The American Diabetes Association (ADA) standards of medical care is a document I refer to from time to time. The document covers so many areas in diabetes care. Going through the document gives you the far-reaching consequences of diabetes. The ADA notes that diabetes is associated with a significantlyincreased risk, and rate, of cognitivedecline and with increased risk ofdementia. In a 15-year prospectivestudy of community-dwelling peopleover the age of 60 years, thepresence of diabetes at baseline significantlyincreased the age- and sex-adjustedincidence of all-cause dementia,Alzheimer disease, and vascular dementiacompared with rates in those withnormal glucose tolerance.The effects of hyperglycemiaand insulin on the brain are areas of intenseresearch interest.

A paper by Cukierman et al titled “Cognitive decline and dementia in diabetes–systematic overview of prospective observational studies” published in Diabetologia2005 Dec; 48(12):2460-9. Epub 2005 Nov 8., noted that compared to people without diabetes, people with diabetes have a greater rate of decline in cognitive function and a greater risk of cognitive decline. Cognitive dysfunction should therefore be added to the list of chronic complications of diabetes.

Type 2 diabetes has consistently been shown to be associated with increased risk forcognitive decline, cognitive impairment and dementia, bothvascular dementia and Alzheimer’s disease (AD). Such results have been demonstrated for diabetes both in midlife and in old age. Even prediabetes stages, namely, insulin resistance, have been shown to be associated with increased risk forcognitive decline and with increased rates of brain atrophy, both of which areassociated with dementia. .

A related paper by Ravona-Springeret al titled “The association of diabetes and dementia and possibleimplications for nondiabetic populations” publishedExpert Rev Neurother.

2011November; 11(11): 1609–1617. doi:10.1586/ern.11.152 noted the importance of diabetes and cognitive decline. The importance of these findings is that diabetes-related characteristics are modifiable, sothat the degree of control of plasma glucose levels, prevention or treatment of insulinresistance and/or specific treatments in diabetic patients could potentially prevent dementiaor delay its clinical onset. With increasing global prevalence of diabetes, such treatments may affect a large proportion of the population.It also noted additional factors such as ageat onset of diabetes, diabetes duration, type and mechanism of action of antidiabeticmedications, presence of other diabetes-related complications and comorbidities.

There are several underlying mechanismsconsistently associated with diabetes and with prediabetes states (the metabolic syndromecomponents, obesity and hypertension, which, by themselves, are associatedwith increased risk for dementia and impaired cognition. Numerous mechanisms have been proposed for the association between diabetes anddementia. These include brain vascular lesions, insulin resistance, advanced glycation endproducts, inflammation, oxidative stress and competition of insulin and β-amyloid on the insulin-degrading enzyme.

Insulin resistance is another mechanism suggested to contribute to neuropathology andcognitive impairment. Formerly, the brain was conceptualized as aninsulin-insensitive organ. Since then insulin receptors have been detected in the brain withhigh concentrations in several brain areas, namely the olfactory bulb, cerebral cortex, hippocampus, hypothalamus, amygdala, septum and the medial temporal cortex.The high concentrations of insulin receptors in the medial temporal cortex and hippo campusare consistent with the role of insulin in cognitive activity and memory.

Insulin has been shown to havea role in aging-related processes, some of which may also be associated with brainaging and neurodegeneration. Although neurons possess mechanisms forinflux of glucose that are not dependent on insulin, in certain brain regions, namely thehippocampus and hypothalamus, insulin has an effect on glucose uptake. Insulin is involved in long-term potentiation and that it affects thelevels of neurotransmitters involved in memory and learning- beneficial for cognition. Therefore, when insulin levels in the brain are low or when tissue response to insulin is decreased (insulin resistance), cognitive processes would be compromised. Peripheral insulinresistance, which is associated with prolonged peripheral hyperinsulinemia and decrease ininsulin transport through the blood-brain-barrier (BBB), may be one of the causes for reduced insulin levelsin the brain.Insulin resistance is therefore consideredthe underlyingcause of several clinical entities in addition to diabetes (metabolic syndrome, hypertensionand cardiovascular disease). Strategies aimed at the counteracting insulinresistanceare considered beneficial in the prevention of AD and dementia in populationsother than diabetic subjects.

Chronic exposure to high glucose levels contributes to the formation of endogenousadvanced glycation end products (AGEs). This is a group of molecules formed byirreversible non-enzymatic reaction between sugars and free amino acids.The accumulationof AGEs occurs during normal aging and is exacerbated in diabetes. AGEs can alsoform from exogenous sources, such as tobacco smoke and food].

The common consequences of exposure to all kinds of AGEs are among others  increased stiffness in protein matrix and resistance to proteolysis affecting tissueremodeling. This, in turn, results in sclerosis of renal glomeruli, thickening of capillarybasement membrane, atherosclerosis and endothelial dysfunction.

The link of high blood sugar levels (hyperglycaemia) to the development of cognitive impairment and dementia is attracting a lot attention. Management of diabetes and dementia entails high costs. High glucose levels result in structural damage and functional impairment of brain cells and nerves, hemorrhage of cerebral blood vessel, and increased accumulation of amyloid beta. Nutrients and natural food components have been investigated as preventive and/or intervention strategy.

In spite of strides made by modern medicine against diabetes, the prevalence of the disease is high.Globally, an estimated 422 million adults were living with diabetes in 2014, compared to 108 million in 1980. It has been estimated that its prevalence could reach more than 10% of world population by 2025. Based on cost estimates from a recent systematic review, it has been estimated that the direct annual cost of diabetes to the world is more than US$ 827 billion. The International Diabetes Federation (IDF) estimates that total global health-care spending on diabetes more than tripled over the period 2003 to 2013 – the result of increases in the number of people with diabetes and increases in per capita diabetes spending.

Dementia has significant social and economic implications in terms of direct medical and social care costs, and the costs of informal care. In 2015, the total global societal cost of dementia was estimated to be US$ 818 billion (World Health Organization-WHO).

There is accumulating evidence that hyperglycaemia is a major risk factor for the development of  cognitive impairment or Alzheimer’s disease (AD). Hyperglycaemia increases amyloid beta accumulation on brain lesions, exacerbates oxidative stress, neuro-inflammation, mitochondrial dysfunction, impairs neuronal integrity and causes neurodegeneration. Daily and regular consumption of polyphenol-rich cocoa reduces/stabilizes blood glucose levels. Cocoa, on weight basis, is the richest food source of anti-oxidants. Polyphenol-rich cocoa is a potent anti-oxidant, counteracts oxidative stress. It has anti-inflammatory effects and offers neuroprotection.




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