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NHS Choices: Behind the headlines   + / -  
last updated: Tue, 22 Aug 2017 17:44:24 GMT

 Tue, 22 Aug 2017 17:30:00 GMT Gum disease linked to increased risk of Alzheimer's disease

"Gum disease sufferers 70% more likely to get dementia," The Times reports. A Taiwanese study found that people with a 10-year or longer history of chronic periodontitis (CP) had a small but significant increased risk of developing Alzheimer's disease (AD).

Gum disease is an umbrella term used to refer to a number of conditions that can affect the gums – ranging from gingivitis, which can cause bleeding gums, to CP, where extensive damage to the gums and underlying bones can lead to tooth loss. This study only looked at CP.

Previous research we discussed in 2016 did find a link between gum disease and worsening dementia symptoms. But because the people taking part in the study had already been diagnosed with dementia, the picture was muddled, as it was hard to determine a causal relationship.

This latest study found that people who had CP for at least 10 years had an estimated 70% higher risk of developing AD than people without CP.

However, although this increase was judged to be statistically significant (not the result of chance), it was still a very small increase. Only around 1 in 100 people with CP who took part in the study went on to develop AD. It was also not possible to tell whether the results were influenced by people having early undiagnosed AD, which could have led to poorer oral hygiene.

These limitations aside, the study gives another good reason to keep your teeth and gums healthy.

Read more about dental health.

Where did the story come from?

The study was carried out by researchers from Chung Shan Medical University and the National Defense Medical Center, both in Taiwan, without a specific source of funding. It was published in the peer-reviewed medical journal Alzheimer's Research and Therapy.

Coverage of the story in the newspapers was mixed. The Times' and the Mail Online's reports didn't make it entirely clear that the risk of AD only applied to people who had CP for at least 10 years.

The Mail Online also implied that brushing your teeth more could reduce the risk of dementia. Although frequent and effective teeth brushing is associated with reducing the risk of gum disease, it wasn't clear from this study whether changing teeth-brushing habits could reduce the risk of AD.

None of the news sources mentioned the possibility that some people with undiagnosed dementia might not take as good care of their teeth, leading to gum disease.

What kind of research was this?

This was a retrospective cohort study, where researchers looked at a national health database to find people who had CP and then checked whether they developed AD at a later date, comparing them with people who did not have CP.

This is an appropriate study design for looking at how different health conditions may be related to each other over time. However, using existing health records can be difficult if data are missing or unclear, as there is rarely an opportunity to go back and clarify things.

The length of the study was determined by how long the database had been running, rather than by how long it would have been useful to follow the people in the study for.

It's also not possible to tell if the gum disease started because of poor dental hygiene due to someone being in the early stages of undiagnosed AD, rather than the other way round.

What did the research involve?

The researchers used data from the National Health Insurance Program of Taiwan, which covers 99% of the country's residents. They analysed data recorded between 1996 and 2013. Rather than looking at everyone in the database, they took a random sample of 1 million people – around 4.5% of the whole database.

From this sample, they selected two groups of people aged 50 or older to compare. The first group was made up of 9,291 people who had a diagnosis of CP. The second group was made up of 18,672 people who were similar to the first group in terms of age, sex and number of years in the dataset, but who had not received a diagnosis of CP in the time period covered by the data. Two people without CP were matched to every one person with it.

People were excluded from the study if:

  • their age or sex was not clear from the data
  • they already had a diagnosis of CP before 1997
  • they already had AD before 1997, or before CP was diagnosed

The researchers analysed the data by looking at how CP was associated with AD after taking into account various other potential confounding risk factors linked with AD. They looked at whether there were differences between the two groups over time.

A further analysis looked only at people who had CP for at least 10 years before developing AD.

What were the basic results?

By the end of the study, 115 people in the CP group (1.24%) and 208 people in the non-CP group (1.11%) had developed AD.

In the initial analysis, the researchers found no difference in the occurrence of AD between those who had CP and those who didn't during the first 10 years of observation. After around 10 years, some differences emerged between the groups.

People who had CP for at least 10 years had a higher risk of developing AD (hazard ratio [HR] 1.707, 95% confidence interval [CI] 1.152 to 2.528).

How did the researchers interpret the results?

The authors noted that the association between CP and AD was only detected in people who had CP for at least 10 years.

They acknowledged that being able to use a national medical database was beneficial for this kind of study, as it gave access to a wide population, but that it also had limitations, such as lack of control over the quality of the data available.


This was an interesting study that identified a possible link between two conditions, but it may not be a strong enough piece of research to provide definitive estimates of the size of the risk.

The study has a number of weaknesses:

  • If the researchers had used more of the data available rather than taking a random sample to select a cohort, there may have been more cases of CP and AD to use in their analysis. This may have given a better insight into any association.
  • The study did not give any details of how CP was treated or managed, so we don't know if there were any differences between people with CP who did go on to develop AD and those who did not.
  • Although the researchers did take into consideration a number of other risk factors that could have affected the results (such as other health conditions), there may be others that affect the risk of developing both CP and AD that weren't taken into account.
  • It's possible the numbers of people with CP and those with AD may have been underestimated because of the way data were recorded in this database and how the conditions were diagnosed. For example, people may have had early AD, which caused them to have poor dental hygiene before a diagnosis of AD was made. Alternatively, CP may have been present in people in the non-CP group, as diagnosis is reliant on regular dental check-ups, which may not have taken place.
  • Further studies that look at larger numbers of people and follow them forwards in time would be needed to clarify any link between CP and AD.

Despite these limitations, it's still a good idea to take good care of your gums through regular brushing and flossing, and avoiding smoking.

Complications of gum disease can be unpleasant, including loss of teeth, and painful abscesses and ulcers.

Read more advice about keeping your mouth healthy.

Links To The Headlines

Gum disease sufferers 70% more likely to get dementia. The Times, August 22 2017 (subscription required)

People with gum disease are 70 per cent more likely to get dementia, scientists say. The Sun, August 22 2017

Gum disease 'raises the risk of dementia by up to 70%': Findings could see regular dental care promoted as a way of warding off Alzheimer's. Mail Online, August 22 2017

Links To Science

Chen C, Wu Y, Chang Y. Association between chronic periodontitis and the risk of Alzheimer’s disease: a retrospective, population-based, matched-cohort study. Alzheimer's Research & Therapy. Published online August 8 2017

 Mon, 21 Aug 2017 16:31:00 GMT Vitamin C injections could play a role in treating blood cancers

"Super-strength vitamin C doses could be a way to fight leukaemia," the Mail Online reports. Research in mice found vitamin C could help combat the effect of a mutated gene that can cause uncontrollable stem cell growth and trigger the onset of acute myeloid leukaemia (AML).

AML is an aggressive cancer of the white blood cells that usually affects older people. It is thought that some cases of AML are caused by a mutation in the Tet Methylcytosine Dixoygenase 2 (TET2) gene. This gene helps mature stem cells into specialised white blood cells. The mutation can lead to uncontrollable growth of cancerous cells leading to AML.

The researchers used mice to explore whether use of vitamin C could restore the TET2 gene to working order and help slow the progression of leukaemia.

The study found that using high doses of vitamin C intravenously did in fact suppress the growth of leukaemia cancer stem cells in the mice.

Although this does pave the way for future therapeutic approaches, this study was very early stage research in mice, and therefore would require further investigation and trials in humans before any treatment based on the findings could be offered to patients.

Also, the dose used was far higher relative to weight, than would be safe in humans. It would be the equivalent of a human taking 300g of vitamin C, which would mean eating more than 5,000 oranges. So scientists would also have to find a way to lower the dose while achieving the same beneficial effect.


Where did the story come from?

The study was carried out by researchers from several institutions, including New York University and Monash University in Australia. It was funded by numerous institutions such as the US NIH, the Leukaemia & Lymphoma Society and the Chemotherapy Foundation.

The study was published in the peer-reviewed scientific journal Cell.

The UK media's coverage on this topic was generally accurate, highlighting that this is not a treatment that would be used by itself, but instead in combination with other approaches, such as chemotherapy.


What kind of research was this?

This was an animal study which investigated whether treatment with vitamin C could restore function of Tet Methylcytosine Dixoygenase 2 (TET2) and therefore block the progression of leukaemia in mice.

TET2 is one of the most frequent mutations in diseases and cancers of the blood such as leukaemia. The TET2 gene encodes a protein involved in the production of bone marrow and blood cells. As a result, defects and mutations of TET2 can negatively affect the process which causes stem cells to turn into blood cells. In turn, this can promote the progression of leukaemia.

The researchers wanted to explore the role of TET2 deficiency in the maintenance of leukaemia stem cells.

The researchers further investigated whether vitamin C could be useful in the treatment of blood cancers. This is because treatment with vitamin C has previously been tested in solid tumours (tumours located in one part of the body, such as the lungs) and in some cases, been found to result in better patient outcomes.

Animal studies such as this are useful for early stage research. But while there are many genetic similarities between mice and humans, we aren't identical. Therefore further testing is required in people to be sure of the effect of any treatment.


What did the research involve?

The researchers implanted leukaemia stem cells, extracted from humans, into mice and also used mice that were deficient in TET2.

To determine the effects of mutations that could reduce TET2 function, the mice were genetically engineered so that the TET2 gene could be switched on or off.

High doses of vitamin C were then administered intravenously to the mice and the function of TET2 and cell behaviour was studied.

The researchers also tested the use of vitamin C alongside PARP inhibitors. PARP inhibitors are a class of chemotherapy drugs that can help repair damaged DNA.


What were the basic results?

The researchers found that when the function of TET2 was switched off in the mice, abnormal stem cell behaviour occurred. This was reversed however once the function of TET2 was switched back on, confirming that loss of function of TET2 would in fact play a role in the formation of cancerous stem cells in diseases such as leukaemia.

In the TET2 deficient mice, the effects of TET2 deficiency were reversed following having intravenous vitamin C administered. The vitamin C treatment also induced the stem cells to mature and suppressed the growth of leukaemia cancer stem cells in the mice implanted with cell lines from human patients with leukaemia.

The researchers also found that following vitamin C treatment, the leukaemia cell lines were more sensitive to treatment with PARP inhibitors.


How did the researchers interpret the results?

The researchers concluded: "We have found that targeted restoration of Tet2 is sufficient to block aberrant self-renewal of pre-leukemic stem cells. Similarly, vitamin C, by enhancing the activity of TET family dioxygenases, acts as a pharmacologic mimic of Tet2 restoration. Moreover, genetic or pharmacological restoration of TET activity confers an emergent vulnerability in leukemia cells, rendering them more sensitive to PARP inhibitors. Together, these results suggest new therapeutic strategies for clonal hematopoiesis, MDS and AML."



This mouse study explored whether treatment with vitamin C could restore function of TET2 and therefore block the progression of blood cancers like leukaemia.

It found that using high doses of vitamin C intravenously did in fact suppress the growth of leukaemia cancer stem cells in the mice implanted with cell lines from human patients with leukaemia.

It also reported that using vitamin C alongside existing treatment with PARP inhibitors helped reduce the progressions of the disease.

The researchers suggest that in the future, vitamin C could be used alongside chemotherapy and other conventional treatment forms.

This is exciting early stage research, with potential to pave the way for future treatment options for leukaemia and other blood cancers.

One of the challenges of treating acute myeloid leukaemia is that patients are usually older so it is often not safe to use very aggressive forms of chemotherapy. Hopefully vitamin C, or a similar substance, could help enhance the effects of milder forms of chemotherapy.

However, because this was an animal study, these results would need further investigation and have to undergo clinical trials in humans before new treatments based on these findings could be offered to patients.

It is far too soon to start taking high doses of vitamin C on the basis of this research, especially as large amounts of the vitamin (more than 1g per day per person) can cause stomach upsets. Some mice in this study received 100 milligrams, which would be equivalent to humans receiving 300g of pure vitamin C.

From what we know about AML, it would seem that the one way to reduce your chances of developing this cancer is to quit smoking.

Links To The Headlines

High dose injections of vitamin C could help to fight blood cancer and stop it from spreading, study claims. Mail Online, August 18 2017

Blood cancer: High doses of vitamin C could encourage stem cells to die. Daily Express, August 17 2017

Vitamin C helps genes to kill off cells that would cause cancer. New Scientist, August 17 2017

Links To Science

Cimmino L, Dolgalev I, Wang Y, et al. Restoration of TET2 Function Blocks Aberrant Self-Renewal and Leukemia Progression. Cell. Published online August 17 2017

 Fri, 18 Aug 2017 16:30:00 GMT 'Junk food' may increase cancer risk in 'healthy weight' women

"Women who eat junk food such as burgers or pizza are increasing their risk of cancer even if they're not overweight, new research has warned," reports the Daily Mail.

The story is based on research from the US looking at the diet of postmenopausal women in the 1990s and then tracking the development of a variety of cancers over about 15 years.

"Junk food" is often defined as food that is rich in calories (energy dense food) but low in nutrients.

Having a diet high in energy dense foods, such as biscuits, chocolate and pizza was found to increase the risk of cancer in these women, specifically in those of a healthy weight, which was defined as having a body mass index (BMI) of between 18.5 and 24.9. This suggests that having a healthy weight does not necessarily protect against cancer risk.

However the connections between diet, lifestyle and cancer outcomes are complex, and while the researchers attempted to adjust their results for other factors, we cannot say with certainty that energy dense foods increase your cancer risk.

The analysis was limited to postmenopausal women and did not consider drink intake, such as sugary drinks and alcohol, which can also be high in calories.

Still, having a healthy, balanced diet will help you get all the nutrients you need and may reduce your risk of developing cancer.

Read more about cancer prevention.


Where did the story come from?

The study was carried out by researchers from the Mel and Enid Zuckerman College of Public Health, the University of Arizona, the University of Iowa, Purdue University, Albert Einstein College of Medicine, Kaiser Permanente Center for Health Research, Harbor-UCLA Medical Center and the University of California, all in the US.

The research was funded by the National Cancer Institute of the National Institutes of Health and The University of Arizona Collaboratory for Metabolic Disease Prevention and Treatment. The Women's Health Initiative (WHI) from which data was sourced is funded by the National Heart, Lung, and Blood Institute; National Institutes of Health; and US Department of Health and Human Services.

The study was published in the peer-reviewed Journal of the Academy of Nutrition and Dietetics.

The UK media's reporting of this US study was generally accurate, although it could have been more explicit about the fact that all women in the study were postmenopausal, meaning the results might not be applicable to all populations.


What kind of research was this?

This was a prospective cohort study, meaning it looked at a large number of women over a number of years, with the aim of finding out if consuming energy dense foods increases the risk of cancer.

Cohort studies such as this are good at looking at trends in large numbers of people over time but cannot on their own prove cause and effect unless the links are strong and consistent.

It cannot be proven from this research that having an energy dense diet will result in increased risk of cancer.


What did the research involve?

The researchers took data from 92,295 women participating in the Women's Health Initiative (WHI) study in the US, a longitudinal study involving healthy, postmenopausal women recruited between 1995-1998 who were between 50 and 79 years old.

The association between an energy dense diet and cancer was investigated over an average 14.6 year follow up period.

The researchers excluded women who had a history of cancer, and those with a lack of dietary data, missing BMI data, or who reported consuming fewer than 600 calories or more than 5,000 calories per day.

Diet was assessed by self-report at the start of the study using a food frequency questionnaire designed to estimate energy, nutrients and food weight.

Dietary energy density (DED) was calculated by dividing the daily energy intake (in kilocalories) from foods (but not drinks) by the portion size reported and corresponding weight in grams of these foods, as per the WHI database.

Cancer assessment at the start of the study was by self-report by participating women and then by self-report on a biannual basis at follow up, with the results also checked against medical records.

Obesity-related cancers were the outcome of interest and were defined using the American Institute of Cancer Research report of diet, physical activity, and cancer. Common obesity-related cancers include breast, colorectal and kidney cancers.

Analysis took into account potentially confounding variables, including:

  • age
  • ethnicity
  • neighbourhood socioeconomic status
  • smoking history
  • physical activity
  • disease history
  • weight change pattern in adulthood
  • alcohol
  • hormone use and use of disease-related medications

BMI and waist circumference were also measured.


What were the basic results?

The total number of women with cancer over the follow up period was 9,565. This included:

  • 5,565 cases of breast cancer
  • 1,639 cases of colorectal cancer
  • 662 cases of ovarian cancer
  • 955 cases of endometrial cancer
  • 347 cases of renal cancer
  • 461 cases of gallbladder cancer
  • 485 cases of oesophageal cancer 
  • 620 cases of pancreatic cancer

Among 28 analyses across two models the risk of any obesity-related cancer was 10% higher in one analysis for the women consuming the highest energy dense diet compared with the lowest (subhazard ratio (sHR) 1.10, 95% confidence interval [CI] 1.03 to 1.20).

  • After accounting for confounders, energy dense diets were not significantly associated with each individual cancer type.
  • When breaking down into BMI subgroups, only women of a normal weight (BMI < 25) had a positive association between energy dense diets and obesity-related cancer. Those in the highest three quintiles for energy dense diets had a 10%, 18% and 12% increased risk of obesity-related cancer for quintiles 3, 4 and 5 (sHR trend 1.2, significance not reported).
  • Higher energy dense diets were associated with higher BMI (29.0 ± 6.0 versus 26.3 ±4.9 for quintile 5 versus 1).


How did the researchers interpret the results?

The researchers concluded that "among normal-weight women, higher Dietary Energy Density may be a contributing factor for obesity-related cancers. Importantly, Dietary Energy Density is a modifiable risk factor. Nutrition interventions targeting energy density as well as other diet-related cancer preventive approaches are warranted to reduce cancer burden among postmenopausal women."



Energy dense diets appear to be associated with a 10% increased risk of obesity-related cancer in those eating the top 205 high density food types.

A sub analysis of postmenopausal women of normal, overweight or obese weight at the start of the study showed a link specifically in those of a normal weight and a weaker link in those who were overweight or obese.

The authors suggest these findings mean weight management alone might not protect against obesity-related cancer if women have a high energy dense diet.

Although this was a longitudinal study involving a large sample of women, it has some limitations:

  • Food intake was self-reported and so might not accurately represent what women were truly eating as there is a tendency to under-report in such questionnaires.
  • There are a range of other factors that might have contributed to the increased risk of cancer that were not accounted for in analysis, such as whether the participants were employed, the type of employment, home life and social factors, levels of activity, as well as consumption of energy dense drinks (which were not considered in the food questionnaire).
  • Women consuming lower amounts of energy dense food tended to have a lower BMI, engage in more physical activity and consume less alcohol and tobacco, indicating that healthy behaviours cluster together and are hard to unpick.
  • Research was limited to postmenopausal women aged 50 to 79 in the US so might be less relevant to women of other ages or women in the UK where food types and eating trends might differ.

Eating a lot of energy dense foods is not recommended as part of a healthy lifestyle as it increases the risk of becoming overweight due to the high number of calories these foods contain.

To cut down on energy dense foods, aim for balanced diet and try these healthy food swaps.

Links To The Headlines

Junk food is still a cancer risk even if you're not fat: Energy-dense meals can raise the risk of suffering certain types of the disease by 10%. Mail Online, August 17 2017

Women who regularly eat junk food increase their risk of cancer by ten per cent - even if they are SLIM. Daily Mirror, August 17 2017

Links To Science

Thomson CA, Crane TE, Garcia DO, et al. Association between Dietary Energy Density and Obesity-Associated Cancer: Results from the Women's Health Initiative. Journal of the Academy of Nutrition and Dietetics. Published online August 17 2017


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