“Grandma, I’m not ______” What’s Happening to Our Memories?

Imagine in you and your two closest friends when your 80. Odds are one of you will have Alzheimer’s. Yes Alzheimer’s, that scary disease where your loved one starts to forget their life including you, or perhaps in the future you start to forget your loved ones. You may be more at risk to getting it than you would think… but you can also combat this pretty easily with diet, exercise, and a love for learning. 

The National Institute on Aging defines Alzheimer’s Disease as “an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks.” The Alzheimer’s Associations 2018 data shows that presently 5.7 million American’s have Alzheimer’s Disease and this number is expected to rise to 14 million by 2050. They note that every 65 seconds another person develops Alzheimer’s, a disease killing 1 in 3 American seniors which is more than breast cancer and prostate cancer combined.

There are two forms: late-onset in which the symptoms appear in their mid-60s, and early-onset where the symptoms can appear between their 30s and mid-60s. Early-onset is very rare, only about 10% of Alzheimer’s cases, and due to genetics.

Image result for alzheimer picturesYet with all our technologies and knowledge about the disease we can’t truly diagnose AD until postmortem as it is determined by physical changes in the brain. These physical changes include build up of plaques and neurofibrillary tangles. Neuronal death and connection loss are also significant changes, these are simply not visible.

The form and severity of Alzheimer’s one has depends on genetic and environmental factors. As I mentioned earlier early-onset is most commonly characterized by mutations in 1 of 3 genes: APP, PSEN 1, and PSEN 2. These mutations play into the breakdown of APP which is part of the production of the harmful forms of amyloid betas that form the amyloid plaques. Early-onset has helped scientists identify some of the key steps in the formations of these brain abnormalities that are generally found in late-onset.

The causes of late-onset are not yet completely understood. They likely contain a combination of genetic, environmental, and lifestyle factors that affect someone’s risk for developing Alzheimer’s. While they haven’t found specific genes that directly cause late-onset they have found a genetic risk factor in the APOE gene that can increase risk depending on the form. By 2015, they had also discovered and confirmed 33 regions of interest in the Alzheimer’s genome.

Environment and lifestyle play significant factors in the risk associated with development. Medical conditions such as obesity and diabetes, toxins, brain injury, and even diet play a role in Alzheimer’s. The risks increase as you age, accumulating up as different changes in the brain occur. Some are changes that can harm the neurons such as shrinking of areas, inflammation, free radical production, and energy production breakdown.

So preventative measures, that is what everyone wants to know. Its pretty easy actually… Diet, exercise, and keep learning! 

Diet & Exercise – I go into depth about Alzheimer’s and Type 2 Diabetes further down, but the gist is healthy diet and exercise keep your body healthy. They decrease you chances of developing other medical conditions in the present and the future.

Learning – This one is surprising isn’t it? It’s actually a lot simpler than you would guess and it is highly important. As Alzheimer’s involves the loss of neural connectivity the more connections you make, by learning, are vital. The more you have means the more you can lose and the less affects you are likely to see. The video below talks about a study that found this, Dr. Genova mentions it towards the end.

Diabetes and Alzheimer’s

Recent studies have shown that there is a link between type-2 diabetes (T2D) and Alzheimer’s disease (AD). One study showed that T2D nearly doubles the risk of dementia and conversely AD patients are at an increased risk to develop T2D. The commonality between them is insulin. Insulin is a hormone, primarily created in the pancreas, that controls blood sugar levels and aids in using and storing energy. In the brain this insulin works to protect the neurons, strengthen connections, plays a role in cognition and is required for long term memory.

This insulin resistance stems from many sources, the image below goes over the similarities between the two diseases.

Because of all this, medications that have been approved to treat diabetes and obesity can help counteract some effects of AD in animal models. The mechanisms above may provide new targets for disease modifying therapies.

Everyone will be impacted with Alzheimer’s somehow at least once in your life. My story was with my great grandmother who suffered from dementia for years until she died this past summer at the age of 98. Even 8 years ago when we went to visit for her 90th birthday, she couldn’t recognize me. She knew who I was once I explained but it did not click. However, until her dying day, even when she couldn’t really take care of herself, out of all her grandchildren, great grandchildren, and great great grandchildren grandma remembered my little brother the most. He was the namesake of her husband and was in a way the favorite because of that special connection. He held that emotional bond, and even with Alzheimer’s those can’t be broken easily. The memories may be lost but the feelings are forever.

Uncovering the Foundations of an Unlikely Couple: The Link Between Alzheimer’s and Type 2 Diabetes

 

The Relationship:

When considering an individual suffering from Alzheimer’s Disease (AD), one doesn’t often associate Type II Diabetes (T2D), or vice versa. However, this may become the new norm as studies are now showing a link between these two diseases. When you take a closer look, many similarities exist, turning this relationship toxic.

What is Alzheimer’s:

Alzheimer’s is a neurodegenerative disorder characterized by progressive mental deterioration due in part to the buildup of amyloid plaques and neurofibrillary tangles in the brain. This type of dementia is the most common worldwide, causing problems with memory, thinking, and behavior. There is no treatment currently capable of reversing, stopping, or significantly slowing down the progression of this disease, making the study of its origination crucial to future treatment.

http://az616578.vo.msecmd.net/files/2016/04/10/635958482997470921934663329_alzheimers1.jpg

 

What is Type II Diabetes:

Type II Diabetes, or noninsulin-dependent diabetes, is a disease that affects the way that the body metabolizes sugar. This disease is characterized by high blood sugar, insulin resistance, and relative lack of insulin. T2D primarily occurs as a result of obesity and lack of exercise and is seen to be becoming far more prevalent in recent years, likely due the poor diet and lifestyle exhibited by the American society.

 

http://www.frontiersin.org/files/Articles/140046/fnins-09-00204-HTML/image_m/fnins-09-00204-g001.jpg

The Connection:

Insulin, as we know, plays a large role in the body as a regulator of blood glucose. However, it also has an important role in brain function. Insulin is now understood to play a large part in neuroplasticity, neuromodulation, as well as memory and cognition. Lack of insulin function, as characterized by T2D, can disrupt these pathways, leading to common symptoms seen in Alzheimer’s disease.

Insulin function has been found to be disrupted by prolonged inflammation in the brain as seen in both T2D and AD. In individuals experiencing T2D, the accumulation of fat causes the accumulation of inflammatory molecules. It is likely that obesity associated systemic inflammation causes excesses circulating free fatty acids. These circulating cytokines, free fatty acids, and immune cells reach the brain and initiate local inflammation, including microglial proliferation. This chronic inflammation not only disrupts the insulin pathway in the brain, but also causes synaptic remodeling and degeneration through the overactivation of microglia.

In Alzheimer’s, prolonged inflammation of the brain is a characterizing factor of the disease. This chronic inflammation is largely due to the overactivation of microglia, as seen in T2D. Microglia work to degenerate the buildup of amyloid plaques commonly found in the brain of individuals suffering from Alzheimer’s. When these macrophage-like molecules can’t keep up, they continue to release pro-inflammatory cytokines in response, often damaging neurons and synapses in close proximity. This leads to neurodegeneration. Inflammation itself, such as from T2D, can also trigger the activation of microglia as they both respond to, and cause, neuroinflammation.

 

https://www.sigmaaldrich.com/content/dam/sigma-aldrich/articles/biology/microglia-in-neuroinflammation/neuroinflammation-microglia.jpg

Importance:

Though there is no cure for Alzheimer’s, we have found that due to its strong link to T2D, diet may play a role in in alleviating the onset and progression of this neurodegenerative disease. It is important for not only your physical heath, but also future neurological heath, to be cautious of the food you put into your body as it may have a long-term effect.

For those of us who have experienced the terrors of watching a loved one suffer through the horrors of AD, we know the impacts that this knowledge could have. Alzheimer’s is not only detrimental for the individual, but also significantly traumatic for the family as well. Though it is easy to say, “that won’t happen to me” or “I’ll deal with that when I get there”, it may be vastly beneficial to both you and your loved ones to be aware and proactive as it could affect your future and quality of life.

Bibliography:

https://www.sciencedirect.com/science/article/pii/S0889159114000889

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237995/

https://en.wikipedia.org/wiki/Diabetes_mellitus_type_2

https://moodle.cord.edu/pluginfile.php/723477/mod_resource/content/0/2018%20AD%20and%20insulin%20signaling.pdf

Can a poor diet lead to Alzheimer’s? The link between type two diabetes and Alzheimer’s.

Alzheimer‘s disease or AD is a degenerative disease that leads to memory loss, and decline of cognitive functions. Type 2 diabetes (T2D) is caused by problems due to insulin resistance. How are these two different diseases related? Is glucose regulation related to neurons dying? Research has shown that having type 2 diabetes is a major risk factor for AD, and vice verses. These two diseases are more alike than they appear. The inflammation and insulin pathway are two molecular mechanisms that explain the correlation between the two diseases.

 The Insulin Pathway

In order to understand the insulin pathway we must first talk about insulin resistance. This resistance takes place in both AD and type two diabetes.

Type 2 Diabetes: In order to breakdown glucose the body needs insulin. In T2D insulin does not work properly. This leads to high levels of glucose in the body, which causes high blood sugar. Having problems with insulin production can lead to other problems in the body, like in the brain for example.

 Alzheimer’s: Insulin resistance can be shown in postmortem brains of people who suffered from AD. This impaired insulin signaling can be seen clearly in the hippocampus region of the brain. It is thought that insulin resistance in an AD brain may be caused by the build up of amyloid beta plaques. However, this is one hypothesis. There are many more hypotheses being developed surrounding the topic of insulin resistance in the brain.

Inflammation

Insulin resistance plays a large role in the inflammation found in type 2 diabetes, and AD.

Type 2 DiabetesObesity, due to poor diet is often linked to the development of insulin resistance, and ultimately T2D. When fat cells accumulate, inflammatory cells follow. One of the main inflammatory cells involved in T2D is the cytokine TNF-α. 

Alzheimer’sChronic inflammation is one of the characteristics of AD. The inflammation seen in AD is caused by the immune cell called microglia. The microglia are responsible for the protection and remodeling of synapses in the brain, and help contribute to neuroplasticity. Microglia often produce inflammatory cells in response to increased accumulation of amyloid beta plaques. Research has shown that in order for amyloid beta to cause insulin resistance, and therefore inflammation the cytokine TNF-α must be present.

What does this have to do with my diet?

Our society values convenience, so when given the choice between fast food and taking the extra time to pack food it is not surprising that many of us would choose the fast food option. These poor dietary choices combined with spending your free time watching Netflix can lead to serious problems. Nearly 40% of Americans are obese, and 30% of those who are overweight or obese have type 2 diabetes. While maybe these statistics alone aren’t enough to change your mind maybe this next statistic will make you question whether that extra piece of cake is truly worth it. Having T2D doubles your chances of developing Alzheimer’s Disease. Now I am not saying to ditch fast food entirely, I enjoy treating myself too, but the next time I am given the option of packing my lunch or get fast food, I’ll be packing my own.

 Why should you care?

There is no cure for Alzheimer’s Disease, so it is important to take preventative steps now. Remember, little changes can make all the difference.

  • Pack a meal for on the go instead of getting fast food
  • Watch TV or Netflix while you work out
  • Find health snacks that you enjoy
  • Take time for yourself!! Whether it by cooking dinner, or working out try to find healthy practices to implement now. Trust me, your future self will thank you.

Image 1  https://www.psychologytoday.com/us/blog/diagnosis-diet/201609/avoiding-alzheimer-s-disease-could-be-easier-you-think

The 5 Proven Ways to Prevent Alzheimer’s

What is Alzheimer’s Disease?

Alzheimer’s Disease (ASD) is a form of dementia that affects memory, thinking, and behavior, primarily in older individuals; the majority of people with ASD are over 65. The most important thing to know about Alzheimer’s is that it is not a normal part of aging, and it can be prevented through lifestyle choices. The disease progresses from mild memory loss during the early stages to inability to carry a conversation or respond to environment as an affected individual approaches death.

What Goes Wrong in the Brain?

 There are two structures that appear in ASD brains that experts point to as primary characteristics of the disease:

  • Beta-Amyloid Plaques – protein fragments that build up in between nerve cells
  • Neurofibrillary Tangles – tangled tau proteins that build up in cells

These plaques and tangles build up specifically in brain areas important for memory before other areas in Alzheimer’s patients, such as the hippocampus. The plaques and tangles are not well understood by scientists, but we do know that they can destroy nerve cells, leading to memory loss.

The two buildups in the brain are caused by a variety of factors, and they are classified into three types of Alzheimer’s Disease:

Type 1 – Genetic and inflammatory based

Type 2 – Hormones and infection based

Type 3 – Brain pathway dysfunction

While the physiological mechanisms that lead to ASD are complex, there are 5 medically proven ways that can prevent all forms of Alzheimer’s.

How Can the Disease Be Prevented?

 The first thing to understand about preventing ASD is that 99% of drugs that have been formulated to treat the disease have failed. In fact, when drugs that target Beta-Amyloid plaque in the brain are used, ASD can get worse because Beta-Amyloid is a protein the brain produces to protect itself against inflammation.

Secondly, some people are more genetically predisposed to develop the disease. The gene that is most commonly associated with late-onset Alzheimer’s is the APOE gene, which can be tested for. However, many people who have this gene don’t get Alzheimer’s, and many people get the disease who don’t have the APOE gene. So, here are the five clinically proven markers to keep under control to prevent ASD.

  1. Inflammation

Most people are aware that chronic inflammation can lead to disease. However, many people don’t know exactly how to avoid and prevent inflammation. The three most important factors to ditch chronic inflammation are diet, exercise, and sleep:

Diet

  • Eat much more omega-3s than omega-6s, which means more fish and flaxseed and less vegetable oil.
  • Avoid processed foods and sugars.
  • Avoid foods that are commonly inflammation triggering, such as gluten and dairy.

Exercise

  • Make sure to strength train at least 2 days a week.
  • However, know how your body responds to exercise and don’t over train.

Sleep

  • Get at least 7 hours of sleep per night, or up to 9 hours depending how much your body needs.
  • Getting the same amount of sleep every night is best.
  1. Nutritional deficiencies

Lab testing can be performed to measure nutritional deficiencies. Common deficiencies include iron, iodine, vitamin B, vitamin B12, calcium, and magnesium. Any of these deficiencies can have adverse health effects, and they can be simply supplemented for when the deficiency is known.

  1. Toxic exposures

There are over 77,000 man-made chemicals in the environment, so it is impossible to avoid all of them, but measures can be taken to reduce toxic exposure.

  • Drink reverse-osmosis water – city water can be contaminated with halogens, antibiotics, and other prescription drugs.
  • Take preventative measures in situations with high toxic exposure risk
  • Use natural health/beauty products – deodorants and soaps are loaded with toxic chemicals
  1. Genetics

Some people are more genetically predisposed for Alzheimer’s (APOE gene mentioned previously). By getting a genetic test, you can learn if you are at risk, and diet and lifestyle recommendations will be made by a health expert.

  1. Viruses and infections

The presence of a virus such as herpes can cause chronic inflammation. Viruses can be repressed if the immune system is functioning properly. The best ways to boost immune function is through proper diet, exercise, sleep, and supplementation.

Food for Thought: The connection between type 2 diabetes and Alzheimer’s

Image result for alzheimers and diabetes

Both Alzheimer’s disease (AD) and type 2 diabetes are products of insulin resistance. Type 2 diabetes has insulin resistance in the peripheral organs, muscle and adipose tissue, while in AD, the insulin signaling pathway in the brain is impaired. This common molecular mechanism between the two diseases is theorized as the reason why 70% of individuals diagnosed with Type 2 diabetes will eventually develop Alzheimer’s. This connection has led to nicknaming AD as Type 3 diabetes. So what is insulin resistance? Is it actually a good theory for the risk of developing Alzheimer’s? Let’s take a look.

Insulin Resistance

Insulin is a hormone that regulates the amount of glucose in the blood. When insulin binds to a tyrosine kinase receptor, the phosphorylation or activation of proteins occurs, sending a signal down the pathway. This signal allows for the uptake of glucose, fatty acids and amino acids into cells where they are stored in the liver, adipose tissue and muscle as nutrients. If these nutrients are not able to be taken up, diabetes occurs. In the case of Type 2 diabetes, the body becomes resistant to insulin, so the signaling pathway never occurs to cause the uptake of these nutrients. The body’s resistance to insulin can be due to the inability of the insulin receptors to bind insulin and unlock the cells to allow glucose and other molecules into the cell.

Type 3 Diabetes

The term “type 3 diabetes” is given to Alzheimer’s because it has the insulin pathway impairment that is a trademark of diabetes, but in AD it occurs in the brain. The brain dysfunction occurring in AD has similar molecular and biochemical mechanisms as type 1 and type 2 diabetes. The reason why AD would be another form of diabetes and not just a symptom of type 2 diabetes is due to the brain specific issues that are disrupted. These issues stem from abnormalities in gene expression that encode insulin, insulin growth factor (IGF), insulin growth factor peptides, receptors and more signaling mechanisms. Problems with gene expression lead to the disruption of signaling pathways that control insulin and insulin growth factor neuronal survival, along with problems with tau expression, energy metabolism, and mitochondrial function. Together, these abnormalities create the symptoms observed in Alzheimer’s.

Is it a viable hypothesis?

There are multiple different studies showing that abnormalities with insulin and IGF signaling mechanisms occur in the early stages of Alzheimer’s, so they likely play a large role in the disease’s pathology. While AD and diabetes have a lot of similarities, it has not yet been entirely determined what the role of having type 2 diabetes plays in the development of AD. However, there are obvious conclusions that can still be drawn. Since issues with insulin pathways stem from poor diet, excess weight and inactivity, having a healthy lifestyle will keep you out of risk for issues with these pathways. Therefore, if these pathways stay healthy and functional, you will be less likely to develop both type 2 diabetes and Alzheimer’s disease. Alzheimer’s does have a genetic component to its development as well, so staying healthy may decrease the chances that these genetic abnormalities causing the development of the disease. While the research into disease pathology continues and more and more connections are found, it is important to remember the role you play in your own health.

Image: https://www.google.com/search?biw=1392&bih=684&tbm=isch&sa=1&ei=BhO9W9ycNc_8jwT6sLz4Bg&q=alzheimers+and+diabetes&oq=alzheimers+and+diabetes&gs_l=img.3..0i10i24.62947.69763..69890…2.0..0.104.1675.24j1……1….1..gws-wiz-img…….0j0i67j0i10.oPF5crPJtJc#imgrc=_0-B23ouAi8HlM:

Bridging the gap between Alzheimer’s disease and type II diabetes

100 million American adults either have type II diabetes or prediabetes (if left unregulated will lead to type II diabetes in 5 years).

It is estimated that 5.7 million Americans are living with Alzheimer’s.

Both represent a significant physical and economic burden to both the impacted individual as well as the remainder of society. At first glance, it may seem like these two diseases are unrelated, however, recent studies have identified a link between the two.

How is type II diabetes characterized?

Type II diabetes is characterized by insulin resistance. Insulin is a hormone your body releases as a response to increased blood sugar levels (which are directly dependent on eating habits). After a meal, blood sugar levels rise, and the body sends insulin to tell cells to store sugar inside the cells rather than in the surrounding bloodstream. Initially, the body will release more insulin to accommodate the increased blood sugar levels, but overtime the body cannot make enough insulin to keep blood sugar levels normal.

How is Alzheimer’s characterized?                                              

Alzheimer’s can only be diagnosed for certain by taking tissue samples and observing a build-up of neurofibrillary tangles and amyloid-beta plaques. A brain with Alzheimer’s also experiences significant brain atrophy, as seen in the image below.

These physical indicators are difficult to diagnose short of taking a tissue sample, therefore an Alzheimer’s diagnosis is determined almost exclusively on the presented symptoms of memory loss as well as mild cognitive impairment.

How are they connected?

  • Inflammation

Insulin resistance as seen in type II diabetes is proposed to be a result of chronic inflammation in peripheral tissues of an increased amount of fat tissue. Although not caused by an excess of fat tissues, brains with Alzheimer’s have increased levels of inflammation as compared to a “normal brain.”

Additionally, amyloid-beta plaques in the hypothalamus (part of the brain that regulates hormones) have been shown to cause dysregulation of metabolism in peripheral tissues. Amyloid-beta plaques also mediate the further release of various inflammatory factors causing a cascade-like inflammatory response.

Evidence points to sustained inflammation being a mechanism of insulin resistance which is present in both type II diabetes and Alzheimer’s disease.

  • Gangliosides

The brain has insulin receptors that are involved in pathways in the brain. Proper signaling is highly dependent on certain molecules being in the correct location. A cell can be portioned into different areas that accomplish different tasks- known as microdomains. An important factor of microdomains is cholesterol which acts akin to glue holding proteins together at the membrane, thereby making a more efficient signal, simply because the necessary molecules are close together. Gangliosides are commonly associated with microdomains and facilitate many reactions in the body; notably, the conversion from a single amyloid-beta molecule to a full blown plaque by having many aggregate together, a trademark of Alzheimer’s.

Diet has been shown to directly modify the type and frequency of gangliosides that become incorporated into a cell. Insulin receptors can be displaced from its proper location in a microdomain, essentially making it ineffective and modifying proper insulin signaling.

Important Takeaways:

  • Type II diabetes and Alzheimer’s disease are related, and one increases the risk for the other
  • Establishing a link between the two provides insight into two very prevalent diseases in the United States, which in turn could be helpful in finding particular therapies or treatments for one or both diseases
  • Inflammation plays a critical role in the development of type II diabetes and Alzheimer’s alike
  • Gangliosides have the potential to displace insulin receptors in the brain contributing to insulin resistance
  • Taking measures to ensure you do not develop type II diabetes lowers your chances of developing Alzheimer’s at an older age

Sources:

https://www.nia.nih.gov/health/alzheimers-disease-fact-sheet

https://www.alz.org/alzheimers-dementia/facts-figures

https://www.cdc.gov/media/releases/2017/p0718-diabetes-report.html

http://www.diabetes.org/diabetes-basics/type-2/

https://www.ncbi.nlm.nih.gov/pubmed/29129775

Insulin and Alzheimer’s: Bridging the Link Between Degeneration, Diet and Diabetes

Source: https://www.ecowatch.com/dr-mark-hyman-why-scientists-now-call-alzheimers-type-3-diabetes-1882174730.html

Alzheimer’s Disease (AD)

Alzheimer’s Disease (AD) is seen throughout popular culture today and is one of the most well known neurodegenerative disease there is. AD is the most common type of dementia, and is what most people often associate the disease with. Symptoms of AD include memory issues, confusion, problems speaking and writing, alterations in mood and personality. Despite how prevalent AD is and how much research is been put behind it, there is still very much that is not known about the progress of AD and why individuals with AD are being affected.

Neurofibrillary tangles

In understanding AD there are several aspects of disease that are essential to bigger picture. Neurofibrillary tangles (NFT) are one of these. In AD one of the major issue that occurs is proteins in the brain called Tau are hyperphosphorylated. This is one of the markers that is used to diagnose AD, as the malformed Tau proteins build up there is so malfunction associated with the cells. Exactly how this happens in not known but scientists are investigating how NFTs are directly associated with AD. It is believed that some or most of the communication between neurons are blocked because of these.

AB plagues

Amyloid is often used to describe proteins that are naturally produced by the body. The specific amyloid that is observed in AD is referred to as beta amyloid (BA) and is built up because the of incorrect cutting on amyloid precursor protein (APP). This incorrect cutting causes there to be longer BA in the brain which accumulates together to form plaques that cannot be broken down.

Figure 1: This image depicts the two most common identifiers of AD in the brain. There is also an observed loss of mass of brain mass, especially in the hippocampus which is an area associated heavily with memory.

Source: http://weeklyhealthtip.blogspot.com/2015/11/the-link-between-type-2-diabetes-and.html

What else do we know?

One of the major players scientists associated with AD are the cytokines of the immune system. Inflammation is seen in individuals who have AD and the response of the immune system to lower this inflammation is to send in cytokines. These are cells that have response on another cell, in this instance to give a response to inflammation. Thinking about the relationship between AD and cytokines is much like pondering the age old question of the chicken and the egg. Increased amounts of cytokines are associated with mutated APP molecules and Tau phosphorylation and eventually leads to neuron death which is a major culprit in neuroinflammation. So was it the inflammation and BA plaques that called the cytokines or excess cytokines that started the inflammation? A bigger question lays behind this, why is there a strong relationship between AD and type 2 diabetes? What about the two strings them together?

Type 2 Diabetes (T2D)

What is it?

Type 2 Diabetes (T2D) which is also known as adult onset diabetes, is when the body no longer processes glucose properly because of insulin resistance or the lack of the production of insulin. Insulin is the molecule in the body that is response for regulating the sugar molecule glucose in and out of the cells. Although T2D is more common in adults, as childhood obesity increases so does the chance of developing the disease. There is no cure for T2D but can be regulated through healthy eating and exercising.  

Figure 2: The connection between the brain and body is undeniable but eating healthy not only helps with the regulation of T2D it also increases the overall sense of wellbeing and may help the brain in the long run, much longer than some people may think.

Source: https://www.medindia.net/patients/lifestyleandwellness/diet-and-alzheimers-disease.htm

Diet and Diabetes

As seen through ways to live with T2D, diet plays a large role. It is important for individuals with T2D to take insulin shots to increase the amount of insulin in the body but in addition to this, as stated above, taking careful notice of the food that you put into your body. As seen with younger individuals, those who experience or are on the verge of obesity are at risk of developing T2D, suggesting there is some relationship between T2D and food associated with obesity. Although the exact reason for T2D diabetes is unknown to researchers there is some evidence to suggest that weight gain and unhealthy eating are apart of the cause. What most people don’t associate with this however, is AD even though there is a clear link between the two.

Figure 3: A venn diagram shows the relationship between T2D and AD by comparing the similarities between the two. As seen above, there are more things in common than many people realize. The major classifiers of AD are seen listed as well but are not observed in T2D.

Source: https://www.mdpi.com/2072-6643/7/9/5341

Insulin in Alzheimer’s Brain: Type 3 Diabetes

Insulin is so well known in the development of T2D, as well as type 1, that many people do not often realize that it plays a major role in other parts of the body, including the brain. Insulin can increase spatial memory, is essential in cognitive and memory functions, as well as influencing feeding behavior. In patients with AD less insulin is seen as well. There is also a correlatory 80% of individuals who have AD also have insulin resistance of T2D, prompting AD to be called type 3 diabetes. Although there is much more research required behind this notion, scientists urge individuals (especially those with T2D or at risk of developing it) to eat better.

Another culprit in the development of both diseases is leptin. Leptin is a hormone that is made by the body to regulate caloric intake and feeding behaviors. In one study in particular, researchers found that there mice with high fat diets did not allow leptin to bind to neurons which never alerted the body that it was full and the mice continued to eat until they were overweight. Leptin also plays a role in the insulin pathway in the brain. Mutated leptin pathways often led to insulin resistance in individuals. This suggests that high fat diets that change the structure and purpose of leptin are not only associated with diseases related directly to insulin, such as T2D, but others like AD that have less information but what is known is the lack of insulin in the brain. This shows that there is no one common link between the three but rather may remain interconnected to each other.

Figure 4: Many individuals with T2D or at least insulin resistance are at risk of developing AD.

Source; https://ediblearia.com/2016/09/11/alzheimers-disease-is-type-3-diabetes/

Many people don’t realize that changing diet now may make a difference later in life. Not only in AD and the progression of the one not only the most debilitating diseases known to man but also the hardest to watch a loved one endure. It is so important for people to understand the connection between these diseases because in doing so it may aid for them to alter their lifestyle now so that they are able to experience the best possible future.

 

References:  

https://www.alz.org/alzheimers-dementia/10_signs

https://www.brightfocus.org/alzheimers/infographic/amyloid-plaques-and-neurofibrillary-tangles

http://www.diabetes.org/diabetes-basics/type-2/

The Brain-Pancreas Connection: An Insulin Resistance Story

 

http://www.mwhomecare.com/diabetes-alzheimers-study/

What is Alzheimer’s Disease? Most likely when you first encountered Alzheimer’s, you heard that it was an individual forgetting things that they had previously known, such as names, events, or even large portions of their lives. The first thought after that is probably: Why? How does this happen in a person’s head? There are two big things that have been found to contribute to Alzheimer’s: neurofibrillary tangles and Aβ plaques.

Neurofibrillary tangles are hyperphosphorylated aggregates of tau protein that come together as insoluble clumps due to problems caused by insulin resistance. These insoluble tangles increase toxicity in the brain and cause neurons in the brain to die. With less neurons in the brain, connections are less easily made and symptoms of Alzheimer’s start to show.

Aβ plaques are collections of amyloid beta peptide oligomers that clump together because of improper cutting of an amyloid precursor protein (APP). This improper cutting is due to a buildup of the GM3 ganglioside. This also causes the insulin receptor to be unable to receive insulin. Then insulin resistance increases.

https://healclinics.com/a-relationship-between-diabetes-and-alzheimers-disease/

Now how does this relate to Type 2 Diabetes? The answer is insulin resistance. Type 2 Diabetes is characterized as your body being unable to use insulin in the correct way. When it can’t be used, it can’t regulate our blood sugar levels causing hyperglycemia, or higher blood sugar levels than normal. We know that insulin is important in maintaining our blood sugar levels; but being a big part of the brain? That is a new idea. Insulin is made in two parts of the body: the pancreas and the brain. It is an important regulator of brain physiology and works as a cognitive enhancer. So if there is resistance to this cognitive enhancer, there will be breakdown in the brain: Alzheimer’s Disease. We see that both the neurofibrillary tangles and Aβ plaques are fundamentally involved in some way, shape, or form with insulin resistance.

http://www.drugood.com/2018/05/30/is-alzheimers-disease-called-type-iii-diabetes/

Now that we have talked a little bit about both Alzheimer’s and Type 2 Diabetes, we can see that there is a connection between the two. That connection being insulin resistance. However, it goes even deeper. Studies show that 70% of all individuals that have Type 2 Diabetes will develop Alzheimer’s Disease at a later time in their lives. That number is staggering to me and it makes me think we need to make some changes at both the individual and societal levels. Individually we need to think about what we eat and get more exercise. Since Type 2 Diabetes is largely characterized by unhealthy eating and lack of exercise, this would be the obvious place to begin. At the societal level, we need to have healthy options available as fast options, not only unhealthy options. Though much of our society is in a “go-go-go” mode, we still need to have a healthy food to fuel us through our days. Though this won’t completely fix the problem, it will likely be worth it to slow down the large numbers that are developing Type 2 Diabetes and in the future Alzheimer’s. I feel that this ‘risk’ of healthy eating and exercise is worth it to remember loved ones and large events that happen in your life.

Alzheimers and diabetes, the consequences of our lifestyle

Alzheimers is a neurodegenerative disease in individuals that are usually of an older age. One of the major components to Alzheimers disease (AD) is the role of insulin. Insulin functions in our bodies to regulate uptake of glucose for cellular processes. In neurological functions, it breaks down Aβ amyloid plaques. though if there is a lack of insulin, this results in plaque formations leading to tau plaques. These plaques result in loss of neurons, as these can prevent the proper function of the neurons.

Insulin resistance develops from an excess of GM3 gangliosides building up in the phospholipid membrane, causing dissociation of the GEM insulin receptors from the caveolae.

This lack of insulin signaling leads to a lack of glucose in individuals with type 2 diabetes, a disease that is more common in obese and overweight individuals. These diseases share many components, such as a resistance to insulin. These diseases prevalence will only become more taxing on our society, as the projected numbers for the US ranks 50% of the population to be classified as overweight or obese by 2030. This increase in the affected population will also increase the number of individuals that are at a much higher risk for AD and type 2 diabetes. The State of Obesity lists the average percentage of adults in the US is 30% in most states. With several states having 35+% of the population being considered obese. In a projected 13 years for that percentage to gradually increase to encompass more of the population.

So what can we do to prevent this?

Our lifestyle choices play a major component in the development of bad habits, which can result in becoming overweight. Once overweight, this greatly increases the risk for type 2 diabetes. Since the relationship with type 2 diabetes and AD, this also increases the chances for someone who has type 2 diabetes or is overweight to be at risk for AD.

So to take preventative measures at a younger age, as preventing one from becoming obese or overweight by being active and eating a healthy and balanced diet. As these factors become more substantial at an older age.

 

Can you EAT your way into Alzheimer’s?

Did you know that 70% of people with type II diabetes are later diagnosed with Alzheimer’s? That is a ridiculous percentage to be coincidental, but what could these two diseases possibly have in common? Well, recent studies have linked both diabetes and Alzheimer’s to unhealthy diets high in fats and sugar. These unbalanced diets can then lead to detrimental factors such as insulin resistance, the degradation of your blood-brain barrier, and inflammation. Let’s take a closer look at how your diet can affect these three ailments.

Insulin Resistance:
Insulin is a natural hormone produced in the body when blood glucose levels are too high. It signals for the uptake and storage of glucose from the bloodstream to cells on the brain, liver, muscles etc. It is a very important biological function that can be disrupted if too many gangliosides (specifically GM3) have been incorporated into one’s diet. Glycosides are modified lipids that are found inside cell membranes and play an important role in cell signaling and communication. Unfortunately, if there becomes an abundance of GM3s in the membrane, they can disrupt insulin signaling by separating insulin receptors from their secondary proteins. This halts the signaling cascade and prevents the cell from intaking excess glucose resulting in insulin resistance. Excess GM3s also play a crucial role in the feedback production of amyloid beta (Ab) peptides. Once GM3 is degraded into GD3, it signals for more Ab peptides to be produced into the extracellular matrix (ECM). Therefore if there is a continuous integration of new GM3 into our membranes, the concentration of GD3s will rise leading to an increase of Ab peptides in the ECM. This can then lead to aggregation of these peptides which results in Ab plaque formation which is a classic trademark of Alzheimer’s.

Blood Brain Barrier and Chronic inflammation:
Another important factor in both Diabetes and Alzheimer’s is chronic inflammation that causes irreversible cell damage over time. The million dollar question is what causes the inflammation? Some research has pointed to clues within the gut-brain-axis which is a model showing how the gut can affect brain function. Simply the gut-brain-axis states that toxins, molecules, or anything else we digest can more easily get into our bloodstream if our gut’s microbiota is out of whack. This then can lead to extreme problems if our blood brain barrier (bbb) is damaged letting dangerous chemicals enter into our brains and cause inflammation. Microbiota imbalance can be caused by numerous factors including genetics and our daily diet. A diet high in fat, sugar, and sodium can also lead to fat accumulation which has also been shown to degrade our bbb. Without the protective covering of astrocytes around our blood vessels, which make up the bbb, the foreign molecules are free to wreak havoc on our brains. The inflammation response then hyper-activates the processing of Ab Proteins placing a higher concentration of Ab peptides in the ECM. With a higher concentration of Ab peptides, comes plaque formation and eventual neuronal death causing impairment in brain function and Alzheimer’s.
Besides the accumulation of plaques, Ab peptides trigger the production of cytokines which are the signaling molecules for inflammation creating a vicious cycle. If we could one day stop the cycle of inflammation in the brain before serious damage has occurred then we could theoretically treat Alzheimer’s. Other interesting fields of study could include bbb repair, fixing the gut microbiota in Alzheimer’s patients, and the degradation of excess Ab peptides.
However, for now, the biggest preventative strategy for Alzheimer’s and type II diabetes is a healthy lifestyle and diet. What we put into our body’s today will come back to affect our quality of life in the future.

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