Monday 28 February 2022

Diminished activation of specific prefrontal brain region may directly contribute to binge eating in bulimia nervosa

 New research conducted by an investigator from the Icahn School of Medicine at Mount Sinai has revealed a key neural mechanism underlying the feeling of being unable to stop eating, the most salient aspect of binge episodes in eating disorders like bulimia nervosa.

The researcher found deficient activation of the medial and lateral prefrontal cortices (brain regions known to play a role in the control of cravings, behaviors, and emotions) during eating-specific response inhibition in participants with bulimia nervosa compared with healthy controls. The findings, published February 25 in Psychological Medicine, provide initial evidence that this dimished activation of the prefrontal cortex may directly contribute to more severe, out-of-control, maladaptive eating behaviorsThis supports the idea that medial and lateral prefrontal cortex dysfunction may be a promising treatment target.

Bulimia nervosa is a serious, common psychiatric disorder that is associated with high rates of disability and mortality. Fewer than half of adults treated with first-line interventions recover. The neural bases of bulimia nervosa's symptoms remain poorly understood, hindering efforts to develop more efficacious treatments. Decades of previous research suggest that the sense of a loss of control over eating is the most important feature of the binge eating that characterizes the disorder. Therefore, pinpointing the brain-based alterations that occur specifically during attempts to control eating could ultimately improve our understanding of, and targeted treatment for, this often chronic condition.

This study, led by Laura Berner, PhD, Assistant Professor of Psychiatry at Icahn Mount Sinai and a leading investigator in the Mount Sinai Center of Excellence in Eating and Weight Disorders and the Center for Computational Psychiatry, is the first to examine brain activation during attempts to control eating behavior in individuals with eating disorders.

Most studies of how we stop or prevent ourselves from engaging in a behavior ask people to perform a task that involves withholding button-pressing responses. But Dr. Berner developed a new task that asks people to withhold eating responses. Using a portable brain imaging technology called functional near-infrared spectroscopy (fNIRS), the research team measured activation of the prefrontal cortices of 23 women with bulimia nervosa (BN) and 23 healthy controls during this novel go/no-go task requiring inhibition of eating responses and during a standard go/no-go task requiring inhibition of button-pressing responses.

They found women with BN made commission errors on both tasks -- they ate and pressed the button when they were not supposed to -- more often than women without an eating disorder. Coupled with this reduced ability to control their eating responses, the subsets of women with BN who had the most severe sense of loss of control over their eating in the last month, and those who felt most strongly that they binge-ate during the task, both showed abnormally reduced bilateral ventromedial (vmPFC) and right ventrolateral prefrontal cortex (vlPFC) activation during eating-response inhibition. Similarly, in the entire sample, lower eating-task activation in right vlPFC was related to more frequent and severe loss-of-control eating, but no group differences in activation were detected on either task when this full sample was compared with healthy controls. Notably, BN diagnosis and severity were unrelated to brain activation during button-pressing inhibition.


Source: ScienceDaily

Sunday 27 February 2022

Singing in the brain

 For the first time, MIT neuroscientists have identified a population of neurons in the human brain that lights up when we hear singing, but not other types of music.

These neurons, found in the auditory cortex, appear to respond to the specific combination of voice and music, but not to either regular speech or instrumental music. Exactly what they are doing is unknown and will require more work to uncover, the researchers say.

"The work provides evidence for relatively fine-grained segregation of function within the auditory cortex, in a way that aligns with an intuitive distinction within music," says Sam Norman-Haignere, a former MIT postdoc who is now an assistant professor of neuroscience at the University of Rochester Medical Center.

The work builds on a 2015 study in which the same research team used functional magnetic resonance imaging (fMRI) to identify a population of neurons in the brain's auditory cortex that responds specifically to music. In the new work, the researchers used recordings of electrical activity taken at the surface of the brain, which gave them much more precise information than fMRI.

"There's one population of neurons that responds to singing, and then very nearby is another population of neurons that responds broadly to lots of music. At the scale of fMRI, they're so close that you can't disentangle them, but with intracranial recordings, we get additional resolution, and that's what we believe allowed us to pick them apart," says Norman-Haignere.

Norman-Haignere is the lead author of the study, which appears today in the journal Current Biology. Josh McDermott, an associate professor of brain and cognitive sciences, and Nancy Kanwisher, the Walter A. Rosenblith Professor of Cognitive Neuroscience, both members of MIT's McGovern Institute for Brain Research and Center for Brains, Minds and Machines (CBMM), are the senior authors of the study.

Neural recordings

In their 2015 study, the researchers used fMRI to scan the brains of participants as they listened to a collection of 165 sounds, including different types of speech and music, as well as everyday sounds such as finger tapping or a dog barking. For that study, the researchers devised a novel method of analyzing the fMRI data, which allowed them to identify six neural populations with different response patterns, including the music-selective population and another population that responds selectively to speech.

In the new study, the researchers hoped to obtain higher-resolution data using a technique known as electrocorticography (ECoG), which allows electrical activity to be recorded by electrodes placed inside the skull. This offers a much more precise picture of electrical activity in the brain compared to fMRI, which measures blood flow in the brain as a proxy of neuron activity.

"With most of the methods in human cognitive neuroscience, you can't see the neural representations," Kanwisher says. "Most of the kind of data we can collect can tell us that here's a piece of brain that does something, but that's pretty limited. We want to know what's represented in there."

Electrocorticography cannot be typically be performed in humans because it is an invasive procedure, but it is often used to monitor patients with epilepsy who are about to undergo surgery to treat their seizures. Patients are monitored over several days so that doctors can determine where their seizures are originating before operating. During that time, if patients agree, they can participate in studies that involve measuring their brain activity while performing certain tasks. For this study, the MIT team was able to gather data from 15 participants over several years.

For those participants, the researchers played the same set of 165 sounds that they used in the earlier fMRI study. The location of each patient's electrodes was determined by their surgeons, so some did not pick up any responses to auditory input, but many did. Using a novel statistical analysis that they developed, the researchers were able to infer the types of neural populations that produced the data that were recorded by each electrode.

"When we applied this method to this data set, this neural response pattern popped out that only responded to singing," Norman-Haignere says. "This was a finding we really didn't expect, so it very much justifies the whole point of the approach, which is to reveal potentially novel things you might not think to look for."

That song-specific population of neurons had very weak responses to either speech or instrumental music, and therefore is distinct from the music- and speech-selective populations identified in their 2015 study.

Music in the brain

In the second part of their study, the researchers devised a mathematical method to combine the data from the intracranial recordings with the fMRI data from their 2015 study. Because fMRI can cover a much larger portion of the brain, this allowed them to determine more precisely the locations of the neural populations that respond to singing.

Source: ScienceDaily

Saturday 26 February 2022

Potential dangers of increased melatonin use for sleep

 

  • A good night’s sleep is essential for good physical health, cognitive performance, and emotional functioning. Numerous sleep studies have documented these facts over time.
  • More and more adults are taking over-the-counter (OTC) melatonin preparations to get a better night’s rest, but some of them may be taking this substance at dangerously high levels, a new study finds.
  • Experts worry that the coronavirus pandemic’s negative effect on sleep has further increased the reliance on melatonin and other sleeping aids.

In the recent study, researchers obtained data from ten cycles of the National Health and Nutrition Examination Survey (NHANES)Trusted Source, covering the years 1999 through 2018. This study included 55,021 adults, 52% of whom were women. The participants had a mean age of 47.5 years.

The results showed that in 2018, adults in the United States took more than twice the amount of this sleep aid than they did a decade earlier, which may pose a health risk in some individuals.

The study revealed that melatonin use increased from 0.4% in 1999–2000 to 2.1% in 2017–2018, with the increase beginning in 2009–2010.

The study evaluated adults who took melatonin at the recommended dosage of 5 milligrams per day (mg/d), as well as those who exceeded that dosage. Before 2005–2006, the authors found that users did not report taking more than 5 mg/d, but the prevalence of taking more than 5 mg/d went from 0.08% in 2005–2006 to 0.28% in 2017–2018.

Although the overall use of melatonin in the U.S. is still relatively low, the study does “document a significant many-fold increase in melatonin use in the past few years,” according to sleep specialist Rebecca Robbins, Ph.D., who is an instructor in the division of sleep medicine at Harvard Medical School and was not involved in this study.

The body’s biological clock regulates hormonal fluctuations, which evolve over a person’s lifespan. As a result, aging often affects activities such as sleep and wake patterns, which, in some cases, become increasingly disrupted and fragmented.

Melatonin is a key hormone that governs the body’s circadian rhythms. Circadian rhythms play an influential role in certain aspects of our bodily functions and behaviors. They also play a significant part in sleep regulation and overall good health in humans, and their disruption can have numerous consequences.

The negative consequences of sleep deprivation can includeTrusted Source lower vigor, a less positive mood, and feeling stressed, cold, or sleepy. These effects can occur in people of any age.

Source: Medical News Today

Friday 25 February 2022

Drug industry undermining WHO plans for vaccine manufacture in Africa

 

  • The World Health Organization (WHO) has created a technology transfer hub in South Africa to produce and distribute COVID-19 vaccines, and vaccines for other diseases in the future, throughout the continent.
  • This is a response to the vast disparity in vaccine distribution between the Global North and the Global South.
  • However, a consultancy hired by the vaccine manufacturer BioNTech has been lobbying against the WHO’s venture.

Since June 2021, the WHO has been coordinating a messenger ribonucleic acid (mRNA) vaccine technology transfer hub in South Africa.

The hub is important because it will increase the availability of mRNA vaccines, including those for COVID-19, in Africa, which currently has access to very few vaccines, compared with areas of the Global North.

In a new investigation, the journalBMJTrusted Source has revealed that a consultancy hired by the vaccine manufacturer BioNTech has attempted to undermine the new mRNA hub by lobbying the South African government against the venture.

The WHO’s technology transfer hub aims to use publicly available information about Moderna’s mRNA COVID-19 vaccine to develop a similar vaccine that could be more cheaply and quickly distributed throughout Africa.

The hub is supported by the Africa Centres for Disease Control and Prevention, the Medicines Patent Pool, and the South Africa Medical Research Council. The vaccine would be manufactured by the South African companies Afrigen Biologics and the Biovac Institute.

Medical News Today spoke with Prof. David Walwyn, at the University of Pretoria’s Graduate School of Technology Management, in South Africa. Prof. Walwyn told us more about the significance of the WHO’s technology transfer hub.

“The hub will develop generic mRNA vaccines for local manufacture. If the initiative is successful, it will improve vaccine access and lower the cost of critical vaccines in the region.”

“This is very important. Vaccines are essential to public health programs, bringing highly cost effective treatments for infectious diseases into widespread use. At present, these novel vaccines are covered by patents, and there are no generic equivalents. As a result, they are available in limited quantities and at high cost.”

“In other words, [they are] out of the reach of countries in the Global South which do not have manufacturing capability or access to alternative vaccine types,” said Prof. Walwyn.

Dr. Tedros Adhanom Ghebreyesus, WHO director-general, explainsTrusted Source that the technology transfer hub “is great news, particularly for Africa, which has the least access to vaccines. COVID-19 has highlighted the importance of local production to address health emergencies, strengthen regional health security, and expand sustainable access to health products.”

Source: Medical News Today

Thursday 24 February 2022

How does COVID-19 affect the heart?

 

  • A new study takes a close look at the incidence of heart problems after COVID-19.
  • The researchers find evidence of a wide range of heart issues for up to 1 year after recovery.
  • Experts recommend that people who have had COVID-19 remain alert for symptoms of heart issues, promptly consulting a doctor if these occur.

Scientists are confident that COVID-19 can cause heart damage. Based on an analysis of national healthcare databases from the United States Department of Veterans Affairs, a new study offers a more detailed look at common post-COVID-19 cardiac issues.

The study found that people who have recovered from COVID-19 are at an elevated risk of developing heart problems within the first year after the disease.

University of California, Los Angeles cardiologist Dr. Gregg C. Fonarow — who was not involved in the study — told Medical News Today, “There was a large spectrum of cardiovascular injury and risks documented.”

The study comes from researchers at Washington University School of Medicine in St. Louis and the Veterans Affairs (VA) St. Louis Health Care System.

The senior investigator is Dr. Ziyad Al-Aly, chief of research and development service at the VA St. Louis Health Care System and clinical epidemiologist at Washington University.

“What we’re seeing isn’t good,” Dr. Al-Aly says. “COVID-19 can lead to serious cardiovascular complications and death. The heart does not regenerate or easily mend after heart damage. These are diseases that will affect people for a lifetime.”

Dr. Al-Aly described to MNT the types of heart damage known to occur after a SARS-CoV-2 infection:

“A broad array of cardiovascular diseases, including cerebrovascular disease, dysrhythmias, ischemic and nonischemic heart disease, pericarditis, myocarditis, heart failure, and thromboembolic disease. The risks were evident even in people who had mild COVID-19 and did not need to be hospitalized during the acute phase of the ​disease.”

It also appears to be the case, Dr. Al-Aly observes, that COVID-19 does not play favorites when it comes to who might experience postinfection heart problems,

“I would also add that the risks were evident in young [people and older adults], females and males, white people and Black people, people who smoke and people who do not, people with comorbidities — diabetes, hypertension, kidney disease — and people without.”

Source: Medical News Today

Wednesday 23 February 2022

Long COVID: Risk factors and how to mitigate them

 After recovering from COVID-19, many experience long-term symptoms, including brain fog, fatigue, and skin rashes. This syndrome is known as long COVID, and researchers are in the early stages of understanding its risk factors.

According to the Centers for Disease Control and Prevention (CDC)Trusted Source, long COVID is a condition in which COVID-19-related health issues last 4 weeks or more after contracting the virus that causes the disease.

Even those who did not have COVID-19 symptoms immediately after contracting SARS-CoV-2 can develop long COVID. Symptoms may last for several weeks or months.

Research suggests that at least 54%Trusted Source of those who develop COVID-19 experience long COVID. According to a 2021 meta-analysisTrusted Source, the most common outcomes and symptoms among those with long COVID include:

  • chest imaging abnormalities for 62.2% of people
  • general functional impairments for 44%
  • fatigue or muscle weakness for 37.5%
  • general pain for 32.4%
  • generalized anxiety disorder for 29.6%
  • sleep disorders for 27%
  • difficulty concentrating for 23.8%

Other symptoms include:

  • brain fog
  • headache
  • skin rashes
  • fever
  • changes to the sense of smell or taste
  • diarrhea

Research is emerging on risk factors for long COVID. To help parse through these studies, MNT has summarized some of the main findings so far. We also spoke with three experts on the best ways to mitigate the risk factors for long COVID.

One studyTrusted Source that followed 309 participants for 2–3 months after contracting SARS-CoV-2 identified four factors that increase a person’s risk of long COVID:

  • a higher viral load
  • the presence of certain autoantibodies that mistakenly attack the body’s own tissues
  • reactivation of the Epstein-Barr virus (EBV)
  • having type 2 diabetes

However, the study authors noted that their research might not be conclusive as they could not confirm causation, and their sample size makes it difficult to establish any specific predictors.

Nevertheless, other studies support their findings. One studyTrusted Source found that SARS-CoV-2 may reactivate EBV and, in turn, lead to long COVID symptoms. Around 95%Trusted Source of the world’s population carries this virus, although EBV largely lays dormant and is asymptomatic.

Another study found that older age, being female, and having preexisting health conditions were also linked to long COVID.

“Clinical risk factors are largely related to the severity of illness, duration of hospitalization, age at the time of infection, and preexisting comorbidities, such as lung disease, asthma, diabetes, etc.,” Prof. Elizabeta Mukaetova-Ladinska, a professor of psychiatry of old age at the University of Leicester in the United Kingdom, told Medical News Today.

“Thus, the severity of the SARS-CoV-2 infection can increase the risk for long COVID by nearly fourfold, preexisting lung disease and asthma increase the likelihood [by] six- [and] nearly 10-fold, respectively, whereas age increases the risk by 67%,” she added.

“In addition, female sex and age under 50 years are now also acknowledged as risk factorsTrusted Source for long COVID. The latter is of importance, since [there] appears to be some overlap of symptoms of long COVID with those of perimenopause and menopause,” she explained.

Prof. Mukaetova-Ladinska further explained that lower levels of immunoglobulin (Ig) antibodies IgM and IgG3Trusted Source, when combined with clinical risk factors, may also increase a person’s risk of developing long COVID.

She also said that researchTrusted Source suggests a link between alterations to the gut microbiome and long COVID: “Namely, COVID-19 patients with healthy gut bacteria and a microbiome similar to [that of a healthy person] appear to be less likely to develop long COVID, whereas those COVID patients who develop long COVID have a less diverse and abundant microbiome.”

Source: Medical News Today

Tuesday 22 February 2022

Dementia: Frequent loneliness may raise risk

 

  • Studies suggesting an association between loneliness and increased risk of dementia have produced inconsistent results.
  • A new study following dementia-free individuals over 10 years shows that people who felt lonely 3 or more days a week were more likely to develop dementia during the follow-up period.
  • Individuals under the age of 80 years and without known genetic risk factors who experienced frequent loneliness were at elevated risk of developing dementia.
  • Loneliness was also linked to poor executive function and brain changes associated with vulnerability to dementia in individuals who did not have the condition.
  • This study highlights the importance of screening for loneliness in routine clinical care and measures to reduce loneliness.

Experiencing feelings of loneliness three or more times a week may increase the risk of developing dementia later in life, according to a recent study in the journal Neurology.

The study showed that individuals experiencing loneliness, who were otherwise at lower risk of dementia due to genetic risk factors and age, had a threefold higher risk of developing dementia.

The study’s first author Dr. Joel Salinas, a neurologist at New York University Langone Health, told Medical News Today: ”[This study] provides Class I level of evidence (the highest level available) that lonely adults, especially those without major age or genetic risk factors, may have an elevated risk and early neurocognitive vulnerability for developing dementia. This magnifies the population health implications of observed trends in the growing prevalence of loneliness.”

The APOE e4 allele, known as apolipoprotein E, is a fat-binding protein involved in the metabolism of fat and glucose regulation. The allele has a major effect on the progression of age-associated diseases, including Alzheimer’s disease (AD), by influencingTrusted Source the brain function pathways.

Even before the COVID-19 pandemic, loneliness was prevalent in the United States. A 2018 survey reports that more than 1 in 5 individuals in the U.S. frequently experienced feelings of loneliness and social isolation. The COVID-19 pandemic has been accompanied by a further riseTrusted Source in the prevalence of loneliness.

Moreover, feelings of loneliness are especially common in older individuals over the age of 60 years, with estimates ranging from 13% to 43%.

“Older people are at a heightened risk of loneliness due to dwindling networks as friends and family die, they live alone or move to an aged care facility where they may be unable to connect to many residents due to communication challenges as a result of dementia. This may result in social isolation, or they may feel lonely,” Dr. Wendy Moyle, the program director of the Healthcare Practice and Survivorship Program at Griffith University, Brisbane, Australia, explained to MNT.

Loneliness can have adverse effects on health and is associated with an increased risk of cardiovascular diseases and all-cause mortalityTrusted Source.

Although some previous studies have shown that loneliness is associated with an increased risk of cognitive decline and dementia, other studies have reported an absence of such an association.

Moreover, whether loneliness causes dementia or is a symptom of these conditions is not understood.

The present study examined the association between loneliness and dementia. To further enhance the understanding of the impact of loneliness on cognitive function, the researchers used data collected from a large sample of dementia-free individuals who were rigorously monitored for dementia over a long follow-up period of 10 years.

Specifically, the researchers obtained data from the Framingham Study, a population-based longitudinal study initiated in 1948 to understand the multigenerational patterns of cardiovascular and other diseases.

To understand the potential role of loneliness in causing dementia, the researchers also examined the association between loneliness and early indicators that precede the clinical symptoms of dementia. To that end, the researchers examined the association between loneliness and early cognitive and brain imaging markers of dementia in healthy individuals.

To examine the potential impact of loneliness on cognitive decline and dementia, the researchers analyzed data from 2,308 individuals enrolled in the Framingham Study.

The study included participants attending the study site for recurrent clinical examinations as a part of the Framingham study between 1997 and 2001. These participants were aged 40–79 years and did not have dementia at the time of the clinical examination, i.e., at baseline.

The participants were rigorously monitored over the 10-year follow-up period for the incidence of dementia.

To understand the relationship between loneliness and dementia, the researchers only included participants aged 60 years and older. They excluded younger participants due to the lower risk of dementia in individuals aged under 60 years.

During the 10-year follow-up period, 14% — 320 out of 2,308 — of the participants were diagnosed with dementia.

The researchers used the Center for Epidemiologic Studies Depression Scale, a standardized questionnaire, to assess the prevalence of loneliness at baseline. Individuals who reported feeling lonely at least 3 days in the week before the administration of this questionnaire were classified as being lonely.

The researchers found that 144 out of the 2,308 participants (6%) felt lonely for at least 3 days during the previous week. These participants who experienced frequent loneliness had an increased likelihood of developing dementia during the 10-year follow-up period than those who were not lonely.

The association between loneliness and increased risk of dementia was not significant in individuals aged 80 years and older. Moreover, participants under 80 years who experienced loneliness were twice as likely as their counterparts who were not lonely to develop dementia.

The researchers also examined the influence of genetic risk factors on the association between loneliness and the risk of dementia. Individuals carrying a specific allele or version of the apolipoprotein E gene (APOE ε4)Trusted Source are at increased risk of dementia.

Among participants aged under 80 years who did not possess the APOE ε4 gene, loneliness was associated with a three-fold increase in the risk of dementia.

The weaker association between loneliness and risk of dementia in individuals carrying the APOE ε4 gene and those older than 79 years may be due to genetic factors and age-associated factors playing a more prominent role in causing dementia in these individuals.

Previous studies have shown that changes in cognitive function and structural changes in the brain precede the manifestation of the clinical symptoms of Alzheimer’s disease and related dementias (ADRD)Trusted Source.

In the present study, the researchers investigated the association between loneliness and early cognitive and brain imaging indicators of ADRD in a subset of 1875 participants aged 40 to 79 years.

Based on cognitive tests conducted at baseline, the researchers found that loneliness was associated with poor executive functionTrusted Source, which includes higher-level cognitive processes such as decision making, planning, and reasoning.

The researchers used brain MRI scans conducted at baseline to measure brain volume and damage to white matter, which consists of nerve fibers or axons.

The researchers found that loneliness was associated with greater white matter injuryTrusted Source and lower brain volume, which are early markers of dementia.

In sum, these results suggest an association between loneliness and early cognitive and brain imaging indicators of vulnerability to dementia in adults aged under 80 years. In other words, this indicates that loneliness may be involved during the early stages of cognitive decline and may thus potentially contribute to dementia.

The authors also noted that the 10-year follow-up period in the study was longer than that required for dementia to develop in individuals with mild cognitive impairment or other related symptoms. This may suggest that loneliness assessed at baseline, instead of being an early symptom of cognitive decline, likely contributed to the decline in cognitive function.

Due to the observational nature of the present study, these results do not establish whether loneliness is a cause or symptom of dementia. Yet, the potential role of loneliness in increasing the risk of dementia highlights the importance of screening individuals for loneliness and interventions to tackle loneliness.

Dr. Moyle said: “This study supports the earlier studies showing the relationship between loneliness and risk of dementia. However, it is no clearer whether loneliness is an early symptom of dementia or an early contributor to cognitive decline and neuropathology. Perhaps until we can identify very early indicators of dementia, we will not be able to address this question.”

“Either way, we need to understand how to manage and reduce the incidence of loneliness in society. This is essential given the incidence of loneliness, according to research, is increasing in older populations. Although loneliness overlaps with social isolation, it is a distinct feeling; one can be socially isolated and not feel the distressing feeling of loneliness. Lonely people can feel lonely even when they are surrounded by hundreds of well-meaning people. It is this that makes loneliness so difficult to manage. Further research on management strategies to address loneliness in older adults is needed,” added Dr. Moyle.

Similarly, Dr. Andrew Steptoe, Professor of Psychology and Epidemiology at University College London, told MNT: “Two issues are unresolved. The first is whether loneliness is a genuine causal factor in the development of dementia, or whether it is an early indicator of degeneration in the brain that will progress to dementia over time.”

Source: Medical News Today

Monday 21 February 2022

What do we know about microplastics in food?

 Most of the plastics produced globally are used for food and beverage packaging. During its use, however, plastic becomes worn and breaks into small fragments called microplastics. In this Honest Nutrition Feature, we explain the potential dangers of microplastics, how food becomes contaminated with them, and ways to reduce exposure.

Globally, 322 millionTrusted Source metric tons of plastics were produced in 2016, of which 60%Trusted Source supplied the food and beverage industry for food packaging. These plastics contain an array of chemicals, including stabilizers, lubricants, fillers, and plasticizers.

Exposure to some environmental conditions, such as heat, causes plastic to break into smaller fragments called microplastics, which can migrate into food.

Single-use water bottles, to-go containers, food cans, and storage wraps are examples of common plastic-based food packaging that contains microplastics.

Heating food in plastic packaging, long storage times, and the type of plastic packaging a person uses all affectTrusted Source the amount of the microplastics and their harmful chemicals that migrates into food.

The microplastic chemicals present in food are a mixtureTrusted Source of those that manufacturers deliberately add, such as fillers and stabilizers, and those that accumulate as byproducts, such as residues and impurities.

Some common microplastics present in food include:

  • bisphenol A (BPA): Manufacturers useTrusted Source this plasticizer to make polyvinyl chloride, the “parent” plastic of many products.
  • dioxin: This is a byproductTrusted Source of herbicides and paper bleaching, which contaminate the environment.
  • phthalatesTrusted Source: These make plastics more flexible, transparent, and durable and are present in many types of food packaging.
  • polyethylene and polypropylene: These make packaging lightweight and durable and are the most commonTrusted Source plastics present in food and the environment.

Microplastics found in smaller quantities in food include BPA and BPF, mono-(3-carboxypropyl), mono-(carboxyisononyl), and mono-(carboxyisoctyl).

Microplastics are the fragments of stabilizers, lubricants, fillers, plasticizers, and other chemicals that manufacturers use to give plastics their desirable propertiesTrusted Source, such as transparency, flexibility, and durability.

However, experts have classified many of these chemicals as toxic and harmful to human health.

Below, we discuss some of the dangers of microplastics in greater detail.

Disrupting hormones

Scientists consider at least 15Trusted Source of the chemicals manufacturers use to make plastic packaging to be endocrine disruptors.

Endocrine disruptors are structurally similarTrusted Source to some hormones in the body — such as estrogen, testosterone, and insulin — and mimic and disrupt their natural functions, leading to adverse health effects and increasing a person’s risk of chronic conditions.

In particular, research has shown that exposure to BPA plays a role in infertilityTrusted Source in males and females alike, as well as in the development of polycystic ovary syndromeTrusted Source.

BPA competes with estrogen and testosterone for their receptors, reducing the amount of these hormones available for reproductive health.

Increasing risk of chronic disease

Research continues to demonstrate that long-term exposure to endocrine-disrupting microplastics increases the risk of developing type 2 diabetesTrusted Source and heart disease.

Experts associate higher blood levels of dioxins, phthalates, and BPs with pre-disease states of inflammationTrusted Source, impaired fasting glucose, insulin resistance, and obesity, significantly elevating the likelihood of type 2 diabetes.

Some researchTrusted Source suggests that exposure to these microplastics in food causes as much harm to a person’s health and raises their risk of chronic conditions to the same degree as following an unbalanced diet.

Impairing immune health

2020 reviewTrusted Source found that the increased inflammation induced by exposure to microplastics leads to poor gut health and, by extension, weakened immunity.

The gut plays an important roleTrusted Source in immunity, with 70–80%Trusted Source of the body’s immune cells being in the gut. This means that any condition that affects gut health interferes with immune health as well.

Persistent exposure to microplastics in the gut is toxicTrusted Source to immune cells, causing dysbiosis — a disruption to the gut microbiota — and leading to an overgrowth of “bad” bacteria.

ResearchTrusted Source associates dysbiosis with the development of such conditions as Parkinson’s disease.

Moreover, the surface of microplastics may harbor harmful bacteria that further compromise immune health.

Source: Medical News Today