Sugar and Your Brain: Is Alzheimer’s Disease Actually Type 3 Diabetes?

It starves your brain, tangles and twists vital cells, and for decades it has been misrepresented as an untreatable, genetically determined disease. Alzheimer's disease is the 6^th leading cause of death in North America¹. The truth, however, is that this devastating illness shares a strong link with another sickness that wreaks havoc on millions of individuals in North America — Diabetes.

We all know that individuals affected by Type 1 and Type 2 Diabetes have a notable resistance to insulin. Type 1 is caused by the body's inability to produce insulin, and Type 2 is caused by the deterioration of the body's insulin receptors and associated with the consumption of too much refined carbohydrate like processed grains and sugar.  But when studies began to appear in 2005 that revealed a shocking correlation between insulin and brain cell deterioration, major breaks were made around Alzheimer's prevention[i]. Health practitioners became curious about a critical question — could Alzheimer's disease simply be Type 3 Diabetes?

Alzheimer's disease has long been perceived as mysterious and inevitable. 5.3 million individuals suffer every year from the disease that appears to be untreatable[ii]. But, if this illness is associated with insulin resistance, this simply isn't the case.

We already know that diabetics are at least twice as likely to experience dementia[iii].  The cells of your brain can become insulin-resistant just like other cells in the body.  What was once considered a mysterious accumulation of beta amyloid plaques characteristic in the Alzheimer brain is now associated with the same lack of insulin that negatively affects cognition[iv].

Where there is knowledge about underlying causes there is the opportunity for prevention. Research that surfaced around problems with insulin and brain cell death offered health practitioners a way to identify useful prevention tactics that help restore the brain's cell function[v].

Your Brain on Carbohydrates

Most people know that a diet high in carbohydrates indicates a relationship to serious diseases like cancer, heart disease, and diabetes. What we haven't always known is the serious affect sugar has on our brain health. When you eat carbohydrates, which break down into sugar in the body, your blood sugar levels sky-rocket[vi]. High blood sugar levels also create inflammation, further causing your brain's health to weaken. Over time, a diet high in sugar translates into the accelerated death of supple, healthy brain cells[vii].

Studies have shown that brain cells shrink and become tangled from high blood sugar levels over time[viii]. This means that your sugar intake could be drastically affecting long-term brain health, inherently increasing the likelihood of developing lesions in the brain, which are linked to the deadly disease process we call Alzheimer's.

The good news is that the brain is very resilient. A handful of well-researched, holistic prevention tools have been shown to restore damaged brain cells, and return a dying brain to its fully functioning state[ix]. 

How do I decrease my risk for Type 3 Diabetes?

Coconut Oil

Many think it an unusual treatment, but it's the leading preventative tool in cognitive health. It doesn't take years or even months — coconut oil takes action on the brain after just one 40 ml dose[x]. Medium Chain Triglycerides (MCTs) are the primary fat found in coconut oil, and they are powerful in rapidly helping to boost brain metabolism and thereby increasing cognitive functioning. Recent, insightful research has shown that patients experienced significant neurological healing after 4-6 weeks of using the oil in their nutritional plans[xi].  

Coconut oil is also a valuable source of fuel for the brain. When brain cells have undergone metabolic deterioration associated with insulin resistance, they can no longer accept glucose, the brain's main fuel source. However, coconut oil is rich in the medium chain fatty acids that break down into ketones in the liver, an alternative fuel for the brain that is as efficient as glucose.

Using coconut oil has been shown to control or even reverse the progression of what has been recently reported as Type 3 diabetes[xii]. Try using extra virgin coconut oil in your cooking, baking, or your morning smoothies to receive exceptional cognitive benefits.

A Maximized Diet

Compelling reports have shown that the nutrition plan offered to individuals seeking Type 2 Diabetes prevention is one of the same plans offered to those looking to decrease their risk of Alzheimer's disease. This dietary prevention plan includes foods that are low in sugar and high in healthy fats, which creates a rich, healing environment for the brain. Your brain will thrive when you load up on friendly fats and decrease your carbohydrate intake[xiii]. Fats that are optimal for the promotion of plasticity in your brain include olive oil, avocados, salmon, and almonds. Even small increments of good fats can make a lasting difference on your brain's health, so implement them into your diet today – and every day!

The Best Carbs – Fruits and Veggies

Modern day Western culture has consumes voluminous quantities of processed carbohydrates and so-called 'whole grains.' As a result, health practitioners are finding strong links between these foods we eat and suboptimal brain health, which makes it imperative for you to adjust your carbohydrate intake. Fruits and vegetables that promote cell growth, are less inflammatory and acidic than are starchy carbs, and, with the exception of a few higher-sugar fruits, they are lower in sugar are ideal for preventing Type III diabetes[xiv]. Maximize your dishes with blueberries, blackberries, raspberries, kale, spinach, avocados, and other dark colored fruits and vegetables for peak cognitive functioning[xv].

Beta Carotene and Vitamin C

Of course a diet low in sugar, plentiful in good fats, and rich in dark colored vegetables is ideal for the health of your brain[xvi]. Increasing your intake of antioxidants has also proven to be beneficial in nurturing and optimizing neural functioning. Research has shown that Vitamin C and Beta Carotene, found in foods like lemons, grapefruits, kale, and bell peppers, aids in the prevention of neurodegenerative diseases[xvii]. Excessive free radical production can create a dangerous atmosphere in the brain (making it rancid!), and antioxidants are a strong combatant against these brain-damaging agents. Increase your intake of antioxidants through fresh fruits and vegetables, or organic health supplements.

Chiropractic Care

Chiropractic research has shown that over time, the body's resistance to outflow from the brain can cause normal pressure hydrocephalus and toxic metabolic edema, which in turn causes the brain to break down[xviii]. This means that a decrease in normal fluid functioning without an increase in brain volume causes the brain to stop functioning. Naturally, in the prevention of Alzheimer's Disease (and any other cognitive disorder), schedule regular chiropractic appointments, and maintain a body system that is functioning at its highest potential.

Knowledge is Power

Recent research around neural deterioration and insulin resistance has been groundbreaking. The most notable, and curious, point is evidence that the disease could in fact, be preventable[xix]. Alzheimer's disease may no longer be a murky, genetically defined illness, if brain-healthy lifestyle choices are created and maintained. 

source: GreenMedInfo

Alzheimer's, Parkinson's, MS, Depression and Bipolar Disorder All Linked To Metal Toxicity

Metal toxicants entering the part of the brain that deals with stress and panic have been linked to disorders dealing with the central nervous system. Increasing evidence indicates that damage to the locus ceruleus (LC), is present in a wide range of neurodegenerative diseases including demyelinating and psychiatric disorders. 

There are a growing number of Clinicians and Scientists who are convinced that excitotoxins and heavy metals play a critical role in the development of several neurological disorders, including migraines, seizures, infections, abnormal neural development, certain endocrine disorders, specific types of obesity, and especially the neurodegenerative diseases; a group of diseases which includes: ALS, Parkinson's disease,Alzheimer's disease, Huntington's disease, and olivopontocerebellar degeneration.

The locus ceruleus (LC) is a nucleus in the pons (part of the brainstem) involved with physiological responses to stress and panic. It is the principal site for brain synthesis of the hormone and neurotransmitter norepinephrine (noradrenaline).

It has been known for many years that toxicants (i.e., poisons that are put into the environment or human body by human activity) that block the uptake of noradrenaline can damage the LC of experimental animals.

The recent finding that a metal toxicant, inorganic mercury, selectively enters the cytoplasm of human LC neuron has prompted researchers to investigate how these toxicants cause many of these CNS disorders.

The Locus Ceruleus Is Upregulated By Stress

An increased output of noradrenaline from the LC can be elicited by a wide range of acute and chronic stressors, in particular those that are physical (e.g., pain), psychological (e.g., anxiety), or social (e.g., isolation). Chronic stressors can keep noradrenergic neurons in a highly active state permanently. Stressors can increase the uptake of circulating toxicants that use neurotransmitter transporters to enter LC neurons.

Stress has been implicated in the onset or relapse of a number of neurodegenerative, demyelinating and psychiatric conditions. The increased activity of the LC during stress, with a concomitant increase in neurotransmitter release and re-uptake, encourage circulating toxicants to enter the terminal axons of LC neurons.

Studies indicating which elements of the LC-Toxicant hypothesis relate to particular CNS disorders.

CNS Regions Are Innervated By The Locus Ceruleus

About 70% of all CNS noradrenaline comes from the LC innervate in particular CNS regions that are involved in Alzheimer’s disease (hippocampus, neocortex, basal forebrain), amyotrophic lateral sclerosis (brain stem and spinal motor neurons), and mood disorders (amygdala). The substantia nigra, which is damaged in Parkinson’s disease, also receives innervation from the LC.

The normal human brain contains about 32,000 LC neurons and is estimated to contain capillaries with a total length of 640 kilometres. This means that, on average, each LC neuron is responsible for innervating 20 meters of capillaries. No other neuronal system has such widespread contact with circulating blood.

Noradrenaline plays an important part in maintaining the integrity of the blood-brain barrier and in responding to stressors by increasing cerebral blood flow. With their large exposure to the blood circulation, LC neurons could take up toxicants even if they were at low levels in the blood.

Noradrenaline also suppresses inflammation, mostly because of its affects on microglia, which have a high expression of adrenoreceptors. Inflammation would be further increased if a permeable blood-brain barrier, caused by noradrenaline depletion, allowed inflammatory cells to enter the CNS. 

The Locus Ceruleus Has Been Shown To Be Damaged In Neurodegenerative, Demyelinating, and Psychiatric Disorders

A man who injected himself intravenously with metallic mercury had mercury staining in the cytoplasm of about 70% of his LC neurons. This individual committed suicide a few months after the mercury injection, so mercury uptake by the LC may have been aided by stress-induced upregulation of the LC neurons. This is the first time that a metal toxicant has been found to be able to enter the human LC selectively.

Neuromelanin, a dark pigment produced neurons in the LC, increases during aging and may influence cell function. Neuromelanin could initially play a protective role by chelating certain circulating metal toxicants such as mercury and lead and when production is inhibited could dramatically affect uptake.

Recent reviews have highlighted the extent of LC damage in neurodegenerative, demyelinating, and psychiatric disorders.

The LC-Toxicant hypothesis can explain a number of puzzling features of neurodegenerative, demyelinating and psychiatric disorders, which are grouped below under the term “neurodegenerative disorders”.

One agent that enters neurons at an early age and cause damage later in life is a heavy metal, since metal toxicants persists within human neurons for many years.

CNS and Neurogenerative Disorders

In Parkinson’s disease, cell loss is more severe in the LC than in the substantia nigra. This fits with suggestions based on animal experiments that in Parkinson’s disease LC damage occurs first, and that the noradrenaline-deficient substantia nigra is then more susceptible to toxic insults.

The topographical distribution of cell loss in the LC varies in Alzheimer’s disease, Parkinson’s disease and depression. he type of pathology differs as well, with LC cell loss in Alzheimer’s disease and Parkinson’s disease, gliosis in multiple sclerosis, and neuronal shrinkage in amyotrophic lateral sclerosis. These topographical and pathological differences suggest that toxicants affect LC neurons in different ways.

Genetic variation is unlikely to account for the variations in incidence of neurodegenerative disorders that have been described between city and country living, or for increases or decreases of disease incidence over time. Here environmental factors are more likely. The LC would be subjected to different toxicants in the city versus the country, and would be exposed to different levels of pollutants over time. Geographic differences in toxicant exposure could interact with other environmental factors in a disorder such as multiple sclerosis, where a reduction in sunlight and vitamin D levels at increased latitudes has been implicated.

Herbicides, pesticides, vaccinations, medications and industrial exposures may be the most effective approach likely to define groups with known exposures to certain toxicants and then look for genetic variants (either single nucleotide, copy number, or epigenetic) in the biological pathways that normally protect individuals from these toxicants. An analysis could then be undertaken to see if these genetic variants are more common in people within these defined groups who have neurodegenerative disorders.

Source: PreventDisease