When every January is dry: The surprising appeal of living without alcohol – CBC.ca
It’s January, a month that many people now observe as ‘Dry January’ — a period to set aside alcohol and focus on health.
It’s not something I will be observing as a special occasion, because I don’t drink at all.
I can’t remember when I decided not to drink.
It was before I turned 19, because my celebration didn’t include the traditional first (legal) bar visit. It was before I started university, because I was able to enjoy being the only sober person at the end-of-orientation-week party, where I banked some wild stories to recount to my friends once they recovered from their hangovers.
I had had the occasional sip of alcohol as a teenager, and I thought it tasted terrible. I never enjoyed the astringent kick of wine, the malty foulness of beer.
But, honestly, who does? Alcoholic drinks taste objectively bad to most people at first. As the saying goes, you don’t drink them for the taste, and it’s likely that if alcoholic beverages were uncoupled from their euphoric effects we wouldn’t drink them at all.
When I declined a glass or bottle, I often found myself in the hot seat, being grilled on my reasons for abstaining.
The difference between me and most of my peers, I suppose, is that I wasn’t enthusiastic enough about the idea of getting buzzed to push through the nasty flavour.
My choice puzzled my friends at the time. After all, in our society we drink alcohol not only for its pleasurable effects but as a rite of passage.
Alcohol is a symbol of our transition into adulthood, and most teenagers are anxious to enjoy adult freedoms and to prove themselves worthy of adult responsibilities. We indulge in alcohol furtively when we begin to feel suffocated by the authority of our parents and guardians. We partake in alcohol openly to celebrate when our numerical age makes us legally (if not actually) independent from them.
When I declined a glass or bottle, I often found myself in the hot seat, being grilled on my reasons for abstaining. Not drinking, I’ve discovered, is one of the few purely personal choices that can make even strangers deeply uncomfortable.
It’s a singular experience to be questioned about why you don’t drink alcohol, because there are a limited number of answers people consider legitimate. An illness, a religious doctrine, a family history of alcoholism — these seem to be acceptable explanations for abstaining.
My reasons? I don’t like the taste, I’m having a good time already, I just don’t feel like it? These never seem to be good enough, so much so that I’ve sometimes fallen back on the excuse that there’s been alcoholism in my family (which is true, but not a factor) just to cut these awkward conversations short.
Why all this public concern over one aspect of my diet? I don’t like spicy food or cilantro either, but no one interrogates me about that.
Reckless libertines or hopeless degenerates?
Not drinking, on the other hand, is often taken as an affront. This is probably a legacy of the temperance movement, the organized crusade against alcohol consumption that snowballed during the 19th and early 20th centuries and eventually led to prohibition.
The temperance movement took a moral stance against alcohol and portrayed drinkers as reckless libertines or hopeless degenerates.
As a result, when you say you don’t drink, even today, the people around you begin to wonder if you’re looking down your nose at them like the temperance teetotallers of yore.
Add to that the fact that our society considers alcohol essential for relaxing, socializing, and partying, and the non-drinker becomes a very suspicious animal indeed. Is she a puritanical square, the sworn enemy of all things fun?
Each of us deserves to assess for ourselves whether drinking works for us, our bodies, and our pocketbooks.
This heap of cultural baggage makes it difficult for each of us to untangle how we really feel about alcohol from how we’re supposed to feel about it, how alcohol really affects our bodies from our expectations of how it should affect them.
I know a number of moderate drinkers who’ve recently given up alcohol after realizing they don’t actually enjoy drinking.
Alcohol is a depressant. It can lower your inhibitions and relax you, but it can also dampen your mood and make you feel gloomier than you did before. If you’re already prone to depression, drinking alcohol may not be a fantastic experience.
Others quit drinking because it’s getting in the way of their fitness goals (many alcoholic beverages are high in calories but, because they’re liquids, don’t fill you up) or because they want to save money. Newfoundlanders and Labradorians spend $1,056 per person on alcohol each year.
Each of us deserves to assess for ourselves whether drinking works for us, our bodies, and our pocketbooks. So, I propose a reality-based reset of our society’s approach to alcohol:
- Alcohol is a depressant, which can be a good thing or a bad thing depending on the circumstances and the individual drinker.
- Alcoholic drinks are not only drugs but food. You may or may not like their taste, and you may or may not want to include them as part of your diet.
- Alcohol might be a social lubricant, but you don’t need it to cut loose, act silly, and have fun. (I should know. I tend to be the friend who dances with abandon and occasionally lands on my face, despite being sober.)
Whether you’ll be enjoying the occasional drink this month or having a dry January, just remember that, if you’re of legal age, drinking is an option, not a requirement.
Read more from CBC Newfoundland and Labrador
CAMH Study Confirms Ongoing Brain Inflammation Associated With Long COVID – muskoka411.com – Muskoka 411
A new CAMH study published in the journal JAMA Psychiatry found elevated levels of inflammation in the brain of patients who report persistent symptoms of long COVID.
Using advanced brain scanning with positron emission tomography (PET) imaging agents developed exclusively by the CAMH Brain Health Imaging Centre, study senior author Dr. Jeffrey Meyer and his study team found elevated levels of the protein TSPO, a brain marker of inflammation, in patients with onset of depression within several months after a COVID-19 infection.
“We already knew that there is brain inflammation in people who died in the midst of a severe, active COVID-19 infection. What’s new about this study is that it shows that inflammation is hanging around for a long time in the brains of people with long COVID even after only mild to moderate symptoms of active COVID-19,” said Dr. Meyer, Head of the Neuroimaging Program in Mood & Anxiety at the Campbell Family Mental Health Research Institute at CAMH. “Inflammation in the brain was suspected of being the critical step in causing neurological and psychiatric symptoms of long COVID so confirming this is vital to develop treatments for people experiencing symptoms.”
It is generally believed that the majority of the world’s population has experienced at least one acute episode of COVID-19, and that at least 5 per cent of those people—more than 200 million globally—may experience lingering neurological symptoms, including depression, loss of enjoyment, memory impairment, slower motor control, low motivation and energy, for months to even years due to brain inflammation from long COVID.
As part of this study, 20 participants underwent brain scanning with specialized PET imaging designed to detect the presence of elevated levels of the TSPO protein. All had at least one documented acute episode of COVID-19 after which they reported symptoms of depression that continued for months. Most participants also experienced a variety of other lingering symptoms associated with long COVID, including extreme fatigue and problems with concentration and memory often referred to as ‘brain fog’.
“What’s also noteworthy is that the regions of the brain that had the most inflammation are the ones involved in the capacity to enjoy things, motivational energy and the ability to think and move quickly. These were often the symptoms of greatest concern among the people with long COVID who took part in the study,” added Dr. Meyer.
In a pioneering 2015 study published in JAMA Psychiatry, Dr. Meyer found that the brains of people with depression had more inflammation—30 per cent more on average—than the brains of people who were not depressed. The greater the inflammation, the more severe the depression. It was the first time an association between depression and brain inflammation had been found. This research was so ground-breaking that it became one of the most highly cited international research studies ever produced to date by CAMH.
Dr. Meyer and his team believe that further study of the association between brain inflammation and depression, as well as further study on the short and long-term impacts of COVID-19 on the brain, could lead to new treatments for long COVID that would also be purposed for depression and other illnesses. “For people who have been suffering from long COVID with lingering symptoms of depression, the hope is that we can use anti-inflammatory medications to see if we can get a reduction in symptoms,” said study first author Dr. Joeffre Braga. “Since inflammation can be in response to injury, it might also give us insight into mechanisms of brain injury in neurodegenerative diseases like Parkinson’s and prompt therapeutic development.”
This study was funded by the Canadian Institutes of Health Research (CIHR).
Read more about this research: https://www.camh.ca/en/camh-news-and-stories/potential-link-between-covid-19-and-brain-inflammation
Tuberculous monoarthritis of the knee joint – CMAJ
Joint tuberculosis (TB) is an uncommon manifestation of TB that typically presents with subacute or chronic atraumatic inflammatory symptoms in single, large, weight-bearing joints.
In Canada, epidemiological risk factors for TB include extended time spent in countries with high burden of TB, known exposure to TB or being part of a population disproportionately affected by TB (e.g., people born outside of Canada, those of Indigenous ethnicity or those with a history of homelessness or incarceration).
Synovial thickening, joint effusions, juxta-articular osteopenia, peripheral osseous erosions and gradual joint space narrowing on magnetic resonance imaging or computed tomography are suggestive of joint TB.
Specialized mycobacterial culture is the gold standard for diagnosis of TB, but nucleic acid amplification tests are increasingly accessible and allow for rapid diagnosis of joint TB.
Treatment for joint TB should be started promptly for preservation of joint function and prevention of irreversible destruction.
A 47-year-old man presented to the emergency department with 2 weeks of acute-on-chronic pain in his right knee. He described a 5-year history of chronic pain in his right knee, with 1 flare-up 3 years before presentation, which had resolved after a few weeks of ibuprofen use. He had not previously sought care for this problem. He was otherwise healthy, with no chronic medical conditions or previous surgeries, and he tested negative for HIV. He had smoked crystal methamphetamine daily for the last 10 years and had no history of intravenous drug use. He had immigrated from the Philippines 16 years before and had not returned.
When examined, the patient was afebrile with normal vital signs. His right knee was swollen with limited flexion and extension. He did not have any overlying erythema or tenderness to palpation of the bursa or the joint line. He had no other inflamed joints. Initial laboratory results showed a leukocyte count of 8.4 (normal 4–11) × 109/L and an elevated C-reactive protein level of 34.4 (normal < 3.1) mg/L. A radiograph of the patient’s right knee showed bony destruction of the knee joint and an irregular lucency of the medial tibial plateau (Figure 1). A computed tomography (CT) scan showed cortical destruction with peripheral osseous erosions and juxta-articular osteopenia (Figure 2). The patient was admitted to the internal medicine service and the initial treating physicians were concerned that he may have had a malignant disease; they ordered a CT scan of the chest, abdomen and pelvis, which showed mild, biapical lung scarring (Figure 3).
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Bloody synovial fluid was aspirated from the patient’s right knee joint, with a leukocyte count of 36.7 × 109/L (79% neutrophils, 15% lymphocytes, 6% monomacrophages) and an erythrocyte count of 150 × 109/L, and no crystals or organisms on Gram stain. Cultures for mycobacteria were negative on acid-fast bacilli staining. Given these findings, bacterial septic arthritis was suspected and he was treated with empirical antibiotic therapy (intravenous [IV] ceftriaxone 2 g daily, and IV vancomycin with a target trough of 10–20 mg/L). After 6 days, the patient’s knee had not improved and bacterial cultures from synovial fluid remained negative. The internal medicine team consulted our infectious diseases team.
We suspected tuberculosis (TB) based on 3 factors, namely the chronic nature of the monoarthritis, the pulmonary apical scarring on chest imaging and that the patient had emigrated from the Philippines — designated as a country with a high burden of TB by the World Health Organization (WHO), with the fourth highest national incidence of TB globally.1 We identified no other identifiable risk factors for TB, such as previous incarceration, homelessness or known close contact with someone with TB.
Nucleic acid amplification testing (NAAT) for TB using the GeneXpert MTB/RIF Ultra assay (Cephied) was performed on samples of synovial fluid, which confirmed the presence of Mycobacterium tuberculosis. Smear testing of sputum samples were negative for acid-fast bacilli. We prescribed standard weight-based dosages of rifampin (10 mg/kg/d), isoniazid (5 mg/kg/d) with pyridoxine (25 mg/d), pyrazinamide (25 mg/kg/d) and ethambutol (15 mg/kg/d) and discharged him to continue this therapy under care of the provincial TB program.
Four weeks later, samples of the patient’s synovial fluid showed growth of M. tuberculosis that was susceptible to the first-line anti-TB medications he was receiving. Mycobacterial cultures from sputum samples were negative, suggesting that he did not have pulmonary TB. At follow-up after the 9-month course of treatment, the patient had considerable improvement of his knee pain (pain only with extended use), periarticular and lower leg swelling and range of motion (full flexion and extension). He had returned to work and was ambulating without need for a mobility aid. Given the extensive destruction of the knee joint, we had planned to refer him to an orthopedic surgeon for consideration of knee arthroplasty. However, he was lost to follow-up, and subsequent knee imaging and surgical referral could not be completed.
In 2020, the incidence of TB in Canada was 4.7 per 100 000 people, consistent with the previous 10 years.2 However, people born outside of Canada and Canadian-born Indigenous peoples are disproportionately affected.2 Bone and joint TB, including both vertebral and extra-axial joint disease, is an uncommon manifestation of extrapulmonary TB. In Canada, this form of TB accounts for about 2.5% of all TB cases per year, and around half of these cases have vertebral disease.3 In low-income regions, bone and joint TB is more commonly seen among children, usually developing shortly after primary infection. In high-income countries, however, it is most commonly seen among adults, resulting from TB reactivation, as we suspected with our patient.3 Extra-axial disease usually presents as a monoarthritis that affects the knee or hip.
Diagnosis may be difficult and is often delayed by many months, particularly in countries where TB is not endemic.4,5 Key features of TB include the presence of risk factors, the long duration of symptoms and constitutional symptoms. Unlike in bacterial septic arthritis, systemic infectious symptoms such as fevers and chills, rigors or elevated heart rate are usually absent in tuberculous arthritis. Other differential diagnoses include bacterial septic arthritis, crystal arthropathy, systemic rheumatic disease (such as rheumatoid arthritis) and osteoarthritis. Poncet disease, a reactive polyarthritis associated with extra-articular TB disease, should also be considered if several joints are involved and the patient has evidence of nonerosive arthritis.6 Findings from physical examination are nonspecific and include restricted range of motion, swelling and joint effusion.7 Joint erythema, warmth and tenderness may be absent, unlike in crystal arthropathy or bacterial septic arthritis.
Typical radiologic findings in early disease show thickening of the synovium and joint effusions — similar to other causes of monoarthritis such as septic arthritis or crystal arthropathy.8 Early TB arthritis may also be misdiagnosed as osteoarthritis if imaging shows only joint space narrowing.8 Later-stage disease has features of juxta-articular osteopenia, peripheral osseous erosions and joint space narrowing, known as the Phemister triad.9 Some chronic cases may have sinus tract formation.8
Plain radiographs may show the Phemister triad in later-stage disease, but magnetic resonance imaging (MRI) and CT are the best imaging modalities for disease characterization. In particular, MRI offers the most specificity for TB arthritis, but timely availability is often limited; therefore, CT may be used as it offers more specific disease characterization than plain radiographs. 8 However, because joint TB has no pathognomonic imaging findings, particularly early in the disease course, the diagnosis cannot be made based on imaging alone and requires microbiological confirmation.
Diagnosis is typically achieved by synovial fluid analysis or synovial biopsy with microscopy for acid-fast bacilli and mycobacterial culture. However, testing synovial fluid for acid-fast bacilli has a low sensitivity of about 30% and cultures take weeks to detect growth. Mycobacterial cultures also require specialized laboratories that are certified for biosafety containment level 3 and have clinical mycobacteriology accreditation to ensure quality assurance.3 Joint fluid analysis often finds a leukocyte count in the inflammatory range, typically 10–20 × 109/L, but may be higher.7
Newer methods for molecular detection of M. tuberculosis such as NAAT are rapid, more geographically accessible and do not require specialized laboratories. The most studied and widely available NAAT assay recommended by WHO is the automated, cartridge-based GeneXpert MTB/RIF and the newer generation, GeneXpert MTB/RIF Ultra. A recent review of the diagnosis of extrapulmonary TB with the GeneXpert assay found a sensitivity of 60%–100%, depending on specimen type, and a specificity of 87.5%–100% for bone and joint specimens.10 We did not diagnose TB in our patient until 5 years after symptom onset, by which time he had considerable destruction of the knee joint. Despite the presence of joint destruction, TB arthritis typically responds well to medical therapy and is usually treated for 6–12 months. Treatment duration should be extended for patients with increased risk of relapse, such as those with extensive disease at presentation.3 Unlike other causes of septic arthritis, TB arthritis does not require acute surgical management; surgery is reserved for treatment of complications related to joint destruction after completion of TB treatment.3
Clinicians should consider joint TB in patients who present with subacute joint pain and swelling with joint fluid analysis suggestive of an inflammatory arthritis, and in patients who do not respond to standard therapy for inflammatory or septic arthritis. In addition to mycobacterial cultures, NAAT may aid timely diagnosis and management.
The section “Cases” presents brief case reports that convey clear, practical lessons. Preference is given to common presentations of important rare conditions, and important unusual presentations of common problems. Articles start with a case presentation (500 words maximum), and a discussion of the underlying condition follows (1000 words maximum). Visual elements (e.g., tables of the differential diagnosis, clinical features or diagnostic approach) are encouraged. Consent from patients for publication of their story is a necessity. See information for authors at www.cmaj.ca.
Competing interests: None declared.
This article has been peer reviewed.
The authors have obtained patient consent.
Contributors: All of the authors contributed to the conception and design of the work. Adrianna Gunton drafted the manuscript, revised it critically for important intellectual content, gave final approval of the version to be published and agreed to be accountable for all aspects of the work.
This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY-NC-ND 4.0) licence, which permits use, distribution and reproduction in any medium, provided that the original publication is properly cited, the use is noncommercial (i.e., research or educational use), and no modifications or adaptations are made. See: https://creativecommons.org/licenses/by-nc-nd/4.0/
Neighborhood deprivation and depressive symptoms linked to premature aging – News-Medical.Net
Feeling depressed and living in a deprived urban neighborhood could be making you age faster, according to a new study led by researchers at McMaster University.
The findings, published June 5 in The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences, showed that living in urban environments marked by material and social inequities, and having depression symptoms, were independently associated with premature biological aging, even after accounting for individual-level health and behavioral risk factors, such as chronic conditions and poor health behaviors.
Parminder Raina, a professor in the Department of Health Research Methods, Evidence, and Impact at McMaster University, led the research team, which included investigators from the Netherlands, Norway and Switzerland.
Our study used two DNA methylation-based estimators, known as epigenetic clocks, to examine aging at the cellular level and estimate the difference between chronological age and biological age.”
Divya Joshi, study’s first author and research associate in the Department of Health Research Methods, Evidence, and Impact at McMaster
“Our findings showed that neighborhood deprivation and depressive symptoms were positively associated with acceleration of the epigenetic age estimated using the DNAm GrimAge clock. This adds to the growing body of evidence that living in urban areas with higher levels of neighborhood deprivation and having depression symptoms are both associated with premature biological aging.”
Depressive symptoms in the study were measured using a 10-item standardized depression scale. The researchers found an acceleration in the risk of death by one month for every point increase on the depressive symptom score. They theorized that emotional distress caused by depression may result in more biological wear and tear and dysregulation of physiological systems, which in turn could lead to premature aging.
The researchers assessed neighborhood material and social deprivation using two indices that were developed by the Canadian Urban Environmental Health Research Consortium (CANUE) based on 2011 census.
Social deprivation reflects the presence of fewer social resources in the family and community, and material deprivation is an indicator of people’s inability to access goods and conveniences of modern life, such as adequate housing, nutritious food, a car, high-speed internet, or a neighborhood with recreational facilities.
The researchers found an increase in the risk of death by almost one year for those exposed to greater neighborhood deprivation compared to lower neighborhood deprivation.
The study did not find that neighborhood deprivation amplified the effect of depressive symptoms on epigenetic age acceleration.
“Our results showed that the effect of neighborhood deprivation on epigenetic age acceleration was similar regardless of depression symptoms, suggesting that depression influences epigenetic age acceleration through mechanisms unrelated to neighborhood deprivation,” Joshi said.
The research examined epigenetic data from 1,445 participants enrolled in the Canadian Longitudinal Study on Aging (CLSA), a research platform following more than 50,000 participants who were between the ages of 45 to 85 when recruited.
“Longitudinal studies, like the CLSA, are important to confirm associations like those found in this study,” said Raina, the study’s senior author and lead principal investigator of the CLSA.
“By following the same group of participants for 20 years, we will be able to determine whether epigenetic changes are stable or reversible over time. We will also gain insight into the mechanisms that are leading to accelerated epigenetic aging.”
Support for the CLSA is provided by the Government of Canada through the Canadian Institutes of Health Research and the Canada Foundation for Innovation. Additional support for this study was provided by the European Union Horizon 2020 Programme.
Joshi, D., et al. (2023) Association of Neighborhood Deprivation and Depressive Symptoms With Epigenetic Age Acceleration: Evidence From the Canadian Longitudinal Study on Aging. The Journals of Gerontology Series A. doi.org/10.1093/gerona/glad118.
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