Summary: The NLPR3 inflammasome and the inflammatory response it triggers play a critical role in the emergence of tau pathology.Source: DZNE
Inflammation drives the progression of neurodegenerative brain diseases and plays a major role in the accumulation of tau proteins within neurons. An international research team led by the German Center for Neurodegenerative Diseases (DZNE) and the University of Bonn comes to this conclusion in the journal Nature. The findings are based on the analyses of human brain tissue and further lab studies. In the particular case of Alzheimer’s the results reveal a hitherto unknown connection between Amyloid Beta and tau pathology. Furthermore, the results indicate that inflammatory processes represent a potential target for future therapies.
Tau proteins usually stabilize a neuron’s skeleton. However, in Alzheimer’s disease, frontotemporal dementia (FTD), and other “tauopathies” these proteins are chemically altered, they detach from the cytoskeleton and stick together. As a consequence, the cell’s mechanical stability is compromised to such an extent that it dies off. In essence, “tau pathology” gives neurons the deathblow. The current study led by Prof. Michael Heneka, director of the Department of Neurodegenerative Diseases and Gerontopsychiatry at the University of Bonn and a senior researcher at the DZNE, provides new insights into why tau proteins are transformed. As it turns out, inflammatory processes triggered by the brain’s immune system are a driving force.
A Molecular Switch
A particular protein complex, the “NLRP3 inflammasome”, plays a central role for these processes, the researchers report in Nature. Heneka and colleagues already studied this macromolecule, which is located inside the brain’s immune cells, in previous studies. It is a molecular switch that can trigger the release of inflammatory substances. For the current study, the researchers examined tissue samples from the brains of deceased FTD patients, cultured brain cells, and mice that exhibited hallmarks of Alzheimer’s and FTD.
“Our results indicate that the inflammasome and the inflammatory reactions it triggers, play an important role in the emergence of tau pathology”, Heneka said. In particular, the researchers discovered that the inflammasome influences enzymes that induce a “hyperphosphorylation” of tau proteins. This chemical change ultimately causes them to separate from the scaffold of neurons and clump together. “It appears that inflammatory processes mediated by the inflammasome are of central importance for most, if not all, neurodegenerative diseases with tau pathology.”
A Link between Amyloid Beta and Tau
This especially applies to Alzheimer’s disease. Here another molecule comes into play: “amyloid beta” (Amyloid Beta). In Alzheimer’s, this protein also accumulates in the brain. In contrast to tau proteins, this does not happen within the neurons but between them. In addition, deposition of Amyloid Beta starts in early phases of the disease, while aggregation of tau proteins occurs later.
In previous studies, Heneka and colleagues were able to show that the inflammasome can promote the aggregation of Amyloid Beta. Here is where the connection to the recent findings comes in. “Our results support the amyloid cascade hypothesis for the development of Alzheimer’s. According to this hypothesis, deposits of Amyloid Beta ultimately lead to the development of tau pathology and thus to cell death,” said Heneka. “Our current study shows that the inflammasome is the decisive and hitherto missing link in this chain of events, because it bridges the development from Amyloid Beta pathology to tau pathology. It passes the baton, so to speak.” Thus, deposits of Amyloid Beta activate the inflammasome. As a result, formation of further deposits of Amyloid Beta is promoted. On the other hand, chemical changes occur to the tau proteins resulting into their aggregation.
A Possible Starting Point for Therapies
“Inflammatory processes promote the development of Amyloid Beta pathology, and as we have now been able to show, of tau pathology as well. Thus, the inflammasome plays a key role in Alzheimer’s and other brain diseases,” said Heneka, who is involved in the Bonn-based “ImmunoSensation” cluster of excellence and who also teaches at the University of Massachusetts Medical School. With these findings, the neuroscientist sees opportunities for new treatment methods. “The idea of influencing tau pathology is obvious. Future drugs could tackle exactly this aspect by modulating the immune response. With the development of tau pathology, mental abilities decline more and more. Therefore, if tau pathology could be contained, this would be an important step towards a better therapy.”
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Source: DZNE Media Contacts:
Marcus Neitzert – DZNE Image Source:
The image is in the public domain.
NLRP3 inflammasome activation drives tau pathology
Alzheimer’s disease is characterized by the accumulation of amyloid-beta in plaques, aggregation of hyperphosphorylated tau in neurofibrillary tangles and neuroinflammation, together resulting in neurodegeneration and cognitive decline1. The NLRP3 inflammasome assembles inside of microglia on activation, leading to increased cleavage and activity of caspase-1 and downstream interleukin-1β release2. Although the NLRP3 inflammasome has been shown to be essential for the development and progression of amyloid-beta pathology in mice3, the precise effect on tau pathology remains unknown. Here we show that loss of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation by regulating tau kinases and phosphatases. Tau activated the NLRP3 inflammasome and intracerebral injection of fibrillar amyloid-beta-containing brain homogenates induced tau pathology in an NLRP3-dependent manner. These data identify an important role of microglia and NLRP3 inflammasome activation in the pathogenesis of tauopathies and support the amyloid-cascade hypothesis in Alzheimer’s disease, demonstrating that neurofibrillary tangles develop downstream of amyloid-beta-induced microglial activation.
HOW MANY LYME DISEASE PATIENTS DON’T MEET STRICT DIAGNOSTIC CRITERIA?
In a recent article published in Open Forum Infectious Disease, Kobayashi and colleagues suggest that Lyme disease is often mistakenly diagnosed as causing various illnesses, which has led to the unnecessary use of antibiotics. The authors conducted a retrospective study of patients with possible Lyme disease, who were referred to an infectious disease clinic in Maryland between 2000 and 2013. ¹
Kobayashi and colleagues concluded that nearly 3 out of 4 patients referred to the clinic did not have Lyme disease. They did not interview the referring doctor at Johns Hopkins University School of Medicine. Instead, they conducted a chart review.
However, to be included in the study, patients had to meet the Infectious Diseases Society of America’s (IDSA) guidelines or the Centers for Disease Control and Prevention’s (CDC) clinical and serological criteria.
The authors found that out of 1,261 patients, all but one were symptomatic when they presented to the clinic, with a median duration of complaints of 558 days, ranging from 1 day to 51 years.
“The 5 most commonly identified symptoms were arthralgia (71.3%), fatigue/malaise (66.8%), headache (42.1%), myalgia (40.8%), and sleep disturbance (34.3%),” writes Kobayashi.
Only a few patients had abnormal physical findings.
“The 5 most common abnormal physical findings were rash other than erythema migrans (6.6%), joint swelling (5.9%), tender points (3%), objective sensory abnormality (2.1%), and motor weakness (1.5%),” the authors explain.
The researchers did not report a number of clinical presentations that can occur in Lyme disease, including:
It may be that many physicians do not recognize or document these types of manifestations, given that the authors didn’t mention any of these presentations.
Approximately 1 in 10 patients had a history of co-infections.
“Although 139 (11%) co-infections were diagnosed before evaluation at the infectious diseases clinic, none of these infections were confirmed or treated based upon the evaluations performed in this study,” writes Kobayashi.
“Of these 139 putative co-infections, 61 (44%) were said to be caused by Babesia microti or B. duncani, 40 (29%) by Epstein-Barr virus, 30 (22%) by Bartonella, 11 (8%) by Ehrlichia spp., and 32 (23%) were attributed to other infectious agents,” writes Kobayashi.
Takaaki Kobayashi, Yvonne Higgins, Roger Samuels, Aurasch Moaven, Abanti Sanyal, Gayane Yenokyan, Paul M Lantos, Michael T Melia, Paul G Auwaerter, Misdiagnosis of Lyme Disease With Unnecessary Antimicrobial Treatment Characterizes Patients Referred to an Academic Infectious Diseases Clinic, Open Forum Infectious Diseases, Volume 6, Issue 7, July 2019.
Logigian EL, Kaplan RF, Steere AC. Chronic neurologic manifestations of Lyme disease. N Engl J Med. 1990;323(21):1438-1444.
Fallon BA, Nields JA. Lyme disease: a neuropsychiatric illness. Am J Psychiatry. 1994;151(11):1571-1583.
Sigra S, Hesselmark E, Bejerot S. Treatment of PANDAS and PANS: a systematic review. Neurosci Biobehav Rev. 2018;86:51-65.
Muehlenbachs A, Bollweg BC, Schulz TJ, et al. Cardiac Tropism of Borrelia burgdorferi: An Autopsy Study of Sudden Cardiac Death Associated with Lyme Carditis. Am J Pathol. 2016.
Kanjwal K, Karabin B, Kanjwal Y, Grubb BP. Postural orthostatic tachycardia syndrome following Lyme disease. Cardiology journal. 2011;18(1):63-66.
Krupp LB, Hyman LG, Grimson R, et al. Study and treatment of post Lyme disease (STOP-LD): a randomized double masked clinical trial. Neurology. 2003;60(12):1923-1930.
Simons LE. Fear of pain in children and adolescents with neuropathic pain and complex regional pain syndrome. Pain. 2016;157 Suppl 1:S90-97.
Klempner MS, Hu LT, Evans J, et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. N Engl J Med. 2001;345(2):85-92.
Krause PJ, Telford SR, 3rd, Spielman A, et al. Concurrent Lyme disease and babesiosis. Evidence for increased severity and duration of illness. Jama. 1996;275(21):1657-1660.
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**Comment**
This article brings up very important points – many patients do not meet the stringent CDC diagnostic criteria to even be accepted into research studies much less be diagnosed with Lyme/MSIDS. For 40 years we’ve had blood serology that misses half of all cases as well as the fact many patients do not present with the “classic” EM rash but either have no rash at all or a rash that presents differently. https://madisonarealymesupportgroup.com/2019/02/22/why-mainstream-lyme-msids-research-remains-in-the-dark-ages/
You’d have to be blind to not see how patients are immediately set up for failure.
While they continue to shout about unnecessary antibiotics, most patients are denied care. Trust me when I say we all have much better things to do besides taking expensive, painful treatment!
Until the CDC/IDSA/NIH admit that they only have a very partial picture of how Lyme/MSIDS presents patients are doomed to the same suffering they’ve been suffering for over 40 years.
It is important as one of the nation’s leaders in chronic Lyme disease complex, and after nearly two decades of helping patients, to point out how the CDC has missed the mark entirely with their current study and publication on prolonged treatment for Lyme disease. Unfortunately this information is quite literally too little and too late. Too little, because it is old information and too late, because it offers nothing new to help the many patients that have been suffering. On its face, this small study is designed to discourage physicians from helping their patients.
Recently, Centers for Disease Control and Prevention (CDC) released statements regarding the treatment of chronic Lyme disease based on a few published studies on a small number of patients and conducted a case study that ultimately provided no new information not already known by most Lyme literate physicians. In the statement, the CDC states that antibiotics were shown not to provide long-term benefits for chronic Lyme patients and rather gave rise to other complications such as CDIF infections.
The CDC inferred, based on these outcomes, that doctors should not treat these patients but rather refer them to other specialists. Referring to the same old rheumatology, psychiatry, pain management, and neurology treatments that never eliminate the root cause which is the infections.
This lack of proper treatments ultimately leaves the patients in a life-time of suffering and in a condition that only worsens over time. That is exactly the opposite direction to health and healing that our team is dedicated to achieving with our patients. But the devil is in the details, and to the untrained physicians and patients, the CDC statements sound reasonable and conclusive. However, IV antibiotics were never effective for numerous reasons as we mentioned in our peer-reviewed published article from 2014 in the Open Journal of Medical Microbiology Chronic Lyme Disease: Persistent Clinical Symptoms Related to Immune Evasion, Antibiotic Resistance and Various Defense Mechanisms of Borrelia burgdorferi.
It is something we hear daily from our new patients when they first walk in, the antibiotics they had taken in the past only provided temporary relief. Therefore, the important question and case study work should help answer why the IV antibiotics alone do not work. This is a topic in which we have done a great amount of medical work and have been speaking and teaching about for years. In fact, we wrote about this: Top 7 Overlooked Factors for Treating Lyme Disease.
We will discuss in this article why personalized integrative medicine and a detailed diagnosis and treatment plans make all difference for chronic Lyme disease patients. As clinicians working in the field, we believe the CDC chose this study with a pre-established belief in the results but this mindset is only a distraction to real advancements that are being made in treating this disease. Let’s take a look at the facts.
Chronic Lyme disease Complex, Not Just Chronic Lyme
Patients with chronic Lyme never have just the one infection, they have multiple infections that have gone untested and untreated for extended periods of time. Antibiotics are not even effective for many of these infections, such as with viral, fungal, and parasitic infections.
When chronic Lyme disease is mentioned, most often they are actually referring to chronic Lyme disease complex which involves the spirochete which causes Lyme, Borrelia burgdorferi, and also associated co-infections, which enter the body with Borrelia in the initial tick bite: Babesia, Ehrlichia, Bartonella, Rocky Mountain Spotted Fever etc. Chronic Lyme disease complex can also include secondary infections which occur as a result of a compromised immune state. This is important to keep in mind because antibiotics do not work against viral infections and similarly, fungal infections require antifungal medication and so on. The secondary and co-infections must be identified in order for treatment to be effective. This is the number one reason why antibiotics alone cannot be used to treat these patients.
It is important to understand that Borrelia has a number of mechanisms both for evading and distracting the immune system and that Borrelia is capable of burrowing and spreading throughout most of the body’s tissues, including the blood-brain barrier. Antibiotics cannot easily pass the blood-brain barrier which allows borrelia and others infections like babesia to attack the brain and central nervous system unimpeded. Borrelia implants itself in tissues and within individual cells to avoid being consumed and lysed by the immune system. The microbe is also adept at countering the adaptive immune system through constant variation in its surface proteins, or antigens, a feat enabled by its complex single chromosome and its circular DNA plasmids. Usually, by the time the body can create antibodies to target Borrelia, its surface has already changed so much that the new antibodies are no longer effective. In serum, Borrelia has the ability to inactivate C3, a protein marker which would normally trigger the immune response for free floating microbes. When Borrelia does find a place to settle down and multiply, the microbe secretes a protein mesh called biofilm which shields it and its progeny from direct exposure to many antibiotics and other compounds that might otherwise harm the infection. Our team has published on this subject extensively and we have assembled a great deal of information on the biology and survival mechanisms used by Borrelia in our published study Borrelia burgdorferi: Cell Biology and Clinical Manifestations in Latent Chronic Lyme.
While the spirochete Borrelia is responsible for causing primary Lyme disease, it is usually not the only factor to consider when approaching treatment for chronic Lyme disease, or more commonly, Lyme disease complex. When a tick bites, various bacteria and parasites enter the wound besides just Borrelia. These simultaneous infections are called co-infections and can include Babesia, HHV-6, Epstein-Barr, and Rocky Mountain Spotted Fever, just to name a few. These co-infections are able to gain a firmer foothold in the body and potentially become chronic since Borrelia excels at distracting and depressing the host immune system. Secondary infections can also be picked up after the initial bite due to a depressed immune response from the infected person. The result is a condition that is chronic and can linger for months or even years, typically worsening over time without proper treatment.
In our published study, Chronic Lyme Disease Complex and Its Commonly Undiagnosed Primary and Secondary Co-Infections, we discuss the various co-infections which can coincide with Lyme to form Lyme disease complex. The presence of multiple different infections in the body simultaneously seriously complicates any potential treatment as is discussed below. Many of these other infections complicate treatment and increase the risk for auto-immune diseases depending on the patient’s genetic background and can also be a precursor to various cancers. Treating these infections in their totality is essential to full recovery and for the patient to achieve health which is why often antibiotics alone don’t work clinically.
Single Antibiotic Treatments Inevitably Fail against Lyme Complex
The organism Borrelia has multiple strategies for evading, inactivating, and depressing the immune response including the ability to insulate itself inside tissues and biofilm to avoid contact with substances which might kill it, like antibiotics. A critical flaw with the four randomized trials funded by the CDC to study chronic Lyme disease is that they all used a single antibiotic regimen (ceftriaxone) compared against placebo. As well, this is not typically the antibiotic of choice with a resistant chronic Lyme. Patients’ co-infections also need to be identified in a case of chronic Lyme disease complex. Each patient should receive a personalized regimen based on their infection profile, neurological involvement, immune state and genomics. Also, their ability to eliminate toxins from the body should be evaluated.
With the advent of multi-drug resistant (MDR) strains of bacteria, we have found in our clinical experience that chronic Lyme disease will not respond effectively to antibiotic regimens without the addition of MDR blockers. In chronic patients, these infections have often become “super bugs” and blocking MDR is essential. Also, multiple organisms can survive and propagate within biofilm communities formed by the Borrelia bacteria. This enables Lyme disease to essentially shield other infections from treatment. Adding compounds which are designed specifically to break up biofilm is part of the treatment often needed to help chronic Lyme disease complex. The signs and symptoms of chronic Lyme and the ways in which it evades treatment by antibiotics is outlined in our published paper Chronic Lyme Disease: Persistent Clinical Symptoms Related to Immune Evasion, Antibiotic Resistance and Various Defense Mechanisms of Borrelia burgdorferi.
Another factor which is not considered in any of the published studies listed by the CDC is the genetic variation in the patients. Each person responds to medication in a slightly different way. A lot of this variation is due to Single Nucleotide Polymorphisms (SNP’s) which also make up a large portion of physical differences between humans. SNP’s will cause each patient to metabolize drugs at a greater or lesser rate than the “average person” which is an amalgamate based off of data from thousands of studies rather than a patient’s own particular medical history. Treating patients based off national averages is always risky, which is why people continue to have adverse reactions to medications prescribed by doctors. This personalized testing is essential for several reasons. Finding blocked genes and variations in HLA-DR are highly common in chronic Lyme disease patients, which is why this disease is often linked to autoimmune diseases. Knowing how to access a genetic profile in the Lyme patient is essential to better tailor the therapy and support pathways of elimination as dealing with biotoxins and neurotoxins is a complex problem.
Other than the terribly flawed placebo-driven studies released, the CDC would have you believe that treatments for chronic Lyme disease complex are risky and potentially life threatening. Below, we point out that…
Treatments for Chronic Lyme Are Not Any More Dangerous than Other IV Therapies
The CDC listed five cases of patients who sought treatment for chronic Lyme disease and experienced adverse events due to intravenous therapy. While the article seems to imply that the resulting infections were due to the treatment for chronic Lyme disease, an impartial reader will notice that each of these adverse events occurred after the installation of a permanent port, in particular PICC’s or Peripherally Inserted Central Catheter. The PICC is essentially an open line directly into a central artery near the heart and thus is extremely prone to infection when proper care is not adhered to. That is why at Envita, our physicians and specialized nursing staff do not prefer to use PICC’s with our patients. Instead, if the patient is to undergo extended intravenous therapy for their condition, an implanted subcutaneous port is recommended and we work with the best interventional radiologist to ensure safety. The implanted port is a soft silicone tube inserted below the skin into which a small needle can be used to deliver drugs in a similar way to a PICC. However, a subcutaneous port is covered by skin which makes it lower maintenance for the patient and reduces the risk of infection drastically. Our nursing staff works in this environment daily and excel at making sure patients ports are properly accessed and maintained.
Whenever the skin is broken for any reason, however, there is always a risk for infection, even in a hospital with trained staff; and nowadays, you may be at greater risk of a MDR infection while in a hospital than not. This risk is reduced when doctors and staff follow rigid sterilization protocols while adverse events tend to occur when discipline relaxes. While the risk continues over a greater length of time in treating a chronic ailment like Lyme, the risk does not inherently grow as a result of the duration and just like at any medical facility, the risks are managed with careful attention to detail and patient compliance. As a facility with many years of helping patients we rarely see any infections because our team is very good at what they do and our facility is clean.
There is nothing inherent about therapy for Lyme that places patients at greater risk than other kinds of treatment. The antibiotics and nutritional IV, immune modulators, phytotheraptics and other medications that are prescribed are commonly used as required. At Envita, we prioritize attention to detail and patient safety, that’s why we personalize our treatments to each individual patient and are confident in our work and outcomes.
The articles released from the CDC seem to imply also that chronic Lyme disease is not even a real phenomenon at all and insist that other factors must be the cause for the patients’ symptoms. However the CDC is sadly mistaken. In our many years of work with these infections, we know that they are the cause of many auto-immune diseases and neurological problems. The message the CDC wants everyone to take home is to get “real” medical care for your problem, to keep using pain medications, neurological drugs, steroids, and deal with being bed ridden while suffering and letting your health decline because the conventional approach is best. The fact is these infections are real and patients can improve. Real hope exists when you treat the cause of your disease and not just the symptoms.
Yet curiously, the CDC does not deny that these symptoms do exist and cause detrimental harm to people’s lives, up to and including hospitalization for pain, fatigue, and neurological problems. The CDC does not discuss why, if Lyme disease is not a contributing factor to these symptoms, the patients do not recover after traditional therapy and why these cases continue to appear in areas prone to tick infestations. To dismiss out of hand a potential explanation with inadequate evidence is unusually irresponsible of this institution responsible for guarding the public against infectious agents. Therefore, in our professional opinion, it’s too little (not enough helpful detailed information), too late (leaving patients to suffer and still question the cause of their illness). Maybe the CDC should read our published studies and look at our materials to help them better design studies for the future instead conducting studies of which they already know the outcomes only to mislead and misdirect the public. We make this statement as the CDC has had a very untrusting relationship with chronic Lyme disease issue in this country.
However, at Envita, we have taken the time to specialize and gather all available information about Lyme disease and its impact on the body. We are proud and blessed to see our patients return to health and we let our success stories speak for themselves. If you are interested in learning more about the risks of Lyme disease, feel free to give us a call at 1-866-457-9956 and one of our trained patient care coordinators will be more than happy to answer your questions. You can also learn more about Lyme disease at our webpage here.
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**Comment**
Envita puts out great materials and we are the better for them. I just love how this article essentially states that the CDC is full of crap – something we all know but it’s nice to hear it from professionals treating this complex disease(s).
This short 7 min. video from Envita explains:The helper T-cells come along and pick up the processed antigen off the dendritic cell and then passes it along to the killer T cells. The Killer T cells follow the spirochete throughout the body and proceeds to destroy healthy tissues and organs because they can’t differentiate between the antigen of the spirochete and the antigen of healthy tissue.As the killer T cells come into contact with the antigen on the healthy tissue it becomes inflamed and destroys healthy tissue and is autoimmune in nature.
Interview With Morgellons Expert, Dr. Ginger Savely
November 8, 2019
You have to fast forward to 8:24 for the start.
Thank God for Dr. Savely. Morgellons patients are believed even less than Lyme disease patients which hardly seems possible yet is. These poor patients are marginalized and told they are making it all up.
WHY IS ASKING FOR HELP SO HARD? SOMETIMES IT’S NECESSARY, ESPECIALLY WHEN YOU ARE CHRONICALLY ILL
Last winter an acquaintance sustained an injury that made it difficult for her to do any heavy lifting. She managed well enough until a big snowstorm hit her area. Her doctor warned her not to shovel her driveway. But because she lived alone, she was either going to have to ask someone else to shovel or stay snowed in.
The solution here seems simple, but it’s actually quite difficult for anyone who is a natural “helper”. As individuals, we are happy to provide help, but we’re not very good at receiving it, and even worse when it comes to asking for it. To ask for help is to show one’s vulnerability; it is to relinquish some control and recognize one’s own limitations. And that makes a lot of us uncomfortable.
A little more than a decade ago, when I was in the throes of a Lyme relapse, I was in a similar situation. I was living alone in Vermont when the state got walloped with more than two feet of snow. Stuck on my couch, barely able to address my basic needs, I wondered how I would ever dig myself out. I saw neighbors huffing and puffing as they unearthed their vehicles and driveways. I hardly knew any of them. How could I possibly ask them for help?
I resigned myself to staying indoors. But my symptoms worsened, and my doctor said I needed to start a new antibiotic. That meant going to the pharmacy, which meant digging out my car.
I paced around my apartment, trying to figure out what to do. I did not have the physical strength to shovel, no matter how badly I wanted to do it or how hard willed I believed myself. I had no choice but to ask for help; I didn’t like being in that position. It brought on feelings of shame and guilt that have often accompanied me on my Lyme journey.
I called my mom. She lived out of state and couldn’t physically help, but she suggested I call an old college friend who lived in my town.
“I can’t do that!,” I said. “He has a family to take care of! I’m sure he’s busy digging out their own cars. He works full time, too. How can I give him this big task on top of everything else he’s got going on?”
I see now that I was projecting my own fears on the response of my friend. I was trying to think of all the ways my request could be a burden on him, without allowing him a say in the matter. I assumed he’d be annoyed or put out, but those assumptions stemmed from my own discomfort.
In the past, I’d had the experience of asking the wrong person for help. Once during my illness, I planned a lunch with former colleagues. I knew I would have more energy if I didn’t have to drive myself to the restaurant, so I asked a colleague who lived nearby if she could pick me up.
“That’s really going to be tough,” she replied. “I have a lot of other things going on that morning, and picking you up would be an extra ten minutes out of my way.” I’d had to swallow my pride and when my request was rejected, I felt embarrassed and ashamed.
In fact, I’d simply asked the wrong person; that sometimes happens, just as sometimes I’m not available to help others as I’d like to. My former colleague wasn’t very understanding when it came to illness. Some people aren’t. Other people are, though, and there was no reason to believe my old friend wouldn’t be compassionate.
Finally, I bit the bullet and called. “Of course I’ll help,” he said without hesitation. “Give me an hour to finish shoveling off our cars, and I’ll be right over.” An hour later there he was, heaving piles of snow with the strength of a lumberjack, and an hour later he was finished. What seemed an insurmountable task to me had truly been no big deal to him, and he said so when I offered to pay him or at least make him some hot cocoa. “Happy to help,” he said. “Let me know if there’s anything else you need.”
I relayed this story to my injured acquaintance who was also snowed in. Together we created a shortlist of people she could ask for help.
A few days later I called to check on her. She was sacked out on her couch, her injury worse, because she’d never called anyone. She had insisted on doing the shoveling herself. She didn’t want to appear weak, she confided. And besides, no one could shovel her driveway as well as she could.
I understood where she was coming from because I’d once been there myself. Over time, though, I’ve realized that asking for help is not a sign of weakness; it actually takes a lot of strength. I also learned that it’s okay to release control over external matters from time to time, like how well the driveway will be shoveled, in order to focus on one’s precious health.
Doing so will allow you to get stronger faster, so you can get back to helping others. Until then, you can still be a natural helper from bed, just by being a good friend, a good listener, and a confident presence. If it feels overwhelming right now, that’s okay; it means that you need to take this time to focus on yourself and get well, so that one day, you can pay it forward.
Jennifer Crystal is a writer and educator in Boston. Her memoir One Tick Stopped the Clock is forthcoming. Contact her at lymewarriorjennifercrystal@gmail.com.
NEUROSCIENCE NEWS
Jennifer Crystal is a writer and educator in Boston. Her memoir One Tick Stopped the Clock is forthcoming. Contact her at 
