Could Artificial Sweeteners Cause Diabetes?

Artificial sweeteners are commonly touted as a healthy alternative to natural sugar. Sweeteners contain low to no calories (read about the types of sweeteners here), and they do not make blood sugars spike in diabetics.   However, a growing body of research lends a growing amount of concern to possible negative side to artificial sweetener use. 

A fascinating set of studies was collected and published recently in Nature, looking at how artificial sweeteners affect the bacteria in our intestines, and how these effects in turn may actually increase the risk of developing diabetes or pre-diabetes.  For the scientist with a couple of hours and a day with a good attention span may want to read the article for themselves – it’s heavy but super.  Here are the key results of their studies:

Both lean and obese mice who were fed artificial sweetener (saccharin, sucralose, or aspartame) were more likely to develop prediabetes compared to mice fed glucose or sucrose. (read more about different types of sugar here).

They showed that the development of prediabetes in these mice was caused by a change in the types of bacteria in the mice’s intestines.  These altered bacteria are better at making calories from food accessible for absorption, meaning that mice (or humans) more readily absorb these calories, thereby contributing to higher blood sugars (and probably weight gain as well).

In humans, survey type studies have shown that people who use artificial sweeteners are more likely to be people with weight struggles and diabetes, but whether the artificial sweeteners cause these problems, or whether it is simply that people who have these problems are more likely to consume artificial sweeteners to help fix these problems, is difficult to separate.    The authors therefore looked at a very small group of seven study participants who didn’t normally consume artificial sweeteners, and they found that when they ate artificial sweeteners for a week, four of the seven participants developed an increase in their blood sugars by the end of the week.  An examination of these people’s stools (oh yes they did) showed a marked change in the bacteria growing in their intestines after a week of artificial sweeteners. When they transplanted the stool of the people who developed higher blood sugars into mice (oh yes they did), the mice then went on to develop higher blood sugars as well.

So, in summary, these elegant studies suggest that artificial sweeteners may change the types of bacteria that grow in our gut, to types of bacteria that cause us to absorb more calories from food into our bloodstream, with the increase in sugar absorption increasing the risk of diabetes.  

So what is the best solution?  Eating added natural sugar undoubtedly increases our risk of diabetes, obesity, and metabolic syndrome, and there is now emerging evidence to suggest that artificial sweeteners may not be good for our metabolism either.

The best answer is to avoid adding added sweetener period, be it sugar or artificial sweeteners. 

Thanks to my friend and colleague, Pam, for the heads’ up on this article.

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Gut Bugs and Obesity

There is a lot of interest and excitement in the research going on about the microscopic organisms that reside in our intestines (called 'gut microbiota').  And so there should be! Did you know that human beings are not actually 100% human, but that we are actually made up of 90% gut microbiota cells and only 10% human cells?  Mind boggling, isn't it.

It turns out that we have evolved to welcome gut microbiota into our own personal ecosystems, such that these bugs actually do some work for us behind the scenes.  For example, while simple and complex polysaccharides (ie, dietary fiber) escape digestion by our upper gastrointestinal (GI) tracts, they can be transformed by bacteria into digestible substances such as sugars or short chain fatty acids.   These short chain fatty acids are involved in regulation of fat storage in the liver and throughout the body via numerous mechanisms that we are only just beginning to understand.

The type of gut bugs we carry is important, but the story is far from clear.  In studies of rodents, obesity seems to be associated with carrying more of the Firmicutes phylum and less of the Bacteroides phylum, but the research is quite conflicted on this when it comes to humans.   If there is a relationship between the type of bacteria and obesity,  it's unclear which is the chicken and which is the egg - in other words, did these bacteria contribute to obesity, or does developing obesity (or eating a poor diet, thus increasing the risk of obesity) change the gut bacteria towards this particular balance?

The gut microbiota also appear to play a role in the production of gut hormones (such as GLP-1) that signal our brains that we are feeling full during a meal, and this response differs depending on what type of bacteria we carry.   Certain types of gut bugs may also stimulate production of inflammatory chemicals by our immune systems that contribute to the risk of insulin resistance, type 2 diabetes, metabolic syndrome, and so forth.

There are probably more unanswered questions than answered ones at this point in the area of the gut microbiome and how it plays into obesity, and thankfully, there is a lot of research ongoing in this area.  A growing body of evidence supports the possibility of prebiotic or probiotic approaches to changing the composition of the gut microbiota in favor of certain types of gut bugs, thereby having a positive impact on obesity and related diseases.    I will be following this area with interest!

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Does Metformin Decrease Heart Risk in Polycystic Ovary Syndrome?

Metformin is a medication that is considered the first line treatment for type 2 diabetes globally.  One of the reasons why is because it is the only diabetes medication that has data to suggest that it decreases the risk of heart disease.  Metformin can also be used to regulate menses in women with polycystic ovary syndrome (PCOS)- could metformin help decrease heart risk in these women as well?   A recent study has endeavored to answer this question.

The study randomized 50 women with PCOS to receive either the birth control pill, or the birth control pill plus metformin, for 6 months, and they looked at the effect these treatments had on the thickness of the inner wall of the carotid artery (called 'carotid intima media thickness') as well as the ability of arteries to dilate (called 'flow mediated dilatation').

While their findings were not significantly different between groups, numerically, the carotid artery wall grew thicker in the women on the pill, whereas it became thinner in women who were also on metformin.  A thicker inner wall is considered a marker for heart disease risk.   The ability of arteries to dilate was also a little better numerically on metformin (but again, not statistically significant); arteries that are better able to dilate are healthier and are associated with lower risk of heart disease.

So, while this was technically a 'negative' study in that no statistically significant difference was shown, I agree with the authors that the numbers may have become significant if the number of patients in the study was larger (50 patients is a very small study).  There is good reason to think that metformin could decrease heart disease risk in these women, as PCOS is a condition where the body is more resistant to the effects of insulin, and metformin works by decreasing the body's resistance to insulin, thereby improving many metabolic parameters.

The ability of metformin to decrease heart disease risk in women with PCOS now needs to be studies in much larger clinical trials, so that we can get an answer to this important question.

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Is Lifespan Shortened By Obesity?

What is the impact of obesity on our lifespan?  The answer may be more complicated than you might think.

An interesting study published in Lancet Diabetes & Endocrinology looked at data from nearly 4.000 people, where they built a statistical model to estimate the effect on lifespan of having a body mass index (BMI) in the overweight category (25-29.9), obesity (BMI 30-34.9), 'very obese' (BMI 35 or higher), compared to an ideal BMI of 18.5-25.

They found that the effect of excess body weight on years of life lost was highest in younger individuals.  For example, very obese men aged 20-39 lost 8.4 years of life, whereas very obese men aged 60-79 years lost only 0.9 years.  Similarly, very obese women aged 20-39 years lost 6.1 years of life, whereas very obese women aged 60-79 lost 0.9 years of life.

The fact that excess body weight has less negative impact on lifespan as we get older may reflect that a little extra body weight may be protective as we age, as we then have more energy supply to sustain us if we become ill with a condition that causes us to lose weight (which could be anything from a bad flu to cancer). It may also be reflective of the obesity paradox - people with certain medical conditions (such as heart disease or kidney failure) with obesity have been found to have better survival than people with these conditions who are lean.  This may be because of the benefit of having extra energy stores on board, or could be because thin people with serious medical problems may simply be sicker.

So, while optimum weight management appears to be most important in our younger years, it is still important throughout our lives, with a slight shift in focus over time.

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Testosterone Treatment In Men - Risk To The Heart?

At the Endocrine Society’s recent ENDO 2015 meeting in San Diego, I managed to score a seat in a packed-to-overflowing symposium discussing some of the controversies surrounding testosterone therapy in men.

At the heart of the discussion ws the fact that testosterone prescribing in men has dramatically increased over the last several years, primarily due to an increase in prescribing of this hormone to men who do not have a medical reason for failure of testosterone production (ie a testicular or pituitary problem), but rather, are men who have a low-ish testosterone due to aging or obesity, in hopes that they may feel better with testosterone therapy.   The prescribing of testosterone in men without a true failure of testosterone production has raised a number of safety concerns – in particular, whether testosterone may increase the risk of heart attacks or stroke.

The first point that was made in the symposium by Dr Alvin Matsumoto is that men may be labelled as having low testosterone, when, in fact, they don’t.  The problem here lies with a number of concerns with the accuracy of measurement of testosterone levels in men:

• First of all, testosterone needs to be measured in the morning, as levels are highest in the morning and fall later in the day; 'normal' ranges have been developed based on the early morning measurements.  
• Second, there are a lot of problems with the accuracy of testosterone measurement - one study looked at over 1000 different labs and found that testosterone levels on the same sample varied by 6 fold (ranging from very low to well within the normal range).  
• Third, testosterone levels are not the same from day to day in one particular man - in fact, in men who have a low testosterone measured initially, about a third will have a normal level on repeat testing.  

Dr Shehzad Basaria then took us through an excellent review of the conflicting data around the effect of testosterone on cardiovascular (CV) risk.  Population studies suggest that testosterone treatment decreases the risk of CV events, but it is possible that it is men more concerned about/interested in their health that were taking the testosterone, so these results may just reflect that healthier men were tending to take testosterone in the populations studied.  Other retrospective studies, on the other hand, have suggested that testosterone treatment increases the risk of CV events – these studies suggested that it is older men, and those with pre-existing heart disease, who had the highest risk.  This is highly relevant to the discussion of whether it is safe to prescribe testosterone to men with age- or obesity-related decline in testosterone, as this is a group of men who are older and more likely to have pre existing heart disease.

We always look to randomized, controlled clinical trials for the answers to these questions if at all possible – and in fact, a recent study called the TOM study was stopped early because they saw a higher risk of CV events in the group of men receiving testosterone treatment.   The TOM study results have been criticized because they were studying muscle strength as their primary endpoint of interest and not CV events per se – but the results are what they are.

As far as how exactly testosterone treatment could increase the risk of heart attacks, we don’t know, but several possibilities have been suggested, including increase in clotting tendency/inflammation, driving testosterone levels too high with treatment, and fluid retention.

Because of the concerns that testosterone treatment may increased the risk of cardiovascular events, the FDA has now stated that testosterone treatment is only approved for men with true failure of testosterone production caused by certain medical conditions (these would include a primary problem with the testicles such as previous injury, mumps, or chromosomal issues; or the pituitary gland such as a pituitary tumor or radiation damage). They go on to state that the benefit and safety of testosterone has not been established for the treatment of low testosterone due to aging, even if a man's symptoms seem related to low testosterone.  The FDA also now mandates that the labeling for testosterone treatments includes a warning that it may increase the risk of heart attack or stroke.

Clearly, much more research is needed to answer our questions in this controversial area.

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Bariatric Surgery For Diabetes Prevention?

Over the last decades, many modalities to prevent type 2 diabetes have been studied.  Lifestyle changes, particularly if they result in weight loss, can be very powerful to prevent this condition.  Of all of the medications studied, only metformin has so far been recommended to decrease the risk of developing diabetes in people who have prediabetes.  Now, studies are coming out, showing that bariatric (obesity) surgery can be very powerful to prevent type 2 diabetes.

One such study, published recently in The Lancet (Diabetes & Endocrinology),  looked at over 2000 patients who had bariatric surgery, and compared them to a group of matched patients who had not had obesity surgery.  They found that, over a median of 2.8 years and a maximum of 7 years of follow up, patients who had bariatric surgery had an 80% lower risk of developing diabetes compared to people who had not had bariatric surgery.

Another recent study was a systemic review and meta-analysis that looked at the power of different interventions to prevent diabetes. In examination of studies of physical activity +/- diet, anti diabetic medications, obesity medications, and bariatric surgery, they found all of these strategies to be of benefit.  Bariatric surgery stood out as being the most effective to prevent diabetes, with a 90% reduction in risk.

So the question then becomes, should we advocate for obesity surgery for the purpose of prevention of diabetes?  Well, as for any treatment or prevention of any medical condition, it's important to balance the benefits vs risks.  Bariatric surgery is invasive, and the most successful modalities (gastric bypass and sleeve gastrectomy) are permanent procedures.  These procedures have a long list of possible complications that need to be taken into consideration.

While bariatric surgery may be the best treatment option for some patients with obesity and existing type 2 diabetes, obstructive sleep apnea, severe high blood pressure, or severe osteoarthritis, it seems that using surgery solely to prevent these conditions may be outweighed by potential risks.  That being said, a marked reduction in risk of developing type 2 diabetes is certainly an added bonus to the patient having bariatric surgery who is having bariatric surgery for other reasons.


Thanks to my friend Gord for the inspiration for this blog post!

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ENDO 2015: Diabetes and Bones

And....we're off!!! ENDO 2015 is off to a fabulous start.  I'm excited to share with you our learnings about diabetes and bone disease from a symposium held this morning.  You'll need a few extra minutes to read this post - it's a little longer than my usual blogs - so much to cover and share!  Grab a cuppa and get comfy. :)


We were first provided an overview of the impact of type 1 diabetes (T1DM) and type 2 diabetes (T2DM) on the skeleton, by Dr Ann Schwartz.  We learned that diabetics are at an increased risk of fracture (broken bones) than people without diabetes. In T1DM, bone density is lower than in non diabetics, suggesting a moderately increased risk of hip fracture.  However, studies have shown that a type 1 diabetic is actually at over a 6 times higher risk of a hip fracture compared to a non diabetic (much higher than differences in bone density would suggest), suggesting that there is much more to the story than a lower bone density.

In type 2 diabetics, the situation is different.  As 90% of T2DM patients struggle with overweight or obesity, bone densities are higher, a result of the higher body weight that the skeleton supports. Despite this, T2DM patients are at 40% higher risk of hip fracture; after adjusting for body mass index (BMI), there is a 70% increased risk of hip fracture compared to non diabetics.  

While diabetics are at a higher risk of falls (see below for more thoughts on this), studies that controlled for falls still show a higher fracture risk – again suggesting that there is something going on in the bones themselves that increase fracture risk.

So why are diabetics at a higher risk of fracture for a given bone density?  Many possibilities have been suggested in terms of differences in bone structure at the microarchitectural level, but as Dr Mary Larsen Bouxsein pointed out, there is little that is currently understood about exactly what is happen at the microscopic level in terms of the damage that high blood sugars could be doing to bone.  Dr Josh Farr showed us data suggesting that cortical bone microarchitecture in women appears to be compromised in T2DM due to decreased bone formation and turnover, but these studies are limited by size and data are not available in men.

As diabetics have a higher fracture risk for a given bone density, our traditional means of evaluating fracture risk may not be appropriate.  It has been shown that bone density testing (using the T score) does predict risk of hip fracture in diabetics, but at a particular T score, the fracture risk is higher than a non diabetic with the same T score.  The FRAX score, which we often use to predict risk of fracture in our patients, underestimates the risk of fracture in T2DM.

Medications that treat type 2 diabetes may have variable effects on bone as well, as reviewed by Dr Christian Meier.  Metformin, our first line treatment for type 2 diabetes, seems to be protective of the bones.  We know that the group of medications called thiazolidinediones increase the risk of fracture in postmenopausal women and older men, and with longer duration of treatment. There is some evidence to suggest that the group of type 2 diabetes medications called incretin therapies may be protective of bone, but much further study needs to be done.  A newer class of medications called the SGLT2 inhibitors may slightly increase fracture risk, but again, much more study is needed in this area.

A few important points that I would like to highlight (from this session, as well as my own thoughts):  

• It is crucially important to avoid low blood sugars in patients with diabetes.  A low blood sugar can cause a fall that can result in a fracture.  
• Prevention of diabetic nerve damage is also crucial, as fall risk increases in those who have loss of sensation to their feet.  
• Being fit and strong is also important to prevent falls. 
• Finally, checking vitamin B12 in patients on metformin is important as well, as low vitamin B12 can cause nerve damage, and metformin can rarely cause vitamin B12 levels to be low.

Follow me on twitter! @drsuepedersen

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