Treatment of Diabetes
Diabetes mellitus is a chronic metabolic disease characterised by chronic hyperglycemia (elevated blood glucose) associated with impaired carbohydrates, lipids, and protein metabolism with lack of insulin secretion or decreased sensitivity to insulin metabolic effects- also known as insulin resistance. The prevalence of type 2 diabetes mellitus is increasing rapidly around the world and parallels the increase in obesity prevalence.
Insulin resistance impairs the ability of muscle cells to take up and store glucose and triglycerides, which results in high levels of glucose and triglycerides circulating in the blood. It is commonly associated with visceral adiposity, glucose intolerance, hypertension (high blood pressure), dyslipidemia, endothelial dysfunction and elevated levels of markers of inflammation. Insulin resistance itself has been shown to significantly increase the incidence and prevalence of cardiovascular disease in individuals with type 2 diabetes mellitus.
Hyperglycaemia causes damage to muscle cells, which results in loss of strength and mass. Loss of muscle strength is also a significant predictor of physical function limitation and disability in type 2 diabetes mellitus. It is associated with excess physical disability in older adults, especially in lower extremity mobility tasks.
Diabetes disease causes impairments in multiple organs, with microvascular and microvascular complications underpinning multi-system damage. These include:
Insulin resistance impairs the ability of muscle cells to take up and store glucose and triglycerides, which results in high levels of glucose and triglycerides circulating in the blood. Insulin resistance plays a significant pathophysiologic role in type 2 diabetes mellitus. It is commonly associated with visceral adiposity, glucose intolerance, hypertension, dyslipidemia, endothelial dysfunction and elevated levels of markers of inflammation. Insulin resistance itself has been shown to significantly increase the incidence and prevalence of cardiovascular disease in individuals with type 2 diabetes mellitus.
Hyperglycaemia causes damage to muscle cells, which results in loss of strength and mass. Loss of muscle strength is also a significant predictor of physical function limitation and disability in diabetes mellitus. It is associated with excess physical disability in older adults, especially in lower extremity mobility tasks.
In an individual experiencing end-stage diabetes co-morbidities will include nerve damage in the toes, hands, kidneys and eyes causing neuropathy, nephropathy and retinopathy. Results can include amputation, blindness and kidney failure. Other conditions that individual can suffer from are hypertension, cardiovascular disease and obesity.
Modern management of diabetes: Exercise
Exercise training and physical activity have been considered a cornerstone in the prevention and treatment of type 2 diabetes mellitus. Along with glycemic control, exercise has a number of benefits, such as decreasing insulin resistance and improving aerobic capacity, muscular strength, body composition, and endothelial functions. Further, exercise is effective in improving glycemic control and blood lipid profiles in type 2 diabetes mellitus.
Exercise training has long been known as an important non-pharmacological tool for the treatment of diabetes, with The American College of Sports Medicine highlighting structured exercises are backed by a substantial body of evidence for treating and managing diabetes. Together, exercise and lifestyle modifications can actually reduce the progression of insulin resistance. Recent evidence suggested that a combination of aerobic and resistance training (combined exercise) is more beneficial than either training modality alone. Aerobic exercise enhances insulin sensitivity, and resistance training may improve blood glucose uptake by increasing muscle mass, with glucose transporter type 4 expression mechanisms appearing to be synergistic.
Modern management of diabetes: Fasting
Fasting is evolutionarily embedded within our physiology, triggering several essential cellular functions.
Researchers from the University of Alabama conducted a study with a small group of obese men with pre-diabetes. They compared a form of intermittent fasting called “early time-restricted feeding,” where all meals were fit into an early eight-hour period of the day (7 am to 3 pm),or spread out over 12 hours (between 7 am and 7 pm). Both groups maintained their weight (did not gain or lose) but after five weeks, the eight-hours group had dramatically lower insulin levels and significantly improved insulin sensitivity, as well as significantly lower blood pressure. Participants in the eight-hours group also had significantly decreased appetite. Just changing the timing of meals, by eating earlier in the day and extending the overnight fast, significantly benefited metabolism even in people who didn’t lose a single pound.
Intermittent fasting, when undertaken for health reasons in patients with diabetes mellitus, both types 1 and 2, has been shown in a few small human studies to induce weight loss and reduce insulin requirements. People with diabetes, however, are not the average individual, and their personal needs require more careful consideration at the beginning of and during the use of a fasting regimen. With proper medication adjustment and self-monitoring of blood glucose levels though, intermittent fasting can be encouraged and safely implemented among people with diabetes.
Best nutritional management considerations for people with diabetes:
Avoid sugars and refined grains. Instead, eat fruits, vegetables, beans, lentils, whole grains, lean proteins, and healthy fats (a sensible, plant-based, Mediterranean-style diet).
Let your body burn fat between meals. Don’t snack. Be active throughout your day. Build muscle tone.
Consider a simple form of intermittent fasting. Limit the hours of the day when you eat, and for best effect, make it earlier in the day (between 7 am to 3 pm, or even 10 am to 6 pm, but definitely not in the evening before bed).
Avoid snacking or eating at nighttime, all the time.
Nitric oxide, exercise and diabetes
Nitric oxide, is a significant component of the insulin-signaling cascade, executing microvascular vasodilation stimulated by local nitric oxide production from the vascular endothelium. Vasodilation has the potential to decrease systemic blood pressure and increase local tissue blood flow in tissues such as muscle. The combination of decreased blood pressure and increased tissue blood flow, together with specific beneficial endothelial effects, may serve to prevent hypertension, cardiovascular disease, and insulin resistance. Read more.
Exercise & nitric oxide
The results that aerobic exercise training increased nitric oxide generation, reduced blood pressure, and induced anti-oxidant enzymes via SIRT3 suggest that exercise training may be an important factor for the prevention of disease by inducing intrinsic nitric oxide and anti-oxidant enzymes. Read more.
NAD+ simulates sirtuins
Sirtuins have a host of metabolic targets, resulting in profound effects on various cellular processes, such as mitochondrial biogenesis, cellular stress response, lipid metabolism, insulin secretion and sensitivity, apoptosis, circadian clock dynamics, inflammation, and aging. Through these targets, sirtuins translate changes in feeding status, DNA damage, and oxidative stress into metabolic adaptations. Read more.
Exercise and NAD+
NAD+ is mainly generated by the NAD+ salvage pathway in which nicotinamide phosphoribosyltransferase (NAMPT) is rate-limiting. NAMPT decreases with age in human skeletal muscle, and aerobic exercise training increases NAMPT levels in young men. Read more.