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.

vitacolumbia.com
info@vitacolumbia.com

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:

Continue reading “Alzheimer’s Disease as Type-3 Diabetes: Hyperinsulinemia as a mechanism in Alzheimer’s Pathology”

Dietary Sugar and the Childhood Obesity Epidemic

Preventing childhood obesity is vital due to its association with lifelong obesity, metabolic disorders such as type-2 diabetes mellitus and hypertriglyceridemia, obesity-related cancers, in addition to psychosocial repercussions and decreased educational attainment. From 1975 to 2016, mean BMI and obesity rates in children and adolescents aged 5-19 years have increased globally and in most regions.

Added sugar consumption is the primary factor associated with childhood obesity trends, in addition to being associated with other detrimental health conditions such as dental caries, asthma, altered lipid profiles, hypertension, and cancer. A 2019 analysis of data compiled from the Centers for Disease Control and Prevention (CDC) from 2011 to 2016 revealed 98% of American toddlers and 60% of infants consume added sugar in sweetened foods and beverages. Sweet bakery products were in the top 3 sources of added sugar for both toddlers and infants. Previous studies examining sugar intake in older children (aged 2-8 years) also reported sweet bakery products to be one of the top three sources for added sugar. Fruit drinks, yogurt, and sugar-sweetened beverages were other important sources of added sugar identified by researchers. In 2015, the World Health Organization (WHO) and the American Heart Association (AHA) recommended limiting added sugars consumption to <10% of total caloric intake for children aged 2 to 19 years. In 2017, the AHA released a statement advising children less than 2 years to old to avoid consuming added sugars entirely. The most recent analysis of CDC data revealed about 70% of American children older than 2 years exceed recommendations for added sugars intake.

Infants and children around the world exhibit a heightened preference for sweetness, most likely a biological underpinning to confer advantage in environments of scarcity. Moreover, emerging research has shown significant similarities in neurochemistry and behavior between consumption of added sugars and drug-like effects, including bingeing, craving, tolerance, withdrawal, cross-sensitization, cross-dependence, reward and opioid effects. Sugar addiction appears to develop as a result of natural endogenous opioids released upon sugar consumption. The opioid-like pain reducing properties of sugar are evident from birth. A sweet solution placed in a newborns mouth, elicits facial relaxation, often accompanied with a smile. Furthermore, something sweet placed on the tongue of a crying newborn produces an instantaneous calming effect. In another study, sucrose consumption delayed pain reporting in children aged 8 to 11 years old undergoing a cold-induced pain stimulus test, whilst having no effect in adult. Evolutionary driven taste preferences, coupled with heightened response to natural endogenous opioids produced upon sugar consumption make infants and children more vulnerable to sugar addiction than adults.

While it may not be reasonable to eliminate sweet foods entirely from a child’s diet, substitution of sugar with an all-natural sweetener such as vitaSWEETis a practical approach to abate the rising trends in childhood obesity and other detrimental health ailments associated with added sugar consumption. vitaSWEET is as sweet as sugar, zero calories, has no effect on blood glucose levels, and is safe for children.

 

 

 

Sugar and Aging: The Role of Advanced Glycation End-Products (AGEs) in Aging & Chronic Disease

Aging is the result of progressive physiologic changes which occur until senescence, due to a decline in biochemical functions and capacity to adapt to metabolic stress. The abnormal accumulation of biological waste plays a significant role in organ or tissues functional deterioration as we age.

Advanced Glycation End-Products (AGEs) are a complex group of compounds consisting of proteins, lipids, or DNA which undergo glycation when exposed to sugars. The human body lacks enzymes to eliminate glycated products, which progressively accumulate as metabolic waste during aging. The glycation reaction results in impaired protein function and reduced elasticity of tissues such as blood vessels, skin, and tendons.

Hyperglycemia vastly accelerates the glycation process, with AGE accumulation playing a significant role in the microvascular and macrovascular damage associated with diabetes mellitus.  In addition to diabetes, many other chronic diseases such as atherosclerosis, chronic kidney disease, rheumatoid arthritis, Alzheimer’s disease, Parkinson’s disease, vascular dementia, cataracts, other degenerative ophthalmic diseases, and many other diseases are associated with the accumulation of AGEs in tissues. Furthermore, there is significant evidence that AGEs contribute to sarcopenia and the loss of bone density and muscle mass associated with aging.

Cooking or consuming sugars with fats or proteins results in the most significant generation of AGEs. A study using a mouse model, given an AGE-rich diet for 16 weeks resulted in a 53% increase in serum AGE levels. Currently there is considerable interest in discovering potential inhibitors of AGE formation or agents that may disintegrate and eliminate AGEs. Of the several AGE inhibitors and breakers discovered including aminoguanidine, N-phenacylthiazolium bromide, and alagabrium, none are in clinical use due to safety concerns. Recently, interest in herbal products has been rising, some of which have similar or even stronger anti-AGE than synthetic drugs, with a much more favorable safety profile. Flavanoids, a class of polyphenols, including kaempferol, genistein, guercitrin, quercetin, and epicatechin appear to have potent anti-glycation properties, and are currently the most promising pharmaceutical approach to manage AGE accumulation.

As with most of medicine, the best treatment is prevention, and thus diet and exercise are the easiest way to reduce AGE accumulation, slow the aging process, and avert the onset of chronic disease. The simplest change one can make is avoiding sugar in cooking, baking, sauces, and beverages, and supplement 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:

Continue reading “Sugar and Aging: The role of Advanced Glycation End-Products in Aging and Chronic Disease”