mother to baby in the womb.

Hinckley and four Public Health Agency of Canada scientists authored a recent report that reviewed 59 cases of pregnant mothers carrying Lyme disease and their pregnancy outcomes. The results were published in the November 2018 peer-reviewed science journal PLOS One, showing that 36 of the 59 fetuses had been harmed. Complications ranged from miscarriage and stillbirth to congenital abnormalities, respiratory distress and heart abnormalities.

“It is clear, however, that pregnant women who suspect that they might have contracted Lyme disease should see their health-care provider as quickly as possible to receive appropriate treatment and reduce the chance of poor fetal outcomes,” said Hinckley.

PHAC denied requests from the Herald to speak with any of the agency’s four scientists that coauthored the study. The Herald contacted the study’s lead author Lisa A. Waddell by email and phone but did not get a response.

The question remains, why do pregnant mothers with untreated Lyme disease risk harming their unborn baby?

Determining cause

The authors of the systematic review failed to provide a specific cause for any of the 36 pregnancies resulting in harm to the fetus, nor could they definitively say whether Lyme disease factored in any of the congenital malformations. The study couldn’t rule out transplacental transmission, that the bacteria causing Lyme disease, B. burgdorferi, could be passed from mother to baby in utero.

“It is biologically plausible that transplacental transmission of B. burgdorferi occurs given our understanding of transplacental spirochete transmission for other species of spirochetes (T. pallidum) in humans,” said the study. “However, the evidence in this systematic review on congenital malformations does not provide sufficient evidence to exclude or confirm a role for B. burgdorferi in congenital malformations.”

The study calls for more research to settle the debate.

But the topic of in utero transmission of Lyme disease is not new and cases of it have been documented over the decades. As far back as 30 years ago the federal Department of Health acknowledged it as a legitimate form of transmission, stating in a June 1988 Canada Diseases Weekly Report that,

“Transplacental transmission of B. burgdoferi has been documented and may be associated with an increased risk of adverse pregnancy outcome.”

That it occurs is not up for debate, argues biologist Vett Lloyd of the Mount Allison University Lyme Research Network.

“There is evidence from epidemiological studies that the Lyme disease bacteria can be transmitted from mother to child,” said Lloyd, who’s also a leading Canadian tick expert. “There is also evidence from case studies of this.

“But what we don’t know are the answers to questions important to pregnant mothers: How often does this occur? Is it with every pregnancy when the mother is infected or one in 10? One in 100? One in a million?”

We know what we don’t know

Ultimately, the study illustrates how much researchers don’t know about the impact of Lyme disease in pregnancy, she says. If in utero transmission occurs and the B. burgdorferi bacterium passes the placenta to the baby what happens then? In children and adults Lyme disease has the potential to target every vital organ.

If it is transmitted in utero to a child, that increases the number of people who can potentially be infected,” said Lloyd. “There is no reason to think that a newborn would be any less affected by Lyme disease than an adult — the opposite would be a reasonable assumption.

This problem is compounded if a mother doesn’t know that she is infected with the Lyme disease bacteria, becomes pregnant while being treated or becomes infected while pregnant.”

The Herald made several attempts to speak to Dr. Robert Strang, the province’s chief medical officer of health, about the findings of the study but he declined to be interviewed. In an email statement Strang reaffirmed one of the main conclusions of the study: “There is not enough evidence to confirm that Lyme disease during pregnancy has any adverse effect on the fetus, Lyme disease can be effectively treated in pregnancy and that further research is needed,” stated Strang.

Strang’s statement also defends the way the province treats Lyme disease, including in pregnant mothers. “Nova Scotia’s approach to the diagnosis and treatment of Lyme disease, including Lyme disease in pregnancy, is based on current scientific evidence and is consistent with national and international evidence-based guidelines.”

Sue Faber, co-founder of LymeHope and a registered nurse, says PHAC is ignoring decades of documented proof of transplacental transmission and insists it’s only a matter of time before the medical community is forced to acknowledge it as a legitimate form of transmission that results in congenital Lyme disease — babies being born with the disease.

Over the year, her Lyme advocacy group has gotten thousands of letters from people across the country convinced family members have fallen victim to congenital Lyme disease. She also says a follow up study is needed to look at some of these families.

When the time comes that the medical community accepts that babies can contract the disease in utero it will be “a game changer,” she says.

“For Lyme disease to be passed from mother to child in pregnancy challenges and deconstructs the status quo from Lyme being only a tick-borne disease to one that can be transmitted from human-to-human, mother-to-baby,” said Faber. “Once we acknowledge that this disease changes and we have a big problem on our hands.”

Anna Maddison, spokeswoman for PHAC, admits more research is required to better understand if there may be adverse effects of Lyme disease during pregnancy. She did not say what current or future research is planned to target questions around transplacental Lyme disease.

But Maddison did point to a new Pan-Canadian Lyme Disease Research Network and that part of its research mandate will include working with patients and families to help address gaps in knowledge. The Society of Obstetricians and Gynecologists of Canada is also reviewing current evidence on the effects of Lyme disease and other tick-borne diseases on pregnancy, she says.

“The aim is to equip health-care providers and women with evidence-based information and tools on Lyme disease and other tick-borne diseases during pregnancy,” said Maddison.

But Faber says she sees little evidence that PHAC is responding to the findings of the study with the urgency it deserves.

Medical and scientific research needs to follow the precautionary principal,” said Faber. “If there’s a risk, it needs to be addressed. We have identified that human-to-human transmission is possible, and even if it’s plausible there’s a social responsibility to protect the public from exposure to harm.”



The truly despicable thing is the potential for congenital transmission has been known about for decades yet nothing has been done.  Authorities continue to deny, deny, deny despite the lack of research.  You’d think that research in this area would be a high priority knowing Lyme is the #1 vector-borne disease in the U.S.  But no.  They want more climate data….

How many have been infected congenitally?  God only knows.

I find it highly interesting that the minute the Zika scare came out, they KNEW it was sexually transmitted and announced it with abandon.

With Lyme/MSIDS……crickets.

We desperately NEED transmission studies.  We need to know ALL the bugs that can transmit it, if it’s spread congenitally, via breast milk, tears and other bodily fluids, via blood transfusion, organ transplants, etc.

We also desperately need to know the cumulative effects of Lyme with the various coinfections (polymicrobial nature).

For more:

Sjogren’s Syndrome: Clinical Benefits of Low-dose Naltrexone Therapy

Sjogren’s Syndrome: Clinical Benefits of Low-dose Naltrexone Therapy

Scott Zashin 1

1. Rheumatology, University of Texas Southwest Medical Center, Dallas, USA Corresponding author: Scott Zashin,



Sjogren’s Syndrome is a chronic autoimmune disorder that causes the inflammation of the lacrimal and salivary glands, resulting in dryness of the eyes and mouth. In addition, fatigue and musculoskeletal pain, often described as aching, is very common. Treatment directed toward alleviating the fatigue and pain associated with Sjogren’s is currently very limited. This report describes a case of a 47-year-old female with suspected Sjogren’s based on long-standing dry eyes, dry mouth, joint pain, fatigue, elevated measures of inflammation, and a positive rheumatoid factor. She failed standard therapy but improved clinically with low-dose naltrexone therapy.


Low-dose naltrexone (LDN) is a unique compound that has pain-relieving and anti- inflammatory properties. Limited studies have shown benefit in helping relieve the pain in patients with fibromyalgia and improving disease activity in autoimmune conditions such as inflammatory bowel disease and multiple sclerosis. As a result, it seems reasonable that the medication might be useful in Sjogren’s Syndrome, an autoimmune condition that is associated with pain and inflammation.

Case Presentation

A 47-year-old female was diagnosed with Sjogren’s Syndrome six years ago by another rheumatologist, based on her history of eye and mouth dryness. She was found to have a negative rheumatoid factor at that time, but her sedimentation rate by modified Westergren (erythrocyte sedimentation rate, ESR) was recorded as low as 48 and as high as 61 (normal: less than 20 mm/h). Her C-reactive protein (CRP) was 1.74 (normal less than 0.80 mg/dl). Two years ago, she saw a second rheumatologist who agreed with the diagnosis of Sjogren’s Syndrome. At that time, her rheumatoid factor was now elevated at 69 IU/ml (normal: less than 14 IU/m/). Her antinuclear antibody (ANA) and Sjogren antibodies (SS-A and SS-B) were absent. Her anti-CCP antibody and 14.3.3 ETA protein were normal. Her ESR was 48 and her CRP was 1.42. Past medical history included a diagnosis of fibromyalgia. She also had a history of breast cancer that had been in remission for 20 years, a generalized seizure disorder, and elevated liver tests with normal biopsy. Additional medical issues included symptoms of neuropathy, anxiety, and depression. A prior sleep study did not reveal evidence of sleep apnea. She first came to see this author 18 months ago, seeking another opinion, with complaints of fatigue, severe musculoskeletal pain, as well as dryness of her eyes and mouth.

Her daily medications to help with her symptoms of Sjogren’s Syndrome and fibromyalgia included Lexapro, Restasis, meloxicam 15 mg, vitamin D3, magnesium, tramadol 100 mg daily prn, salagen 5 mg tid prn, and hydroxychloroquine 400 mg daily. Her exam demonstrated widespread trigger points affecting both sides of her body, above and below her waist. Her blood work was remarkable for an ESR of 37 and a CRP of 0.77. Her alanine aminotransferase (ALT) was 40 U/L (normal 6-29 U/L).

She elected to try low-dose naltrexone (LDN), which was compounded using a short-acting filler and started at 1.5 mg daily with instructions to increase the medication weekly by 1.5 mg. She came back to see me two weeks after starting the medication and was taking 3 mg daily. She stated that she felt terrific. Her lab was remarkable for a normal ESR of 25 and a CRP of 2.33. Her ALT was normal.

She was seen in follow-up 16 months ago and remained on 3 mg of naltrexone. She felt well but complained of neuropathic pain. Her ESR was now 20. CRP was not ordered. Her ALT was 31 U/L. She was seen in follow-up 14 months ago and remained on 3 mg of naltrexone and continued to feel well without stiffness or pain. She noted that, previously, it would take her all day to feel better. Her ESR remained at 20 and CRP was only minimally increased at 0.87.

She was then seen in follow-up 11 months ago with complaints of increased achiness. She had widespread tender points. She was given a short course of corticosteroids with symptomatic improvement in place of meloxicam. Naltrexone was increased on that visit to 4.5 mg. On the day of that visit, her ESR was 40 and CRP was 25.7 ( current normal value less than 8 mg/L). She was again seen in follow-up nine months ago, doing well on 4.5 mg of naltrexone. Hydroxychloroquine was discontinued a few weeks earlier due to a prolonged QTc interval. Her ESR was back down to 20 and CRP was down to 10.9.

Overall, the patient noted significant clinical benefit with her fatigue and pain within two weeks of starting low-dose naltrexone but no significant change in her dry eyes or mouth. She continues to do well on low-dose naltrexone four months after stopping hydroxychloroquine due to the electrocardiogram (EKG) abnormalities. While her symptoms improved, what is most interesting about this case is that her clinical improvement was associated with an improvement in her inflammatory markers.


In the initial pilot study that used low-dose naltrexone in the treatment of fibromyalgia, the baseline sedimentation rate was a significant predictor of clinical response to LDN [1]. It was of interest to note that this patient’s dramatic clinical response to LDN correlated with an improvement in her ESR. It is postulated that low-dose naltrexone has a beneficial effect on the immune system due to the following mechanisms.

Low-dose naltrexone blocks mu-, delta-, and other opioid receptors. These receptors are present in the cells of the immune system. This inhibition may result in an upregulation of endorphins, which in addition to decreasing pain, may have a beneficial effect on the immune abnormalities by suppressing cell growth [2].

Low-dose naltrexone inhibits microglia activity. Microglia are immune cells in the central nervous system that, when stimulated, produce inflammatory products that may be associated with pain, fatigue, cognitive dysfunction (brain fog) sleep, and mood disorders. Low-dose naltrexone inhibits toll-like receptors that are found in microglia cells. As a result, the production of inflammatory substances declines with resulting symptomatic improvement [3- 4]. The inhibition of these toll-like receptors has been postulated to be responsible for the effectiveness of hydroxychloroquine, a standard therapy in diseases such as Sjogren’s Syndrome and systemic lupus.

Overall, LDN is well-tolerated. The 50 mg standard dose of naltrexone is Food and Drug Administration (FDA) approved in the treatment of alcohol dependence and for inhibiting the effects of opioids. Low-dose naltrexone is sometimes used to help alleviate the symptoms of patients with chronic conditions, including fibromyalgia [1], Crohn’s disease [5-6], and multiple sclerosis [7]. The use of LDN at this low dose and for these indications is considered “off-label” use. In other words, it has not undergone the rigorous testing needed to get the approval of the FDA. Side effects include but are not limited to vivid dreams (most patients take the medication in the evening, but morning dosing of the medication may help with this issue). Patients may experience a reduction in pain relief from narcotics for at least six to 24 hours after taking low-dose naltrexone. In addition, low-dose naltrexone should not be used in patients who are currently receiving opioid analgesics due to the possibility of acute opioid withdrawal. The medication should be avoided until it is felt that the narcotics are out of the patient’s system. Those patients taking thyroid replacement may require a lower amount of thyroid medication so periodic monitoring is indicated. The elevation of liver enzymes is a potential risk with naltrexone treatment but is not felt to be common with low-dose therapy. Other potential side effects may include but are not limited to gastrointestinal disturbances, such as stomach cramps and diarrhea, agitation, anxiety, flu-like symptoms, and headaches. The drug should be compounded with short-acting fillers, so calcium carbonate should be avoided. The most common starting dose is 0.5 mg daily in the evening and increased weekly up to a target dose of 4.5 mg. The drug can be started at higher doses. The drug should be stopped at a minimum of 24 hours prior to the time narcotics may be needed for pain relief for a scheduled surgical procedure. In my practice, I will ask patients to temporarily discontinue low-dose naltrexone 72 hours in advance of taking narcotics if the patient is new to therapy, to ensure pain relief [8-11].


Based on a Medline review, this is the first peer-reviewed case report of a patient with Sjogren’s Syndrome who was treated with low-dose naltrexone and obtained clinical benefits. As a result of this case, further study is needed to determine if low-dose naltrexone will subsequently prove to be a useful medication for treating Sjogren’s Syndrome.

Additional Information


Human subjects: Consent was obtained by all participants in this study. Conf licts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: I prescribe low dose naltrexone to patients in my medical practice.

  1. Younger J, Mackey S: Fibromyalgia symptoms are reduced by low-dose naltrexone: a pilot study. Pain Med. 2009, 10:663-672. 10.1111/j.1526-4637.2009.00613.x
  2. Wang D, Sun X, Sadee W: Different effects of opioid antagonists on μ-, δ-, and κ-opioid receptors with and without agonist pretreatment. J Pharmacol Exp Ther. 2007, 321:544-552.10.1124/jpet.106.118810
  3. Younger J, Parkitny L, McLain D: The use of low-dose naltrexone (LDN) as a novel anti-inflammatory treatment for chronic pain. Clin Rheumatol. 2014, 33:451-459. 10.1007/s10067-014-2517-2
  4. Watkins LR, Hutchinson MF, Ledeboer A, Wieseler-Frank J, Milligan ED, Maier SF: Glia as the ‘bad guys”: implications for improving clinical pain control and the clinical utility of opioids. Brain Behav Immun. 2007, 21:131-146. 10.1016/j.bbi.2006.10.011
  5. Smith JP, Stock H, Bigaman S, Mauger D, Rogosnitzky M, Zagon I: Low-dose naltrexone therapy improves active Crohn’s disease. Am J Gastroenterol. 2007, 102:820-828.
  6. Raknes G, Simonsen P, Smabrekke L: The effect of low-dose naltrexone on medication in inflammatory bowel disease: a quasi experimental before-and-after prescription database study. J Crohns Colitis. 2018, 12:677-686.
  7. Gironi M, Martinelli-Boneschi F, Sacerdote P, et al.: A pilot trial of low-dose naltrexone in primary progressive multiple sclerosis. Mult Scler. 2008, 14:1076-1083.10.1177/1352458508095828
  8. Low dose naltrexone. (2018). Accessed: 2018:
  9. LDN Research Trust. (2018). Accessed: 2018:
  10. Dickson, Windham, Smith, et al.: The LDN Book . Linda Elsegood (ed): Chelsea Green Publishing, White River Junction, VT; 2016.
  11. Moore E, Wilkinson S: The Promise of Low Dose Naltrexone Therapy. McFarland & Company Inc, Jefferson NC; 2009


For an overview of Sjogren’s:  (3 Min Video)  Please notice symptoms are quite similar to Lyme/MSIDS.  

Sjögren’s Syndrome is an autoimmune disease that is found primarily in women, where inflammation at the salivary and lacrimal glands causes dryness of the eyes and mouth. However, it’s also a systemic disease that affects the entire body, producing joint pain and fatigue, and damaging internal organs. As many as four million Americans suffer from Sjögren’s Syndrome, which often overlaps with other rheumatic diseases making it very common to misdiagnose or overlook. Unfortunately, many patients are not diagnosed on time, which makes it much more difficult to treat. In this video, the Director of the Jerome L. Greene Sjögren’s Syndrome Center, Dr. Alan Baer, discusses the symptoms and problems that many patients with Sjögren’s Syndrome face.

If you search the internet with the words Lyme & Sjogren’s, tons of blogs will pop up with people with both. There isn’t much if any science on the two, however. This is another problem with research in Lyme-land – nobody is studying the effects of Lyme triggering or in conjunction with other syndromes within the body.  A big problem.

Excerpt from The Lyme Book:

Lyme disease can trigger autoimmunity, so some people will present with rheumatoid arthritis, lupus, Sjogren’s, Hashimoto’s thyroiditis or any number of autoimmune diseases. It may not be that these diagnoses are incorrect; it may just be that the Lyme infection has unbalanced the immune system sufficiently to trigger the autoimmune mechanism. Where there is autoimmune disease with sufficient evidence of Lyme disease (either through lab work or clinically), treating the Lyme will often improve, if not eliminate, the autoimmunity.

The key concept to grasp here is that of underlying cause. Western medicine has somehow distanced itself from the quest for discovery of the underlying cause of illness. As is the case with bromyalgia or chronicfatigue syndrome, the diagnosis describes a set of symptoms but does not explain why they occur.

For more:  Very informative documentary put out by the LDN Research Trust on Lyme/MSIDS.  Dr. Horowitz, Dr. Toups, Dr. Schweig, Dr. Windham, Dr. Holtorf, & Dr. Schwarzback, speak on everything from testing, to diet, to inflammation, and how LDN can help Lyme/MSIDS patients.












First Case of B. corocidurae in Native European Presenting as Meningitis With Cranial Polyneuritis & Cavernous Sinus Thrombosis

Meningitis with cranial polyneuritis and cavernous sinus thrombosis by Borrelia crocidurae. First autochthonous case in Europe.

Malincarne L, et al. Int J Infect Dis. 2019.


Borrelia crocidurae is endemic in West Africa, where it represents the leading cause of tick-borne relapsing fever (TBRF). TBRF typically presents with high fever and systemic symptoms, followed by recurrent episodes. Neurological complications may occur during febrile relapses. B. crocidurae is considered the most neurotropic agent of TBRF and is associated to severe neurological manifestations i.e. meningitis and encephalitis.

To date, European cases of B. crocidurae infection have been reported in travelers returning from endemic areas. We report the first autochthonous case in Europe of B. crocidurae infection, presenting as meningitis with cranial polyneuritis and cavernous sinus thrombosis that were not preceded by classical febrile recurrences.



This is important as it shows again that Borrelia burgdorferi is not the only borrelia we need to be concerned about.  While endemic in Africa, this case is in a non-traveling European demonstrating the prolific spread of ticks and subsequently the pathogens they carry:

It also demonstrates once again that current CDC 2-tiered testing will NEVER pick this up.  

Cranial polyneuritis = inflammation of many nerves simultaneously.

Cavernous sinus thrombosis =  when the immune system creates a blood clot to prevent bacteria or other pathogens from spreading within a cavity at the base of the brain which drains deoxygenated blood from the brain back to the heart. Typically it is caused by an infection. The clot increases pressure inside the brain which can cause damage.  Mortality is 30%.  

Symptoms of cavernous sinus thrombosis may include:

Tests for Cavernous Sinus Thrombosis

Doctors may order brain scans, including CT and MRI scans, to look for cavernous sinus thrombosis. They may also test blood or spinal fluid to check for signs of infection.

Treatment of Cavernous Sinus Thrombosis

Doctors treat cavernous sinus thrombosis with high-dose antibiotics. These are usually given though an IV drip.

Corticosteroid medications may also be used to reduce swelling. Blood thinners are sometimes given.

Surgery may be needed to drain the site of the initial infection.







Toxicity & Impact of Environment on Chronic Illness – Dr. Neil Nathan

 Approx. 1 Hour

Toxicity and the Impact of Our Environment on Chronic Illness With Dr. Neil Nathan

Published on Mar 15, 2019

Learn more at Cindy Kennedy, FNP, is joined by Dr. Neil Nathan, who discusses his book, Toxic, and how the environment can impact chronic illness.
Neil has been practicing medicine for 47 years, and has been Board Certified in Family Practice and Pain Management and is a Founding Diplomate of the American Board of Integrative Holistic Medicine and a Board member of The International Society for Environmentally Acquired Illness. With Dr. Rich van Konynenburg he did the ground-breaking clinical research which demonstrated the importance of methylation chemistry in Chronic Fatigue Syndrome, and he has recently completed a study with Dr. Robert Naviaux on the metabolomics of Chronic Fatigue Syndrome. He has written several books, including Healing is Possible: New Hope for Chronic Fatigue, Fibromyalgia, Persistent Pain, and Other Chronic Illnesses and On Hope and Healing: For Those Who Have Fallen Through the Medical Cracks.
He has hosted an internationally syndicated radio program/podcast on Voice America called The Cutting Edge of Health and Wellness Today. He has been working to bring an awareness that mold toxicity is a major contributing factor for patients with chronic illness and lectures internationally on this subject which led to the publication of his book, Mold and Mycotoxins: Current Evaluation and Treatment, 2016 and now to his most recent book Toxic: Heal Your Body from Mold Toxicity, Lyme Disease, Multiple Chemical Sensitivities and Chronic Environmental Illness.
His current medical practice is the Redwood Valley Clinic in Northern California. He can be contacted most easily through his website,, through which consultations are available. Neil has been treating chronic complex medical illnesses for 25 years now, and Lyme disease for the past 15 years. As his practice has evolved, he finds himself increasingly treating the patients who have become so sensitive and toxic that they can no longer tolerate their usual treatments, and his major current interest is in finding unique ways of helping them to recover. The recent findings that mast cell activation and porphyria are more common than has been appreciated by the medical profession are of particular importance in this regard.


Lyme in Slovak Republic

Association of seroprevalence and risk factors in Lyme disease

Andrea Bušová1, Erik Dorko1, Eva Feketeová2, Kvetoslava Rimárová1, Jana Diabelková1, Tímea Rovenská1, Tomáš Csank3

Cent Eur J Public Health 2018, 26(Supplement):S61-S66 | DOI: 10.21101/cejph.a5274

Objective: The aim of the presented cross-sectional seroepidemiological study was to determine the current presence of antibodies against B. burgdorferi s.l. in the groups of Slovak population, and to identify potential risk factors to Lyme borreliosis.

Methods: A group of 261 adults (patients from the Neurological Clinic with possible symptoms of LB and healthy persons with possible working exposure to tick bite: gardeners and soldiers working in afforested areas) were examined in order to assess the seroprevalence of anti-Borrelia antibodies. Sera were screened by commercial enzyme-linked immunosorbent assay (ELISA). The respondents completed questionnaires with general demographic, epidemiological and clinical data.

Results: We detected 17.2% presence of positive IgG and 5.7% presence of positive IgM antibodies in all investigated groups. Our results confirmed that the following risk factors such as age and gender are significantly associated with the presence of positive specific antibodies against investigated disease.

Conclusion: The results of seroprevalence obtained in the present study confirm the possibility of infection with B. burgdorferi among respondents exposed to contact with ticks.



Imagine the percentages if they used direct microscopy or even the MISDS questionnaire, not serology which misses half of cases:

Key quote:  “These serologic tests cannot distinguish active infection, past infection, or reinfection.”

In plain English, these tests don’t show squat.

Please spread the word that Dr. Horowitz’s MSIDS questionnaire has been validated and predicts Lyme much better than serology:  The results support the use of the HMQ as a valid, efficient, and low-cost screening tool for medical practitioners to decide if additional testing is warranted to distinguish between Lyme disease and other illnesses.

Here it is.  You can print it off and fill it out yourself:  Excerpt:

There has been an ongoing record of suppression of microscopy for Lyme.  In an interview with now retired professor of microbiology Morten Laane, the facts come rolling out on how he was fired, his lab was closed down, and his published article disappeared without a trace after presenting his findings at a scientific conference on how microscopy showed spirochetes as well as other organisms like Babesia in a number of patients (12).  Laane is far from alone.  Dr. Sin Hang Lee has even filed a $57.1 million lawsuit against the CDC for suppressing direct detection tests, and for employing ‘Lysenkoism,’ a term used for a Russian political campaign using bogus science to suppress true biological and medical sciences and to punish scientists and doctors who don’t follow Party Line (13).

BTW:  The Lyme Good Old Boys aka The Cabal own patents on Lyme serology testing:

Employees of the U.S. Centers for Disease Control hold patents on Lyme tests:  For nearly four decades now the only FDA approved test for Lyme disease is the indirect two-tiered antibody test.

Dr. Allen Steere filed a patent in 2013 for yet more antibody detection tests for Lyme disease: (Application #20150219646) Compositions and Methods for the Detection of Bacterial Infections Associated with Lyme Disease

Anybody smell a rat yet?

The other issue with this study is the fact they are STILL looking this as a ONE pathogen illness when it’s typically not:  Key Quote:  Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes.” 


Melatonin: Benefits & Uses

waking up from healthy sleep


  • Melatonin is a hormone produced by the pineal gland, which helps regulate your circadian rhythm
  • Taking a melatonin supplement may be helpful for people who are experiencing sleep disorders due to various environmental or social factors
  • Aside from promoting sleep, melatonin supplements may help boost cardiovascular health, manage fibromyalgia, lower the risk of gallstones and decrease the symptoms of tinnitus

Sleeping is an essential human function, and at the heart of it is your circadian rhythm, also known as your body clock. It’s a natural, biological timer that helps your body recognize sleepiness and wakefulness over a period of 24 hours.

By sticking to a regular bedtime schedule, such as sleeping and waking up at the same time each day, you can maintain a steady circadian rhythm that will allow you to maximize your productivity while you’re awake, and get the right amount of sleep when nighttime arrives.1

Your circadian rhythm is largely dictated by your pineal gland. This gland is located near the center of your brain, with a shape that looks similar to a pine cone, hence the name. It’s estimated to be one-third of an inch long, and is made up of unique pineal cells and neuroglial cells that help support the gland.

Despite its small size, it plays a crucial role in your health because it produces a single hormone called melatonin, which is vital for controlling your body clock and, ultimately, your sleeping patterns.2

What Is Melatonin?

Melatonin, or N-acetyl-5-methoxytryptamine, is a hormone produced by the pineal gland.3 Your brain usually starts secreting melatonin around 9 p.m., which is the time most people go to bed. By increasing the amount, your body begins to recognize that bedtime is fast approaching, allowing you to sleep at an ideal time.4

To do this properly, you need to be aware of your exposure to light throughout the day and especially at night, because melatonin production depends on how much light your body absorbs.

If you stay awake past dark, light emitted by electrical devices hampers your body’s ability to produce melatonin. Ideally, you want to stop using gadgets an hour before sleeping to help increase melatonin production and maintain a steady circadian rhythm. Nightshift workers usually have it worse and constantly suffer from disrupted body clocks, because of their poor melatonin production.

3 Main Uses of Melatonin in Your Body

What is the role of melatonin anyway? Based on published research, it has been discovered to perform three main functions:

Controls your circadian rhythm — Melatonin works as a sleeping aid by normalizing your circadian rhythm by convincing your body to prepare itself for bedtime.5 It’s a hormone that only “signals” your body to prepare for sleep, not one that actually makes you fall asleep.

Functions as an antioxidant — Recent studies have found that melatonin not only affects your body clock, but also functions as an antioxidant that can help support your health. Specifically, it may help different aspects of your brain, cardiovascular and gastrointestinal health.6 It may even lower your risk of cancer, in some cases.7

Boosts your immune system — Melatonin may benefit your immune system in various ways. In one study, researchers suggest that melatonin may help improve the treatment of bacterial diseases such as tuberculosis.8 In another study, melatonin has been suggested as a potential tool against inflammation, autoimmune diseases and Type 1 diabetes.9

6 Ways to Optimize Your Melatonin Levels Naturally to Improve Sleep Quality

According to the Centers for Disease Control and Prevention (CDC), an estimated 50 to 70 million Americans are suffering from a sleeping or wakefulness disorder.10 As a result, many of them turn to various remedies, such as behavioral and environmental changes, to get a good night’s rest.11

One of the first things you can do is to make sure that your body is producing enough melatonin. Optimizing your melatonin levels naturally is important because it helps keep your body functioning normally without relying on outside factors. So, instead of immediately relying on melatonin supplementation, here are a few lifestyle changes I suggest you try first to boost your melatonin production:

Avoid using electronic devices an hour before sleeping — Gadgets such as cellphones, TVs and computers emit blue light, and exposure to it tricks your body into thinking it’s still daytime. By avoiding gadgets an hour before bed, your body can produce the melatonin needed to help you sleep at your intended time.

Make sure to get regular sunlight exposure — Getting regular sun exposure in the morning or at noontime helps your body reduce its melatonin production, so that when nighttime arrives, your pineal gland produces the correct amount to induce sleepiness.

Try to sleep in complete darkness — If possible, try to remove immediate light sources from your room to help improve your sleep quality. The slightest exposure to light can interfere with your body’s melatonin production and keep you up later than you need. Keep gadgets 3 feet away from your bed or use blackout window shades.

Remove sources of electromagnetic fields (EMFs) in your bedroom — EMFs emitted by certain devices such as Internet routers can disrupt your pineal gland’s melatonin production. Ideally, you should turn off your wireless router, as well as other wireless devices connected to the Internet before sleeping.

If you need a nightlight, use a low-wattage yellow, orange or red bulb — Low-wattage bulbs with a yellow, orange or red color do not interfere with melatonin production the same way that white and blue bulbs do.

Wear blue light-blocking glasses — This special device can help keep your eyes from absorbing blue light that can affect your melatonin levels. It can be a useful tool to have around the house, especially if you’re constantly surrounded by gadgets and artificial light sources.

In addition, the following foods are known to contain small amounts of melatonin. Making them a part of your regular diet while practicing the aforementioned sleeping tips may help improve sleep quality:12

  • Grass fed meat (lamb, beef and pork)
  • Wild-caught salmon
  • Pasture-raised chicken and eggs
  • Raw, grass fed milk
  • Pineapple
  • Banana
  • Apple
  • Pomegranate
  • Mulberry
  • Tart cherries
  • Grapes
  • Onion
  • Garlic
  • Cauliflower
  • Turnip
  • Cucumber
  • Carrot
  • Radish
  • Beetroot
  • Tomatoes
  • Seeds (Flax, sunflower, fennel, mustard, alfalfa, celery and fenugreek)
  • Nuts (pistachio, almonds and walnuts)

If you’ve already tried everything, including incorporating melatonin foods in your diet, and you’re still having difficulty getting quality sleep, you may consider taking a melatonin supplement. In 2016 alone, 3.1 million adults in the United States turned to melatonin supplementation to help them sleep peacefully.13

Studies Regarding the Use of Melatonin Supplements

Since the discovery of melatonin, various studies have been conducted to discover how using it as a supplement can benefit your health. According to the Journal of Pineal Research, the melatonin secreted by your pineal gland enters every cell in your body and can even cross morphophysiologic barriers.

As a result, not only may it help you improve sleep quality,14 it also has certain anti-inflammatory compounds that may help reduce your risk of cardiovascular diseases, such as atherosclerosis and hypertension.15

In addition, a study published in Endocrine Journal reports that increasing melatonin intake may help improve your overall health, as this hormone can be an effective antioxidant that can help fight free radicals in your body.16

Another study suggests that melatonin may help obese people manage their weight. The researchers indicate that certain lifestyle factors suppress melatonin production, which results in sleep disruption that can lead to weight gain. By increasing melatonin production, adequate sleep can be reintroduced as part of a healthy lifestyle, along with other positive lifestyle changes, to help curb obesity.17

8 Potential Benefits of Melatonin Supplement

Melatonin may help boost your health in various situations, as shown in the table below. While each benefit is backed up with scientific research, always consult with a doctor before giving melatonin supplements a try:

Insomnia — Melatonin is primarily used to help treat people who have sleeping disorders by inducing sleepiness quicker.18

Jet lag — Melatonin may be used to help treat jet lag by adjusting your body to a new time zone. However, it’s generally recommended only for travelers who cross four to five time zones.19

Heart disease — People who are struggling with heart disease may benefit from melatonin. A study has found that it may help lower your bad cholesterol levels by as much as 38 percent.20

Menopause — Increasing melatonin consumption in menopausal women 42 to 62 years old may help improve mood and stave off depression.21

Autism — Children diagnosed with autism who are also plagued with sleeping problems may benefit from melatonin supplementation. Research indicates that taking the hormone can lead to deeper sleep and better daytime behavior.22 However, I advise consulting your health care provider before giving any melatonin supplement to children.

Fibromyalgia People affected with fibromyalgia are believed to have lower levels of melatonin. A group of researchers found that increasing the melatonin levels of fibromyalgia sufferers through supplementation helped alleviate their symptoms and improved sleep quality.23

Gallstones Melatonin can help lower your risk of gallstones by inhibiting cholesterol absorption across the intestinal epithelium, as well as increasing the conversion of cholesterol into bile.24

Tinnitus — If you have tinnitus, slightly increasing your melatonin may help improve your symptoms. In one study, participants who took 3 milligrams of melatonin supplements every night experienced a decrease in tinnitus intensity after the testing duration.25

Do Not Take Melatonin if You Have These Conditions

Here’s a crucial question you should ask yourself: Are you fit to take melatonin? While there are valid reasons for taking this supplement, remember that it can exacerbate certain health conditions as well. If you’re taking any of the following medications, you should not take melatonin as the mixture can have adverse effects to your health:26

Anticoagulants and anti-platelet drugs


Contraceptive drugs

Diabetes medications


Taking melatonin while pregnant should be avoided as well, since there’s little knowledge in this field.27 If you’ve recently developed pregnancy-related sleeping problems, I advise you to consider behavioral and dietary changes before considering melatonin or other similar types of supplement.

Refrain from giving melatonin to children, including babies and toddlers, unless approved by your physician. While a 2016 study found that children with sleep difficulties who took melatonin did not develop any concerns or adverse side effects,28 it’s better to be safe.

10 Side Effects of Melatonin You Should Know About

Some of melatonin’s potential side effects include:29,30

  • Daytime sleepiness
  • Short-term depression
  • Irritability
  • Vivid dreams, or possibly nightmares
  • Mild anxiety
  • Headaches
  • Abdominal discomfort
  • Confusion
  • Body clock disruption
  • Dizziness

If you are already taking a melatonin supplement and begin to experience any of the mentioned side effects, stop taking it immediately and consult with a doctor for safer alternatives. In addition, melatonin and alcohol should not be taken together, as it can increase your chances of accidents because the sedative effects are amplified.31

Remember: Consider Optimizing Your Melatonin Levels Naturally Before Taking a Supplement

Melatonin is a crucial hormone that performs few but important functions. Low levels of it can lead to sleep disruption, increase your risk of certain diseases and lower your antioxidant capabilities. However, remember to always try and improve your sleeping habits and environment before attempting melatonin supplementation.

While there’s an abundance of scientific evidence that suggest melatonin supplementation can be beneficial to your health, too much of it can actually make you more wakeful. By primarily focusing on natural strategies, you forego this risk, as well as the chances of developing unpleasant side effects that can further disrupt your quality of sleep. If you do decide to take a melatonin supplement, seek guidance from a doctor first.

Frequently Asked Questions About Melatonin

Q: Is melatonin addictive?

A: Currently, there’s very little information regarding melatonin supplement addiction. However, beware that it can still be abused, although the chances of becoming dependent are lower compared to other types of medications or supplements.32


Q: How long does it take for melatonin to work?

A: The average time for melatonin supplements to work is generally 20 minutes. If you’re about to take melatonin for the first time, it’s recommended that you take it one to two hours before your bedtime.33


Q: Can you take melatonin supplements while pregnant?

A: As of the moment, there is a lack of scientific evidence regarding the use of melatonin supplements on pregnant women, but it’s theorized that it may hamper sex drive, reduce ovarian function and increase the risk of developmental disorders. If you’re pregnant, it is best that you avoid using this supplement and resort to natural remedies to correct sleeping problems.34


Q: Is melatonin safe to use for kids?

A: Melatonin supplements are generally safe for children. According to a study published in Canadian Family Physician, children with sleep difficulties who took melatonin had no concerns or adverse side effects, according to their parents.35 However, consult with your child’s pediatrician before giving them any type of melatonin supplement.


Q: When is the ideal time to take melatonin?

A: Taking a melatonin supplement two hours before bedtime can help you maximize its effectiveness.36


Q: How long does the effects of melatonin last?

A: The half-life of melatonin is very short, around 59 to 65 minutes only.37


Q: Can you overdose on melatonin?

A: Yes. While there are no reported deaths related to overdosing from melatonin, consuming more than the recommended amount can cause side effects, such as autoimmune hepatitis, a psychotic episode, seizures, headaches or skin eruption.38



Besides helping sleep, melatonin is known for protecting the brain. Research has shown starting to supplement in middle age protects against Alzheimer’s, reduces the risk of Parkinson’s, shrinks the size of the infarct area in a stroke, minimizes brain swelling & dysfunction after head injury, and increases the “longevity protein” SIRT1.

  • Melatonin has been proposed as a treatment for numerous brain and neurological diseases as it helps reduce oxidative stress and inflammation inside the brain and strengthens the blood-brain barrier.  A leaky blood-brain barrier can contribute to issues like brain fog, anxiety, depression, and even Alzheimer’s.
  • It also increases brain-derived neurotrophic factor (BDNF) – which is a protein that promotes survival of nerve cells & helps regular synaptic plasticity.  Mouse studies have shown melatonin relieves symptoms of ALS by preventing cell death and slowing disease progression.  
  • Melatonin is needed for normal eye development, decreases pressure in the eye and lack of it may be a cause of glaucoma.
  • A rat study showed melatonin prevents against cell death in optic neuritis, a manifestation of MS, Lyme, and Bartonella.
  • Regarding tinnitus, (noise in the ears), melatonin was 150 times more effective than other tinnitus drugs in reducing symptoms.
  • Melatonin may help prevent and treat cancer by improving immune function, increasing tumor suppressor proteins, acting against cancer stem cells, and by suppressing cells that block the activity of immune cells. Supplementation also reduced incidence and size of breast cancer tumors.
  • Melatonin concentration is 400 times higher in the gut than the brain and controls behavior of gut bacteria.  It’s been shown to be protective against lesions caused by H.pylori infection and speeds ulcer healing.  It protects and strengthens the intestinal barrier and can help prohibit inflammation in the stomach which can in turn protect against colitis, irritable bowel, and various cancers.














Small Fiber Neuropathy & PTLDS

Association of small fiber neuropathy and post treatment Lyme disease syndrome

Peter Novak , Donna Felsenstein, Charlotte Mao, Nadlyne R. Octavien, Nevena Zubcevik

Published: February 12, 2019



To examine whether post-treatment Lyme disease syndrome (PTLDS) defined by fatigue, cognitive complaints and widespread pain following the treatment of Lyme disease is associated with small fiber neuropathy (SFN) manifesting as autonomic and sensory dysfunction.


This single center, retrospective study evaluated subjects with PTLDS. Skin biopsies for assessment of epidermal nerve fiber density (ENFD), sweat gland nerve fiber density (SGNFD) and functional autonomic testing (deep breathing, Valsalva maneuver and tilt test) were performed to assess SFN, severity of dysautonomia and cerebral blood flow abnormalities. Heart rate, end tidal CO2, blood pressure, and cerebral blood flow velocity (CBFv) from middle cerebral artery using transcranial Doppler were monitored.


10 participants, 5/5 women/men, age 51.3 ± 14.7 years, BMI 27.6 ± 7.3 were analyzed. All participants were positive for Lyme infection by CDC criteria. At least one skin biopsy was abnormal in all ten participants. Abnormal ENFD was found in 9 participants, abnormal SGNFD in 5 participants, and both abnormal ENFD and SGNFD were detected in 4 participants. Parasympathetic failure was found in 7 participants and mild or moderate sympathetic adrenergic failure in all participants. Abnormal total CBFv score was found in all ten participants. Low orthostatic CBFv was found in 7 participants, three additional participants had abnormally reduced supine CBFv.


SFN appears to be associated with PTLDS and may be responsible for certain sensory symptoms. In addition, dysautonomia related to SFN and abnormal CBFv also seem to be linked to PTLDS. Reduced orthostatic CBFv can be associated with cerebral hypoperfusion and may lead to cognitive dysfunction. Autonomic failure detected in PTLDS is mild to moderate. SFN evaluation may be useful in PTLDS.



Keep in mind, researchers by nature have to obtain as close to ground zero as possible.  In this case they chose to use the unscientific and abysmal CDC 2-tiered blood serology which research has shown misses over half of all cases.  It was also never intended for diagnosis but for surveillance purposes only.  Lyme should be a clinical diagnosis.  We desperately need a better form of accurate testing for this very reason.  Nearly ALL research is based upon 2-tiered serology which leaves out a huge subset of patients.  

Some of the sickest people NEVER test positive using CDC criteria.

Also, please note:  

All patients had received a course of antibiotics for Lyme disease including 3 weeks of oral doxycycline as recommended by Infectious Diseases Society of America (IDSA) guidelines [13,30]. Because of symptoms persistence, all participants were treated with additional antibiotics (data in S1 Table). The list may not be accurate and may underestimate the antibiotic therapy as many participants were treated in multiple institutions and as such medical records may be incomplete.

Many would argue that the entire premise of this research article is flawed in that the CDC moniker of PTLDS is not taking into account persistent/chronic infection.  For a fantastic read on that:

Until this issue is resolved, people will be put into two camps based on a false premise, 1) Acute cases 2) PTLDS.  There are numerous subsets of people.  See link above.

Parasympathetic failure & low orthostatic CBFv  was noted in 7 out of 10 patients and abnormal total CBFv score was found in all 10!
All of you out there suffering with dry eye & mouth, inability to digest food, and having colitis type symptoms (either diarrhea or constipation – usually alternating) this study reveals why.
Lyme loves the spine!  

By OpenStax College – Anatomy & Physiology, Connexions Web site., Jun 19, 2013., CC BY 3.0,

You can visualize where on the spine the various organs receive information from.  Notice all the things connected to the cranial nerves at the top.  Please know Bartonella and other coinfections can affect these areas as well.  Dr. Ericson’s found Bart all over the place:  Take a gander at her slides where she’s found Bart in collagen, where a PIC line was removed, skin biopsies (including the brain), cartilage, and blood cells.

Lastly, besides the spinal involvement, notice ALL of the patients had an abnormal Total CBFv score.  This is cerebral blood flow velocity from the middle cerebral artery.  Not enough blood flow = not enough oxygen, which is required for normal functioning.  It alone can account for brain fog and fatigue.  Too much blood flow = swelling and inflammation which can cause severe pain and even lead to Chiari:  In one week I met 3 Lyme patients with a Chiari diagnosis.  I had an MRI to rule it out myself.

One drug that was most effective for me for this issue was Minocycline: