Living in a suboptimal culture and following blindly along. In the most paper-money wealthiest societies, sickness could not be so widespread, rampant and ever-increasing across all demographics unless it was tied to the very foundations of a society and all its systemic branching ideologies and institutions. By environmental, I am referring to the natural world, human interaction with it and destruction of it. At least one of the articles below refers to environmental as smoking, diet, physical activity and health conditions. 2. Maafa Racism 3. Methodological Shortcomings
a) Due to methodological differences, presuppositions and flaws, the resulting non-scientific method process causes risk factors to vary across studies. Differences in methodology include, but are not limited to things such as length of follow-up, adjustment for confounders, and different diagnostic criteria of dementia. b) Studies of dementia are hampered by certain methodological issues inherent to [not understanding] the disorder. These methodological issues may influence the results of studies and be partly responsible for variability in results across studies. Here are four of the many methodological issues associated with the study of dementia:
Diagnostic procedure - The most important problem with respect to studying dementia and Alzheimer Disease (AD) is defining the outcome, [defining context, defining the disease and defining the criteria for diagnosis]. As yet, there is no single diagnostic test for AD or most of the other types of dementia. The diagnosis of AD is based on clinical criteria, and can be graded as possible, probable, or definite. Several sets of criteria are available, of which the criteria of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) and the Alzheimer’s Disease and Related Disorders Association (ADRDA), dating from 1984, are the most commonly used. The diagnostic work-up of dementia is time and cost intensive. In large population based studies, it is impossible to assess every subject with a complete diagnostic work-up. Using medical records to identify cases would lead to an underestimation of the number of individuals with dementia, as many of the cases of dementia are never diagnosed in a formal setting. Therefore, large population based studies usually employ one of two possible stepwise approaches, each one having drawbacks. The use of different criteria to diagnose dementia, and the variable approaches to apply these criteria in large samples, can result in highly varying estimates of frequency. The difficulty of diagnosing mild dementia can lead to an additional problem in incidence studies, as cases that are very mild and therefore not recognized at baseline may be wrongly counted as incident cases at follow up, resulting in biased estimates. Insidious (slow or gradual) onset - Neuropathological changes, eventually leading to the clinical syndrome of dementia, may start as early as decades before the disease becomes clinically overt. The moment when dementia is diagnosed is arbitrary because there is no moment when the person goes from healthy to sick, instead the process is gradual. Biomarkers - There is a complex relationship between Dementia Syndrome and the underlying diseases. When we talk of AD, we refer to the syndrome that is characterized by progressive memory problems, which usually has an insidious onset. However, at the moment the diagnosis of AD is made, we assume to know the underlying neuropathological substrate—that is, neuritic plaques and neurofibrillary tangles. We assume to know this, because during a person's lifetime, it is impossible to directly measure neuropathology. In fact, post-mortem studies have shown that this assumption in many cases is wrong. In a report of the MRC CFAS of the first 209 subjects (48% demented) who came to necropsy, Alzheimer-type pathology and vascular pathology were equally common, and both correlated with cognitive decline. Most subjects had mixed pathology. Approximately one third of clinically demented patients did not fulfill neuropathological criteria for definite AD, whereas an equally large proportion of non-demented elderly subjects did fulfill these criteria.
In other words, a significant number of people diagnosed with Dementia did not have brain plaques and a significant number of people not diagnosed with Dementia, did have brain plaques. Furthermore, a significant number of people who did not have Dementia Syndrome symptoms, did have brain plaques.Thus then, what we must conclude, is that brain plaques are not a primary way of diagnosing Alzheimer's Dementia, not even post-mortem. Also then, the use of plaques as a determinant is likely also unreliable in determining Lewy Body Disease. This then indicates the whole approach to dealing with Dementia is deeply flawed. This we knew early on in this delving deeper series when we discovered the problems with definition and added to it the worldview under which the society and medical industry operates.Neuropathologically, the distinction between different types of dementia, and even between demented and non-demented, seems to be very difficult. The question arises that if it is useful to make clinical distinctions between subtypes of dementia, neuropathology may not even exist. A step towards directly measuring disease, rather than clinical phenotype, would be to take biomarkers as outcome of studies. Both neuroimaging and cerebrospinal fluid can provide useful surrogate markers that give a more direct impression of the pathology. In this way, the possibility of different types of pathology coexisting within one subject is appreciated. For example, magnetic resonance imaging (MRI) measures suggestive of Alzheimer-type pathology and vascular pathology can be evaluated simultaneously. Cross sectional versus longitudinal studies - Studies with a longitudinal design are preferred over studies with a cross sectional design for several reasons. It is conceivable that information about risk factors may be systematically different between patients and controls. Patient data must come from a proxy, who might recall the medical history differently than a proxy of a control or the control himself. In addition, prevalence is determined by both the number of new cases over a given period of time, and by the duration of survival once patients have the disease. In analogy, findings of cross sectional studies can reflect the contribution a risk factor makes to developing dementia as well as to surviving after the dementia starts. Another important issue in this respect is that risk factors may change over time. Risk factors such as blood pressure change with age. Furthermore, the disease, once it has started, may in turn influence risk factors. For example, the diet of a demented individual may change, when the person forgets to eat his or her meals on a regular basis. Therefore, the relationship between a risk factor and disease may differ depending on the age the risk factor is measured relative to the outcome. Risk factors should be measured as early as possible. c) Conclusions Regarding Epidemiology & Methodology Of Dementia Syndrome
Dementia has reached epidemic proportions, [yet there is no national or global shift in order to deal with it, just as there is none to deal with annual influenza epidemic and many other types of pandemics]. Dementia Syndrome affects about 6% of individuals over 65 years of age and has a strong age dependent prevalence. AD is the most prevalent [diagnosis assigned to] dementia, responsible for about 60–70% of cases. VaD (vascular disorder) is the second most [diagnosis assigned], accounting for 15–20%. Any time you hear the words, study, research, report, trial, investigation, clinical trial, expert, scientist, researcher, authorities, you should be very aware of how many variables go into the information they are presenting, including the variable of honesty.. 4. Age-related
a) Per mentalhealth.org.uk, we do not know what causes Alzheimer’s Disease but we do know that aging is the main factor. The disease most commonly affects people over 60 years old. Even though risk increases with age, Dementia Syndrome is not a normal part of aging. I wonder what set of conditions are we cultivating that catch up with us after 60 years? The answer must be tied to lifestyle, which is, culture, the predictable avalanche of of being snowballed.
In contradiction to saying “aging is the main factor,: this same article goes on to say scientists believe many different genetic, health, lifestyle and environmental factors may influence when and how the disease develops. Thus I say, how can aging be positively said to be the main factor when instead it is most likely a set of conditions that is that main factor, i.e., the perform storm of imperfection. b) Although older people are vastly more likely to develop Alzheimer's Disease, the vast majority of older people do not develop Alzheimer's Disease. Thus old age cannot be the main risk factor. It's like saying saying the longer you live the more susceptible to sickness you will be. This is patently false in civilizations but true in societies. So then, what is the difference? 5. Genetic Risk
a) A multitude of factors beyond genetics contribute to the development and course of Alzheimer’s Disease. For this reason, Ohio State University does not recommend genetic testing.
b) A specific gene that causes Alzheimer’s Disease has not been found.
However, having the APOE ε4 form of the apolipoprotein E (APOE) gene is said to increase a person’s risk of developing Alzheimer's Disease and increases the risk of developing Alzheimer's Disease at an earlier age. However, having the APOE ε4 gene does not mean a person will definitely develop Alzheimer’s Disease. In fact, most people with the APOE ε4 gene do not develop Alzheimer's. The APOE gene and E4 allele combination is neither necessary nor sufficient to cause Alzheimer Disease, In fact, most people who develop Alzheimer’s do not have APOE ε4 gene.
All this considered, then why do so many studies, websites and media articles try to make it seem like Dementia Syndrome, especially Alzheimer's Disease is genetic related and racial related and African-American females are at a greater risk of developing the disease?.
c) The APOE e4 gene is a false positive indicator of Dementia Syndrome risk, just as is age, gender and brain plaques. 6. So I'll say it again. Maafa Racism targets Africans with falsely constructed studies, constant terrorism that causes disease development, misrepresentations of facts, misdiagnosis and inappropriate treatment that is then said in a deceitful oversimplified way that Alzheimer's affects African-Americans at twice the rate of European-Americans. For these reasons and more, Maafa Racism causes Africans to suffer greater health disparities. Some of these disparities are real and some are numerically fudged smoke of okie doke.
If the African genetic seed was inherently more unhealthy, then all races that sprung up out of Africans could not be any more healthy than the seed that spawned them. And in fact, an unhealthy seed could not proliferate for hundreds of thousands of years and achieve what it did if it was genetically susceptible to everything imaginable that could weaken and sicken and kill the human organism. Are we to think Africans proliferated during “primitive” times of low IQ and populated the world with knowledge and people, yet, during this Age of so-called high intelligence and the best cultures, that Africans would then become the sickest just because they are African? The answer is yes, with a twist of covid whiteness and their wannabes. There is no conclusive evidence to suggest that any particular group of people are at a greater risk or lesser risk to develop Alzheimer's dementia. Ethnicity, profession, geographical and socio-economic situation are not determinants of the condition. 7. In September 2019, Harvard University stated that most genetic studies have predominantly focused on white individuals in the US and abroad. The article distinguishes between association and causation. Thus I say that being African might be associated with higher proportional incidences of Dementia Syndrome and sickness in general; however, this does not mean African genetics is a cause. Rather African Genetics are targets of war. Gender
8. Although more women are affected by Alzheimer's dementia, women live longer, thus gender is not the cause of Alzheimer Disease. There must be lifestyle differences that women engage in that contribute to their higher incidence of developing Dementia Syndrome. This might be things such as types of medical care and medication given to women, personal care products and cosmetics. The fact that women live longer is not sufficient to explain the higher difference of Dementia diagnosis assigned to females than males. Formal Education Misperception & Higher Education Misperception
9. There is mounting evidence to suggest that people with a higher level of education are at less risk than those with a lower level of education. I say this is a false positive because how can formal education be a better brain stimulant than informal education or being self-taught? Does the brain know from what source learning is taking place? This flies in the face of saying that staying mentally active can help stave off mental decline. Based on what this article is saying, then only formal mental activity will help, i.e., being taught by a European to think like them.
Still keeping this 100, understand clearly that The European & Wannabe Worldview is deeply invested in their superior intelligence. Thus anything dealing with the mind, brain and cognitive functioning, they will always find ways to suggest they know best, thus their emphasis on formal education as better than informal while contradicting themselves every step of the way when speaking about early childhood learning, lifelong learning and late-stage learning. Geographical Risk
a) Per the Journal of Neurology, Neurosurgery and Psychiatry, there are substantial differences in possible risk factors for dementia between regions. Another Study, Another Set Of Mixed-Matched Results Contradictory Juxtaposed published in one of the libraries of scholars, the article states
the greatest risk factors for Alzheimer's are older age, genetics, and having a family history of Alzheimer's. Variations in medical conditions, health‐related behaviors and socioeconomic risk factors across racial groups likely account for most of the differences in risk of Alzheimer's and other dementias.
Then the article backtracks and says, despite some evidence that the influence of genetic risk factors on Alzheimer's and other dementias may differ by race, genetic factors do not appear to account for the large differences in prevalence or incidence among racial groups.
Then the article, in the same paragraph doubles back and says, instead, health conditions such as cardiovascular disease and diabetes, which are associated with an increased risk for Alzheimer's and other dementias, are believed to account for these differences, as they are more prevalent in black/African American and Hispanic/Latino people.
Then the article gives it all back and ends up mostly on the right track by saying, socioeconomic characteristics, including lower levels and quality of education, higher rates of poverty, and greater exposure to adversity and discrimination, may also increase risk in black/African American and Hispanic/Latino communities (and may in turn contribute to the health conditions mentioned above). Some studies suggest that differences based on race and ethnicity do not persist in rigorous analyses that account for such factors.
