Peeing At Night? Could Be Sleep Apnea

Many people get up to pee at night.  This could simply be a reflection of drinking water before bedtime, caffeine, or alcohol, or it could be a symptom of a medical problem, one of which is sleep apnea.

Obstructive sleep apnea (OSA) is a condition where the upper airway is obstructed during sleep, causing pauses in air intake despite an effort to breathe.  The severity of OSA is determined by the number of apnea (no airflow) or hypopnea (decreased airflow) during an hour, measured during overnight testing:

• mild OSA: 5-15 events per hour
• moderate OSA: 15-30 events per hour
• severe OSA: over 30 events per hour

Obesity is a common cause of OSA, but it can also be caused by decreased muscle tone of the upper airway (due to neurologic conditions or substances such as alcohol, sedatives, or muscle relaxants), or variance in the structure of the upper airway. 

So how does OSA cause a person to pee excessively at night?  Research has shown us that the negative pressures generated in the chest by trying to inhale against a blocked airway cause increased blood return to the right side of the heart.  This, in combination with other pressures placed on the heart by OSA, cause the heart to release a hormone called atrial natriuretic peptide (ANP) that tells our kidneys to excrete more sodium and water.  

Other common symptoms of OSA include daytime sleepiness, morning headaches, difficulty concentrating, restless sleep, and snoring. OSA is not thought of or tested for enough, and as a result, there are many unrecognized cases of OSA out there.

There are many other medical problems that can cause a person to pee at night, ranging from bladder issues, to prostate problems, to uncontrolled diabetes, to congestive heart failure, to several others.   For health care providers, it's important to consider obstructive sleep apnea on this list when a patient tells us they are urinating often at night.   If you are a patient urinating excessively at night, be sure to speak to your doctor about it.

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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!

Follow me on twitter! @drsuepedersen

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