Heart Failure Diet: Foods To Eat and Avoid - Health Essentials

“Heart failure” is as serious and life-threatening as it sounds. It’s the medical term for when your ticker can’t pump enough oxygenated blood to meet your body’s needs.

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There isn’t a cure for heart failure. But what you eat can help you manage the lifelong condition and minimize its impact on your life. Basically, your choices at mealtime can help you stay active and healthier.

So, what food should and shouldn’t be on your plate? Registered dietitian Julia Zumpano, RD, LD, has some definite menu recommendations. (SPOILER ALERT: There’s a big focus on reducing sodium intake.) 

The need for a heart failure diet

Researchers estimate that more than 64 million people around the world are in various stages of heart failure. To put that in perspective, that’s a group nearly equal to the population of France.

Heart failure also stands as the leading cause of hospitalization for those aged 65 and older. Put bluntly, it’s a condition that often steals years off lives.

Given all of that, it’s no wonder some experts refer to heart failure as a global pandemic.

Successfully living with heart failure often requires immediate lifestyle changes, with dietary choices topping the list. Think of your meals as medicine. What you eat can help or hurt your weakened heart.

“Everything you eat affects your entire body, including your heart,” says Zumpano. “Making good dietary choices — especially when it comes to sodium — is critical if you’ve been diagnosed with heart failure.”

Why is reducing sodium important with heart failure?

A bit of sodium is essential within your diet, as the mineral helps your body maintain fluid levels. “Consuming sodium helps your body absorb and hold onto the fluid it needs,” explains Zumpano.

But take in too much sodium, and you can retain excess water. If you have heart failure, that’s a big issue. Here’s why.

With heart failure, your struggle to adequately pump blood can lead to fluid buildup in your body. This excess fluid can be anywhere, from your arms and legs to areas around critical organs such as your lungs.

So, if you have heart failure and consume high amounts of sodium, you’re basically boosting fluid retention in a system that’s already flooding. That can send blood pressure numbers soaring.

“You’re putting extra strain on a heart that’s already having trouble keeping up,” says Zumpano.

But reducing sodium in your diet lessens extra fluid retention, which can take some pressure off your hard-working heart. Basically, it’s a way to help a compromised cardiovascular system.

How much sodium is too much?

Someone living with heart failure should try to limit sodium consumption to less than 2,000 milligrams (mg) per day, advises Zumpano. To put that in perspective, that’s less sodium than what’s in a teaspoon of table salt.

(Quick science lesson: Salt and sodium are often used interchangeably, but they’re different. Salt is a combination of sodium and chloride. Sodium, meanwhile, is just … well, sodium, and one of the most common elements on Earth.)

Should fluid consumption be limited?

Does it make sense to cut back on drinking cups of water and other beverages if your body is struggling with too much fluid? Sometimes, says Zumpano.

“Some people with heart failure do need to restrict how much they drink because they’re holding onto so much fluid,” she says. “But not everyone needs to follow a low-fluid diet. It’s on a case-by-case basis.”

Zumpano recommends talking to your healthcare provider before cutting back on fluid consumption to address heart failure symptoms.

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10 tips to adopt a low-sodium diet

So, how do you cut back on sodium intake to slow the progress of heart failure? Zumpano offers 10 suggestions to ease the transition into a low-sodium diet.

#1: Hide your salt shaker

Kind of obvious, right? Eliminating the habit of shake-shake-shaking salt onto your plate can bring an instant reduction in sodium consumption. (FYI, too: While sea salt and kosher salt are less processed than ordinary table salt, they aren’t low in sodium.)

#2: Use fresh herbs

Fresh herbs and spices can add flavor to meals without any sodium. But be wary of prepackaged spice and seasoning blends. “Salt usually gets mixed in with the herbs and spices — and the sodium adds up quickly,” notes Zumpano.

#3: Read nutrition labels

Food labels in the United States include a section that tells how much sodium is in a single serving of the food item. “My general rule is to try to keep that number below 140 mg of sodium,” says Zumpano. (Be mindful of what is classified as a serving size, too.)

“Take the time to read labels,” she adds. “The more you look, the more surprised you may be as to where sodium pops up.”

#4: Search out low-sodium or sodium-free products

Food manufacturers have definitely noticed that there are millions of people looking to cut sodium — and they’ve responded with product offerings that can better fit within a low-sodium diet, says Zumpano.

Shelves are loaded with products labeled “Low Sodium” or “No Sodium.” Low sodium means that food has 140 mg or less of sodium per serving. No sodium means that food has less than 5 mg of sodium per serving.

#5: Don’t confuse lower with low

Be cautious of foods labeled “lower, “reduced” or “less” sodium.” These products do offer lower sodium content than the regular version of the food, but that doesn’t mean they’re actually “low” when it comes to sodium content.

An example would be soy sauce, where a splash of the “reduced sodium” flavoring still may amount to a significant amount of sodium.

“This is where reading nutrition labels at the store becomes so important,” stresses Zumpano. “Be mindful of the milligrams of sodium that are actually in a serving — not just that it’s less than normal.”

#6: Focus on fresh foods

If you’re wondering where to steer your grocery cart to find food low in sodium, Zumpano has a map: “I often suggest that you try to shop the outside of the grocery store, where you’ll find your fresh produce, fresh meats and fresh dairy,” she says.

Ideal foods to grab include:

• Fruits and vegetables. No shocker here, right? “Fresh fruit and vegetables are packed with nutrients and have no or very, very little natural sodium,” notes Zumpano. (If you go the frozen or canned route, look for no-salt-added options.)
• Fresh meats. Fresh beef, pork, poultry and fish are just … well, raw meat with minimal amounts of natural sodium. “The best options for meat are where there has been little to no extra processing,” she says. (More on that in #7!)
• Dairy. Yogurt and milk aren’t very high in sodium. Cheese can be tricky, but there are varieties (Swiss, fresh mozzarella, brick and goat cheeses) that are naturally lower. There are some reduced sodium options, too.
• Nuts and seeds. Look for unsalted nuts and seeds to keep these nutritional powerhouses in your diet.
• Fresh grains and dried beans. Can it take a little longer to prepare dried beans or fresh grains like brown rice, wild rice and oats? Yes. But the payoff is healthier food for very little sodium compared to many convenience options. (For a shortcut, check the freezer section. Some of these foods can be found cooked and frozen without any added salt.)

#7: Limit processed and convenience foods

The majority of sodium in the average American’s diet comes from processed foods and convenience foods. By some estimates, more than 70% of consumed sodium is added during commercial processing.

Check the labels and you’ll often see high sodium content in canned soups, luncheon meats, breads, pasta and rice mixes, frozen dinners, instant cereals, puddings and many, many more items.

“Sodium is one of the best ways to preserve convenience foods and extend their shelf life,” explains Zumpano. “It’s simple, inexpensive and effective, which is why so much of it ends up in processed food.”

Dodging this sodium comes down to spending more time in the kitchen cooking with fresh ingredients. Is that less convenient? Without question.

But eating smarter and healthier is key to living better with heart failure. “Adding a few steps to your food preparation process can help you eliminate a tremendous amount of sodium from meals,” encourages Zumpano.

#8: Cook smartly

Getting low-sodium food items into the house won’t help if you use high-sodium sauces, dressings and seasonings during preparation. Do an ingredient inventory of your fridge, pantry and cupboards to get a sense of what’s there.

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“Take an extra look at what you’re using while cooking,” advises Zumpano.

And if you have a favorite recipe that includes salt, experiment and try reducing how much you use to minimize sodium content. Using a bit less often won’t seriously change the taste of the dish.

#9: Go simple when eating at restaurants

Let’s be realistic: Odds are you aren’t going to eat every meal at home. Grabbing a bite at a restaurant or hitting the buffet table at a party is part of life.

When you do eat out, look for more simply prepared foods. The more processed the food is, the more likely it is high in sodium. So, opt for a baked potato instead of mashed potatoes, or choose a side salad (dressing on the side) over a bowl of soup.

“Cut the sodium where you can while still finding joy in what you’re eating,” says Zumpano. “Every little bit helps.”

#10: Be patient

Reducing sodium in your diet can be difficult at first. As you make changes, it might help to keep a record of how much sodium you’re eating every day. You can write it down or use a meal-tracking app to make things easier.

“The idea isn’t deprivation,” notes Zumpano. “Look for adjustments you can make so you can enjoy the foods you want to eat while backing off of others. It’s about building knowledge about sodium so you can make the best choices.”

And as you make changes to your diet, your taste buds will adjust. (FYI: That’s a good thing!)

“Something that didn’t taste salty to you in the past will taste extremely salty to you after adhering to a low-sodium diet for just a week or two,” Zumpano continues. “It will help reinforce your good choices and it will become easier to follow sodium restrictions.”

An added bonus to better eating? High-sodium foods often are high in fat and calories, too, so you may drop some pounds after cutting back on items like processed meats, chips and snack foods, fried foods and breads.

Research shows that losing weight can ease stress on your heart and extend your life with heart failure, particularly if you have obesity.

Low-sodium diet sample menu

Going low-sodium doesn’t mean you won’t eat fabulous food. In fact, your meals can be amazing while adjusting to help manage heart failure. Just consider this example of a one-day meal plan:

Breakfast

• 1 cup fresh fruit.
• 1 slice of sprouted grain bread.
• An egg white omelet made with 1/2 cup egg whites, veggies (mushrooms, bell pepper and onion) and 2 tablespoons feta cheese or nutritional yeast.

Lunch

• 3 ounces grilled salmon.
• 2 cups of grilled veggies.
• 1 tablespoon extra virgin olive oil and vinegar dressing.
• 1/2 cup berries.
• 2 tablespoons salt-free slivered almonds.

Dinner

• 4 ounces grilled chicken.
• 1 cup roasted red-skin potatoes in rosemary and olive oil.
• Steamed green beans.
• 2 cups tossed salad with low-sodium dressing.
• 1 cup fresh melon.

Snack

• 1 small banana with 1 tablespoon unsalted natural peanut butter.

Note: For a diet in which you consume 2,000 mg of sodium per day, a sample plan might involve eating 300–400 mg at breakfast, 200 mg for snacks twice daily, 600 mg for lunch and 600–700 mg for dinner.

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Heart Failure Diet: Foods To Eat and Avoid - Health Essentials
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Mother-to-baby HIV transmission shouldn't be happening in Canada, researchers say - Prince George Citizen

A new study concludes a few pregnant women in Canada are passing HIV to their babies, despite the fact that this country has all the tools needed to stop it from happening.

Researchers combed through an HIV surveillance database and found 33 babies born in Canada between 2012 and 2021 were infected during pregnancy or delivery. 

Pediatric infectious diseases specialist and study co-author Dr. Fatima Kakkar says pregnant women with HIV can take antiretroviral treatment to prevent transmission to their babies. 

She says all pregnant women should be screened for HIV infection, but that sometimes doesn't happen if they don't have access to good prenatal care. 

In other cases, women who immigrated to Canada during their pregnancies didn't have their HIV status discovered until it was too late to prevent transmission. 

Kakkar says there are also women who tested negative at the beginning of their pregnancies but became infected by an HIV-positive partner later. 

She says it's important to fight the stigma that still exists around HIV so that pregnant women won't be afraid to be tested and treated. 

Kakkar and her colleagues presented the findings at the Canadian Conference on HIV/AIDS Research that wrapped up on Sunday.  

This report from The Canadian Press was first published May 1, 2023.

———

Canadian Press health coverage receives support through a partnership with the Canadian Medical Association. CP is solely responsible for this content.

Nicole Ireland, The Canadian Press

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Mother-to-baby HIV transmission shouldn't be happening in Canada, researchers say - Prince George Citizen
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Mother-to-baby HIV transmission shouldn't be happening in Canada, researchers say - Squamish Chief

A new study concludes a few pregnant women in Canada are passing HIV to their babies, despite the fact that this country has all the tools needed to stop it from happening.

Researchers combed through an HIV surveillance database and found 33 babies born in Canada between 2012 and 2021 were infected during pregnancy or delivery. 

Pediatric infectious diseases specialist and study co-author Dr. Fatima Kakkar says pregnant women with HIV can take antiretroviral treatment to prevent transmission to their babies. 

She says all pregnant women should be screened for HIV infection, but that sometimes doesn't happen if they don't have access to good prenatal care. 

In other cases, women who immigrated to Canada during their pregnancies didn't have their HIV status discovered until it was too late to prevent transmission. 

Kakkar says there are also women who tested negative at the beginning of their pregnancies but became infected by an HIV-positive partner later. 

She says it's important to fight the stigma that still exists around HIV so that pregnant women won't be afraid to be tested and treated. 

Kakkar and her colleagues presented the findings at the Canadian Conference on HIV/AIDS Research that wrapped up on Sunday.  

This report from The Canadian Press was first published May 1, 2023.

———

Canadian Press health coverage receives support through a partnership with the Canadian Medical Association. CP is solely responsible for this content.

Nicole Ireland, The Canadian Press

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Mother-to-baby HIV transmission shouldn't be happening in Canada, researchers say - Squamish Chief
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Wildfire smoke increases risk of heart issues within hours, study finds - CBC.ca

The B.C. Centre for Disease Control is again warning British Columbians of the negative health impacts of wildfire smoke, in the wake of new research that suggests air pollution can immediately increase risk of several heart problems.

For every 10 micrograms more of PM2.5 — the primary particle in B.C.'s wildfire smoke — in one metre cube of air, a person's combined odds of experiencing at least one of four heart issues was 5.5 per cent greater, a study published Monday in the Canadian Medical Association Journal found.

The four arrhythmia studied are all significant risk factors for heart attacks and heart disease, the study notes, supporting decades of evidence that shows higher rates of cancer, chronic disease and premature death in communities that live with poor air quality.

The findings highlight the urgency of limiting even short-term exposures to wildfire smoke amid smoke-related rises in heart attacks and respiratory issues researchers and health care workers are already observing in B.C., says one BCCDC expert.

"When there is wildfire smoke in the province, we do see increases in those types of negative outcomes within hours of the smoke arriving," said Sarah Henderson, scientific director of environmental health services at the BCCDC.

Heart attacks, breathing problems, and weakened heart walls increased by about 1 to 2 per cent within an hour of exposure to more PM2.5, according to a 2020 study Henderson co-authored.

"It's a small but important number," Henderson noted.

Dr. Lori Adamson, a member of the Canadian Association of Physicians for the Environment, says more needs to be done by government at all levels to prepare people for the health impacts of wildfires. (Photo courtesy of Lori Adamson)

Dr. Lori Adamson, an emergency physician in Salmon Arm, B.C. — about 111 kilometres north of Kelowna — says she sees first-hand the influx of patients struggling to breathe who come to hospital on smoky days, and that in turn puts pressure on their hearts.

"My patients are very distressed about the situation and they come in kind of feeling desperate and hopeless … because it feels like a really big problem and outside of their control," said Adamson.

Adamson adds the majority of — as well as the most vulnerable — people she admits to hospital are infants and children, whose lungs are more delicate and who breathe faster than adults, and people with pre-existing respiratory conditions like asthma and chronic obstructive pulmonary disease that are exacerbated by the smoke.

'Action at a broader scale' needed

The peer-reviewed study is based on data from nearly 200,000 patients in 322 cities in China between 2015 and 2021, where coal-burning means air pollution is more persistent and of different chemical proportions than in B.C.

The findings are concerning for B.C. because the size of the particle matters more than the composition, Henderson said. PM2.5 is smaller and can penetrate further than other molecules, blocking even more oxygen exchange.

"We don't know much about this right now but if you protect yourself from these exposures in the short-term, you're also protecting yourself in the long-term," said Henderson.

Henderson suggests using air purifiers with HEPA filters to clean air at home, wearing well-fitted N95 and KN95 respirators if spending time outside, and to avoid exercise and heavy breathing on smoky days.

Anyone struggling to breathe, particularly young children and older adults, should seek medical care. "We do have to look at these individual level interventions and behaviours to help reduce exposure and impacts within the population," said Henderson.

For Adamson, a member of the Canadian Association of Physicians for the Environment, more needs to be done by government at all levels to prepare people for the health impacts of wildfires and move away from fossil fuel-based energies that drive climate change and worsen wildfires.

"There needs to be action at a broader scale … so we're not just figuring out how to deal with smoke in our faces."

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Hourly air pollution exposure and the onset of symptomatic arrhythmia: an individual-level case–crossover study in 322 Chinese cities - CMAJ

Arrhythmia is caused by disordered electrical activity in the heart, often occurs abruptly and can lead to severe cardiovascular diseases such as heart failure, acute myocardial infarction, stroke and death.1^–3 The Global Burden of Disease study estimated a prevalence of around 59.7 million cases of atrial fibrillation and atrial flutter globally in 2019, and the disability-adjusted life years related to these 2 conditions increased from 3.79 million in 1990 to 8.39 million in 2019.4 Furthermore, the Cardiovascular Health and Diseases Burden Study in China reported that about 4.87 million people had atrial fibrillation in 2019.5 Given the considerable disease burden of arrhythmia, identifying modifiable risk factors is important.

Air pollution has been reported to be a modifiable risk factor for cardiovascular diseases;4^,6 therefore, clarifying the effects of air pollution on arrhythmia is important. Air pollution is a complex mixture of particulates and gases that varies by time and location.7^,8 Common air pollutants tracked by the World Health Organization (WHO) and government agencies are typically known as “criteria” air pollutants.9^–12 Particulate matters in air pollution are broadly categorized by aerodynamic diameter as inhalable particles (< 10 μm, PM₁₀), fine particles (< 2.5 μm, PM_2.5) and coarse particles (2.5–10 μm, PM_2.5–10). Criteria air pollutants that are gaseous generally include nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon monoxide (CO) and ozone (O₃). These pollutants have varied physicochemical properties and have been reported to negatively affect human health in different ways.1^,13

Previous epidemiological studies have linked short-term exposure to air pollution with arrhythmia, but the results have been inconsistent.14^–21 In addition, most of these studies evaluated the associations only at a daily level;22^–24 few have considered the effects of hourly exposure to air pollution before symptom onset. Associations have generally been observed in ecological time-series analyses, leading to difficulty in making causal inferences.23^–26 Furthermore, no previous studies have systemically evaluated associations of criteria air pollutants with the acute onset of various types of arrhythmia episodes at a national level.

China has air pollution levels well beyond the WHO guidelines for air quality and those measured in other countries.9^,27 Accordingly, we sought to evaluate the association of hourly exposure to air pollution with the acute symptomatic onset of arrhythmia in China.

Methods

Study design and setting

We conducted a time-stratified, case–crossover study at the individual level to evaluate the association between hourly exposure to ambient air pollution and the onset of symptomatic arrhythmia in China among patients admitted to certified chest pain centres from 2015 to 2021.28 This study design has been widely used in epidemiological studies of air pollution.29^,30 It allows patients to serve as their own controls, and, therefore, factors that remain relatively stable over a short period (e.g., in the same month) such as sex, age, body mass index, comorbidities and socioeconomic and behavioural factors, can be automatically controlled by design.31^,32

We reported this study according to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) checklist for case–control studies.33

Data source

We obtained data for patients with symptomatic arrhythmia from the Chinese Cardiovascular Association (CCA) Database — Chest Pain Center, from Jan. 1, 2015, to Dec. 31, 2021. Established in 2015, this nationwide network uses a standardized registry system to monitor the quality of care provided to patients seen in emergency departments for chest pain or discomfort. The CCA database has been described previously.23^,34^,35 Several strategies, including an internal reporting checklist, are used to ensure validity and quality of the data (described in Appendix 1, available at www.cmaj.ca/lookup/doi/10.1503/cmaj.220929/tab-related-content). To ensure data quality, we included only data from hospitals with a chest pain centre certified by the National Chest Pain Center Program.35

Study population and case ascertainment

We extracted medical records for patients admitted to a certified chest pain centre with symptoms (chest pain or discomfort) arising from a primary diagnosis of 1 of 4 main subtypes of arrhythmia — namely, atrial fibrillation, atrial flutter, premature beats (atrial or ventricular in origin) and supraventricular tachycardia — during the study period. We excluded patients with chest pain or discomfort and arrhythmia secondary to another diagnosis (e.g., acute coronary syndrome, pulmonary embolism, aortic dissection). Therefore, we included only those with a principal diagnosis of symptomatic primary arrhythmia in this study.

In these centres, cardiologists diagnose chest pain or discomfort using common clinical practice guidelines and according to symptoms, laboratory biochemical tests and electrophysiological measurements such as electrocardiograms. The principal diagnoses are entered into the database.

Although more specific diagnostic information on the symptomatic arrhythmia is not recorded in the database, only patients with acute symptoms are typically admitted to the chest pain centres. Hence, our study population likely represents patients with a new onset of symptomatic arrhythmia or an acute worsening of pre-existing arrhythmia resulting in chest pain or discomfort, regardless of whether these episodes were diagnosed as intermittent, persistent or permanent.

We excluded patients with symptomatic arrhythmia who did not report the timing of symptom onset, were admitted by referral from other hospitals, or had a second admission of arrhythmia in the same month. We also excluded cases reported by hospitals without nearby air pollution monitoring stations (< 50 km in distance). More information about case ascertainment is described in Appendix 1.

We extracted information on sex, age, self–reported time and location of symptom onset, disease history, principal clinical diagnoses and address of the reporting hospital.

Environmental exposure assessment

We obtained hourly concentrations of 6 criteria air pollutants — PM_2.5 (μg/m³), PM₁₀ (μg/m³), NO₂ (μg/m³), SO₂ (μg/m³), CO (mg/m³) and O₃ (μg/m³) — during the study period from the National Urban Air Quality Real–time Publishing Platform. We calculated PM_2.5–10 (μg/m³) by subtracting the concentrations of PM_2.5 from PM₁₀ at the same station.29

Since the database did not include the location of symptom onset (complete address) for nearly three-quarters (73.2%) of the study population, we used concentrations of air pollutants measured at the nearest monitoring station to the reporting hospital to represent exposure for all participants, a proxy widely used in epidemiological studies of air pollution.29^,36 The median distance between the included hospitals and the nearest monitors was 4.4 km (range 0.04–49.9 km).

We obtained hourly ambient temperature and relative humidity for each hospital from the nearest meteorological station (median distance 19.0 km), recorded in the China Meteorological Data Service Center (http://data.cma.cn/). If data at the nearest monitoring station were not available, we used data from the next nearest station.

The final missing rates ranged from 1.1% to 3.1% for various environmental variables; we omitted data from patients with missing environmental variables before statistical descriptions and analyses. To avoid the possible influences of outliers in concentrations of air pollutants, we removed the highest and lowest 2.5% of hourly concentrations during the study period.37

Case and control periods

For our case–crossover study design, we defined the case period as the hour of symptom onset of arrhythmia for each patient. We selected the corresponding control periods for each patient to be in the same hour, day of week, month and year to control for time trends such as circadian rhythms and seasonality.38 For example, if a patient had an onset of symptomatic arrhythmia at 7:00 pm on Monday, Nov. 2, 2020 (defined as the case period), eligible control periods were 7:00 pm on Nov. 9, 16, 23 and 30, 2020. We matched each case period to 3 or 4 control periods, depending on the number of the same days of the week within the month of symptom onset.

Statistical analysis

We used conditional logistic regression models to evaluate the associations between hourly ambient air pollution and arrhythmia onset. Previous studies have shown lagged effects of air pollution on cardiovascular diseases within the first few hours or days after exposure.24^,29^,39 Therefore, after matching exposure and arrhythmia onset at the hourly level, we considered lag periods of less than 1 day (e.g., 0–6 h, 7–12 h, 13–24 h), and daily lag periods, including 0 days (i.e., lag 0–24 h), 1 day (i.e., lag 25–48 h), 2 days, (i.e., lag 49–72 h) and 3 days (i.e., lag 73–96 h).40

We first hypothesized linear exposure–response relationships by fitting separate models with a linear term for each pollutant at each lag period.24^,41 To control for potential confounding by time-varying factors, we included a binary indicator of public holidays and natural cubic splines with 6 and 3 degrees of freedom for temperature and relative humidity, respectively, both of which were included using the 96-hour average (lag 0–3 d), in the models.29 To evaluate possible nonlinear exposure–response relationships, we replaced the linear term for each air pollutant with a natural cubic spline with 3 degrees of freedom. In addition, to determine whether some confounding was present in relation to diurnal or seasonal patterns, we calculated the number of arrhythmia cases and average concentrations of the 6 air pollutants at the hourly or seasonal level, plotted their relationships and reported the Spearman correlation coefficients.

To explore potential effect modifications, we conducted stratified analyses by sex (male and female), age (< 65 and ≥ 65 yr), season and region of the country. We defined the season as warm (April to September) and cold (October to March), and the region as north and south based on the geographic marker of the Qinling–Huaihe line.29

We conducted 2 interaction analyses. First, we added an interaction term between the grouping variable (i.e., sex, age group, region, season) and air pollutants into the main model. Second, we fit separate models in each group and examined the statistical significance of potential effect modifications by 2–sample z tests using the following formula:

where β₁ and β₂ and were the stratum-specific coefficients of point estimates, and SE and SE₂ were the corresponding standard errors. Finally, we conducted a supplementary analysis by adding an interaction term of PM_2.5 and O₃ into the main model to explore potential interaction effects of air pollutants as reported in previous studies.42^–44

We conducted several sensitivity analyses to determine the robustness of the associations between air pollutants and arrhythmia onset. First, to control for potential confounding of coexposures, we fit pairwise 2-pollutant models. Second, we reran the main models separately for patients for whom complete address of symptom onset was available, using exposure data based on both hospital address and onset address. Third, we analyzed the relationship between levels of air pollution and initial visits (before admission) in the chest pain centres (thereafter defined as emergency department visits), matched by the time of first medical contact. Finally, we compared the fit of linear and nonlinear models using likelihood ratio tests, to evaluate the linear assumption used in the main analyses.45

All analyses were 2 sided, with an α level of 0.05. We presented results as percent change and 95% confidence intervals (CIs) for the risk of arrhythmia onset associated with an interquartile range (IQR) or a 10 μg/m³ (1 mg/m³ for CO) increase in concentrations of air pollutants.29 To correct for multiple testing, we used the Benjamini–Hochberg procedure for the set of 24 (6 pollutants × 4 arrhythmia subtypes) main analyses and the set of 48 (6 pollutants × 8 subgroups) subgroup analyses, with a false discovery rate of 0.05.46 More information on our analysis methods is available in Appendix 1.

We performed all analyses in R (version 3.6.3, R Project for Statistical Computing) with the survival package for conditional logistic regression.

Ethics approval

The study protocol was approved by the Institutional Review Board of the School of Public Health, Fudan University (no. 2021–04–0889). All data were anonymized, with access to the database authorized by the CCA Database — Chest Pain Center.

Results

We included a total of 190 115 patients with symptomatic primary arrhythmia in this analysis, of whom 96 133 had atrial fibrillation, 5300 had atrial flutter, 41 613 had overall premature beats (including atrial or ventricular) and 47 069 had supraventricular tachycardia (Figure 1). The mean age of the study participants was 64 (range 18–98) years, with 47.1% younger than 65 years. Demographic characteristics are summarized in Table 1. We included data from 2025 certified hospitals in 322 Chinese cities. These hospitals are most densely distributed in the eastern region of the country, followed by the central region and the western region, a distribution that is largely consistent with socioeconomic and air pollution characteristics in China (Appendix 2, Supplemental Figures S1 and S2, available at www.cmaj.ca/lookup/doi/10.1503/cmaj.220929/tab-related-content).

Figure 1:

Flow chart.

View this table:

Table 1:

Patient demographic characteristics

During the study period, the 24-hour average concentrations of PM_2.5, PM_2.5–10, NO₂, SO₂, CO and O₃ were 34.4 μg/m³, 25.5 μg/m³, 27.5 μg/m³, 8.9 μg/m³, 0.7 mg/m³ and 59.0 μg/m³, respectively. The 24-hour average temperature was 17.5°C and the relative humidity was 71.4% (Table 2). We found weak-to-moderate correlations between air pollutants and meteorological conditions, with Spearman coefficients ranging from –0.45 to 0.63 (Appendix 2, Supplemental Table S1).

View this table:

Table 2:

Descriptive statistics of air pollutants and meteorological factors over the 24 hours before arrhythmia onset

Diurnal and seasonal patterns

At the diurnal level, we did not observe any significant correlations between hourly concentrations of air pollutants and hourly numbers of arrhythmia onset (Appendix 2, Supplemental Figure S3 and Table S2). Likewise, no significant relationships were found between average concentrations of air pollution and numbers of arrhythmia cases at the seasonal level (Appendix 2, Supplemental Figure S4 and Table S2).

Lag period patterns

Short-term exposure to ambient air pollution was associated with higher risk of the onset of symptomatic arrhythmia, but the magnitude differed by lag period. Generally, the effects occurred during the first several hours and either persisted or attenuated thereafter; exposures at a lag period of 0 days (0–24 h) showed the highest risks compared with other daily lags. The risks attenuated greatly after 24 hours, except the association between exposure to PM_2.5 and atrial flutter, which was strongest at lag 2 days (Appendix 2, Supplemental Figures S5–8). Therefore, we reported results primarily using a lag period of 0 days in subsequent analyses (Figure 2).

Figure 2:

Change in the odds of arrhythmia onset per interquartile range increase in concentration of air pollutants. The exposure duration was an average lag period of 0–24 hours preceding the onset for all analyses other than the analysis for PM_2.5 and atrial flutter, which used a lag period of 49–72 hours. Note: CI = confidence interval, CO = carbon monoxide, NO₂ = nitrogen dioxide, O₃ = ozone, PM_2.5 = particulate matter with an aerodynamic diameter ≤ 2.5 μm, PM_2.5–10 = particulate matter with an aerodynamic diameter between 2.5 and 10 μm, SO₂ = sulfur dioxide.

Associations between specific air pollutants and arrhythmia subtypes

Exposure to ambient air pollution showed stronger associations with atrial flutter and supraventricular tachycardia than the other 2 subtypes. At lag periods of 0–24 hours, exposure to PM_2.5, NO₂, SO₂ and CO was associated with the onset of atrial fibrillation, atrial flutter and supraventricular tachycardia. Exposure to PM_2.5–10 showed positive and significant associations with atrial flutter and supraventricular tachycardia at lag 0 days. We found no evidence of an association between the pollutants and onset of premature beats except for NO₂. At lag periods of 0–24 hours, exposure to O₃ was associated only with supraventricular tachycardia (Figure 2 and Appendix 2, Supplemental Figures S5–8).

Among the relationships of the pollutants with onset of different types of arrhythmias, NO₂ consistently showed the strongest associations. Specifically, an IQR increase in the concentration of NO₂ was associated with increases in the odds of atrial fibrillation (3.4%, 95% CI 1.8% to 5.1%), atrial flutter (11.4%, 95% CI 3.6% to 19.7%), premature beats (3.7%, 95% CI 1.1% to 6.4%) and supraventricular tachycardia (8.9%, 95% CI 6.2% to 11.6%) (Figure 2). The effect estimates per 10 μg/m³ (per 1 mg/m³ for CO) increase in concentration of air pollutants at a lag period of 0 days are presented in Table 3.

View this table:

Table 3:

Change in the odds of onset of symptomatic arrhythmia associated with a 10 μg/m³ (1 mg/m³ for CO) increase in air pollutant concentrations during lag 0 to 24 hours

The curves depicting the exposure–response relationship between all air pollutants and arrhythmia onset increased monotonically and were, in general, approximately linear, without any apparent concentration thresholds (Figure 3 and Appendix 2, Supplemental Figures S9–10). Furthermore, we found no statistically significant differences between linear models and nonlinear models (Appendix 2, Supplemental Table S3).

Figure 3:

Exposure–response curves for the concentrations of 6 air pollutants and atrial fibrillation (panels A–F) and supraventricular tachycardia (panels G–L). The associations are presented as percentage change in the odds of the outcome in comparison to the odds at the median concentration over a lag period of 0–24 hours. The solid red lines represent the point estimates, and the intervals between dashed red lines represent 95% confidence intervals (CIs). The other dashed lines represent the concentration of air pollutants (green = 25th percentile, blue = 75th percentile, black = 95th percentile). Note: CO = carbon monoxide, NO₂ = nitrogen dioxide, O₃ = ozone, PM_2.5, = particulate matter with an aerodynamic diameter ≤ 2.5 μm, PM_2.5–10 = particulate matter with an aerodynamic diameter between 2.5 and 10 μm, SO₂ = sulfur dioxide.

Stratified and interaction analyses

Stratified analyses showed that the associations of the 6 pollutants with overall onset of arrhythmia was stronger among patients who were male or younger than 65 years. In addition, exposure to air pollution exposure had stronger associations among patients located in the north region and during the cold season (Appendix 2, Supplemental Table S4).

Analyses for the inclusion of interaction terms showed some significant effect modifications. Specifically, higher risks of arrythmia onset were found among males (significant difference for SO₂), patients younger than 65 years (significant difference for PM_2.5–10), patients located in the north region (significant difference for SO₂) and during the cold season (significant difference for all air pollutants) (Appendix 2, Supplemental Tables S5). We did not find any statistically significant interactions between PM_2.5 and O₃ for the 4 types of arrhythmias (Appendix 2, Supplemental Table S6).

Sensitivity analyses

Analyses using 2-pollutant models showed similar results after simultaneously controlling for co-pollutants (Appendix 2, Supplemental Figures S11–14). Furthermore, for patients who provided complete onset address (n = 51 331), the estimates were not significantly different in analyses using exposures assigned according to the onset address and those assigned according to the hospital address (Appendix 2, Supplemental Table S7). Compared with the main analyses, we observed a slightly stronger association between exposure to air pollutants and arrythmia onset using exposures matched by the time of initial visit to the emergency department (Appendix 2, Supplemental Table S8). Finally, the estimated associations between exposure to air pollutants and arrhythmia onset (including subgroup analyses) remained statistically significant after we corrected for multiple testing (Appendix 2, Supplemental Table S9–10).

Interpretation

We evaluated the association between hourly exposure to air pollution (PM_2.5, PM_2.5–10, NO₂, SO₂, CO and O₃) and symptom onset of 4 common arrhythmias, and found that acute exposure to ambient air pollution was associated with increased risk of symptomatic arrhythmia. The risks occurred during the first several hours after exposure but attenuated greatly 24 hours after exposure. Among the 6 pollutants, NO₂ showed the strongest association with all 4 arrhythmias, while O₃ was associated only with supraventricular tachycardia. We did not observe any concentration thresholds for the exposure–response relationships.

Previous findings on the association of air pollutants with arrhythmia have been mixed.24^,26^,47^,48 Most studies were subject to the ecological fallacy (the bias that may occur when associations that exist between variables at the aggregate level may not represent the true associations that exist at the individual level),49^,50 and were limited in sample size, geographical coverage and time specification.21^,23^,24^,26 Our case–crossover study strengthens previous findings by providing large-scale, individual-level evidence.

Some studies have shown positive associations between exposure to PM (PM_2.5 and PM₁₀) and risk of arrhythmia, but results have varied in different countries and regions.51^,52 Consistent with previous studies,15^,53^,54 we found that exposure to PM_2.5 increased the risk of arrhythmia. We also found that PM_2.5–10 increased the risk of atrial flutter and supraventricular tachycardia but had little effect on atrial fibrillation and premature beats.

The existing evidence on the association of gaseous pollutants with arrhythmia is also inconsistent.15^,55^–60 Several studies have reported no association,14^,54^,60 but we found NO₂ had the strongest associations with arrhythmia, compared with other pollutants. The inconsistency of these findings may be explained by the difference in air pollution mixture, climate conditions and population susceptibility, as well as the study design, statistical power and exposure lags that were used in the various studies.21^,47^,48

We found the strongest associations of air pollution with atrial flutter and supraventricular tachycardia, followed by atrial fibrillation and premature beats. Although the exact mechanisms are not yet fully understood, the association between air pollution and acute onset of arrhythmia that we observed are biologically plausible. Some evidence has indicated that air pollution alters cardiac electrophysiological activities by inducing oxidative stress and systemic inflammation, affecting multiple membrane channels, as well as impairing autonomic nervous function.1^,61^–65

Among numerous epidemiological studies of air pollution, few have explored the interactive effects for 2 or more air pollutants, likely because of intractable problems in relation to multi-collinearity and exposure measurement. The interactive effects of PM and O₃ have been most commonly investigated in previous studies but the results have been mixed.42^,43^,66^,67 For example, a time-series study from Shanghai reported that higher levels of PM₁₀ strengthened the association between exposure to O₃ and mortality.66 Another study from Moscow also observed increased mortality from all causes, ischemic heart disease and cerebrovascular disease, associated with exposure to PM₁₀ at concurrent higher levels of O₃.67 In contrast, a study from Hong Kong observed that exposure to O₃ may alleviate the adverse effects of particulate air pollution on cardiovascular and respiratory morbidity; 42 another study in Seoul also observed attenuated associations of exposure to O₃ with stroke mortality in conjunction with higher levels of PM₁₀.43 Our study did not find any statistically significant interactions between PM_2.5 and O₃ for all types of arrhythmias, and further studies are warranted to evaluate these possible interactions.

Given the nature of our database and study design, the observed triggering effect of air pollution could be the result of an acute worsening or a recurrent episode of a pre-existing arrhythmia (including a previously undiagnosed arrhythmia) induced by exposure to pollutants within 24 hours. Some previous studies linking short-term air pollution exposure and arrhythmia have reported comparable effect sizes to our study.21^,24^,47^,48 For example, Halldorsdottir and colleagues21 conducted a time-stratified, case–crossover study in Reykjavik, and found that an increase in NO₂ of 10 μg/m³ increased the risk of atrial fibrillation at a lag period of 0 days (odds ratio [OR] 1.03, 95% CI 1.01 to 1.05). Another study observed that an IQR increase in PM_2.5 levels was associated with an increased risk of atrial fibrillation (OR 1.05, 95% CI 1.01 to 1.09) at a lag of 48–72 hours.⁴⁸⁸

These effects appeared to be appreciably smaller than those of other well-known and established risk factors for arrhythmia. For example, the Framingham Heart Study and 2 other systematic reviews indicated that the prevalence of diabetes, obesity and some cardiovascular diseases (e.g., hypertension, congestive heart failure, valve disease) was associated with increased risk of developing atrial fibrillation, with hazard ratios (or risk ratios) ranging from 1.2 to 5.9,68^–70 which were about 1–6 times greater than those associated with air pollution. Despite the smaller effect sizes associated with exposure to air pollution, the disease burden could still be considerable because of the ubiquitous exposure.

Stratified analyses in our study showed that the association of exposure to air pollutants and arrhythmia was stronger among male patients, which is consistent with previous studies.23^,71 It is unclear why male patients may be more vulnerable, but this may be owing to a higher prevalence of lifestyle-related risk factors for arrhythmia (e.g., smoking, alcohol intake) or more exposure to air pollution through outdoor activities, including work.7 Furthermore, the associations were stronger in the cold season, which may be owing to a higher level of pollution during this period from central heating in China.72 In addition, low temperature has been found to enhance the harmful effects of air pollution on the cardiovascular system.29

In previous studies, older adults have generally been found to be more vulnerable to air pollution;29^,45 however, we found that older patients had lower risks of arrhythmia related to air pollution. We postulate that this may be a result of a blunted response to exposure to air pollution from pre-existing diseases or age-related impairment.73

Understanding the timing of exposure and symptom onset is important from a clinical and public health perspective. However, previous evidence on sensitive exposure windows was uncertain.14^,41^,74 We found evidence on lag patterns, which indicated that air pollution was associated with the onset of symptomatic arrhythmia within the first hours of exposure.

We observed approximately linear exposure–response relationships, without apparent thresholds, which was similar to previous results.24^,41 The State of Global Air 2020 study27 and another previous study75 reported that the annual average level of PM_2.5 in China was 31.4 μg/m³ in 2019, which is much higher than in Canada (7.1 μg/m³),27 and the WHO guidelines for global air quality (5 μg/m³).9 Although our study was conducted in China, where exposure levels are very high, the results may still be relevant to other countries because of the “no threshold” findings we observed in the exposure–response relationships. Our findings also highlight the necessity of more stringent air pollution control, as well as prompt responses for susceptible populations during episodes of air pollution.

Limitations

As with most previous epidemiological studies on short-term health effects of air pollution,29^,48 we obtained all exposure data from fixed site monitors nearest to the reporting hospitals; consequently, errors in exposure measurement were inevitable. However, the patients in our study were usually taken to the nearest hospital for timely treatment, and the resultant non-differential misclassification could only cause Berkson bias, which would not influence the mean estimates of the associations but could lead to an inflation of confidence intervals.36^,76

We studied patients with symptomatic arrhythmia who visited participating chest pain centres and, thus, we did not include those who had asymptomatic arrhythmia, were admitted by other hospital departments or died before arriving at hospital. In addition, the database we used did not collect information on patients with ventricular tachycardia, ventricular flutter or ventricular fibrillation. Therefore, our population may not be a representative sample of patients with arrythmia in China, and our results may have limited generalizability to other regions. The lack of detailed information on disease history and diagnosis prevented us from conducting some clinically important stratified analyses.

We cannot exclude the possibility of diagnostic or reporting errors in such a nationwide analysis. We deemed such errors to be random and not related to variations in air pollution, so they were not likely to bias our results. The varying sample size for different subtypes of arrhythmia attenuated the comparability in their associations with air pollution. Finally, although we used a time-stratified, case–crossover study design, we could not fully exclude residual confounding, especially from time-varying, individual risk factors (such as emotional shock and strenuous exercise).

Conclusion

Acute exposure to ambient air pollution was associated with increased risks of symptomatic arrhythmia. The risks occurred during the first several hours after exposure but attenuated greatly after 24 hours. The exposure–response relationships were, in general, approximately linear without discernable thresholds of concentrations of air pollutants, but the magnitude varied by type of air pollutant, arrhythmia subtype, subpopulation and geographic or seasonal features. Our study adds to evidence of adverse cardiovascular effects of air pollution, highlighting the importance of further reducing exposure to air pollution and of prompt protection of susceptible populations worldwide.

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What You Need To Know About Flavonoids - Health Essentials

You’ve probably heard the saying, “Add some color to your plate” when it comes to a healthy diet. 

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Well, if your body’s health was a vibrant tapestry, flavonoids would be just one of the many threads to choose from. These plant compounds can be found in everything from common grocery store fruits and veggies to flowers, herbs and spices. In fact, the chemical is what’s responsible for the bright color in many popular produce. 

Dietitian Bailey Flora, RDN, LD, explains what flavonoids are, their subgroups and how your body may benefit from them. 

What are flavonoids?

OK, back to high school biology for a second. Flavonoids are a type of phytochemical or plant chemical that are widely distributed in the plant kingdom. They create the vibrant colors of many fruits, vegetables and flowers, and have been found to have a variety of health benefits.

“Flavonoids aren’t really digested or absorbed the same as other nutrients like protein or carbohydrates,” explains Flora. Instead, our gut bacteria break down flavonoids and use them to benefit different parts of our bodies, such as providing antioxidant and anti-inflammatory properties.  

Flavonoids are further grouped into different subclasses based on their own chemical structure and how they’re broken down. This is why the type of flavonoid you’re getting will depend on the foods you’re eating. (More on that in a moment).

“The color of the food will actually give you a hint of what subgroup of flavonoid it is,” notes Flora. 

Benefits of flavonoids

Research has shown that flavonoids have a range of health benefits, including antioxidant, anti-inflammatory and anti-cancer properties. They’ve been linked to a reduced risk of chronic diseases such as cardiovascular disease, as well as improved cognitive function. 

Here are some of the known benefits of flavonoids:

Anti-carcinogenic properties 

A research study from 2011 found that flavonoids play an important role in fighting cancer. 

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According to Flora, flavonols — a type of flavonoid — can help with promoting the cell life cycle and even discouraging the growth in some cancers. 

Heart health

Your heart can benefit from a flavonoid-rich diet as well. Specifically, they’ve been shown to help with relieving symptoms of hypertension (high blood pressure). A 2021 study found an association between lower blood pressure and a higher intake of flavonoid-based foods like apples, berries and pears. This is largely why you’ll notice a lot of the flavonoid-rich fruits in the Mediterranean diet, which is known for benefiting your heart. 

“They do this by helping with blood vessel relaxation and preventing blood clots from forming,” states Flora. 

Brain health 

Flavonoids are also linked to promoting brain health, decreasing neuro-inflammation and improving blood flow to the brain. A 2022 review found that having a flavonoid-rich diet was associated with higher cognitive and memory function, especially for aging adults. 

How much do you need?

There isn’t any established recommended daily intake or daily value for flavonoids. But research suggests that a higher intake of flavonoids may have health benefits, and consuming a diet rich in flavonoid-containing foods is generally recommended for overall health and well-being. The amount of flavonoids needed in your diet will vary depending on individual factors such as your age, sex and overall health status. 

How to get flavonoids from food

The best way to get flavonoids into your system is directly from food and drink sources. Foods that are rich in flavonoids include berries, citrus fruits, tea, wine, onions and cocoa. 

Here’s what you should eat or incorporate into your diet based on some of the well-known subgroups of flavonoids: 

Anthocyanins 

Anthocyanins are the specific type of flavonoids that give most flowers their vibrant color — specifically those with a purple hue. Similarly, they’re found in the skin of most berries, thus giving them their shades of purple, pink and red. 

You can find these in foods like: 

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Flavanones 

High in antioxidant power, this flavonoid family holds stock over most citrus fruits you know and love. 

Find them in foods like: 

• Lemons.
• Limes.
• Grapefruit.
• Oranges.

Flavanols

These types of flavonoids are best known for having high antioxidant properties and can help with cardiovascular health. 

These can be found in foods like: 

Flavones

Along with being responsible for the vibrant pigments in blue and white flowers, flavones are mostly found in different types of herbs as well as some vegetables. So, when you’re looking to refill your spice rack again, look for the ones that are high in these types of flavonoids to get some of their anti-inflammatory benefits.

These can be found in ingredients like: 

Isoflavones

Finally, you can get isoflavones from your favorite soy products. Reach for recipes with tofu or edamame. 

Be careful with supplements

As you can see from the lengthy list above, you can get more than enough flavonoids from what’s in your fridge and pantry. While there are supplements out there touting to fill the gap for flavonoids, it’s better to stick to getting them through delicious dishes and recipes. 

“I always recommend choosing food over supplements,” advises Flora. “The more that you can include some of these plant-based flavonoids through dense foods, it’s just going to provide that extra benefit.”

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What You Need To Know About Flavonoids - Health Essentials
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‘Every joint, muscle, nerve started aching’: People share their struggles living with fibromyalgia - The Indian Express

In 2018, Hina Arora, a software engineer, experienced widespread pain in her neck and shoulders, which gradually spread throughout her body. The excruciating pain affected her daily activities, and was often accompanied by episodes of anxiety attacks, mood swings, and periods of feeling low, “which worsened during the menstrual cycle”. “All this, in the absence of any understanding and support from others, led me to feel extremely isolated,” she told indianexpress.com.

Eventually, she joined physiotherapy sessions, which provided some relief. She also incorporated exercise into her daily routine and tried to prioritise rest and self-care, which helped her manage her ailment, which was diagnosed as fibromyalgia.

Similarly, Arushi Lohiya, a marketing and branding consultant, developed fibromyalgia in 2015, after she felt intense headaches multiple times a day, which “incapacitated me”. “There was acute pain in my hip, which made it impossible for me to sit in one place. Subsequently, every joint, muscle, and nerve started aching and rendered me immobile. I had to quit my job as I was unable to perform even basic tasks like writing, brushing my teeth, and combing my hair,” she recollected.

However, her condition only made her stronger, and she decided to help others with the condition setting up India Fibromyalgia Foundation, which is dedicated to creating awareness and advocating for patients with the illness.

What is fibromyalgia?

According to a study published in the Dialogues in Clinical Neuroscience, fibromyalgia is characterised by chronic widespread pain, unrefreshing sleep, physical exhaustion, and cognitive difficulties. It occurs in all populations throughout the world with a prevalence between 2-4% in general populations.

Elucidating, Dr Ilavaran S, Orthopaedic Surgeon, Apollo Spectra Hospital, Chennai said that the brain and spinal cords of fibromyalgia patients change as a result of ongoing nerve stimulation. “This alteration entails an aberrant elevation of specific pain-signaling molecules in the brain. As a result, the brain’s pain receptors appear to form a kind of painful memory and grow more sensitive, causing them to overreact to both painful and nonpainful signals. An event that results in either physical stress or emotional (psychological) stress is frequently what sets off fibromyalgia,” he told indianexpress.com.

Along similar lines, Vishnu Priya Bhagirath, Counselling Psychologist said that the pain associated with fibromyalgia is often described as a deep, persistent ache that is accompanied by tenderness in specific points on the body known as “trigger points”. “Cognitive dysfunction or ‘fibro-fog’ can cause difficulty in concentrating, memory issues and trouble with word recall,” she said.

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Other factors which can lead to fibromyalgia are a family history of the condition, psychological stress and trauma, musculoskeletal conditions and fatigue.

However, Saumya Pahwa, Consultant Clinical Psychologist, said, “Fibromyalga is a contested diagnosis and many health professionals believe it does not exist as a true disease, and that it is in the patient’s minds, making it psychological or psycho-somatic in nature. ” She added that fibromyalgia is more commonly seen in women than men, possible due to the way both genders feel and react to pain as well as societal expectations. “It can also be triggered due to past trauma, abuse and domestic violence, especially in women,” she continued.

Adding to this, Vishnu Priya said, “One possible cause of fibromyalgia is abnormal pain processing in the brain and spinal cord, which can result in an exaggerated response to pain signals.”

Diagnosis of fibromyalgia

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Even a modest amount of pressure on tender spots causes discomfort. (Source: Freepik)

Physicians typically rely on a combination of patient history, physical examination, and laboratory tests to make an accurate diagnosis.

“Typically, the disease is accompanied by 18 painful spots. Even a modest amount of pressure on tender spots causes discomfort. A doctor will use their fingertip to push the spots on the body to perform a tender point examination. They’ll use enough force and inquire as to whether the patient is in pain. They will also rule out associated conditions such as tension and migraine headaches, irritable bowel syndrome, restless leg syndrome, chronic fatigue, lupus and rheumatoid arthritis,” said Dr Ilavaran.

While there is no known cure for fibromyalgia, quality treatment can provide significant relief and remission from pain. This includes a combination of medication and lifestyle modifications such as:

*Get plenty of sleep: People with fibromyalgia frequently experience daytime fatigue and a drowsiness in the morning. One can improve sleeping patterns by avoiding coffee at night, keeping the room at a cool, comfortable temperature and turning off electronic devices before sleeping.

*Exercise regularly: Although fibromyalgia can make exercise challenging, maintaining an active lifestyle is an excellent way to manage the condition. One does not have to undertake strenuous activity. Start out by swimming, strolling or engaging in low-impact aerobics, and gradually increase the length and intensity of the workouts.

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*Medications: Pain relievers such as acetaminophen, ibuprofen and antidepressants like Duloxetine have been shown to be helpful. Anti-seizure medications such as Gabapentin are known to bring relief in some patients.

*Therapies: Physical therapy which included exercises to condition and strengthen muscle groups, occupational therapy and psychotherapy such as cognitive behavioral therapy helps with mental health.

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*Self-care strategies: A healthy diet, meditation and yoga can help.

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‘Every joint, muscle, nerve started aching’: People share their struggles living with fibromyalgia - The Indian Express
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