BMJ: Continuous glucose monitoring in pregnant women halves adverse birth effects

Freestyle libre

Adapted from the BMJ article by Susan Mayor 23 Sept 17

A study has shown beneficial effects in type one pregnant patients. One in two babies born to such women have complications such as prematurity, stillbirth, congenital anomalies, and being too big. These are due to high blood sugar levels in the womb and there has been no reduction in these in the last 40 years.
Denise Feig, the author of the study, based at the University of Toronto, says, “Keeping blood sugar levels in the normal range during pregnancy for women with type one diabetes is crucial to reduce risks for the mother and child. As insulin sensitivity varies through the pregnancy adjusting insulin accurately is complex. Since our results have come through we think that continuous blood sugar monitoring should be available to all type one women.”
In the international study 325 women who were planning a pregnancy or pregnant took part. Two thirds were randomised to get the monitors and the rest had standard treatment. Large newborns were halved and so was neonatal intensive care admissions and hypoglycaemia. Women had a small but significant reduction in HbA1c. They had more time in the normal blood sugar range and hypoglycaemia was not increased.
The extra cost of the monitors could be offset to some extent by the reduced cost of medical care after the birth.

Lifestyle changes add up to a longer life

Adapted from an article by James Hamilton in the Herald 14th October 2017

If you want to improve your life expectancy you can do the sums and see just how much extra time you can have according to Scottish researcher Dr Peter Joshi.
Obesity levels are now three times more than in the 1980s. At that time six percent of men and eight percent of women were affected. This has spurred an Edinburgh team to look into the genes affecting longevity in families and the lifestyle factors that affect life span in individuals. The old nature/ nurture debate again. Overall 600,000 people were tested and their family histories explored.
When it comes to longevity the balance comes down much more to lifestyle than your genes.
Educate yourself: add a year to every year educating yourself beyond school. That’s really like going to university for free. You get the time back at the other end!

Graduated!.jpg
Get slim: add a year for every surplus stone you lose. Diabetes complications is the main factor in causing the reduced life expectancy.
Stop smoking or don’t start: add seven years to your life if you don’t smoke those 20 cigarettes a day.
Praise the parents: some people have a gene that improves their immune function giving an extra six months life expectancy.
Blame the parents: Addiction to drugs and alcohol are somewhat genetically based.
Blame the parents (again): A gene that affects cholesterol reduces lifespan by about eight months.

The full report is the journal Nature Communications.

Which medicines work most effectively for diabetic neuropathy?

What treatments can improve pain and quality of life?

This comprehensive report was first published in April 2017 by Diabetes in Control and discusses what old and new medicines work for diabetic neuropathy and importantly which ones don’t.

Pharmaceutical Products and Drugs
Diabetic neuropathy is a nerve disorder that the National Institute of Diabetes and Digestive and Kidney disease estimates affects about 60 to 70% of diabetic patients in some form, with the highest rates of neuropathy occurring in patients who have had diabetes for over 25 years.

Although diabetic neuropathy can affect almost any organ in the body, the most common type of diabetic neuropathy is peripheral neuropathy. Peripheral neuropathy, which is often worse at night, results in tingling, numbness, and pain occurring in the hands, arms, fingers, legs, feet, and toes.

The best way to prevent diabetic neuropathy is keeping glucose under control and maintaining a healthy weight, but for those who experience this painful condition, finding the best relief can often be difficult and confusing.
Building upon a previously published study from 2014, a new systemic review was conducted to “systemically assess the effect of pharmacological treatments of diabetic peripheral neuropathy (DPN) on pain and quality of life” plus a search of PubMed and Cochrane Database of systemic reviews (reviews from 2011 – March 2016).
A total of 106 randomized controlled trials were used in the final systemic review, including trials analyzed by the previously published study. Only two medications, duloxetine and venlafaxine, had a moderate strength of evidence (SOE) compared to the low strength of evidence found with the remaining 12 study medications. As a class, serotonin-norepinephrine reuptake inhibitors (SNRIs) was found to be an effective treatment for diabetic neuropathy with the most commonly reported adverse effects of dizziness, nausea, and somnolence. Venlafaxine and tricyclic antidepressants were also determine to be effective at relieving pain compared to placebo using the previous analysis’ data.

Pregabalin was determined to be effective at reducing pain compared to placebo but found to have a low SOE due to the inclusion of four unpublished studies causing potential bias. Pregabalin, as well as the other anticonvulsants included, had adverse effects of dizziness, nausea, and somnolence.

Oxcarbazepine was also found to be an effective neuropathy pain reliever compared to placebo.
Atypical opioids have a dual mechanism of action, norepinephrine reuptake inhibition and mu antagonism, which aids in a class wide effective pain relief compared to placebo, and more specifically tramadol and tapentadol were found to be effective vs placebo. The most common adverse effects reported for opioids were constipation, somnolence, and nausea.

The last medication that was determined to be an effective pain reliever of diabetic neuropathy compared to placebo was botulinum toxin

Gabapentin, using five randomized controlled trials, was determined at two different doses to be ineffective at treating pain when compared to placebo. Other agents that were determined to be ineffective treatments for diabetic neuropathy were typical opioids (oxycodone), topical capsaicin 0.075%, dextromethorphan, and mexiletine.

Practice Pearls:
Pregabalin, oxcarbazepine, and tapentadol have shown to be effective vs placebo at relieving pain due to diabetic neuropathy and are also FDA approved for this indication.
Serotonin-norepinephrine reuptake inhibitors may be a good choice for relief of diabetic neuropathy pain and have the additional benefit of relieving depression that is commonly associated with diabetic neuropathy
Additional studies are needed to assess long-term pain relief effectiveness.

References:
“Nerve Damage (Diabetic Neuropathies) | NIDDK.” National Institutes of Health. U.S. Department of Health and Human Services. Web 05 April 2017
Julie M. Waldfogel, Suzanne Amato Nesbit, Sydney M. Dy, Ritu Sharma, Allen Zhang, Lisa M. Wilson, Wendy L. Bennett, Hsin-Chieh Yeh, Yohalakshmi Chelladurai, Dorianne Feldman, Karen A. Robinson. “Pharmacotherapy for diabetic peripheral neuropathy pain and quality of life”. Neurology, 2017; 10.1212/WNL.0000000000003882 DOI: 10.1212/WNL.0000000000003882
 
Mark T. Lawrence, RPh, PharmD Candidate, University of Colorado-Denver, School of Pharmacy NTPD

 

 

 

BMJ: Continuity and individualised care matter more to patients than guidelines

old woman walking

By Martin Rowland and Charlotte Paddison
Adapted from article in BMJ 18 May 2013
As the population rises more people are living with multiple medical conditions. These can be diabetes, rheumatoid arthritis, macular degeneration, depression, cancer, coronary heart disease and dementia among others.

These cause complex health, emotional and social problems which make their management difficult, especially in socioeconomically deprived areas. A new model of care is needed to manage patients optimally in these circumstances.
Although this seems obvious, care seems to be moving in the wrong direction for these patients.
Evidence based guidelines are really geared to patients with single conditions. They don’t cater to someone who has multiple conditions. Over treatment, and overly complex surveillance and assessment routines result. Older, less well educated and less affluent patients cope particularly poorly with these regimes. Guidelines also fail to recognise that patients get more frail as they age. The burdens of illness and treatment are different for a 100 year old compared to a 50 year old.
An individualised regime for each patient needs to be developed to focus on what matters most to each one.
Unfortunately doctors often feel that they can’t deviate from a guideline for fear of criticism and litigation. Perhaps guidelines should only be applied when they are clearly being used in the patient’s best interests, instead of the doctor’s? Exception reporting is a mechanism that allows doctors to deviate from guidelines and maybe should be used more.
Medical training does not as yet focus on this sort of individualised care. Medicine of old age comes the closest.
Listening to patients is the key thing that can help a doctor understand what their needs and goals are. The most appropriate care can then be built around that. The biggest barrier to this seems to be the over emphasis on single conditions.  This prevents rather than enhances goal oriented care.
Longer consultations are needed to help guide patients talk about their needs and think through complex decisions.
Satisfaction and outcomes are improved if this can be achieved. Despite this patients still often complain that they never see the same doctor twice both in hospital and primary care. It is also particularly difficult to provide a good quality of care when a doctor does not  know the patient and does not see the patient for follow up.
Young adults say they want to see the same doctor 52% of the time, but this increases to over 80% in those aged over 75.  More than a quarter of patients however say they struggle to see the doctor of their choice. This seems to be getting worse over time rather than better. Perhaps this is due to nurses taking over a lot of the care regarding chronic illness. Doctors are also increasingly working part time and may be involved in other tasks other than direct patient care. Shift systems in hospitals limit continuity a great deal.
In primary care, advanced access schemes give faster access but at the expense of continuity of care.
Older patients are particularly keen on waiting a few days longer to see the GP of their choice. Booking systems need to allow for both access and continuity.
This can be improved by receptionists attempting to book patients with their “own” doctor rather than simply the first available. Two or three doctors can share lists and try to see each other’s patients if one is not available.  E-mail booking of doctors directly can help. E-mail consultations can help.  Time for these must be built into the working day. The number of doctors who deal with  particularly complex needs may need to be restricted. Monitoring continuity of care can help. What gets monitored tends to get done more often after all.
As guidelines need to become less important for patients with multi-morbidity, a doctor’s clinical judgement becomes more critical.  There can be squads of other health care professionals involved in a patient’s care and deciding what ones are necessary and what ones are not is a useful task.  As the need for the traditional UK General Practitioner is increasing, sadly, their availability and time commitments to patient care seem to be decreasing.

Kris Kresser: Why has the American approach to heart disease failed?

Why Has the American Approach to Heart Disease Failed?
on April 18, 2017 by Chris Kresser 

Tsimane 2

A recent New York Times article correctly suggests that diet and lifestyle changes are far more effective ways to prevent and treat heart disease than statins and stents. But what diet, and what lifestyle? Is it as simple as avoiding “artery-clogging saturated fat,” as the author suggests? Read on to find out why the American approach to heart disease has really failed.
Jane Brody wrote an article in The New York Times called “Learning from Our Parents’ Heart Health Mistakes.” She argues that despite decades of advice to change our diet and lifestyle in order to reduce our risk of heart disease, we still depend far too much on drugs and expensive procedures like stents.
She says:
Too often, the American approach to heart disease amounts to shutting the barn door after the horse has escaped.
To support this argument, she refers to a recent paper published on the Tsimane, an indigenous population in the Bolivian Amazon. The study found that the rate of coronary atherosclerosis in the Tsimane was one-fifth of that observed in the United States (and the lowest that has ever been measured). Nearly nine in 10 Tsimane had unobstructed coronary arteries and no evidence of heart disease, and the researchers estimated that the average 80-year-old Tsimane has the same vascular age as an American in his mid-50s.
I certainly agree with Ms. Brody so far, and her analogy that the American approach to heart disease amounts to shutting the barn door after the horse has escaped is spot on.
The problem is what comes next, as she attempts to answer the question of why the Tsimane have so much less heart disease than Americans:
Protein accounts for 14 percent of their calories and comes primarily from animal meats that, unlike American meats, are very low in artery-clogging saturated fat. [emphasis mine]
Does saturated fat “clog” your arteries?
Artery-clogging saturated fat? Are we still using that phrase in 2017?
As I’ve written before, on average, long-term studies do not show an association between saturated fat intake and blood cholesterol levels. (1) (I say “on average” because individual response to saturated fat can vary based on genetics and other factors—but this is a subject for another article.)
If you’re wondering whether saturated fat may contribute to heart disease in some way that isn’t related to cholesterol, a large meta-analysis of prospective studies involving close to 350,000 participants found no association between saturated fat and heart disease. (2)

Does saturated fat really “clog” your arteries?

Are “clogged arteries” the cause of heart disease?
Moreover, as Peter Attia eloquently and thoroughly described in this article, the notion that atherosclerosis is caused by “clogged arteries” was shown to be false many years ago:
Most people, doctors included, think atherosclerosis is a luminal-narrowing condition—a so-called “pipe narrowing” condition.  But by the time that happens, eleven other pathologic things have already happened and you’ve missed the opportunity for the most impactful intervention to prevent the cascade of events from occurring at all.
To reiterate: atherosclerosis development begins with plaque accumulation in the vessel wall, which is accompanied by expansion of the outer vessel wall without a change in the size of the lumen. Only in advanced disease, and after significant plaque accumulation, does the lumen narrow.
Michael Rothenberg also published an article on the fallacy of the “clogged pipe” hypothesis of heart disease. He said:
Although the image of coronary arteries as kitchen pipes clogged with fat is simple, familiar, and evocative, it is also wrong.
If heart disease isn’t caused by “clogged arteries,” what does cause it?
The answer to that question is a little more complex. For a condensed version, read my article “The Diet-Heart Myth: Why Everyone Should Know Their LDL Particle Number.”

For a deeper dive, read Dr. Attia’s article.
Here’s the 15-second version, courtesy of Dr. Attia:
Atherosclerosis is caused by an inflammatory response to sterols in artery walls. Sterol delivery is lipoprotein-mediated, and therefore much better predicted by the number of lipoprotein particles (LDL-P) than by the cholesterol they carry (LDL-C).
You might think that I’m splitting hairs here over terminology, but that’s not the case. It turns out that this distinction—viewing heart disease as caused by high LDL-P and inflammation, rather than arteries clogged by saturated fat—has crucial implications when it comes to the discussion of how to prevent it.
Because while it’s true that a high intake of saturated fat can elevate LDL particle number in some people, this appears to be a minority of the population. The most common cause of high LDL-P in Americans—and elsewhere in the industrial world—is almost certainly insulin resistance and metabolic syndrome. (I explain why in this article.)
And what is one of the most effective ways of treating insulin resistance and metabolic syndrome? That’s right: a low-carbohydrate, high-fat diet!
News flash: diets high in saturated fat may actually prevent heart disease.
Perhaps this explains why low-carbohydrate, high-fat diets (yes, including saturated fat) have been shown to reduce the risk of heart disease.
For example, a meta-analysis of 17 low-carb diet trials covering 1,140 obese patients published in the journal Obesity Reviews found that low-carb diets were associated with significant decreases in body weight, as well as improvements in several CV risk factors, including decreases in triglycerides, fasting glucose, blood pressure, body mass index, abdominal circumference, plasma insulin, and C-reactive protein, as well as an increase in HDL cholesterol. (3)
(In case you’re wondering, low-carb diets in these studies had a null effect on LDL cholesterol: they neither increased nor decreased it.)
Saturated fat is a red herring.
Instead of focusing so much on saturated fat intake, which is almost certainly a red herring, why not focus on other aspects of the Tsimane’s diet and lifestyle that might contribute to their low risk of heart disease?

For example:
They are extremely active physically; Tsimane men walk an average of 17,000 steps a day, and Tsimane women walk an average of 15,000 steps a day—and they don’t sit for long periods. Ms. Brody does mention this in her article.
They don’t eat processed and refined foods. We have been far too focused on calories and macronutrient ratios and not enough on food quality. We now know that hunter–gatherers and pastoralists around the world have thrived on both high-carbohydrate, low-fat diets (like the Tsimane, who get 72 percent of calories from carbohydrate) and low-carbohydrate, high-fat diets (like the Masai and Inuit).

But what all hunter–gatherer diets share in common is their complete absence of processed and refined foods.
Perhaps if we stopped focusing so much on the amount of fat and carbohydrate in our diet and started focusing more on the quality of the food we eat, we’d be better off.
And of course we also need to attend to the many other differences between our modern lifestyle (which causes heart disease) and the ancestral lifestyle (which prevents it), including physical activity, sleep, stress, light exposure, play/fun, and social support.
The Tsimane study illustrates exactly why an evolutionary perspective on diet, lifestyle, and behavior is so important. It helps us to generate hypotheses on what aspects of our modern way of life may be contributing to chronic diseases like atherosclerosis and gives us ideas about what interventions we need to make to prevent and reverse these diseases.

Thinking clearly: What is mindfulness all about?

Do you ever just wish you could get someone who knows virtually everything that’s known about the brain and quiz them about mindfulness? Well, I do – a lot – and I just got my wish!

It is my pleasure to present this interview with John McBurney MD. A practicing physician with of over 35 years’ experience, he is board certified in Neurology, Clinical Neurophysiology and Sleep Medicine. Dr. McBurney maintains a daily mindfulness meditation practice as well as home yoga practice.

Could you describe the neurological response to mindfulness practice?

Mindfulness practice ultimately comes down to the concept of neuroplasticity.

In mindfulness, in cultivating awareness of the breath and voluntary moment by moment awareness of the brain, we are training the brain – just like when you are learning to play the violin or any other complex skill – we are training to break out of those self-referential ruminative recursive mental states and to achieve an orientation toward the outer world and in the present moment rather than anticipating the future or reliving the past.

contemplative neuroscience mechanisms behind mindfulness

 Could we be losing something by focusing more on the external realities rather than the self?

Occasionally, we do hear of adverse experiences arising from mindfulness. With any robust intervention there are always potential risks.

How long does it take for mindfulness to have a noticeable effect?

The results can happen almost immediately, however, they are also cumulative. We are still figuring out what the minimum effective dose is. 

What is the relevance of the changes in functional connectivity in the brain in someone who has devoted  a monumental amount of time to meditation, such as Tibetan monks, who may put in more than 10,000 hours in to their practice, compared to the likes of you and me?

A very neat study was published by David Cresswell in Biological Psychiatry in 2016. They invited individuals with high level of stress, unemployed adults, to a weekend retreat experience. They were randomised to in 2 groups:

  • a 3 day mindfulness retreat (the treatment group) and
  • a 3 day relaxation retreat where they read stories, told jokes and had a good time (the control group).

The study was conducted in one centre over one weekend, so it is well controlled. Initially, both groups rated the interventions as being equally helpful to them, subjectively.

The researchers looked at the functional connectivity between the dorsolateral prefrontal cortex and the cingulate gyrus. They also looked at Interleukin-6, a known marker of inflammation, that has been previously shown to be elevated in stressed out unemployed people.

Even with this brief weekend mindfulness intervention, the treatment group developed increased connectivity between the dorsolateral prefrontal cortex and the cyngulate gyrus. There was a neuroplastic response even after a 3 day mindfulness retreat. This was also associated with a decrease in the marker IL-6. Even after 4 months, IL-6 was decreased in the treatment group, but in the control group, IL-6 levels continued to rise, independent of whether they managed to get a job or not.

This is also relevant to doctors, who are at high risk for burnout. Because of their work commitments, the mindfulness retreat for doctors was condensed from the standard 8 week model developed by John Kabat-Zinn to a weekend intervention. The question was: does the weekend model work? The research at the University of Wisconsin where this was developed was reassuring: the residents are less stressed out, more effective and have a greater level of satisfaction.

We still don’t know the absolute minimum dose, but it seems that a weekend of mindfulness can be life-changing for the brain.

Another paper published in PLOS ONE from the Benson-Henry Institute for Mind Body Medicine in Harvard looked at the practices such as meditation, prayer, mindful yoga, Tai-Chi, Qi Gong, etc, i.e. ones that elicit a relaxation response (as opposed the stress response).

This study showed that in both novice and experienced practitioners of relaxation response modalities, there were changes in the epigenetic transcription of the genome. There was upregulation of pathways associated with mitochondrial integrity, downregulation of inflammatory pathways, improved insulin-related metabolism and improved nitric oxide signalling.

Long term potentiation, the standard mechanism for memory formation, strengthens existing neural connections. This happens immediately, as you read this. Over time, long term potentiation leads to formation of new connections,through synaptogenesis, dendritic arborisation and neurogenesis i.e. brain structure changes. In turn, this affects the most neuroplastic neurons located in the hippocampus.

mindfulness minimum effective dose response neurology

In reference to this fascinating recent study of the fight or flight response, it seems plausible that breathing regulates our stress levels much more than conscious thought. Could you explain the significance of this in terms of mindfulness?

The ancients believed that emotions reside in the body. This comes up a lot in serious yoga classes.

This highly innovative study shows that the control of the adrenal medulla – the main effector of the stress response – is not from the conscious ruminating thinking centres, but by the motor and sensory cortex.

This explains why breathing, as well as yoga and Tai-Chi, are an important part of meditative practice. In my experience, these kind of interventions do affect the stress response in a beneficial way.

Mindful exercise exists in many form. For example, weightlifters need to be very mindful to maintain perfect form. Cycling is another example: it is vital to concentrate on every pedal stroke and maintain an even cadence. Once you start to day dream, you notice straight away that your output is way worse. This overlaps with the concept of flow. It is about getting in the zone. There is a very inspiring TED talk by Judson Brewer MD, Ph.D. that explains the physiology behind flow and how it is augmented by mindfulness. Mindfulness is work, and it does require discipline. There is a paradox here of non-striving and non-doing while also being disciplined.

You are a sleep medicine expert. Could you comment on the relationship between mindfulness and sleep?

Insomnia is a complex problem with many causes. However, for most people with idiopathic insomnia, the cause is these self-referential recursive ruminations. They aren’t able to “turn their brain off”. Through mindfulness practice, they are generally able to tame the default mode network that’s responsible for ruminating and daydreaming. A simple strategy would be to lie in bed and concentrate on the breath. This would ease the transition between wakefulness and sleep.

mindfulness default mode network neurological basis for the self

Mindfulness is a mainstay treatment for many mental health disorders. What about use of mindfulness in the treatment for organic pathology of the brain usually treated by neurologists?

There is some preliminary data that mindfulness training has a beneficial effect of seizure frequency in patients with epilepsy. It is a medical condition associated with tremendous anxiety and stress, so mindfulness could have a significant benefit in more than one way. It may even have a benefit it terms of remembering to take medication on time, etc.

Some robust studies show that the frequency of relapse in multiple sclerosis decreases with mindfulness intervention. The effect from mindfulness is similar in magnitude to the effect from beta-interferon. 

John Kabat-Zinn used to take the patients who suffered from chronic pain or had diseases for which we had no answer, and those patients got better. Even beyond neurology, there is some evidence that mindfulness can have benefits in psoriasis. We are probably only at the bottom of this mountain.

Dr McBurney has given me so much to think about. I will follow up with part 2 of our discussion that focuses more on the philosophical and life experience aspects of mindfulness once I wrap my head around it.

neurological path mindfulness default mode network adrenal medulla

Sheri Colberg: Joint health is critical to staying active

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Joint Health Is Critical to Staying Active

Diabetes in Control

Without properly functioning joints, our bodies would be unable to bend, flex, or even move. A joint is wherever two bones come together, held in place by tendons that cross the joint and attach muscles to a bone on the other side and ligaments that attach to bones on both sides of the joint to stabilize it. The ends of the bones are covered with cartilage, a white substance formed by specialized cells called chondrocytes. These cells produce large amounts of an extracellular matrix composed of collagen fibers, proteoglycan, elastin fibers, and water. Tendons and ligaments are also made up primarily of collagen.

Joints can be damaged, however, making movement more difficult or painful. Joint cartilage can be damaged by acute injuries (i.e., ankle sprain, tendon or ligament tears) or overuse (related to repetition of joint movements and wear-and-tear over time). Damage to the thin cartilage layer covering the ends of the bones is not repaired by the body easily or well, mainly because cartilage lacks its own blood supply.

Aging alone can lead to some loss of this articular cartilage layer in knee, hip, and other joints—leading to osteoarthritis and joint pain—but having diabetes also potentially speeds up damage to joint surfaces. Although everyone gets stiffer joints with aging, diabetes accelerates the usual loss of flexibility by changing the structure of collagen in the joints, tendons, and ligaments. In short, glucose “sticking” to joint surfaces and collagen makes people with diabetes more prone to overuse injuries like tendinitis and frozen shoulder (1; 2). It may also take longer for their joint injuries to heal properly, especially if blood glucose levels are not managed effectively. What’s more, having reduced motion around joints increases the likelihood of injuries, falls, and self-imposed physical inactivity due to fear of falling.

Reduced flexibility limits movement around joints, increases the likelihood of orthopedic injuries, and presents a greater risk of joint-related problems often associated with diabetes, such as diabetic frozen shoulder, tendinitis, trigger finger, and carpal tunnel syndrome. These joint issues can come on with no warning and for no apparent reason, even if an individual exercises regularly and moderately, and they may recur more easily as well (3). It is not always just due to diabetes, though, since older adults without diabetes experience inflamed joints more readily than when they were younger.

So what can you do to keep your joints mobile if you’re aging (as we all are) and have diabetes? Regular stretching to keep full motion around joints can help prevent some of these problems, and also include specific resistance exercises that strengthen the muscles surrounding affected joints. Vary activities to stress joints differently each day. Overuse injuries occur following excessive use the same joints and muscle in a similar way over an extended period of weeks or months, or they can result from doing too much too soon.

Doing moderate aerobic activity that is weight-bearing (like walking) will actually improve arthritis pain in hips and knees (4). People can also try non-weight-bearing activities, such as aquatic activities that allow joints to be moved more fluidly. Swimming and aquatic classes (like water aerobics) in either shallow or deep water are both appropriate and challenging activities to improve joint mobility, overall strength, and aerobic fitness. Walking in a pool (with or without a flotation belt around the waist), recumbent stationary cycling, upper-body exercises, seated aerobic workouts, and resistance activities will give you additional options to try.

Finally, managing blood glucose levels effectively is also important to limit changes to collagen structures related to hyperglycemia. Losing excess weight and keeping body weight lower will decrease the risk for excessive stress on joints that can lead to lower body joint osteoarthritis (5). Simply staying as active as possible is also critical to allowing your joints to age well, but remember to rest inflamed joints properly to give them a chance to heal properly. You may have to try some new activities as you age to work around your joint limitations, but a side benefit is that you may find some of them to be enjoyable!

References:

  1. Abate M, Schiavone C, Pelotti P, Salini V: Limited joint mobility in diabetes and ageing: Recent advances in pathogenesis and therapy. Int J Immunopathol Pharmacol 2011;23:997-1003
  2. Ranger TA, Wong AM, Cook JL, Gaida JE: Is there an association between tendinopathy and diabetes mellitus? A systematic review with meta-analysis. Br J Sports Med 2015;
  3. Rozental TD, Zurakowski D, Blazar PE: Trigger finger: Prognostic indicators of recurrence following corticosteroid injection. J Bone Joint Surg Am 2008;90:1665-1672
  4. Rogers LQ, Macera CA, Hootman JM, Ainsworth BE, Blairi SN: The association between joint stress from physical activity and self-reported osteoarthritis: An analysis of the Cooper Clinic data. Osteoarthritis Cartilage 2002;10:617-622
  5. Magrans-Courtney T, Wilborn C, Rasmussen C, Ferreira M, Greenwood L, Campbell B, Kerksick CM, Nassar E, Li R, Iosia M, Cooke M, Dugan K, Willoughby D, Soliah L, Kreider RB: Effects of diet type and supplementation of glucosamine, chondroitin, and msm on body composition, functional status, and markers of health in women with knee osteoarthritis initiating a resistance-based exercise and weight loss program. J Int Soc Sports Nutr 2011;8:8

 

In addition to my educational web site, Diabetes Motion (www.diabetesmotion.com), I also recently founded an academy for fitness and other professionals seeking continuing education enabling them to effectively work with people with diabetes and exercise: Diabetes Motion Academy, accessible at www.dmacademy.com. Please visit those sites and my personal one (www.shericolberg.com) for more useful information about being active with diabetes.