President Ronald Reagan
Archive | September 2022
QUOTE FOR THE WEEKEND:
“Lewy bodies are clumps of abnormal protein particles that, for reasons that are not fully understood, accumulate in the brain. These deposits cause a form of dementia called Lewy body dementia, or LBD — which is what the late actor and comedian Robin Williams suffered from.
LBD is not the same as Parkinson’s, but the two are closely related: LBD causes some or all of the motor symptoms of Parkinson’s. More than 1 million people in the U.S. are affected by Lewy body dementia, according to the Lewy Body Dementia Association.”
John Hopkins Medicine
Part II Lewy Body Dementia-How its diagnosed, risk factors, prognosis and stages!
How to Diagnose for LBD:
1-Most important is getting an experienced clinician within the medical community who should perform a diagnostic evaluation. If one is not available, the neurology department of the nearest medical university should be able to recommend appropriate resources or may even provide an experienced diagnostic team skilled in Lewy body dementia.
A thorough dementia diagnostic evaluation includes physical and neurological examinations, patient and family interviews (including a detailed lifestyle and medical history), and neuro-psychological and mental status tests. The patient’s functional ability, attention, language, visuospatial skills, memory and executive functioning are assessed.
Than further diagnostic tooling to help diagnose LBD:
2- A brain imaging (CT or MRI scans)
3-Blood tests
4-Other laboratory studies may be performed.
The evaluation will provide a clinical diagnosis. Unfortunately, currently, a conclusive diagnosis of LBD can be obtained only from a postmortem autopsy for which arrangements should be made in advance. Some research studies may offer brain autopsies as part of their protocols. Participating in research studies is a good way to benefit others with Lewy Body Dementia. Though it is hard to do this if you only get diagnosed with this after you die being misdiagnosed previously when alive, like Robin Williams through a autopsy. So the point is when symptoms resembling dementia or better Lewy Body Dementia go to an expert doctor in this
Medications
Medications are one of the most controversial subjects in dealing with LBD. A medication that doesn’t work for one person may work for another person. Become knowledgeable about LBD treatments and medication sensitivities.
Prescribing should only be done by a physician who is thoroughly knowledgeable about LBD. With new medications and even ‘over-the-counter,’ the patient should be closely monitored. At the first sign of an adverse reaction, consult with the patient’s physician. Consider joining the online caregiver support groups to see what others have observed with prescription and over-the-counter medicines.
Risk Factors
Advanced age is considered to be the greatest risk factor for Lewy Body Dementia, with onset typically, but not always, between the ages of 50 and 85. Some cases have been reported much earlier. It appears to affect slightly more men than women. Having a family member with Lewy Body Dementia may increase a person’s risk. Observational studies suggest that adopting a healthy lifestyle (exercise, mental stimulation, nutrition) might delay age-associated dementias.
Clinical Trials
The recruitment of LBD patients for participation in clinical trials for studies on LBD, other dementias and Parkinsonian studies is now steadily increasing.
Prognosis and Stages
Defining the stages of disease progression for LBD is difficult. The symptoms, medicine management and duration of LBD vary greatly from person to person. To further complicate the stages assessment, LBD has a progressive but vacillating clinical course, and one of its defining symptoms is fluctuating levels of cognitive abilities, alertness and attention. Sudden decline is often caused by medications, infections or other compromises to the immune system and usually the person with LBD returns to their baseline upon resolution of the problem. But for some individuals, it may also be due to the natural course of the disease.
Come back tomorrow to learn treatments for LBD!
QUOTE FOR FRIDAY:
“Lewy body dementia, also known as dementia with Lewy bodies, is the second most common type of progressive dementia after Alzheimer’s disease. Protein deposits, called Lewy bodies, develop in nerve cells in the brain regions involved in thinking, memory and movement (motor control). Lewy body dementia causes a progressive decline in mental abilities. People with Lewy body dementia might have visual hallucinations and changes in alertness and attention.”
MAYO CLINIC
Part I Lewy Body Dementia – A type of dementia
Learn the S/S Robin Williams had,which where 3 of 4 of these:
“Who was Lewy? In the early 1900s, while researching Parkinson’s disease, the scientist Friederich H. Lewy discovered abnormal protein deposits that disrupt the brain’s normal functioning. These Lewy body proteins are found in an area of the brain stem where they deplete the neurotransmitter dopamine, causing Parkinsonian symptoms.
In Lewy Body Dementia [LBD], these abnormal proteins are diffuse throughout other areas of the brain, including the cerebral cortex. The brain chemical acetylcholine is depleted, causing disruption of perception, thinking and behavior. Lewy body disease exists either in pure form, or in conjunction with other brain changes, including those typically seen in Alzheimer’s disease and Parkinson’s disease.”
We all know Robin Williams and initially he was presented in the news as committing suicide but in the past few years it has been presented by doctors that he died of LBD which makes more sense, for a man who had it all to many with Parkinson’s Disease. Robin all his life wanted to make others smile and laugh, never did he come across as a depressed unhappy man. We all have our ups and downs along our journey living, which is a part of life. Killing yourself is a severe extreme and you know the news (jump at the first juicy article to make it big or and if we are wrong will admit it or possibly apologize later, sad). The disease killed him in making him think to do suicide.
LBD is not a rare disease. It affects an estimated 1.4 million individuals and their families in the United States. Because LBD symptoms can closely resemble other more commonly known diseases like Alzheimer’s and Parkinson’s, it is currently widely underdiagnosed. Many doctors or other medical professionals still are not familiar with LBD.
Lewy body dementia (LBD) is a progressive brain disorder in which Lewy bodies (abnormal deposits of a protein called alpha-synuclein) build up in areas of the brain that regulate behavior, cognition, and movement.
A complex disease, LBD can present with a range of symptoms including problems with thinking, memory, moving, sleep and/or changes in behavior, to name a few of the physical, cognitive, and behavioral symptoms.
LBD also affects autonomic body functions, such as blood pressure control, temperature regulation, and bladder and bowel function. Progressively debilitating, LBD can also cause people to experience visual hallucinations or act out their dreams.
What is the Difference Between LBD and Dementia with Lewy Bodies?
LBD is an umbrella term for two closely related clinical diagnoses: Parkinson’s disease dementia and dementia with Lewy bodies (DLB).
What Causes LBD?
The causes of LBD are not yet well understood, but research is ongoing in this area. There are probably multiple factors involved, including genetic and environmental risk factors that combine with natural aging processes to make someone susceptible to LBD.
What are the Signs and Symptoms of LBD?
This condition impairs thinking, such as memory, executive function (planning, processing information), or the ability to understand visual information. Patients with LBD may have fluctuations in attention or alertness; problems with movement including tremors, stiffness, slowness and difficulty walking; hallucinations; and alterations in sleep and behavior.
Come back tomorrow for Part II!
QUOTE FOR THURSDAY:
“Suicide is the second leading cause of death among young adults and for every youth suicide it is estimated that 100 to 200 others attempt suicide. Young adulthood is a time when many people experience significant stress from life transitions such as gaining more independence and responsibility when moving from home and beginning college or a career. That stress has been amplified by the COVID-19 pandemic. Yet, we’ve seen striking glimmers of resilience – the ability to bounce back from a negative experience or difficult challenge. ”
JED Foundation
Quote for Wednesday
Alzheimer’s Disease Awareness
Alzheimer’s Disease considered by some as Diabetes 3=Brain Diabetes.
At one time Alzheimer’s disease was a disease considered with unknown etiology (or cause). Today it is considered different in the eyes of many in the medical profession. WELCOA =Wellness Council of America blog site considers this Month, June, Alzheimer’s and Brain Awareness Month! It is national month in November as well.
While we know that certain diseases, like type 2 diabetes, are definitively connected to the foods you eat, Alzheimer’s is generally thought to strike without warning or reason.
That is, until recently.
Now, a growing body of research suggests there may be a powerful connection between the foods you eat and your risk of Alzheimer’s disease and dementia, via similar pathways that cause type 2 diabetes. Some have even re-named Alzheimer’s as “type 3 diabetes.””
Can You Eat Your Way to Alzheimer’s?
In a recent animal study, researchers from Brown University in Providence, Rhode Island were able to induce many of the characteristic brain changes seen with Alzheimer’s disease (disorientation, confusion, inability to learn and remember) by interfering with insulin signaling in their brains.
Know that faulty insulin (and leptin, another hormone) signaling is an underlying cause for insulin resistance, which, of course, typically leads to type 2 diabetes. However, while insulin is usually associated with its role in keeping your blood sugar levels in a healthy range, it also plays a role in brain signaling. When researchers disrupted the proper signaling of insulin in the brain, it resulted in dementia.
What does this have to do with your diet? Let us go back to one of my articles on diabetes and how it impacts your diet. It states “The foods we eat that contain starches, carbohydrates, calories are made up of sugar. When food reaches our stomach in time digestion starts to take place where these foods are broken down in the stomach into individual or complex sugar molecules ( glucose being one of the most common and important ones). The glucose then passes from our stomach into our bloodstream when it reaches the liver 60 to 80 % of the glucose gets stored in that organ turning glucose into inactive glucose that’s converted to glycogen. The purpose for glycogen is when our glucose is low and our body needing energy we have this extra stored sugar, glycogen, to rely on. This is done by the liver which allows the sugar to be stored and released back into the bloodstream if we need it=energy, since nothing is in our stomach at that time, in that case scenario). When glucose=an active sugar, it is our energy for our cells and tissues and is a sugar ready to be utilized by the body where it is needed, by many organs. Think of a car for one moment, and what makes it run? That would be gas/fuel for it to function. The same principle with glucose in your bloodstream=fuel for the human body so we can function, for without it we wouldn’t survive. That is the problem with a person that has diabetes. They eat, they break the food down, the glucose gets in the blood but the glucose fuel can’t be used due to lack of or NO insulin at all. Insulin allows glucose to pass into our cells and tissues to be used as energy/fuel for the body parts to work. Glucose is used as the principle source of energy (It is used by the brain for energy, the muscles for both energy and some storage, liver for more glucose storage=that is where glucose is converted to glycogen, and even stored in fat tissue using it for triglyceride production). Glucose does get sent to other organs for more storage, as well. Insulin plays that vital role in allowing glucose to be distributed throughout the body. Without insulin the glucose has nowhere to go.”
So how does this impact your brain thinking? “This new focus on the Alzheimer’s/Diabetes/Insulin connection follows a growing recognition of insulin’s role in the brain. Until recently, the hormone was typecast as a regulator of blood sugar, giving the cue for muscles, liver and fat cells to extract sugar from the blood and either use it for energy or store it as fat. We now know that it is also a master multitasker: it helps neurons, particularly in the hippocampus and frontal lobe, take up glucose for energy, and it also regulates neurotransmitters, like acetylcholine, which are crucial for memory and learning.” What is effected with Alzheimer’s disease? Your memory and learning, So your diet plays a big role in Alzheimer’s disease.”
Over-consumption of sugars and grains is what ultimately causes your body to be incapable of “hearing” the proper signals from insulin and leptin, leaving you insulin resistant in both body and brain. Alzheimer’s disease was tentatively dubbed “type 3 diabetes” in early 2005 when researchers learned that the pancreas is not the only organ that produces insulin. Your brain also produces insulin, and this brain insulin is necessary for the survival of your brain cells.
If You Have Diabetes, Your Risk of Alzheimer’s Increases Dramatically
Diabetes is linked to a 65 percent increased risk of developing Alzheimer’s, which may be due, in part, because insulin resistance and/or diabetes appear to accelerate the development of plaque in your brain, which is a hallmark of Alzheimer’s. Separate research has found that impaired insulin response was associated with a 30 percent higher risk of Alzheimer’s disease, and overall dementia and cognitive risks were associated with high fasting serum insulin, insulin resistance, impaired insulin secretion and glucose intolerance.
A drop in insulin production in your brain may contribute to the degeneration of your brain cells, mainly by depriving them of glucose, and studies have found that people with lower levels of insulin and insulin receptors in their brain often have Alzheimer’s disease (people with type 2 diabetes often wind up with low levels of insulin in their brains as well). As explained in New Scientist, which highlighted this latest research:
What’s more, it encourages the process through which neurons change shape, make new connections and strengthen others. And it is important for the function and growth of blood vessels, which supply the brain with oxygen and glucose.
As a result, reducing the level of insulin in the brain can immediately impair cognition. Spatial memory, in particular, seems to suffer when you block insulin uptake in the hippocampus… Conversely, a boost of insulin seems to improve its functioning.
When people frequently gorge on fatty, sugary food, their insulin spikes repeatedly until it sticks at a high level. Muscle, liver and fat cells then stop responding to the hormone, meaning they don’t mop up glucose and fat in the blood. As a result, the pancreas desperately works overtime to make more insulin to control the glucose – and levels of the two molecules skyrocket.
The pancreas can’t keep up with the demand indefinitely, however, and as time passes people with type 2 diabetes often end up with abnormally low levels of insulin.”
Alzheimer’s Might be “Brain Diabetes”
It’s becoming increasingly clear that the same pathological process that leads to insulin resistance and type 2 diabetes may also hold true for your brain. As you over-indulge on sugar and grains, your brain becomes overwhelmed by the consistently high levels of insulin and eventually shuts down its insulin signaling, leading to impairments in your thinking and memory abilities, and eventually causing permanent brain damage.
Regularly consuming more than 25 grams of fructose per day will dramatically increase your risk of dementia and Alzheimer’s disease. Consuming too much fructose will inevitably wreak havoc on your body’s ability to regulate proper insulin levels.
Although fructose is relatively “low glycemic” on the front end, it reduces the affinity for insulin for its receptor leading to chronic insulin resistance and elevated blood sugar on the back end. So, while you may not notice a steep increase in blood sugar immediately following fructose consumption, it is likely changing your entire endocrine system’s ability to function properly behind the scenes.
Additionally, fructose has other modes of neurotoxicity, including causing damage to the circulatory system upon which the health of your nervous system depends, as well as profoundly changing your brain’s craving mechanism, often resulting in excessive hunger and subsequent consumption of additional empty carbohydrate-based calories.
In one study from UCLA, researchers found that rats fed a fructose-rich and omega-3 fat deficient diet (similar to what is consumed by many Americans) developed both insulin resistance and impaired brain function in just six weeks.
Plus, when your liver is busy processing fructose (which your liver turns into fat), it severely hampers its ability to make cholesterol, an essential building block of your brain crucial to its health. This is yet another important facet that explains how and why excessive fructose consumption is so detrimental to your health. Decreasing fructose intake is one of the most important moves you can take in decreasing the risk of Alzheimer’s disease in your lifetime.
More Tips for Avoiding Alzheimer’s Disease:
The beauty of following a healthy diet is that it helps treat and prevent all chronic degenerative diseases, from the common ones like heart disease, cancer, diabetes, obesity and Alzheimer’s to the ones you have never heard of or can’t even pronounce.
The first step is to eat healthy, maintaining exercise balanced with rest and practice healthy habits in addressing Alzheimer’s disease, which is currently at epidemic proportions, with 5.4 million Americans – including one in eight people aged 65 and over – living with the disease.By 2050, this is expected to jump to 16 million, and in the next 20 years it is projected that Alzheimer’s will affect one in four Americans. People we need to live healthier if not to help ourselves our future young ones.
In spite of how common memory loss is among Westerners, it is NOT a “normal” part of aging. While even mild “senior moments” may be caused by the same brain lesions associated with Alzheimer’s disease and other forms of dementia, these cognitive changes are by no means inevitable! People who experience very little decline in their cognitive function up until their deaths have been found (post-mortem) to be free of brain lesions, showing that it’s entirely possible to prevent the damage from occurring in the first place and one of the best ways to do this is by leading a healthy lifestyle.
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Fructose. As mentioned, most everyone will benefit from keeping their total fructose consumed to below 25 grams per day.
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Improve Magnesium Levels. There is some exciting preliminary research strongly suggesting a decrease in Alzheimer symptoms with increased levels of magnesium in the brain. Unfortunately most magnesium supplements do not pass the blood brain levels, but a new one, magnesium threonate, appears to and holds some promise for the future for treating this condition.
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Optimize your vitamin D levels with safe sun exposure. Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed. Researchers believe that optimal vitamin D levels may enhance the amount of important chemicals in your brain and protect brain cells by increasing the effectiveness of the glial cells in nursing damaged neurons back to health.
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Vitamin D may also exert some of its beneficial effects on Alzheimer’s through its anti-inflammatory and immune-boosting properties. Sufficient vitamin D is imperative for proper functioning of your immune system to combat inflammation that is also associated with Alzheimer’s.
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Vitamin B12: According to a small Finnish study recently published in the journal Neurology, people who consume foods rich in B12 may reduce their risk of Alzheimer’s in their later years. For each unit increase in the marker of vitamin B12 (holotranscobalamin) the risk of developing Alzheimer’s was reduced by 2 percent. Very high doses of B vitamins have also been found to treat Alzheimer’s disease and reduce memory loss.
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Eat a nutritious diet, rich in folate. Vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day.
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High-quality animal-based omega-3 fats, such as krill oil. (I recommend avoiding most fish because, although fish is naturally high in omega-3, most fish are now severely contaminated with mercury.) High intake of the omega-3 fats EPA and DHA help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression, and lowering your risk of developing the disorder.
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Avoid and remove mercury from your body. Dental amalgam fillings, which are 50% mercury by weight, are one of the major sources of heavy metal toxicity, however you should be healthy prior to having them removed.
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Avoid aluminum, such as antiperspirants, non-stick cookware, vaccine adjuvants, etc.
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Exercise regularly. It’s been suggested that exercise can trigger a change in the way the amyloid precursor protein is metabolized,10 thus, slowing down the onset and progression of Alzheimer’s. Exercise also increases levels of the protein PGC-1alpha. Research has also shown that people with Alzheimer’s have less PGC-1alpha in their brains11 and cells that contain more of the protein produce less of the toxic amyloid protein associated with Alzheimer’s. I would strongly recommend reviewing the Peak Fitness Technique for my specific recommendations.
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Avoid flu vaccinations as most contain both mercury and aluminum, well-known neurotoxic and immunotoxic agents.
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Eat plenty of blueberries. Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against Alzheimer’s and other neurological diseases.
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Challenge your mind daily. Mental stimulation, especially learning something new, such as learning to play an instrument or a new language, is associated with a decreased risk of Alzheimer’s. Researchers suspect that mental challenge helps to build up your brain, making it less susceptible to the lesions associated with Alzheimer’s disease.
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Avoid anticholinergic and statin drugs. Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.
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Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of coenzyme Q10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.
** Before making any changes check with your doctor or endocrinologist first.**
QUOTE FOR TUESDAY:
“Leukemia is the most common cancer in children and teens, accounting for almost 1 out of 3 cancers. Most childhood leukemias are acute lymphocytic leukemia (ALL). Most of the remaining cases are acute myeloid leukemia (AML). Chronic leukemias are rare in children. ”
American Cancer Society
QUOTE FOR MONDAY:
“Lymphoplasmacytic lymphoma (LPL) is a low-grade (slow-growing) non-Hodgkin lymphoma. It develops from B lymphocytes (a type of white blood cell) that become abnormal and grow out of control. The abnormal cells in LPL can produce large amounts of abnormal antibodies (sometimes called ‘paraprotein’). In most cases of LPL, this is an IgM abnormal antibody. LPL with IgM detectable on blood tests is called Waldenström’s macroglobulinaemia (WM). It is named after the scientist who first described it. All types of LPL are treated in the same way.”.
Lymphoma Action (https://lymphoma-action.org.uk)