Australian Physiotherapy Association Aquatic Group - Diabetes Information Pack 2010

By Darren Elliot and Lisa Gilkes

Diabetes is a very large problem in Australia. To give the reader a tangible and relevant idea of the extent of the problem, the following statistics have been taken from Diabetes Australian Facts 20081:

  • The prevalence of diagnosed diabetes more than doubled between 1989–90 and 2004–05.
  • Diabetes and its complications were responsible for around 8% of the total burden of disease in Australia in 2003.
  • People with diabetes were twice as likely as people without diabetes to have a heart attack and three times as likely to have a stroke.
  • People with diabetes were twice as likely to have cataracts or glaucoma as those without diabetes and nearly a third of end stage kidney disease was caused by diabetic nephropathy.

It is an even more serious problem in the Aboriginal and Torres Strait Islander population as these peoples are 3 times as likely as non-Indigenous people to have diabetes and have much greater hospitalisation and death rates than other Australians1.

In 2003, type 2 diabetes was the second leading specific cause of health loss in males and the fourth in females in Australia3.

Diabetes has quite a large health burden in Australia. The following stats are again from Diabetes Australian Facts 2008.

  • An estimated 700,000 Australians (3.6% of the population) had diagnosed diabetes in 2004–05. It was also estimated that for every diagnosed person with diabetes there was one undiagnosed person with diabetes in Australia.
  • In 2005, nearly 3% of deaths in Australia were directly due to diabetes and it contributed to another 6% of deaths - nearly 12,000 deaths in total.
  • Diabetes was responsible for 5.5% of the total burden of disease in Australia in 2003; 92% of this burden was due to Type 2 diabetes, which is by far the most common type. When the contribution of diabetes to stroke and heart disease is also included, it accounted for 8.3% of the total disease burden.

Diabetes Australian Facts 2008 also found that diabetes in Australia was becoming more prominent

  • Between 1989–90 and 2004–05, the proportion of people with diagnosed diabetes more than doubled from 1.3% to 3.3%. The rise is largely driven by an increase in the prevalence of Type 2 diabetes;
  • Between 2000–01 and 2004–05, the rates of diabetes hospitalisation increased by 35%, from 1,932 hospitalisations per 100,000 people to 2,608 per 100,000.

Diabetes effects are widespread

  • It was treated in over 500,000 hospitalisations in 2004–05.
  • More than half (56%) of the people with diagnosed diabetes in 2003 also had a disability. A quarter considered diabetes as the main condition causing their disability.
  • In 2004–05 there were 3,394 lower limb amputations among people with diabetes.
  • 1999–2000 about 30% of men with self-reported diabetes were suffering from impotence, which is likely to be linked to their diabetes.

What is Diabetes?

Diabetes mellitus is a group of chronic metabolic conditions, all of which are characterized by elevated blood glucose levels (BGL) resulting from the body s inability to produce insulin or resistance to insulin action, or both 2.  Diabetes can be classified thus:

  • Type 1 - an absolute deficiency of insulin due to autoimmune destruction of the pancreatic beta cells
  • Type 2 - a lifestyle disease that develops when there is abnormal levels of insulin resistance and the pancreas cannot produce enough insulin to offset the resistance. About 83% of self-reported cases of diagnosed diabetes in 2004–05 were Type 2. Type 2 diabetes is more common among people aged 45 years or over1.
  • Gestational diabetes - which is diagnosed routinely with screening during pregnancy. No specific cause has been identified, but a theory is that the pregnancy hormones increase insulin resistance, resulting in impaired glucose tolerance.
  • A group of other types of diabetes caused by specific genetic defects of beta-cell function or insulin action, diseases of the pancreas, drugs or chemicals.2

Gestational diabetes and type 1 account for 10% of diabetics.

While diabetes type 1 and type 2 used to be (and still is by some people) described as insulin dependent and non - insulin dependent, these terminologies are not accurate, as many type 2’s who have insufficient insulin production are increasingly being prescribed insulin. 50% of patients will require insulin 6 years post diagnosis, and most will eventually need to take it due to the natural course of the disease - this is regardless of which type of drug they take earlier in the course of the disease4.

Type 2 diabetes is no longer being called adult onset diabetes either, with more and more children being diagnosed with this lifestyle disease. McMahon et al (2004) studied diagnosed type 2 adolescents between 1990 and 2002 at PMH and found mean age at diagnosis of 43 patients was 13 years. Also, of these children, 59% had hypertension and 24% had hyperlipidemia5.


Short-term effects of diabetes may be polyuria, polydipsia, and polyphagia. The body’s short-term response to hyperglycemia is to try and dilute the glucose concentration. To achieve this, the body can increase water intake (polydipsia) and or excrete glucose from the urine (polyuria). The Polyphagia is thought to be the result of insufficient glucose transporting into the body’s cells, leaving the cells “hungry” and stimulating a need for food.

Long Term Complications:

Hyperglycemia causes damage to the endothelial lining of blood vessels. This damage can lead to atherosclerosis, macrovascular and microvascular disease. The vascular damage that occurs causes many flow on effects that could be seen as much more detrimental than the hyperglycemia itself. Diabetes has been found to be an independent risk factor of Cardiovascular Disease death rates when controlling for other risk factors such as current smoking, hypertension, or high cholesterol8.

Haffner et al (1998) compared fatal and non-fatal myocardial infarctions in a Finnish diabetic population with those of a non diabetic population9. The authors found the seven-year incidence rates of myocardial infarction in nondiabetic subjects with and without prior myocardial infarction at base line were 18.8 percent and 3.5 percent, respectively. The seven-year incidence rates of myocardial infarction in diabetic subjects with and without prior myocardial infarction at base line were 45.0 percent and 20.2 percent, respectively

Atherosclerosis is a chronic inflammatory condition initiated in the endothelium in response to injury and maintained through the interactions between modified lipoproteins, particularly low-density lipoprotein (LDL) cholesterol, T-lymphocytes, monocyte-derived macrophages, and the normal constituents of the arterial wall6. Once the LDL crosses the endothelium, the ensuing inflammation stimulates a chain of events within the artery walls that results in adhesion of circulating white blood cells to the endothelium, and smooth muscle proliferation within the artery walls. The collagen and water binding properties within the artery wall are also modified, and the smooth muscle cells within the walls proliferate in response to the changes resulting in arteries which have thickened, non functional smooth muscle walls. Overall, the arteries have a more permeable endothelium, a thickened fibrous cap and are at a resting state of inflammation. This has serious implications for people with diabetes and helps to understand why coronary artery disease, stroke, and peripheral vascular disease occur. Interestingly post prandial hyperglycemia, (hyperglycemia after meals) may be more predictive of atherosclerosis than fasting glucose or HbA1c7.

The microvascular complications that occur in people with diabetes occur as these smaller vessels have similarly weakened walls, which cause increased leakage of blood, protein and can rupture. Brownlee (2001) explains that such changes lead to oedema, ischemia, and hypoxia induced neovascularisation in the retina, proteinuria, glomerulosclerosis in the kidney and axonal degeneration in peripheral nerves7.

A growing body of evidence shows that endothelial dysfunction might even precede the development of type 2 diabetes and modify the progression of vascular atherosclerotic alterations10. Any further elaboration of this vast subject matter is beyond this document.

Musculoskeletal Complications of Type 2 Diabetes

The misconception within some circles of healthcare and physiotherapy is that diabetes is seen as not being relevant as some clinicians view diabetes as a “sugar problem” that has no widespread effects on other bodily systems. Diabetes is unfortunately becoming increasingly prevalent in all areas of physiotherapy including musculoskeletal physiotherapy, and its effects and associated trends are becoming more obvious. This section has been included to enable the reader to see that diabetes might be included in the clinical picture in many physiotherapy settings including musculoskeletal clinics.

Due to increased glucose in the blood, normal metabolic glucose transport is circumvented (normally glucose requires enzymatic transport), and what ensues is non-enzymatic glycosylation of tissues11. This in turn creates a byproduct in affected tissues that modifies protein structure and function, leading to angiogenesis and increased extracellular matrix synthesis. This cascade can lead to many complications in the musculoskeletal system (and otherwise).

Browne, et al (2001) identifies this glycosylation of connective tissue as one of the 6 possible reasons for increased incidence of musculoskeletal disorders within the type 2 diabetic population12. The other 5 potential mechanisms for musculoskeletal disorders within the type 2 diabetic population are:

  1. Increased CT deposition due to proliferation of myofibroblasts
  2. Neuropathy
  3. Vascular insufficiency
  4. Abnormal levels of insulin
  5. Obesity

Brown et al (2001) reviewed commonly seen musculoskeletal disorders within the diabetic population and found the following trends:

  • Shoulder adhesive capsulitis: defined as shoulder pain with decreased range of movement, occurring in up to 30% of patients with diabetes, compared with 2.5% of non diabetic population
    • More commonly bilateral in Diabetes
  • Shoulder hand Syndrome: adhesive capsulitis, painful, swollen, tender hands associated with vasomotor and skin changes.
    • Large overlap with reflex sympathetic dystrophy
    • 7.4% of patients with SHS had diabetes
  • Cheiroarthropathy skin is thickened and tight, patients may exhibit the ‘prayer sign’ due to flexor tendon contracture
    • Cheiroarthropathy is more known for its associations rather than its symptoms, with proliferative retinopathy and neuropathy having a 9.3 and 3.3 fold risk increase13.
  • Dupuytren’s: focal flexor contracture and thickened palmar fascia
    • Associated with a 2x higher risk of vision threatening retinopathy and a 5x increase in foot ulceration
  • Carpal Tunnel Syndrome
    • Fibrosis of flexor retinaculum of wrist, along with neural ischemia in diabetes
    • Corticosteriod injection is less helpful in diabetes as the aetiology is usually non inflammatory, and this treatment can prolong hyperglycemia
  • Hyperostosis
    • Due to the anabolic effects of insulin on bone, vertebral hyperostosis which mirrors ankylosing spondylitis causes ossification of the vertebral ligaments
  • Gout, and arthritis
    • Hyperuricemia is associated with insulin resistance even prior to the development of diabetes, along with diuretics which predispose to gout

Annemans et al (2008) studied gout retrospectively in UK and Germany GP practices and found that in Germany the most common co-morbidity was diabetes (25.9%)14.

Riedel et al (2004) in their study of gout and prescription medication point out that the medications used to treat common co-morbidities, particularly diuretics and prophylactic aspirin, could potentially contribute to development of gout.15

Due to the high proportion of overweight and obese individuals who have type 2 diabetes, osteoarthritis is commonly found within this patient group. Diabetes and osteoarthritis do not have a causative relationship, once adjusted for weight within this population12.

Approximately 82 000 lower-extremity amputations directly related to diabetes are performed in the USA annually16. Of these amputations, the majority (80%) are preceded by foot ulceration. The prevalence of lower limb amputations in Australia was 13.97 per 100 000 total population between 1995 and 199817.

The risk for Diabetic Foot Syndrome increases with age, height and diabetes duration, but not with current glycaemic control or blood pressure16.

Diabetic osteoarthropathy (also known as Charcot arthropathy) is a severe, destructive form of degenerative arthritis resulting from a loss of sensation in the involved joints12. It most commonly affects the pedal bones. Loss of sensation leads to inadvertent (and unnoticed) repeated microtrauma to the joints, which leads to degenerative changes. Fractures ensue, and due to the decreased/absent sensation and pain the patient continues to walk on the foot causing severe deformities and eventually amputation

Abdominal adipose tissue: not just a storage site

Adipose tissue is no longer thought of as a passive storage site. It is made up of biologically active cells and can be thought of as an endocrine organ. It produces many molecules including leptin (appetite suppresant); adiponectin (hypothesised to contribute to decreased insulin sensitivity); cytokines (low level chronic inflammation and insulin resistance) which increases the risk of cardiovascular disease, high blood pressure, and blood clotting.

Fat is the largest endocrine organ in the body18 and it secretes hormones and other factors that travel throughout the body signaling the musculoskeletal system, pancreas, liver, heart, adrenal glands, and central nervous system. It can also release aberrant factors that can cause or amplify metabolic disorders. Thus, adipose tissue may play a role in causing diseases such as type 2 diabetes and cardiovascular disease18.

Exercise and diabetes

Exercise is intricate in managing type 2 diabetics, and as shown below has many benefits outside of ‘weight loss’ – which may have been thought of in the past as the only benefit to exercise.

  • Reduces cardiovascular risk factors 26
  • Improves the control of blood glucose levels 28, 22, 21, 23, 24, 20
  • Helps decrease waist measurement 23 and in particular, body fat 22, 20
  • Decreases visceral adipose 22
  • Every percentage point reduction in mean A1C correlates with a 37% reduction in risk of micro-vascular complications and a 21% reduction in risk of any diabetes-related end point and diabetes-related deaths 30 (note sub 6 HbA1c is not clinically beneficial, and can lead to complications also 32)
  • Improves QOL 28
  • Significantly increases the body’s response to insulin (endogenous and exogenous) 21
  • Improves body composition 22, 21 muscle strength 21, 29 and workload capacity
  • Reduces blood pressure 21
  • Significantly reduces plasma triglycerides 22


  • If a pt has moderate weight loss soon after diagnosis, but then puts all the weight back on 18 months later, patients can still enjoy benefits such as decreased blood glucose level and decreased blood pressure years later 30
  • 3-7 hours per week of structured walking at a moderate to fast pace can reduce the risk of death due to diabetes complications by 40-60% 25

Recommendations to avoid complications

In 2004 the ADA recommended that before increasing physical activity or beginning an exercise program, diabetic patients should undergo a detailed medical evaluation with appropriate diagnostic studies. The medical examination should screen for the presence of both macro- and micro-vascular complications and for signs and symptoms of cardiovascular, renal, and ocular disease.19

For therapists working with or prescribing exercise to type 2 diabetic patients, the following recommendations may be of value to avoid complications:

  • Pre and post exercise testing of BGL - particularly if patients take insulin, or any medication that increases their natural insulin production (particularly sulfonylureas)
  • If patients take insulin, or any medication that increases natural insulin production, they should carry fast acting carbohydrates such as carbotest 75g/300ml (Lomb Scientific) or jelly beans to each exercise session.
  • Patients should always complete an adequate warm up and cool down to ready the body for exercise and transition to rest much more gradually
  • Patients need to avoid breath holding during exercise/exertion – as this may increase blood pressure – straining the already compromised blood vessels
  • Adequate water needs to be drunk before, during and after exercise
  • Footwear that is closed, comfortable and supportive should be worn
  • Patients should inspect their feet after each exercise session for pressure areas, colour changes andbetween their toes for any fungal infection (especially after using public showers)
  • If exercising in a pool, socks (with grip on the bottom) or reef shoes may be worn to minimize risk of infection and cuts
  • If exercising in a heated pool, it is advised that patients have a cool shower afterwards to help the body maintain temperature regulation (a problem in patients with diabetes)
  • Heart rate monitoring should be performed with more vigorous exercise or if cardiac autonomic neuropathy is suspected.
  • Patients and therapists need to watch for signs of hypotension post exercise particularly on exiting a pool.

Aquatic Physiotherapy specifically

Hooper (1999) found that pure immersion in a heated pool from 37 to 40 degrees can result in reduction in medication, weight and BGL 31. Increasing skeletal muscle blood flow facilitates insulin mediated glucose uptake, and this is the hypothesis as to why patients may benefit from immersion in a heated pool. More recently, a study by De Leon et al (2005) found that aquatic exercise, specifically a six-week exercise program with participants working at 40-60% of their heart rate reserve capacity, normalised blood glucose in both men and women with Type 2 diabetes. Despite this positive long-term benefit, prevention of hypoglycaemia in the immediate stages after exercise is essential, as capillary glycaemia mean values were shown to be 27% lower after each exercise session than before.32  This re-enforces the importance of BGL monitoring pre and post exercise. 

Patients with decreased sensation (peripheral neuropathy) and reduced peripheral blood flow may not notice when they are getting too hot, and their neurovascular mechanisms for dissipating heat are decreased. This can therefore cause burns to occur at much lower temperatures than one would usually expect.This is not an issue in thermo-neutral pools (32-36°) but patients should be advised of the risks of exercising in spas and the option of wearing foot protection.

Compensatory sweating can occur in the face and trunk of type 2 diabetic patients if there is damage to the sympathetic neural system, which decreases the perspiration ability of the peripheral areas of the body. This is a great way that therapists can determine whether a diabetic patient is exercising at an intensity that might be too vigorous. Generally, exercise intensity should be gradually progressed and caution exercised if sessions are lasting more than 30 minutes to avoid overheating and excessive drops in BGLs.

While no known research has been done comparing land based exercise to water based exercise and its effect on BGL, anecdotally patients who exercise in the pool typically have faster and more pronounced drops in their BGL. As a precaution, fast-acting carbohydrates (carbotest 75g/300ml or jelly beans) should be kept close to the pool in case of hypoglycaemia. If BGL monitoring is not possible poolside, ensure the patient has eaten in the hour prior to immersion and that they have slow acting carbohydrates on hand to help restore glucose levels post exercise. In Type 1 diabetics, delayed onset hypoglycaemia can occur 4-24hrs after exercise, so a light snack before bed or reduced insulin dose before sleeping may be warranted to avoid nocturnal hypoglycaemia. 33

Self-monitoring of BGL's provides critical information on the impact of exercise and is recommended for all patients before and after exercise34.  At the very least patients should be asked about their BGLs for that day and when they last ate prior to commencing each aquatic physiotherapy session. Regular testing will also provide patients and aquatic physiotherapy staff with increased awareness of the effect of strength based versus cardiovascular exercise, and dietary intake, on BGL's.

More frequent monitoring is recommended for those with poor awareness of hypoglycaemia or those performing high-intensity exercise. Essentially, clinicians and patients must work together to maximise the benefits of exercise whilst minimising risks of negative consequences.34

It is known that immersion in water increases the central blood volume by 20-40% 35 thereby increasing the work and output of both the heart and kidneys (diuresis.)36 This is likely to further reduce BGLs and contribute to dehydration. It is therefore imperative that diabetic patients drink regularly during their exercise session.

Another important consideration is the increased incidence of autonomic neuropathy, retinopathy, cardiovascular and kidney disease in these clients and the possible implications these conditions may have for exercise prescription.

If autonomic neuropathy is present, blood pressure control may be impaired,   hypotension or hypertension possibly occurring post exercise.19 Given that a drop in BP usually occurs with immersion, greater care needs to be taken with diabetic clients. Heart rate recovery after exercise may also be reduced.37 Although immersion normally reduces heart rate 10-15 BPM 38, diabetic patients may not respond in the same way. Monitoring of heart rate is advisable during and after exercise at the initial appointment and with higher intensity exercise. However if patients are on Beta Blockers, an RPE scale should be used to prescribe exercise intensity instead of HR.39

In the presence of proliferative diabetic retinopathy, vigorous exercise and valsava-like manoeuvres can increase blood pressure and increase the risk of retinal and vitreal haemorrhage and detachment. Therefore, those patients with proliferative diabetic retinopathy, overt nephropathy or severe cardiovascular disease should restrict their exercise to moderate intensity.19

Many Australians are at risk of developing Type 2 diabetes and it is predicted that 50% of cases are undiagnosed. Early diagnosis or identification of impaired glucose tolerance is critical to the optimal management and prevention of further complications.

Aquatic physiotherapists are recommended to familiarise themselves with risk factors for Type 2 diabetes and make available the AUSDRISK (Australian Diabetes Risk Assessment Tool)40 to all aquatic physiotherapy patients as appropriate.

Diabetes Australia has some excellent information sheets available via the internet in both English and other languages.41  

The position statement from the American Diabetic association provides some guidelines for exercise prescription.19


Aquatic Physiotherapy can be a useful treatment regime in type 2 diabetes as many patients have other chronic conditions such as osteoarthritis. Also, the moderate intensity and low impact of aquatic physiotherapy allows complications to be kept to a minimum specifically regarding: retinopathy, nephropathy, and neuropathy. For the obese diabetic client with co-morbidities, aquatic physiotherapy may be the only form of exercise that they can tolerate initially.


Wounds/ lesions of the skin particularly the feet are susceptible to infection in hydrotherapy settings. Hydrotherapy pools can be sources of bacteria, and if patients have cuts, or any broken skin there is a large risk of infection. This is more critical in the type 2 diabetes population than in the general population due to decreased healing rates. Healing rates are decreased in patients with diabetes due to the hyperglycemic (increased viscosity) state of their blood, atherosclerosis, and neural changes such as decreased pain and sensation. Something as simple as wearing reef shoes, or other modified footwear (such as socks with rubber soles) can therefore save diabetic patients from possible infection, and amputation.


Hyperglycemia in type 2 diabetics is a fasting level of greater than 6mmol/L, and greater than 8mmol/L 2hrs post prandial.

Symptoms may include: polyphagia, polyuria, polydipsia, dry mouth, itchy skin, stupor. Treatment for hyperglycaemia typically involves getting a better balance between medication, exercise and diet. This is a gross oversimplification, however.

Hyperosmolar nonketotic state can occur in dehydrated patients with type 2 diabetes that have severely high BGL (>30mmol). The kidneys preserve water and the BGL level continues to rise, therefore water and electrolytes are drawn out of the body’s cells to compensate leading to electrolyte imbalances and potential coma. Type 2 diabetics should be exercised with caution when BGL is above 15mmol/L, but an experienced clinician may exercise a patient who is above 15mmol/L (and well hydrated) without complication if monitored closely. Typically a patient with BGL above 20mmol/L should not be exercised.

Type 1 diabetics should not be exercised when they are above 15mmol. The metabolic state is different in type 1’s compared to type 2’s as there is an absolute deficiency in insulin. If these patients exercise whilst hyperglycemic, the body’s cells can’t use glucose efficiently, so the body responds by releasing more glucose (via the breakdown of fat), creating ketone bodies. Normally ketones may occur periodically with the breakdown of fat and this is non problematic, but if breakdown of fat is prolonged (as it is when hyperglycemic type 1’s exercise) the body’s pH level is disrupted and results in ketoacidosis, which is a medical emergency.


Hypoglycemia or abnormally low blood glucose (<4mmol/L), can be a complication of several diabetes treatments. It may develop if the glucose intake does not match the medical treatment (or the medication is too aggressive), or if exercise is not timed correctly, is too vigorous or is for an extended period of time without adequate glucose intake. Less frequently, patients may forget or miss a meal and continue to take their hypoglycaemic medication.

Hypoglycaemic events can occur in patients who take insulin and/or sulfonylureas to manage their glucose levels (sulfonylureas are a drug class that stimulates the islets of Langerhans to produce more insulin). The increased insulin, which occurs as a result of taking these drugs, can cause blood glucose levels to drop much quicker, and much lower than prior to taking these medications (note in patients not taking insulin or sulfonylureas, the body’s homeostatic mechanisms are able to keep BGL above 4mmol/L). Because exercise is a hypoglycaemic agent, patients are particularly vulnerable to dangerous drops when exercising and on these drugs. It is worth noting also that hypoglycaemic symptoms can be observed and experienced within the chronically hyperglycaemic population during and post exercise if their blood glucose level has significantly reduced as a result of exercise. These patients may not have a BGL that is below 4mmol/L but as a result of a rapid and/or large drop in BGL the body exhibits symptoms of a similar nature as a patient with hypoglycaemic values.

Symptoms of a hypoglycaemic attack can be quite obvious to observe (but not always – particularly if the patient’s autonomic system is damaged in the more poorly controlled patients, or if the patient is on beta blockers). Patients may lose coordination, become agitated, lose consciousness, become sweaty, panic, and may exhibit other symptoms of sympathetic nervous system activation. More extreme consequences can be coma, seizures, or even brain damage and death.

Pre exercise, a patient that is at risk of hypoglycaemia needs their BGL to be at least 6mmol/l (as a general guideline) to prevent hypoglycaemic events during exercise (approximately 30 minutes of moderate intensity exercise). If a patient is below 6mmol/L but above 4mmol/L treatment involves administering 15g of slow acting carbohydrate (2 Tbspn raisins, 8 lifesavers, 1 ounce of energy bar); if they are below 4mmol/L administering 15g of fast acting carbohydrates (1/2 cup of soft drink or fruit juice), retesting 10 minutes later and applying the appropriate treatment from that point until they reach non hypoglycemic BGL. Once above 4mmol/L the slow acting carbohydrate regime above is applied to this patient also.

Post exercise, if a patient is hypoglycaemic, a therapist needs to administer the same regime until the patient’s BGL is above 4mmol/L. It is good safe practice to administer the slow acting carbohydrate post exercise once a BGL of above 4mmol/L has been achieved as the hypoglycaemic effects of exercise can continue once exercise has ceased. If patients are exercising for the first time, therapists should pay extra attention and be sure to note any signs and symptoms associated with hypoglycaemic BGLs. Not all patients respond the same way, and the same patient might respond differently given time of day, medication and/or meals; unknown sickness; mode of exercise and duration of exercise.


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Other useful websites

International Diabetes Federation (IDF) website,