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Do vitamin D supplements reduce cancer, cardiovascular risk?

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A new study searches for links between vitamin D supplements, cancer, and heart disease. Raymond Forbes LLC/Stocksy
  • Initial research has suggested that vitamin D may reduce the risk of developing cardiovascular disease and cancer.
  • However, there have been few large, higher-quality randomized controlled trials (RCTs) to corroborate this.
  • A recent RCT examined the effects of vitamin D supplementation in Finland.
  • It found no association between vitamin D supplementation and reduced risk of cardiovascular disease or cancer.

Vitamin D helps the body absorb calcium, which improves bone strength. Among other roles, it also contributes to the functioning of muscles, nerves, and the immune system.

Many scientists have set out to understand how vitamin D deficiency and supplementation may influence disease. According to the World Health Organization (WHO), there is some evidence that vitamin D may help protect against respiratory tract infections, for example.

Over the past 2 years, researchers have also explored whether vitamin D reduces the risks associated with COVID-19. Although investigations are ongoing, there seems to be some evidence that these supplements might improve intensive care unit admission rates.

Two other areas of particular interest are vitamin D’s potential effects on cardiovascular disease and cancer risk. However, few RCTs have looked into this. These types of studies are the gold standard for identifying causal relationships in scientific research.

A recent study, which appears in The American Journal of Clinical Nutrition, goes some way toward addressing this knowledge gap.

Speaking with Medical News Today, Vimal Karani, a professor of nutrigenetics and nutrigenomics at the University of Reading, in the United Kingdom, confirmed that there has been a gap between the initial research and findings from clinical trials.

Prof. Karani was not involved in the recent study but has worked with some of its authors.

He explained that past large epidemiological studies “have established a link between vitamin D deficiency and the risk of [cardiovascular disease] traits in various ethnic groups.” This, he said, suggests that vitamin D supplements might lower cardiovascular risk.

“However,” he continued, “clinical trials have not provided convincing evidence of the blood pressure-lowering effect of vitamin D supplementation.”

Prof. Karani said that there could be a wide range of reasons for this, including “differences in the sample size, duration of supplementation, dose of the supplementation, age of the participants, geographical location, sun exposure, and the outcome measures. Further research is required to replicate the findings in multiple ethnic groups.”

To provide further evidence of the relationship between vitamin D, cardiovascular disease, and cancer, the researchers behind the present study conducted the Finnish Vitamin D Trial.

This took place between 2012 and 2018, and it was double-blind, randomized, and placebo-controlled.

“When we started to plan the trial, there was a lot of evidence from observational studies that vitamin D deficiency would be associated with nearly all major chronic diseases, such as [cardiovascular disease], cancer, type 2 diabetes, and also mortality,” said Dr. Jyrki Virtanen in an interview with Medical News Today.

Dr. Virtanen is an associate professor of nutrition and public health at the University of Eastern Finland, and a co-principal investigator of the study.

“Also, we had shown that among [the] Eastern Finnish population, low vitamin D content of the body was associated with higher risk of mortality and glucose metabolism disturbances. However, these kinds of studies do not give evidence for causality.”

“At that time, there was little evidence from RCTs that improvement of [the] vitamin D status of the body with vitamin D supplementation reduced the risk of diseases.”

“Therefore, our aim was to start a long-term vitamin D supplementation trial in Finland, where vitamin D insufficiency had been quite prevalent due to the long winter, and investigate whether vitamin D supplementation could reduce the risk of major chronic diseases and death.”

The researchers looked at data from 2,495 people, including male participants 60 years or older and female participants who were postmenopausal and 65 years or older. The participants also had no history of cardiovascular disease or cancer.

The participants either took a placebo, vitamin D at a dosage of 1,600 international units (IU) each day, or vitamin D at a dosage of 3,200 IU each day.

Compared with the placebo, neither dosage of vitamin D reduced the incidence of cardiovascular disease or cancer in this cohort, the team determined.

One factor that complicated this analysis was that the participants tended to have high levels of vitamin D at the start of the study. This, the authors believe, stems from the implementation of policies to fortify foods with vitamin D in Finland, which began in 2003–2011.

“It is likely that vitamin D supplementation does not provide major health benefits, especially in populations where the vitamin D situation is already good at the start of the trial.”

– Dr. Jyrki Virtanen

“A ‘problem’ with most large vitamin D supplementation trials has been that the starting levels of vitamin D have been pretty high in a large part of the study populations,” explained Dr. Virtanen.

“This may reflect the well-known fact that people who take part in these kinds of studies tend to be more health-conscious and more interested in their health, so they are, on average, healthier than the average population.”

“They may have a better diet and are more likely to take supplements and exercise, which all are associated also with higher serum vitamin D levels,” he told MNT.

“Those who might benefit from the vitamin D supplementation — i.e., those with low serum vitamin D levels — are a small minority in the trials. It is tricky to target this deficient population, though, because for ethical reasons it would not be possible to screen people and only admit people with low vitamin D levels in the trial. It would not be ethical to keep a part of the study population, the placebo group, deficient [in] vitamin D for several years.”

MNT spoke with Prof. Sean Strain, Dr. Emeir McSorley, and Dr. Pamela Magee, of the Nutrition Innovation Centre for Food and Health, at Ulster University, in Northern Ireland.

They explained that despite the low recruitment levels — the study authors had hoped to recruit 30,000 participants — the results showed some signs that vitamin D had health benefits.

“Even though recruitment was challenging and didn’t meet expectations, there is some indication that the cohort investigated had lower incidence of both [cardiovascular disease] and cancer, compared to national statistics, which would have been gathered prefortification.”

“This may indicate that improvements to vitamin D status nationally are having benefits to the overall health of the population over and above the well-known bone and muscle health effects. Because of the low numbers recruited, the cohort may not be nationally representative, and care should be taken when interpreting these findings,” said the scientists.

According to Prof. Karani: “The unique feature of this RCT was the use of two different vitamin D doses to see the dose-response effect over a period of 5 years. Despite the large doses, the study failed to see any effect of the supplementation on lowering the incidence of [cardiovascular disease] and cancer.”

“The findings have significant public health implications,” continued Prof. Karani. “However, the findings cannot be generalized to other populations, given that [the] Finnish population is a well-known example of an isolated population, where multiple bottlenecks resulting from consecutive founder effects have led to the gene pool of current-day Finns.”

Dr. Virtanen said that while there is some evidence of broader health benefits from vitamin D supplementation, there were also conflicting findings.

“At the moment, there is no consensus [about] what would be the optimal vitamin D intake and [whether it is] the same for all health outcomes and for all people. For example, there is some evidence that high-dose vitamin D supplementation may modestly reduce the risk of cancer death, but not overall cancer incidence.”

“And although there, so far, is no evidence that vitamin D supplementation could prevent [SARS-CoV-2] infection, it is well-documented that those, especially with the severe form of COVID-19, have low serum vitamin D levels.”

“It is also possible that this is a consequence of the [SARS-CoV-2] infection rather than the cause, because it is known that acute infection leads to lower serum vitamin D levels, and many of the COVID-19 patients are overweight or obese or have a chronic disease like type 2 diabetes, which all are associated with lower serum vitamin D levels,” explained Dr. Virtanen.

Prof. Strain, Dr. McSorley, and Dr. Magee highlighted the role that vitamin D may play in a healthy immune system.

“There is recent strong evidence that vitamin D supports your immune system, and given the global pandemic, it does appear that those who are vitamin D replete don’t have as severe a response to COVID-19 as those who are deficient — and importantly, recover quicker.”

“Vitamin D plays a key role in musculoskeletal health. Vitamin D can be obtained via sunlight and dietary sources. However, a vitamin D supplement may be required to meet the recommended dietary intakes — that is, 600 IU per day in the United States for those aged 1–70 years, and 800 IU per day for those over 70 years — in order to maintain a sufficient status.”

“Supplementation may be particularly relevant in populations residing at northerly latitudes, where vitamin D cannot be synthesized from sunlight during the winter months, and in populations that spend little time outdoors and/or obtain limited amounts of vitamin D from food sources.”

“It is very difficult to obtain vitamin D from food intake alone, unless that food is fortified with vitamin D. Furthermore, those with illnesses that affect vitamin D absorption may require vitamin D supplementation,” said the scientists.

Prof. Strain, Dr. McSorley, and Dr. Magee suggested that the research could be developed by studying a population with low levels of vitamin D.

“This research needs to be undertaken in a suitable population, where many have a low vitamin D status and can therefore benefit from vitamin D supplementation.”

“It would be important to explore whether vitamin D supplementation can decrease the incidence of [cardiovascular disease] and cancers, as that would make a strong case for mandatory vitamin D fortification or promotion of fortified foods in the population.”

“There is some tantalizing evidence that the Finnish national [vitamin D] fortification program is having benefits by decreasing the incidence of [cardiovascular disease] and cancers, as well as the expected beneficial effects on bone health.”

“Another very important area that needs to be explored further is the link between sufficient vitamin D status and a fully functional immune system, especially in light of the current COVID-19 pandemic.”

As Prof. Karani notes, “A similar RCT with a longer duration of vitamin D supplementation is highly warranted in ethnically diverse populations to see if the findings from the present study could be generalized.”

Dr. Virtanen told MNT that his current focus is on further analyzing the results from the Finnish Vitamin D Trial.

“At the moment, we don’t have plans to start another vitamin D trial, but we are of course going to publish several other results from the Finnish Vitamin D Trial, for example effects [on] heart arrhythmias, infections, type 2 diabetes, falls and fractures, pain, [and] mood changes.”

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Covid May Raise the Risk of Diabetes in Children, Study Says

Children who have recovered from Covid-19 seem to be at appreciably improved risk of developing Form 1 or Kind 2 diabetic issues, scientists at the Facilities for Disorder Manage and Prevention documented on Friday.

A heightened risk of diabetic issues has now been seen among grown ups who recovered from Covid, in accordance to some scientific tests. Researchers in Europe have described an boost in the variety of youngsters being diagnosed with Sort 1 diabetic issues due to the fact the pandemic commenced.

But the C.D.C. review is among the initial to look at huge coverage declare databases in the United States to estimate the prevalence of new diabetes diagnoses in children underneath age 18 who experienced Covid or were being acknowledged to be contaminated with the coronavirus.

The analyze employed two claim databases from U.S. health and fitness strategies to look at diabetes diagnoses created in youngsters underneath 18 more than the program of a 12 months or more, starting up in March 1, 2020, comparing all those who experienced Covid with those people who did not.

The researchers observed improves in diabetes in both knowledge sets, though the relative premiums have been fairly diverse: they found a 2.6-fold raise in new diabetic issues instances between children in a single, and a scaled-down 30 p.c improve in a further.

“Even a 30 p.c increase is a major boost in hazard,” mentioned Sharon Saydah, a researcher at the C.D.C. and lead creator of the analyze. The differences likely end result from distinct methods of classifying children as owning Covid, she additional.

Dr. Saydah claimed it was not however crystal clear no matter if write-up-Covid diabetes would be a persistent affliction in these children, or a transient ailment that resolves. Most of the young children ended up only adopted about four and a 50 percent months.

The acquiring underscores the worth of vaccinating all eligible small children from Covid, she extra, and using steps like masking and distancing, primarily to guard the youngest, who cannot nevertheless be vaccinated.

“It’s genuinely important for clinicians, pediatricians and dad and mom to be mindful of the signs and indications of diabetes, so they can get their young children identified,” Dr. Saydah mentioned. Greater thirst, recurrent urination, accidental weight reduction and tiredness are between the telltale signs.

She pointed out that weight gain and sedentary behavior, which have elevated all through the pandemic, are also possibility components for diabetes.

Many of the young children in the examine ended up only diagnosed soon after getting an episode of diabetic ketoacidosis, a life-threatening complication that takes place when the entire body does not have ample insulin to enable blood sugar into cells to use for energy.

Dr. Saydah and her colleagues did not distinguish between kinds of diabetic issues, which include each Type 1 and Variety 2 in their analysis. The will increase ended up witnessed the two between all those who had been sick with Covid, and individuals who were being asymptomatic but analyzed positive.

A further study, also introduced on Friday by the C.D.C., located that two doses of the Pfizer-BioNTech vaccine secured hospitalized children concerning the ages of 12 and 18 from critical multisystem inflammatory syndrome, or MIS-C, which can establish two to 6 weeks immediately after an infection with the virus.

The examine looked at 24 hospitals in 20 states concerning July and Dec. 9, 2021, through the period of time when the Delta variant was dominant. It concluded that vaccination experienced an efficacy fee of 91 p.c from MIS-C, and pointed out that among the 38 hospitalized clients aged 12 to 18 who required life assist, all were unvaccinated.

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Does the Omicron variant increase risk of reinfection?

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A woman getting tested for COVID-19 at a mobile testing site at Times Square in New York City on December 6, 2021. Anadolu Agency/Getty Images
  • Omicron, which is the latest SARS-CoV-2 variant of concern, is spreading globally.
  • A South African study has found high rates of reinfection among those with previous confirmed SARS-CoV-2 infections since the beginning of November. This was when scientists discovered the Omicron variant there.
  • These observations suggest that Omicron can evade immunity from prior infection.

A preprint study from South Africa suggests that the Omicron variant of SARS-CoV-2 is more than three times as likely to reinfect people than previous variants.

This ability to evade immunity from prior infection may be causing its rapid spread.

For the study, which has not yet undergone peer review, researchers rapidly analyzed 2,796,982 confirmed SARS-CoV-2 cases in South Africa. All first infections had occurred at least 90 days before November 27, 2021.

The researchers identified primary infections and suspected repeat infections. They considered anyone who tested positive again more than 90 days after their first positive test to have a reinfection with SARS-CoV-2.

The team analyzed whether or not there were differences in reinfection risk during the first, second, and third waves. The second wave was dominated by the Beta variant, the third wave was dominated by the Delta variant, and experts assume that the Omicron variant has dominated reinfections since November 2021.

They judged a higher relative risk of reinfection among the population in any wave as indicating immune escape by the virus. Immune escape means that the virus can evade immunity acquired through either infection or vaccination.

Of the sample, 35,670 people (1.3{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809}) had two confirmed SARS-CoV-2 infections. There were peaks of reinfection in January and July 2021, which corresponded with the peak of waves two and three in South Africa, along with a spike in reinfections in November 2021, which corresponded with the detection of the Omicron variant there.

The researchers suggest that this means that Omicron can evade prior immunity. They call for in vitro studies to test this.

They also note that although in vitro studies for the Beta and Delta variants suggested that they could evade prior immunity more effectively than the original Alpha variant, their own analysis did not show this at a population level. This is because there was no increased risk of reinfection in either the second or third waves compared with the first.

The authors suggest that scientists need to design better experiments to determine the risk of immune escape in vitro.

Dr. Chris Coleman — an assistant professor of infection immunology at the University of Nottingham in the United Kingdom — told Medical News Today: “This is a clear sign that the new variant is escaping immune responses, as this is evading the ‘natural’ response — which may be more complex than vaccine-induced response.”

These findings may have implications for public health planning. For example, if Omicron is more transmissible and can evade immunity, the potential for spread is enormous. The authors question whether or not immune escape will mean that people are less protected against severe COVID-19.

Experts have noted that most Omicron infections have, so far, led to only mild symptoms, and there have been no recorded deaths yet. However, the ability of Omicron to reinfect is worrying.

Dr. Arturo Casadevall, Ph.D. — chair of the Molecular Microbiology & Immunology Department at Johns Hopkins Bloomberg School of Public Health in Baltimore — highlighted that concern.

He said: “These results imply that Omicron has changed so much relative to the other variants that prior COVID-19 immunity is not as protective. This finding is very concerning because it implies that whatever immunity was built up by prior COVID-19 is not sufficient to protect against Omicron.”

In speaking to the Science Media Centre, Prof. Paul Hunter — a professor of medicine at the Norwich School of Medicine in the U.K. — agreed.

“Unlike previous waves that were because the variants were intrinsically more infectious, Omicron appears to […] have substantial immune escape, at least from immunity caused by a natural infection. Whether Omicron is also more infectious is possible but cannot be answered by this analysis.”

– Prof. Paul Hunter

The authors point out that their study cannot answer the question about whether or not the current vaccines will be effective against Omicron. At the time of the study, vaccination levels in South Africa were very low.

However, experts believe that — as with other variants — even if vaccines do not prevent infection, they should prevent severe COVID-19 from Omicron.

The vaccination status of those with suspected reinfections in this study was not known.

“One key question, of course, is if this [increased risk of reinfection with Omicron] also applies to vaccinated individuals and, as they say, the public health implications (e.g., is the infection milder with reinfection?).”

– Dr. Chris Coleman

Dr. Casadevall stressed: “These findings heighten the concern that the same [immune escape] may happen in those vaccinated. Omicron is showing itself to be a very dangerous new variant with the potential to set back some of the progress we have made against COVID-19.”

So, until we have more data about Omicron, experts are clear that the priority is to get as many people vaccinated as possible.

Dr. Michael Head, Ph.D. — a senior research fellow in global health at the University of Southampton in the U.K. — told the Science Media Centre: “[While] we await more data to emerge over the coming days and weeks, the message to the general public has to be — go and get all the doses you are eligible for.”

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.

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COVID-19 survivors have higher risk of death 12 months after infection

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New research examines the effects of severe COVID-19 a year after the infection. Heath Korvola/Getty Images
  • The negative impact of COVID-19 on patients’ health has been recognized but not yet clearly quantified.
  • Previous research has looked at the effects of the disease at 6 months, and scientists have now explored the impact on overall health at 12 months.
  • The relative increase in the risk of death after COVID-19 is higher for under 65s than over 65s.

The total number of recorded COVID-19 deaths has passed 5 million globally, with over 750,000 deaths in the United States alone. However, these figures are unlikely to reveal the true impact of COVID-19 on the population.

Scientists have now shown an increased risk of death among COVID-19 survivors 12 months after the infection.

For people younger than 65 who were hospitalized with COVID-19, the risk of death in the 12 months after the infection was 233{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} higher than it was for people who did not have the disease, results published in the journal Frontiers in Medicine have shown.

Nearly 80{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of all deaths of people in the study who had recovered from COVID-19 in the past 12 months were not due to cardiovascular or respiratory causes, suggesting that the impact of the virus is significant and wide-ranging, even after the initial infection has been fought off.

Prof. Arch Mainous, an author of the paper, told Medical News Today in an email: “A lot of interest in the scientific community has focused on what happens to patients after having an episode with COVID-19. Some people are focusing on ‘long COVID’ or persistent symptoms like brain fog or lack of smell. We were interested in the hard outcome of death after COVID-19 recovery.”

“We thought that the impact of COVID-19 would be significant enough to engender complications. The overall trauma or psychological insult to the body would be dramatic enough to create lasting damage.”

To measure the impact of COVID-19 on long-term health, researchers from the University of Florida looked at electronic healthcare records from patients tested for COVID-19 in any setting in the University of Florida health system, both in Gainesville and Jacksonville. People who died within 30 days of their COVID-19 tests were excluded from the analysis.

Out of 13,638 people tested for COVID-19 between January 1 and June 30, 2020, 424 people were found to have COVID-19. Of this number, 178 people were classified as having severe disease. The rest were negative for SARS-CoV-2, the virus that causes COVID-19, as determined by polymerase chain reaction (PCR) testing.

The researchers then evaluated the electronic healthcare records of these people, following them for 365 days after the first PCR test. They found that 2,686 people in the cohort had died.

The team then analyzed the healthcare records to determine cause of death and compared the risk of death for people who had had COVID-19 with that of people who had not tested positive for SARS-CoV-2.

They found that the vast majority of deaths among people who had had COVID-19, nearly 4 out of 5 of these deaths, were not due to cardiovascular or respiratory illness, despite much existing research into the impact of COVID-19 on these systems.

Prof. Mainous said, “Treatment in the hospital is [fine for surviving] the initial episode, but our strategy should focus on keeping people out of the hospital in the first place.”

“Taking your chances that you might get COVID-19 but that it will be mild, or that you will just rely on treatments to pull you through a severe episode is a course of action with big risks.”

These figures demonstrate that the impact of COVID-19 could last longer than we had originally anticipated. However, they do not tell us why.

Prof. Mainous continued, “Although there are a variety of theories floating around about why there are post-acute complications from COVID-19, and more work needs to be done to establish definitively the mechanism, it seems likely that the intense level of inflammation in the body affects multiple parts of the body.”

Children were not included in this study, but Sammie Mcfarland, founder and CEO of Long Covid Kids, told MNT in an interview that the study shed some light on a topic that should get more attention — and that we still do not understand the long-term impact of COVID-19 on children.

In the United Kingdom, she said, “We don’t know if the children coming out of hospital go on to recover, go on to die, or go on to get long COVID, we just don’t know.”

She also pointed out that while cases of pediatric multisystem inflammatory syndrome, a rare complication that can occur in children with COVID-19, have been recorded, we do not know what has happened to many of these kids.

Mcfarland told us: “Those children are living now with some severe impairment, and some of them have died. And those children aren’t recorded as COVID deaths. And they’re not recorded in the COVID data. But it’s still from COVID.”

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.

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Does diet influence dementia risk? What we know

Dementia is a leading cause of disability and death worldwide. There is no cure. Recent research has focused on whether diet might influence the risk and progress of dementia. In this Special Feature, Medical News Today assesses the evidence and looks at how you might help reduce your risk of dementia.

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What does the latest research say about the link between diet and dementia risk? We investigate. Image credit: Luis Manuel Matias/Addictive Creative/Offset

According to the World Health Organization (WHO), dementia affects more than 55 million people worldwide, with 10 million people receiving a diagnosis each year. About 60-70{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of people globally with dementia have Alzheimer’s disease, which affects almost 6 million people in the United States.

It may be the third leading cause of death after cancer and heart disease in certain age groups.

With an aging global population, the WHO predicts that the number of people with dementia will rise to 78 million by 2030 and 139 million by 2050.

According to existing research, diabetes, obesity, and heart disease, which can increase the risk of developing dementia, are all rising in number.

The main symptoms of dementia are memory problems, loss of cognitive function and coordination, and personality changes. The most significant risk factor for dementia is aging — more than 90{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} of people with dementia are over 65 — but other factors are also involved.

There is currently no cure for dementia, and most treatments alleviate symptoms without slowing the progress of the disease. So are there ways reduce to reduce this risk?

Keeping fit and healthy can reduce the risk of dementia — and diet is a large part of keeping fit.

In a comment for MNT, Dr. Christopher Weber, director of global science initiatives at the Alzheimer’s Association, noted that:

“Research looking at the relationship between diet and cognition is well-established. There is strong evidence to suggest that what is good for the heart is good for the head, and we know a healthy diet is good for the heart.”

Some studies have suggested that a Mediterranean diet can improve cognitive function. This diet includes plenty of fruit and vegetables, nuts and seeds, olive oil and fish, with small amounts of dairy, eggs, and red meat, together with a moderate amount of red wine.

Recent research showed that a Mediterranean diet has associations with improved cognitive functioning and slowed the progression from mild cognitive impairment to dementia.

An alternative to the Mediterranean diet is the MIND diet (Mediterranean-DASH Intervention for Neurodegenerative Delay). The diet is similar but focuses on green leafy vegetables, other vegetables, nuts, berries, beans, whole grains, seafood, poultry, olive oil, and wine.

This diet highlights the importance of foods and nutrients that have an association with dementia prevention.

A problem with diet studies is that they are observational, and people usually assess their diet through self-reported questionnaires. However, researchers have demonstrated an association between these diets and improved cognitive function.

One study showed a substantially slower cognitive decline in those following the MIND diet. A 2021 study found a positive correlation between MIND diet score, cognitive resilience, and cognitive function.

Interestingly, the researchers found that improved cognitive function was independent of brain pathologies that post-mortems identified in participants.

Dr. Weber commented: “The Mediterranean diet and the MIND diet have been shown in clinical studies to be beneficial to brain and heart health. The Alzheimer’s Association encourages everyone to eat a healthy and balanced diet as a way to help reduce the risk of cognitive decline.”

Processed food is one of the current bad guys. Experts tell us to eat a balanced and varied diet containing plenty of fresh food to stay healthy. But could a diet high in processed food increase your dementia risk?

“There is […] strong evidence linking poor diet (for example, eating a diet high in unhealthy fats and sugar) and increased risk for dementia.”

– Dr. Christopher Weber

In animal models, a diet high in refined carbohydrates increases the risk of dementia and Alzheimer’s. A human study in France replicated this effect and confirmed that older participants who ate a daily snack high in refined carbohydrates were more likely to develop dementia.

Another study has linked processed meat products, such as sausages, salami, and bacon, with dementia. Regular consumption of processed meat increased the relative risk of all dementias by 44{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809} and Alzheimer’s disease by 52{cfdf3f5372635aeb15fd3e2aecc7cb5d7150695e02bd72e0a44f1581164ad809}.

However, like all the other dietary studies, this was observational and the risks reported are relative rather than absolute. One expert commented that the results “would not persuade me to give up my breakfast bacon.”

Proponents of vitamin and mineral supplements often tout them as a way of compensating for a less than optimal diet, but is there any evidence that they might help combat dementia?

A recent study gave older male rats a processed food diet high in refined carbohydrates and found that their learning and memory skills suffered. Another group of rats on the same diet but with omega-3 supplements showed no memory problems.

The authors of the study explained their findings in terms of the inflammatory response provoked by processed foods. Scientists know that omega-3 resolves inflammation, which might explain the effect in the rats who received it.

However, there is little other evidence to suggest that supplements affect dementia. The WHO advises that a healthy diet and regular exercise will likely have more significant effects.

The link between alcohol and dementia is not entirely clear. While heavy alcohol consumption has strong associations with the development of dementia, the effect of moderate alcohol intake is still open to question.

The majority of studies show an association between low to moderate alcohol use and reduced risk of dementia, particularly for red wine drinkers.

Two systematic reviews, one of which analyzed results from 26 studies, concluded that reducing heavy alcohol use could be an effective dementia prevention strategy.

However, they also noted that those who abstained from alcohol entirely had a higher dementia risk than those who drank in moderation.

Therefore, it is possible that drinking in moderation may have some protective effect, but no observational study can exclude all other factors. It may be that those who drink moderately have a better diet, do more exercise, or are generally in better health.

One study into the effects of moderate drinking in older adults in New Zealand controlled for socioeconomic status but found no evidence for a link between moderate drinking and better health.

So perhaps that protective effect is just wishful thinking from those of us who enjoy an occasional drink!

Research has linked memory decline with inflammation, and this is an area that is attracting a lot of interest.

According to Prof. Tim Spector, Professor of Genetic Epidemiology, King’s College London and Zoe Study lead, “This fits with the ‘inflammaging’ theory that is gaining a lot of traction.”

There are links between inflammation and the gut microbiome. Several clinical studies have seen an association between the gut microbiome and dementia.

One cross-sectional study in Japan found a significant difference between the microbiome of people with dementia and those without the disease.

Those with dementia had a much lower number of Bacteroides, a species known to reduce inflammation. They also had much higher numbers of microbes (enterotype III) that have associations with dementia.

Two other studies back up these findings. One analyzed gut microbiome metabolites, finding that people with dementia had significantly different metabolites from those without the disease.

A second stressed the links between the gut microbiota and dementia development, observing effects on the microglia and cytokine release, which have implications in inflammation and dementia.

“There are large numbers of studies that are pointing in the same direction. People with dementia have sub-optimal microbiomes. The picture is of not only reduced numbers of species but also increased numbers of inflammatory species.”

– Prof. Tim Spector

The gut microbiome and diet have links, and this could be why the Mediterranean and MIND diets have shown positive effects in reducing dementia risk and progression.

“Reduced [microbiome] diversity and [more] inflammatory species are related to poor diet, generally low in fiber and diversity of plants,” Prof. Spector told us. “With elderly people, there’s often a tipping point, such as losing a partner. The diet reduces in quality and diversity. That can accelerate cognitive decline.”

He did, however, stress that there may be a reverse causality. People in the early stages of cognitive decline might reduce the quality of their diet and thereby accelerate the process.

“Studies of centenarians have found that they generally live in areas with a good food culture and lots of socializing,” he added. “It’s not about fats. It’s not about carbohydrates or calories, but can you get fresh, varied food? You need your gut microbes to keep your immune system suppressing inflammation?”

The short answer is probably; that diet may well play a part. Evidence is growing that a varied diet rich in plants will support a varied gut microbiome. And a varied gut microbiome helps to reduce the inflammation implicated in dementia.

“Poor diet harms microbes, which harms the immune system with these knock-on effects of cognitive decline. In dementia, inflammatory aging is the current theory. It’s partly triggered by the immune system which involves the microbes and diet.”

– Prof. Tim Spector

So until randomized control trials can prove how diet influences dementia, it is probably best to eat a diet that reduces the risk of heart disease and supports your microbiome, combining it with regular exercise.

The jury is still out on moderate alcohol consumption, but there is clear evidence that too much alcohol increases the risk of many health conditions, including dementia.

Dr. Weber concluded: “While we continue to learn more about lifestyle factors that have the greatest impact on our overall risk, there are things we can do today that may decrease our risk of cognitive decline as we age. Eating a heart-healthy diet, exercising regularly, and staying cognitively engaged are just a few.”

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Exposure to air pollutants may amplify risk for depression

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A new study looks at the impact of pollution on depression risk in people with a genetic susceptibility. Jelena Jojic Tomic/Stocksy
  • Exposure to air pollution is associated with cognitive deficits and an increased risk of depression.
  • A recent study examined how air pollutants impact brain networks to mediate changes in cognitive function and enhance the risk of depression.
  • The results suggest that genetic susceptibility to depression combined with high levels of exposure to air pollution have a disproportional effect on brain networks involved in cognition and stress.
  • Exposure to air pollutants was associated with activation of brain networks expressing depression-associated genes, suggesting that exposure to air pollution may cause adverse mental health effects by acting on the same brain networks related to genetic mechanisms of depression.
  • This suggests that individuals with a genetic susceptibility to depression may be more vulnerable to the adverse effects of air pollution on mental health.

Besides having a detrimental effect on physical health, prolonged exposure to air pollutants is also associated with adverse mental health effects.

Exposure to air pollutants, including fine particulate matter, may be associated with impaired cognitive functioning and depression.

Fine particulate matter, also known as PM2.5, consists of tiny inhalable particles smaller than 2.5 microns. These particles commonly come from industrial sources and vehicles.

How exposure to PM2.5 might increase the risk of depression is not well understood.

Also, scientists do not know whether air pollution can interact with a genetic predisposition for depression to increase the likelihood of depression.

Individuals with a genetic predisposition for a particular disease may have an increased likelihood of developing the condition in the presence of certain environmental factors or due to behaviors such as smoking.

A recent study investigated the effects of PM2.5 exposure, in combination with a genetic predisposition for depression, on brain networks involved in cognition and social stress.

The study’s lead author, Dr. Hao Yang Tan, a scientist at the Lieber Institute in Baltimore, MD, told Medical News Today:

“The study reveals for the first time how air pollution and genes interact with one another to impact important cognitive and emotional circuitry of the brain. Air pollution is changing the expression of genes that are conducive to depression.”

“Previous studies have observed air pollution’s link to depression, but our results are the first to show a direct, neurological cause,” he explained.

“What is most intriguing is that the two factors are linked in such a way that they have a multiplier effect on one’s risk of depression. That is, together, risk genes and bad air raise the risk of depression much more than either factor does in isolation.”

The study appears in the journal Proceedings of the National Academy of Sciences.

The study recruited 352 healthy participants residing in Beijing, China. Beijing has relatively high levels of air pollution, including high concentrations of PM2.5.

For each participant, the researchers studied several specific genetic variants that are associated with depression. From this information, they estimated their genetic susceptibility to depression.

To estimate the PM2.5 exposure levels for each individual, the researchers used air monitoring data obtained from the city air quality monitoring station closest to each person’s home for 6 months before the study.

Depression is associated with cognitive deficits and higher levels of anxiety-depression. In other words, these individuals have an increased tendency to react anxiously or with depressive symptoms to a situation. The scientists evaluated each participant’s levels of anxiety-depression using a questionnaire.

The researchers first examined the effects of PM2.5 exposure on cognition and characteristics associated with depression.

They found that PM2.5 exposure was associated with poor performance on cognitive tests involving reasoning and problem-solving. Higher anxiety-depression was also associated with PM2.5 exposure.

Next, the researchers examined brain networks involved in cognition and processing stress-related information and their association with PM2.5 exposure and genetic risk for depression.

The researchers measured the participants’ brain activity while conducting a simple cognitive task using functional magnetic resonance imaging.

To evaluate the influence of social stress on brain activity during the cognitive task, researchers showed the participants the image of a competitor and compared their performance with that of the competitor.

Higher levels of PM2.5 exposure were associated with slower reaction times during the cognitive task, and this effect of PM2.5 exposure became amplified during social stress.

Social stress had a more pronounced effect on brain networks in individuals with a genetic predisposition for depression and greater PM2.5 exposure.

The effect of social stress on brain networks due to the combination of genetic risk and air pollution was greater than the sum of the effects produced by each factor alone. These results suggest that air pollution may interact with genetic risk for depression to influence brain networks.

The dorsolateral prefrontal cortex is a brain region involved in several processes, including cognition. It was one of the key regions whose connectivity changed during the cognitive task in individuals with higher PM2.5 exposure and a genetic predisposition for depression.

Significantly, scientists have observed changes in the dorsolateral prefrontal cortex activity of healthy individuals with a genetic predisposition for depression and individuals with depression.

To further examine the interaction between genetic risk for depression and air pollution, the researchers investigated whether the combination of these factors differentially influenced brain networks involved in depression.

The researchers mapped the brain networks involved in depression by identifying brain regions expressing high levels of depression-associated genes.

The researchers used the online database Allen Brain Atlas, which provides detailed gene expression data for brain regions. They then identified brain regions that showed correlated expression of genes associated with depression.

The researchers examined if this pattern of coexpression of depression-associated genes in brain regions obtained using the atlas was similar to the brain connectivity patterns of the participants during the cognitive tests.

The pattern of coexpression of depression-associated genes derived using the atlas predicted brain connectivity patterns observed during the cognitive task. However, this was only the case for those with greater exposure to PM2.5 levels and a higher genetic predisposition for depression.

The correlation was weaker in individuals with a lower genetic risk of depression or lower exposure to PM2.5.

This suggests that exposure to PM2.5 air pollutants affects brain network functions associated with the genetic mechanisms of depression.

The researchers also conducted similar analyses focused on the association between the connectivity patterns of the dorsolateral prefrontal cortex with other brain regions and the coexpression of depression-associated genes in these regions.

The co-expression of depression-associated genes tracked the connectivity patterns to and from the dorsolateral prefrontal cortex in individuals with a genetic risk for depression, higher PM2.5 exposure levels, or both.

Interestingly, the co-expressed genes that correlated with brain connectivity patterns of the prefrontal cortex included some involved in neuroinflammation.

Depression is associated with chronic, low-grade inflammation, further suggesting that PM2.5 exposure may interact with depression-associated genes to increase the risk of depression.

“This is possibly the first study to directly implicate how genes for brain disorders operate in concert with each other and affect important cognitive and emotional functions in the live functioning brain, and the impact of air pollution and genes in multiplying the effects of each on these brain functions,” Dr. Tan told MNT.

“It is now [in] much less doubt that there are direct impacts of air pollution on how genes operate in the brain to affect risk for these neuropsychiatric disorders,” he added.

Dr. Tan noted: “Individuals can limit their outdoor activities when pollution is high and be mindful of their risk. Our study would strongly suggest that individuals with genetic risk, e.g., [a] family history of brain disorders, may need to be more careful, and minimize [as much as] possible their exposures to any air pollution.”

“Armed with this knowledge, leaders and public health officials around the globe have ample evidence that additional air pollution controls will lead to lower rates of depression — particularly in densely populated urban areas where air pollution is highest, and stress from socioeconomic and other inequities are greater.”

– Dr. Tan

Dr. Perry Sheffield, an environmental health researcher at Icahn School of Medicine at Mount Sinai, New York, noted that this study “helps drive home the point that when we talk about vulnerable groups — and here I mean groups of people who are more likely to experience negative health effects from a certain environmental exposure — we are ultimately talking about all of us. Each of us is vulnerable probably in multiple ways, and our specific vulnerabilities change during our lives.”

“Vulnerability can certainly be socially and unjustly determined — as we see driving racial and ethnic health disparities — but it can [also be] influenced by underlying genetics, as we see here in relation to air pollution and depression, and certainly by life stage or age,” she continued.

“The value of illustrating these associations in a study like this is that it helps tell the story of why clean air, water, and the overall environment matter for the health of people and communities.”

– Dr. Sheffield

Dr. Tan explained to MNT, “An important strength is that we have studied the brain impacts of air pollution using arguably the most direct measurements of live human brain function, which is MRI technologies.”

“We have studied a large sample of individuals. We have also eliminated many other factors that could have interfered with the study.” For instance, their sample was “socioeconomically homogeneous.”

“We have additionally examined patterns of how risk genes for depression operated in concert with each other in postmortem human brains and found that these patterns corresponded well with how the live human brain operated, and especially so in individuals with genetic risk for depression and exposed to high air pollution.”

Dr. Tan acknowledged that there were a few limitations to their approach, saying the team “studied only a limited set of genes for depression, and that’s likely only the tip of the iceberg.”

“There are likely many other genes [for] neuropsychiatric disorders implicated in the brain impacts of air pollution. Understanding these more comprehensively would enable us to better identify people at risk, and perhaps identify various pharmacological or other ways to protect the vulnerable,” he concluded.