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last updated: Fri, 21 Oct 2016 16:04:07 GMT

 Fri, 21 Oct 2016 17:30:00 GMT Sweetened drinks, including diet drinks, may raise diabetes risk

"Drinking more than two sugary or artificially sweetened soft drinks per day greatly increases the risk of diabetes, research has shown," The Guardian reports.

The research was a Swedish cohort study of sweetened drink consumption over the past year for people diagnosed with type 2 diabetes. They also looked at people with an uncommon form of diabetes known as latent autoimmune diabetes in adults (LADA) which shares features with type 1 and 2 diabetes.

Both groups were then compared with a diabetes-free control group.

Drinking more than two sweetened drinks per day was linked with being roughly twice as likely to have diabetes.

For type 2 diabetes the link was similar when separately analysing sugary and diet drinks. The link with LADA was a little weaker and did not stand up to statistical significance when separately analysing sugary and artificially-sweetened drinks.

However, this study cannot prove that sweetened drinks alone have directly caused these conditions. Other unhealthy lifestyle factors like smoking and poor diet in general were also linked with the two forms of diabetes.

Also, one of the hallmark symptoms of diabetes is increased thirst so it could be possible that in some cases the diabetes came first and was then followed by increased consumption of sweetened drinks.

These uncertainties aside, the results broadly support our understanding of the risk factors for diabetes, which also apply to several other chronic diseases.

To reduce your risk of diabetes, eat a healthy diet, exercise regularlystop smoking and cut down on alcohol consumption.

Read more about diabetes prevention.


Where did the story come from?

The study was carried out by researchers from the Karolinska Institutet, Stockholm and other institutions in Sweden and Finland. Funding was provided by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, AFA Insurance and the Swedish Diabetes Association.

The study was published in the peer reviewed European Journal of Endocrinology and is openly available to access online.

The UK media gives slightly confused reporting by dividing between reporting on diet drinks or sugary drinks.

All the media reports mentioned two drinks per day. The significant links were actually for more than two drinks per day – for example, two-and-a-half or three.

There were no links for two or fewer drinks of any type. In any case, with food frequency questions there is the chance that estimates on portion size or frequency may be inaccurate.


What kind of research was this?

This was a case-control study within a population-based Swedish cohort study that aimed to see whether consumption of sweetened drinks was associated with risk of a rare form of diabetes called latent autoimmune diabetes in adults (LADA).

LADA has features of type 1 diabetes, where the body's own immune cells destroy the insulin-producing cells in the pancreas. But unlike type 1 diabetes, which normally develops in childhood, in LADA the cell destruction is much slower.

Also, the condition often develops later in life and shares many features with type 2 diabetes. For example, the person doesn't always need treatment with insulin straight away. This study reports that in the Swedish diabetes registry, LADA accounts for 5% of all cases.

The researchers compared drink consumption between cases with LADA or conventional type 2 diabetes and diabetes-free controls. The difficulty with this study design is that it's always going to be difficult to prove that a single factor, such as sweetened drinks, is definitely the cause of the condition. 


What did the research involve?

The study used data from the population-based cohort study ESTRID (Epidemiological Study of Risk Factors for LADA and Type 2 Diabetes) which started in 2010.

This study invited people with LADA or Type 2 diabetes from the Swedish diabetes registry to take part, along with a random selection of people aged 35 or over who were free from diabetes to act as controls.

Participants were set to be recruited in a ratio of four people with type 2 diabetes and six controls for every one person with LADA.

All people with diabetes were diagnosed by a doctor. There are said to be no definite criteria for LADA diagnosis, but the study used criteria in line with other literature.

Participants completed a health and lifestyle questionnaire. This included information on weight and height, physical activity, smoking, alcohol intake, family history of diabetes and educational level.

These factors were considered as potential confounders.

They also completed a 132-item food frequency questionnaire. Participants were asked to report their normal food consumption in the preceding year. Three questions asked about intake of sweetened drinks:

  • cola
  • diet cola
  • other diet soft drinks/soda (for example diluted syrups)

They were asked to report the number of 200ml servings per day or per week. Questions on fruit juice weren't analysed in the study.

The researchers analysed the difference in sweetened drink consumption between cases and controls, adjusting for the other confounders.


What were the basic results?

Data was available for 1,136 people with type 2 diabetes, 357 people with LADA, and 1,371 diabetes-free controls.

Average age was 59 for people with LADA and controls, and 68 for those with type 2 diabetes.

Just under two-thirds of all people reported consuming sweetened (including artificially sweetened) drinks.

In general they found that consumption of sweetened drinks was linked with higher body mass index (BMI) and other poor lifestyle factors like smoking, low physical activity and consumption of processed meat and sugary foods.

In adjusted analyses, people drinking more than two servings of any sweetened drinks a day had almost doubled odds of LADA compared with non-consumers (odds ratio [OR] 1.99, 95% confidence interval [CI] 1.11 to 3.56). Each extra daily serving was linked with 15% increased risk (OR 1.15, 95% CI 1.02 to 1.29).

For type 2 diabetes, the link was a little stronger. More than two servings a day was linked with more than twice the odds of type 2 compared with non-consumers (OR 2.39, 95% CI 1.39 to 4.09), and each extra daily serving conferred a 20% increased risk (OR 1.20, 95% CI 1.07 to 1.34).

When separately analysing both sugar-sweetened and artificially-sweetened drinks, the findings were similar and still significant for type 2 diabetes. However, for LADA all links fell short of statistical significance on separate analysis.

Drinking two or fewer drinks per day – either sugar-sweetened or artificially-sweetened drinks – was not linked with either LADA or type 2 diabetes. 


How did the researchers interpret the results?

The researchers conclude: "High intake of sweetened beverages was associated with increased risk of LADA. The observed relationship resembled that with type 2 diabetes, suggesting common pathways possibly involving insulin resistance."



This study primarily aimed to see if consuming sweetened drinks was associated with the rarer condition of LADA, as it is with type 2 diabetes.

The researchers found that having more than two drinks per day was linked with increased odds of both conditions – though the link with LADA was a little weaker and not statistically significant when separately analysing diet and sugary drinks.

They also found that high BMI and other poor lifestyle choices were also linked with the conditions.

The findings generally support what is understood about type 2 diabetes, that high sugar intake, poor diet, low activity and high BMI increase risk. They similarly show that this is also likely to be the case with this rarer variant of the condition.

There are a couple of points to note:

  • This study design cannot prove that sweetened drinks are the direct cause of diabetes in these people. It is likely that high consumption of sweetened drinks is part of a wider picture of generally poor lifestyle habits. Though the researchers have adjusted their analyses for confounding factors, it is difficult to fully account for each health and lifestyle variable that could be having an influence.
  • The results are based on a food frequency questionnaire assessing intake over the past year. Though this is the best way you can look at this, it may not be entirely accurate – particularly when questioning regular portion size – or reflect longer term patterns over the course of the person's lifetime.
  • Several of these analyses deal with small numbers. For example, only 14 people with LADA drank more than two servings of diet drinks a day. Analyses based on small numbers are generally less reliable than those based on larger numbers of people.
  • This is a Swedish cohort. Lifestyle and environmental differences may mean the study is not completely representative of the UK population.

One expert from the University of Cambridge also considers another possibility that increased drink consumption could be due to increased thirst before diabetes is diagnosed – that is, the study can't rule out that this finding could be a symptom rather than a cause of diabetes.

The researchers did try and take account of consumption of water and other drinks as a general marker of thirst, but this is still a possibility the study design can't rule out.

Nevertheless, the findings support current understanding of the risk factors for diabetes, which apply to several other chronic diseases.

To reduce your risk of diabetes (as well as heart disease, stroke and some cancers), eat a healthy diet, exercise regularlydon't smoke and cut down on alcohol consumption.

Read more about diabetes prevention.

Links To The Headlines

Just two sugary drinks a day greatly increases diabetes risk, study shows. The Guardian, October 21 2016

Two diet drinks a day could double the risk of diabetes, study finds. The Daily Telegraph, October 21 2016

Diet Coke WON’T stop you getting diabetes: Two glasses of calorie-free drinks a day 'doubles the risk'. Mail Online, October 21 2016

Links To Science

Löfvenborg JE, Andersson T, Carlsson P, et al. Sweetened beverage intake and risk of latent autoimmune diabetes in adults (LADA) and type 2 diabetes. European Journal of Endocrinology. Published online October 21 2016

 Thu, 20 Oct 2016 14:28:00 GMT 'Statins in a tube': Could a new toothpaste prevent heart disease?

"Brushing teeth thoroughly to remove plaque could help prevent heart attacks … by reducing inflammation," The Daily Telegraph reports.

A study found that "Plaque HD" toothpaste was related to a drop in inflammation levels (but this could have been coincidental), but it did not investigate if this had any long-term effects on cardiovascular outcomes such as heart attacks or stroke.

The "HD" toothpaste is designed to turn plaque (clumps of bacteria) green so you can spot areas where you need to focus your brushing.

The study included 61 people who used either "Plaque HD" toothpaste or a standard toothpaste for 60 days. Researchers measured changes in the amount of dental plaque seen on people's teeth, and in a marker for inflammation in the body called high sensitivity C-reactive protein (hsCRP).

They showed that people who used the "Plaque HD" toothpaste had a bigger reduction in dental plaque than those using normal toothpaste. Analysis of a sub-group of 38 people found that those who used plaque identifying toothpaste had lower levels of hsCRP at the end of the study, while people who used normal toothpaste had higher levels.

The link between poor dental hygiene, high levels of hsCRP and increased heart disease was made in 2010, as we discussed at the time, although there's no direct evidence that one causes the other.

This study doesn't contribute any new findings. There is no evidence that this specific toothpaste is proven to reduce serious cardiovascular outcomes.


Where did the story come from?

The study was carried out by researchers from the University of Illinois and the Florida Atlantic University in the US (and possibly other institutions as not all author affiliations were reported). It was funded by TJA Health, which makes the toothpaste used in the study. The study was published in the peer-reviewed American Journal of Medicine.

The Telegraph reports the study accurately, although it doesn't make clear that the reduction in hsCRP levels was based on just 38 people, nor does it question whether this reduction was caused by lower levels of plaque. The Mail Online calls the toothpaste "revolutionary", although plaque-revealing technologies such as chewable tablets have been around for decades.

It also says that the "special" toothpaste removed twice as much plaque. You could argue that the toothpaste is no more effective at plaque removal, but that people removed more plaque while using it because they could see where the plaque was.

Neither the Telegraph or the Mail mention the potential conflict of interest in regards to the study's funding.


What kind of research was this?

This was a small randomised controlled trial. These types of studies are good ways to compare the effects of treatments. However, in this study, the effects were not actual events (such as heart attacks or strokes) but levels of markers of inflammation, and levels of plaque. This means we have to be careful how much we read into the results.


What did the research involve?

Researchers recruited 61 adults described as "apparently healthy" and randomly assigned them to either 60 days use of plaque identifying toothpaste or what they describe as "identical non-plaque identifying toothpaste".

Their plaque levels were assessed before and at the end of the study using a plaque-revealing mouthwash and photographs taken of the mouth. They had blood tests to measure CRP at the start and end of the study.

The study report is short and does not include much detail about methods. So we don't know, for example, how people were recruited, or how they were randomly assigned to the two groups.

We don't know what instructions they were given about using the toothpaste. The report says they were told to "follow the same brushing protocol", but this is not specified.

We also don't know what happened when people's plaque levels were assessed at the start and end of the study – was that immediately after brushing teeth, after eating, or did researchers specify a certain period of time since last brushing teeth or eating?

Researchers compared the reduction in plaque levels between all 30 people using normal toothpaste and 31 people using plaque identifying toothpaste. However, for hsCRP levels, they concentrated on results from 38 people (19 from each group) because, they say, some people had hsCRP levels of less than 0.5%, which means they would not reasonably expect to see a reduction in their levels.

They also excluded people with very high levels (over 10) which they said were due to "extraneous causes of inflammation," although they don't say what these were.


What were the basic results?

On average, people using plaque identifying toothpaste had a 49% reduction in plaque levels, while those using normal toothpaste had a 24% reduction (confidence intervals not given).

Looking more closely at these results, people who used "Plaque HD" toothpaste had higher levels of plaque at the start of the study, which might mean there was more scope for their levels to reduce. Levels of plaque were about the same when you compare the two groups at the end of the study.

Results for hsCRP were more complicated. When results for everyone in the study were included, the type of toothpaste used made no statistically-significant difference to the reduction in hsCRP levels.

When looking at the 38 people the researchers identify as the "pre-specified subgroup", levels of hsCRP reduced by 29% in people using plaque identifying toothpaste and increased by 25% in those using normal toothpaste (confidence intervals not given).


How did the researchers interpret the results?

The researchers say their toothpaste "produced a highly significant reduction in dental plaque" and "decreased inflammation as measured by hs-CRP." They say that their findings "support the hypothesis that this plaque identifying toothpaste reduces risk of cardiovascular disease."

They add that directly testing the hypothesis would require a large-scale randomised controlled trial big enough and long enough to find out whether use of the toothpaste actually reduces the incidence of heart attacks and strokes.



This study adds some weight to the theory that better oral hygiene may reduce inflammation in the body. However the size of the study and some concerns about its methods and findings mean we should be cautious about hailing plaque identifying toothpaste as a revolutionary new treatment to prevent heart disease.

The study does seem to show that people were able to remove more plaque from teeth while using a plaque identifying toothpaste, which is no doubt a good thing for dental health. However, we don't know exactly which sort of toothpaste was used as the comparison, or how people were told to use it.

If people were told to use the normal toothpaste as they would a plaque identifying toothpaste – for example to brush for a minute, look for signs of plaque then brush again to remove those signs – then they might stop brushing after one minute if they saw no signs of plaque. That could result in them brushing less well than they would normally.

The results on hsCRP are less convincing. Firstly, the statistically-significant results are based on only 19 people from each group. They are hard to interpret, because of the surprising increase in hsCRP among those who used normal toothpaste.

It's unclear why using normal toothpaste would be linked to an increase in hsCRP levels, especially as people using normal toothpaste did reduce their plaque, and had average plaque levels at the end of the study very similar to those who used plaque identifying toothpaste. These findings call into question whether hsCRP levels are linked to plaque levels in this study.

Looking at hsCRP results for everyone in the study (including those with low levels at baseline), average levels start off very similar, then double in the placebo group while staying much the same in the plaque identifying toothpaste group.

These results are not explained. We know that hsCRP levels rise and fall with inflammation anywhere in the body – for example after an injury or an infection. It is possible that these normal day-to-day fluctuations, rather than any reduction in plaque, are behind the results found in this study.

Due to the considerable uncertainty around the methodology of the study it may be sensible not to put too much weight into considering the results of this industry-funded study.

Questions over this study do not mean that it's not important to brush your teeth and reduce plaque, however. Good oral hygiene can prevent painful tooth decay and gum disease.

To keep your mouth healthy:

  • brush teeth twice daily with fluoride-containing toothpaste
  • floss between your teeth
  • eat less sugar and avoid sugary drinks
  • have regular dental check-ups

Read more advice about how to take care of your teeth.

Links To The Headlines

How brushing your teeth could help prevent a heart attack. The Daily Telegraph, October 19 2016

Revolutionary new toothpaste not only removes more plaque but could save you from a heart attack. Mail Online, October 19 2016

Links To Science

Fasula K, Evans CA, Boyd L, et al. Randomized trial of Plaque identifying Toothpaste: Dental Plaque and Inflammation. The American Journal of Medicine. Published online October 19 2016

 Wed, 19 Oct 2016 16:30:00 GMT Anti-inflammatory arthritis drugs may help with depression

"Arthritis pills could help beat depression," The Sun reports. A review of studies suggests anti-cytokine drugs, currently used to treat inflammatory conditions such as rheumatoid arthritis, could have a role in treating depression.

Cytokines are proteins released by cells when the immune system is activated and are linked to inflammatory diseases such as rheumatoid arthritis and psoriasis.

Scientists think there may also be a link between levels of inflammation in the body and symptoms of depression as previous research has found some people with depression have high levels of cytokines.

Researchers decided to look at the effect the treatment had on people's symptoms of depression in studies designed to show improvements to physical symptoms of conditions such as arthritis and psoriasis.

They also wanted to see whether people only felt less depressed if their symptoms of arthritis or psoriasis were better.

They found 20 studies, seven of them comparing anti-cytokine drugs to a placebo. When they pooled the data, they found a small to moderate improvement in depression scores for people taking anti-cytokine drugs. This improvement was not linked to improvements in physical illness symptoms.

We now need to see studies designed to assess the effect of anti-cytokine drugs on people with depression, but no physical illness, to see whether these drugs are safe and effective as a treatment for depression.

It is important to stress that researchers were looking at specialised anti-inflammatory drugs, like infliximab, and not at more widely used anti-inflammatories like ibuprofen. The use of ibuprofen is not recommended for depression.


Where did the story come from?

The study was carried out by researchers from the University of Cambridge, University College London and the University of Texas.

There is no information about specific funding for the study, although the researchers had grants from organisations including the Wellcome Trust, Academy of Medical Sciences and Royal College of Psychiatrists.

The study was published in the peer-reviewed journal Molecular Psychiatry on an open-access basis, so it's free to read online.

The Sun and the Daily Mail cover the study fairly accurately, although neither point out that the effect of the treatment was small in terms of relieving symptoms of depression. However, both make it clear that we don't yet know if the drugs are safe and effective for people with depression.


What kind of research was this?

This is a systematic review which includes three meta-analyses of studies. Meta-analyses are a good way to pool the research in an area, although they are only as good as the individual studies included.

In this case:

  • seven studies were randomised controlled trials (RCTs) comparing cytokine modulator drugs with placebo
  • three were RCTs of cytokine modulator drugs added to other drugs
  • 10 were either not randomised or not placebo-controlled

Only one of the studies looked primarily at the effect of the drugs on depression.


What did the research involve?

Researchers looked for studies of cytokine modulators which measured depression or depressive symptoms. They grouped the studies together and carried out separate meta-analyses of the three different types of study, looking at changes in depression scores between those who took cytokine modulators and those who did not.

They then looked at the RCTs to see whether the change in depression scores could be explained by changes in the physical illnesses being treated. They also carried out analyses to see whether severity of depression symptoms, length of study, sex and age of participants, affected the results.

They did various sensitivity analyses to check for major discrepancies between the study results (heterogeneity), and to see if any individual study had a big influence on the overall results.


What were the basic results?

Seven randomised controlled trials in 2,370 people showed that those taking cytokine modulator drugs had a "small to moderate" improvement in depression symptoms, compared to people who took placebo.

The results were expressed as a "standard mean difference" between symptoms scores of 0.40 (95% confidence interval [CI] 0.22 to 0.59).

However, these figures are hard to interpret as they are the result of combining results from six different depression symptom scoring scales. It's hard to know how clinically important this difference is. The researchers said there was a lot of difference between the degree of symptom improvement in the studies (heterogeneity).

The findings from RCTs comparing cytokine modulator drugs plus another drug to the other drug alone also showed a small to moderate improvement in depression scores. The same was true for non-RCT studies, which showed a bigger standard mean difference – although this was probably because they could not take account of the placebo effect.

Analysis showed no clear link between improvement in depression scores and improvement in physical symptoms. The main focus of the trials was treatment for psoriasis, Crohn's disease, atopic dermatitis, complex regional pain syndrome and rheumatoid arthritis.

Only one study, of 55 people, looked at depression as a primary outcome. This study looked solely at people for whom antidepressants hadn't previously worked. It showed no improvement in depression scores for people taking cytokine modulators, compared to those who took placebo.

Age and sex made no difference to people's likelihood of benefiting from the drugs. Those with more severe depression, however, seemed to benefit more.


How did the researchers interpret the results?

The researchers say their study showed "robust improvements in depressive symptoms after anti-cytokine therapy" with a "small to moderate size effect".

They say the results "suggest inflammatory cytokines may have a key role" in how depression comes about, and that "anti-cytokine drugs may be effective for some patients with depression".

They suggest the antidepressant effect of anti-cytokine drugs should be tested first among people with depression who haven't responded to antidepressants, and who have high levels of inflammatory proteins circulating in their blood.



This study suggests some useful paths for future research into depression, but is not robust enough to allow doctors to start using these drugs to treat people with depression.

Because all but one of the studies included in the review were primarily intended to assess the effect of the drug on another condition, we don't know if they were big enough to reliably assess the effect of the drugs on depression.

Depression symptoms were assessed as secondary outcomes and we need to see trials designed with depression as the primary focus, to get truly reliable results.

It's worth noting that, in all but one study, people were not diagnosed as having depression – the researchers just looked at their scores for depression symptoms. These scores might fall short of a depression diagnosis.

The idea that depression can be triggered by inflammatory proteins in the blood is interesting, and is supported by this study. A recent study looked at non-steroidal anti-inflammatory drugs (NSAIDs, for example ibuprofen) and also found some evidence that they may have an effect on depression.

Many people with depression (about one third) are not helped by usual antidepressant drugs, which alter levels of messenger chemicals in the brain. Treatments targeting inflammatory proteins – another possible cause of depression – might offer hope to some of these people.

Cytokine modulators, including adalimumab, etanercept and infliximab, are more often used for conditions such as rheumatoid arthritis and can have significant side effects. These include making people more vulnerable to infection, severe allergic reactions, cancer and auto-immune diseases. These side effects should make us cautious about using these drugs to treat depression until we know how effective they are.

It is always important to be sure that the potential benefit of a new treatment approach isn't outweighed by associated side effects and complications.

Treatments for depression are not always drug-based. Talking therapies and exercise are often a useful alternative or addition to drug treatments.

Read more about treatments for depression.  

Links To The Headlines

Arthritis pills could help beat depression, new study suggests. The Sun, October 19 2016

Could drugs used to treat arthritis cure depression? New pills for joint pain also found to ease symptoms of the blues. Daily Mail, October 19 2016

Links To Science

Kappelmann N, Lewis G, Dantzer R, et al. Antidepressant activity of anti-cytokine treatment: a systematic review and meta-analysis of clinical trials of chronic inflammatory conditions. Molecular Psychiatry. Published online October 18 2016


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