How Parkinson's Dementia and Lewy Body Dementia Are Related Diseases
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The answer to that question has to do with the One-Pill-for-One-Disease paradigm that Big Pharma developed many years ago as a way to market conventional medicine. As a result of the marketing that’s been done over the years, there is a quiet, unspoken belief that, when you go to the doctor, he or she will be able to prescribe a pill, just one pill, that you will take to overcome your diseased state. Indeed, this idea of One-Pill-for-One-Disease, has been propagated in part by combining drugs into one pill when they are normally prescribed together by doctors. Of course, simplicity can be beneficial. Patients don’t always follow their doctor’s orders even when there is only one pill involved in their treatment. But the idea here is that, if there is only One-Pill-for-One-Disease, you have to have a lot of different diseases – or rather, a lot of different diagnostic labels in order to ensure that patients receive a drug that targets the specific presentation of disease that’s manifesting in their body. Unfortunately though, this One-Pill-for-One-Disease paradigm is often more about making profit than about finding the perfect drug to fit a particular disease. The One-Pill-for-One-Disease idea was meant to simplify medicine, but often, it creates a muddled mess. For example, is Lewy body dementia actually different from Parkinson’s disease or are these two diseases actually made up of the same underlying physical issues? The gold standard for diagnosing dementia with Lewy bodies is a PET scan and single-photo emission computed tomography (SPECT) tracers. Dopamine transporter loss in the brain is the signature feature of LBD. The loss of dopamine transporters helps to differentiate this disease from other types of dementia such as Alzheimer’s, but Alzheimer’s, is a neurodegenerative brain disorder that most impacts memory and language. In contrast, LBD and PD tend to impact movement and coordination. Alzheimer’s begins with memory loss, but Parkinson’s patients typically complain about physical stiffness and tremors as their first set of symptoms. LBD patients begin with symptoms that resemble Alzheimer’s, but the disease progresses more in the direction of eventual Parkinson’s symptoms. Alzheimer’s patients, in contrast, are unlikely to eventually develop movement-related issues.Click here to do a free trial of EMDR to Release Trauma.
The boundary between Lewy body dementia and Parkinson’s disease is not clear cut even if high-tech PET or SPECT diagnostics claim to tell the difference. While researching Parkinson’s disease in the early 1900’s, Friederich, H. Lewy discovered abnormal protein deposits that disrupt the functioning of the brain. When these proteins are found in the substantia nigra of the brain stem, they deplete dopamine and cause symptoms of Parkinson’s disease. But when these Lewy bodies (proteins) are found in other areas of the brain, they deplete acetylcholine levels which causes disturbances in how the patient perceives the world, behaves, and thinks.These two diseases share many symptoms and clinical features including Lewy bodies. Indeed, if the patient first presents with the symptoms of dementia, the diagnosis is Dementia with Lewy Bodies (DLB). Patients who are diagnosed with this form of dementia often develop many of the clinical symptoms of Parkinson’s disease eventually. On the other hand, if the patient first develops tremors and other classic symptoms and clinical features associated with Parkinson’s disease, the diagnosis is Parkinson’s. But someone with Lewy body dementia might also be diagnosed with Alzheimer’s disease depending on subjective reports and the attending doctor’s perception of the problem. Older doctors may have one way of viewing a patient’s symptoms while younger doctors may tend to diagnose patients through a very different lens. A complicating fact is that PD is a disease that seems to have changed over the course of time. About 50 years ago, patients who were diagnosed with Parkinson’s disease had about a 3% chance of developing dementia. Today, the odds of developing dementia after getting diagnosed with Parkinson’s is much higher at 78%. This fact indicates that something has changed in terms of nutrition, the environment, or another unknown variable over the past 50 years that has had quite an impact on the progression of Parkinson’s disease. The moment a patient arrives at a clinic for diagnosis could literally change the patient’s diagnosis.Click here to learn more about the DreamLight.app, a guided meditation and brain-entrainment tool for natural trauma-release.
Age-ism in Dementia Diagnoses
Let’s consider vascular dementia. Vascular dementia happens as a result of damaged or blocked blood vessels that restrict blood flow to the brain, ultimately starving the brain of oxygen and nutrients. While Alzheimer’s (a disease involving amyloid plaques as opposed to a hypoxic brain) begins with memory loss, vascular dementia typically begins with slowed thinking, confusion, and difficulty making decisions. But any issue in the brain that involves dopamine is going to look like difficulty making decisions. And let’s face it…some people ruminate for years before making relatively simple decisions while other people are impulsive in their decision-making strategy. Doing a differential diagnosis to separate vascular dementia from Alzheimer’s is a lot more difficult in practice than most patients realize. But now, just for fun, let’s think about diagnoses that are given to younger people who have similar neurological issues. In young people, poor decision making on one’s own behalf often involves addiction in terms of drugs, behaviors, or toxic relationships. We don’t diagnose young people who have poor decision-making with dementia. We diagnose them with depression, anxiety, psychosis or any number of “young-person mental health issues”. A younger individual who develops memory issues might be diagnosed with dissociative identity disorder / DID (once known as multiple personality disorder), for example. Lydi and I acknowledge that the presentation of a young person’s diseased state can be radically different on the surface, but we also acknowledge that underneath it all, these diagnostic labels for aging individuals are perhaps designed to funnel them into long-term care through a particular drug-administration strategy. While a young person might be given a “chemical-restraint” drug that keeps their behavior under control, a person with dementia might be given drugs that reduce movement-related issues, but that set the patient up for an eventual, fast decline that will land them in a convalescent home. Frontotemporal dementia is a relatively new diagnostic label that didn’t show up until 1994. That was the time period when I (Jennifer) was working in long-term care facilities. But even after 5 years of working in long-term care from 1993 through 1998, I never heard “frontotemporal dementia” as a diagnosis for one of my patients. I also never encountered Lewy body dementia. I worked in a big city and I was an agency-worker which meant that I went to any one of up to 10 different facilities on any given day. I was exposed to a lot of patients. I worked on many Alzheimer’s wings. And I took care of a lot of younger-than-usual patients with Parkinson’s disease, but patients were often given the diagnosis “organic dementia” or “vascular dementia” when their behaviors didn’t fit what insurance companies required in order for them to receive an Alzheimer’s or Parkinson’s diagnosis. Frontotemporal dementia is a disorder that’s given to middle-aged patients who are between 45 to 64 years. Frontotemporal dementia involves personality and behavior changes and issues with language skills rather than early memory loss. But again, one has to wonder why we’re using the word “dementia” to diagnose these relatively young patients. How is it that one patient is diagnosed with frontotemporal dementia while another is diagnosed with psychosis? One of the defining criteria for frontotemporal dementia is age. Psychosis and schizophrenia is diagnosed when it takes shape in a younger patient and that’s fine, but why not label frontotemporal dementia as “frontotemporal psychosis” instead? When we tag the “frontotemporal” with “dementia” we’re suggesting long-term care as an option to loved ones. It’s a grim suggestion. “Psychosis” as a label, in contrast, suggests a mental health facility or some kind of home care. I find that it’s hard to disentangle these labels from the subtle suggestion for “treatment” that they embody. The word “psychosis” has more hope attached to it than “dementia” and I suppose that’s purposeful. If you’re trying to figure out how to overcome frontotemporal dementia, I would definitely recommend that you don’t focus on the word “dementia” and instead simply look at the neurological symptoms without any kind of age-ism clouding up your lens.Click here to subscribe to the Living Database now.
The Evolution of Dementia
Parkinson’s disease progression has changed over the past 50 years and that’s important. Why? Because if the disease progression has changed, there has to be a reason why. If we can study the ways in which life has changed over the past 50 years, we may be able to come up with environmental changes or changes in the patient’s life that may underlie the dementia symptoms. For example, “screen time” is a phrase that didn’t even exist 50 years ago. Fifty years ago, in my home, there was one screen: the TV. It was in the living room. We had just one heavy TV and screen time was limited because there were things to do beyond the living room. This is a major change that’s taken shape over the past 50 years, but there are other major changes that are important too. Nutrition has changed dramatically in the past fifty years. Some of these important changes include:- The end of iodine fortification of bread. Instead iodine is now added to salt, a poor carrier for iodine. Read more here about how a deficiency of iodine can cause cancer and lead to other health problems.
- The addition of bromine to all commercial bread products as well as to soft drinks (especially citrus drinks like Mountain Dew and Gatorade). Bromine competes with iodine in the body and has a negative impact on the brain and nervous system.
- The hybridization and genetic modification of fruits to exclude seeds. Seeds contain vitamin B17 (also known as laetrile or amygdalin) a medicinal substance that prevents and treats cancer.
- The criminalization of vitamin B17. It is illegal to buy or sell vitamin B17 supplements in the United States because this vitamin has been shown to prevent and in some cases cure all degenerative diseases including cancer. Many Americans eat apricot kernels (20-40 per day throughout the day-not all at once- usually 5 kernels which should be eaten only on an empty stomach. If they’re mixed with food, they become less potent).
- Inaccessibility of Vitamin B12. Vitamin B12 should be taken sublingually or as a shot. Vitamin B12 supplements taken by mouth are often ineffective. Symptoms of vitamin B12 deficiency are similar to and/or mimic symptoms of dementia.
- Choline and Phosphatidylcholine - Choline is a precursor of phosphatidylcholine and acetylcholine. Acetylcholine plays a role in Alzheimer’s, Lewy body dementia as well as Parkinson’s.
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Other important changes that might be relevant to the development of dementia:
- Adding bromine to swimming pools instead of chlorine for water purification. Symptoms of bromine intoxication mimic and include symptoms of dementia. Bromine builds up in the body over time.
- The use of bromine as a fire retardant in furnishings and pajamas as well as vehicle interiors.
- While mercury amalgam fillings are not used in most of the world, the U.S. has continued to endorse the use of amalgam for dental fillings. Mercury and other heavy metals have been implicated by many studies as a possible cause of various types of dementia.
