Pharmaceutical companies have spent billions of dollars to find a treatment for Alzheimer’s Dementia. Unfortunately, all recent clinical studies have failed and the potential for the approval of an efficacious treatment in the foreseeable future remain slim.

A particular area of hope, is that researchers have identified a significant connection between diabetes and Alzheimer’s disease. Approximately 80% of people with Alzheimer’s disease also have some form of diabetes, insulin resistance, or disturbed glucose metabolism. The connection between Alzheimer’s disease and diabetes is so close, that researchers have now begun referring to Alzheimer’s as “type 3 diabetes”. This finding is significant because it suggests that the risk of developing Alzheimer’s dementia can be reduced through dietary and lifestyle modifications.

Dementia currently afflicts more than 35 million people worldwide. Almost half of people with dementia have Alzheimer’s disease, the most common form, characterized by progressive memory, cognitive and behavioral deficits. With aging demographics and current trends, the number of people affected by dementia is expected to reach 115 million by 2050. This trend is not only devastating for individuals burdened with the disease, but also families forced to care for their loved ones. Furthermore, the economic impact on society is immense, with the Alzheimer’s Organization predicting Alzheimer’s and other dementias could cost the United States of America almost $1.1 trillion by 2050.

Vita Columbia Clinical Research Inc. is taking the initiative to educate society on the new findings correlating Alzheimer’s disease with diabetes, and the possibility for prevention through lifestyle modifications, such as dietary changes.

A simple method to reduce added sugar consumption, is by substituting table sugar and high fructose corn syrup with vitaSWEET in cooking, baking, and beverages. vitaSWEET tastes like sugar, but is 0 on the glycemic index, meaning that it has no effect on blood glucose levels.

vitaSWEET is formulated with two simple ingredients: monk fruit and erythritol. Monk fruit or luo han guo is native to southern China and northern Thailand, and has almost 300 times natural sweetness than that of sugar. It has been used for centuries in traditional Chinese medicine as a cold and digestive aid, and was first mentioned in the records of 14th century Chinese monks. Erythritol is a naturally occurring sugar alcohol derived from fruits and plants. Vita Columbia’s unique blend of both monk fruit and erythritol is as sweet as sugar and can be used as a 1-to-1 replacement in recipes.

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Type-3 Diabetes as Alzheimer’s Disease: Hyperinsulinemia as a mechanism in Alzheimer’s Pathology

The world is currently facing a diabetes epidemic, affecting over 400 million people worldwide. This figure is more likely to be double, as one in two people currently living with diabetes are undiagnosed. Type 2 diabetes is the most commonly known form of diabetes and without prompt diagnosis and management can lead to complications such as blindness, limb amputation, kidney disease, heart attack and stroke. In congruence with the rise of diabetes mellitus (DM) in the past century, humanity is facing another epidemic, dementia, which currently afflicts more than 35 million people worldwide. Almost half of people with dementia have Alzheimer’s disease (AD), the most common form, characterized by progressive memory, cognitive and behavioral deficits.

In a 2016 study published in the journal Diabetologia (the journal of the European Association for the Study of Diabetes), researchers uncovered that genes responsible for the production of toxic neuroproteins not only lead to Alzheimer’s symptoms, but also lead to diabetic complications. In response to the study results, lead researcher, Professor Bettina Platt stated, “Many people are unaware of the relationship between diabetes and Alzheimer’s disease, but the fact is that around 80% of people with Alzheimer’s disease also have some form of diabetes or disturbed glucose metabolism. This is hugely relevant as Alzheimer’s is in the vast majority of cases not inherited, and lifestyle factors and comorbidities must therefore be to blame.” The connection between Alzheimer’s disease and diabetes is so close, that researchers have now begun referring to Alzheimer’s as “type 3 diabetes”.

Scientists hypothesize that the pathological process leading to the development of AD encompasses two main features: amyloid plaques and neurofibrillary tangles. Amyloid plaques form as a result of the extracellular accumulation of beta-amyloid (Aβ), believed to trigger a cascade of events leading to neurodegeneration, and is the primary therapeutic target in AD pharmacotherapy. Neurofibrillary tangles (NFTs) on the other hand are intracellular inclusions, formed by the aggregation of tau proteins, which are microtubule-associated proteins that function to stabilize microtubules. Cognitive decline in AD is closely correlated with the progressive pathological accumulation of NFTs, believed to directly cause neuronal malfunction and cell death. Extensive clinical research has focused on Aβ or tau proteins as therapeutic targets, but clinical trials have had disappointing results thus far. The most promising therapeutic strategy, on the other hand, may be focusing on risk factors such as DM.

Science has only recently accepted the role of insulin in the brain, which include neuronal development, synapse formation, learning and memory, glucoregulatory function and feeding behavior. Researchers suspect that the high concentration of insulin found in the brain is the result of local production in the brain and active transported across the blood-brain-barrier via a specific transporter, affected by hyperglycemic states such as diabetes.

Several independent research groups have shown insulin resistance to have a significant effect on Aβ synthesis, aggregation, and clearance mechanisms. The studies demonstrated that diet-induced insulin resistance increases Aβ synthesis on a molecular level, and also correlated excessive sucrose intake with increased cerebral Aβ peptide levels and worsened learning impairment in Alzheimer’s transgenic mice. Furthermore, insulin-degrading enzyme (IDE) is an important enzyme involved in the proteolytic degradation of accumulated Aβ in the brain. In states of hyperinsulinemia, as in DM, excessive insulin levels directly compete with Aβ for IDE, reducing Aβ degradation and increasing Aβ levels.

Physiologically, tau proteins are involved in stabilizing neuronal microtubules. In pathological states, such as AD, tau proteins undergo phosphorylation leading to aggregation, the formation of neurofibrillary tangles and neuronal toxicity. Glycogen synthase kinase-3 (GSK-3) is an important regulator of tau phosphorylation. Studies have shown that diabetes and obesity-induced insulin resistance cause excessive activation of GSK-3β which induces tau hyper-phosphorylation, leading to the formation of neurofibrillary tangles responsible for the cognitive changes in AD. Activation of GSK-3 is another suspected mechanism in which diabetes triggers the development of or accelerates the progression of AD.

With aging demographics and current trends, the number of people affected by dementia is expected to reach 115 million by 2050. This trend is not only devastating for individuals burdened with the disease, but also families forced to care for their loved ones. Furthermore, the economic impact on society is immense, with the Alzheimer’s Organization predicting Alzheimer’s and other dementias could cost the United States of America almost $1.1 trillion by 2050.

A optimal method to reduce the personal, social, and economic impacts of the DM and AD epidemics is through prevention, which can be best achieved through dietary changes and physical exercise. One simple dietary change involves substituting sucrose or table sugar for low-glycemic alternatives such as vitaSWEET in cooking, baking, and beverages. vitaSWEET is all-natural and as sweet as sugar, but without the metabolic consequences.

References:

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The Role of Hyperglycemia-Induced Endothelial Dysfunction in Diabetes, Atherosclerosis and Inflammatory Disorders

The prevalence of type 2 diabetes mellitus (T2DM) has tripled in the past three decades, with 2014 figures estimating 422 million diabetics worldwide. Additionally, half of those with diabetes are currently undiagnosed. Hyperglycemia is the primary feature of T2DM, and is most often caused by metabolic abnormalities. Pre-diabetes precedes the onset of T2DM by several years and encompasses early metabolic changes called impaired fasting glucose. Vascular complications in T2DM increase in proportion to the duration of hyperglycemia. Chronic hyperglycemia triggers endothelial dysfunction, the primary factor in the pathogenesis of diabetic vascular complications. Furthermore, emerging research has identified hyperglycemia induced endothelial disfunction to play a significant role in the pathogenesis of atherosclerosis and other inflammatory disorders.

Endothelial cells (ECs) line the internal surface of all blood vessels, and serve as a barrier between circulating blood and tissues. ECs are crucial in the regulation of vascular tone and maintenance of vascular homeostasis. Under normal physiological conditions, ECs exist in a dormant state, but under various mechanical and chemical stimuli, ECs synthesize and secrete many vasoactive substances and growth modulators. ECs are particularly sensitive to changes in blood glucose levels, and hyperglycemic conditions induce acute endothelial inflammation, and a prolonged pro-inflammatory state leading to endothelial dysfunction.

Endothelial dysfunction is characterized by a loss of balance between vasoconstrictors and vasodilators, growth promoting and inhibiting factors, pro-atherogenic and anti-atherogenic factors, and pro-coagulant and anti-coagulant factors. This disruption in vascular homeostasis is caused by reduced nitric oxide production, increased endothelial permeability, increased expression of adhesion molecules, and increased apoptosis. Endothelial dysfunction is responsible for the vascular complications associated with T2DM, and is believed to play a significant role in the pathogenesis of inflammatory disorders such as rheumatoid arthritis, asthma, cerebral small vessel disease, and autoimmune disorders such as inflammatory bowel disease. Furthermore, emerging research has identified endothelial dysfunction as an early pivotal event preceding the development of coronary artery atherosclerosis.

Researchers hypothesize the risk of developing autoimmune diseases, diabetes, and atherosclerotic coronary artery disease to be directly related to the number, intensity and duration of hyperglycemic events. The modern diet is rampant with refined sugar products and beverages with high-fructose corn syrup which cause massive spikes in blood glucose levels. A simple dietary modification to reduce hyperglycemic episodes and associated endothelial dysfunction is to supplement sugar with low-glycemic alternatives such as vitaSWEET, an all-natural sugar alternative, that is as sweet as sugar, bakes like sugar, but without the metabolic consequences.

References:

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Autism and Gestational Diabetes: The Importance of Managing Pre-Pregnancy Prediabetes

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance a woman develops during gestation, typically recognized during the latter half of pregnancy. A review of the global prevalence of GDM on the basis of studies between 2005 and 2018, estimated the global prevalence of GDM to range from 1% to > 30% depending on region and country, as seen in Figure 1.0 below.  The majority of women are normoglycemic after delivery, but as many as 20% have impaired glucose tolerance in the early postpartum period. Furthermore, after the development of GDM, women have an up to 70% risk for recurrent GDM in future pregnancies, a seven-fold higher risk of overt diabetes in the proceeding 5-10 years, and an increased risk of cardiovascular diseases. The short-term perinatal consequences of GDM include pre-eclampsia, preterm delivery, primary caesarean delivery, shoulder dystocia or birth injury, high birthweight, high neonate body fat percentage, neonatal hypoglycemia, and newborn intensive care admission. Long-term outcomes of the offspring include obesity and glucose intolerance. Additionally, emerging research has linked prenatal diabetes as a significant risk factor for long-term neuropsychiatric morbidity, in particular Autism spectrum disorder (ASD) in children.

ASD is a neurodevelopmental disorder characterized by impairments in socialization, communication and language, and repetitive or unusual behaviors. ASD typically appears during the first 5 years of life and persists into adulthood. Individuals with ASD often have co-exiting neuropsychological conditions such as epilepsy, depression, anxiety, and attention deficit hyperactivity disorder (ADHD). The prevalence of ASD has increased dramatically since the 1960s and continues to rise annually at an exponential rate. ASD diagnoses in children have increased from 1 in 150 in the year 2000, to 1 in 59 in 2018, with autism prevalence increasing by 119.4% in this time period. On average, autism costs families $60,000 USD per year, and the cost of taking care of Americans with ASD is expected to reach $451 billion by the year 2025.

The prevalence rates of ASD and GDM have both increased dramatically since the 1960s, in congruence with the global epidemics of diabetes and obesity and societal trend for childbearing at a later age. In the United States, 29.3% of adults 20-22 years of age have detectable pre-diabetes, and it is highly possible that many of GDM cases are actually undiagnosed pre-pregnancy hyperglycemia of varying severity. In addition to pre-pregnancy prediabetes and obesity, other risk factors for GDM include childbearing after the age of 30, positive family history, cigarette smoking, psychological stress, exposure to organic pollutants and endocrine disrupters, and pre-pregnancy dietary factors. Data from observational studies suggests that as many as 45% of GDM cases may be preventable by adherence to a healthy lifestyle.

With the emerging evidence of GDM as an independent risk factor of ASD in children, there is an urgent need to address the epidemics of prediabetes, diabetes, and obesity in women of childbearing age. Emphasis on lifestyle modifications is currently the best approach to reduce GDM and hence the risk of ASD in children. Added sugar consumption is one of the most significant causes of glucose abnormalities and appears to increase the risk for GDM, as seen in a study by Chen et al. whom identified a 22% greater risk for GDM in women consuming five or more servings of sugar-sweetened cola per week. One simple method to reduce dietary sugar consumption is through the substitution of sugar for an all-natural alternative such as vitaSWEET, which is as sweet as sugar, zero calories, has no effect on blood glucose levels, and is safe during pregnancy.

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