I guess we all realize there is no money to be had in prevention. At least not of the global scale witnessed by limited curative therapies and bottomless R&D efforts, especially in neurodegenerative diseases--I am talking to you Alzheimer's disease.
Shareholders are mesmerized by "expanding market share" and the financial opportunities on the horizon. The rest of us scratch our heads and wonder--wouldn't prevention be a better service? What is causing the expanding "customer base" for Pharma and how can we mitigate the tide or better yet reverse the trends?
We are observing the rise of obesity and metabolic derangements in lock step with projected increases in rates of Alzheimer's disease. Perhaps the 90+ billion investment in commodity farming is suspect?
I would be remiss if I didn't mention the US farm bill. Simply put the bill is a comprehensive, multi-year legislation that includes "federal farm, food, fiber, forestry, and rural policies and programs". And yes the Supplemental Nutrition Assistance Program (SNAP) is the largest part of the Nutrition Title.
Okay hats off for investing in economic benefits for our domestic hunger safety net but look at the proportion of crops assigned to vegetables and healthy alternatives. Data Products USDA
Metabolic derangements mediate cognitive impairment and Alzheimer's disease: role of peripheral insulin-resistance diseases
The positive (and destructive) feedback loop leads to the accumulation of toxic ceramides (lipid or fat molecules) and downstream myelin breakdown (neurodegeneration) and dysregulated lipid metabolism--propagating chronic diseases.
Alzheimer's disease (AD) should be regarded as a degenerative metabolic disease caused by brain insulin resistance and deficiency, and overlapping with the molecular, biochemical, pathophysiological, and metabolic dysfunctions in diabetes mellitus, non-alcoholic fatty liver disease, and metabolic syndrome.
Although most of the diagnostic and therapeutic approaches over the past several decades have focused on amyloid-beta (Aβ42) and aberrantly phosphorylated tau, which could be caused by consequences of brain insulin resistance, the broader array of pathologies including white matter atrophy with loss of myelinated fibrils and leukoaraiosis, non-Aβ42 microvascular disease, dysregulated lipid metabolism, mitochondrial dysfunction, astrocytic gliosis, neuro-inflammation, and loss of synapses vis-à-vis growth of dystrophic neurites, is not readily accounted for by Aβ42 accumulations, but could be explained by dysregulated insulin/IGF-1 signaling with attendant impairments in signal transduction and gene expression.
This review covers the diverse range of brain abnormalities in AD and discusses how insulins, incretins, and insulin sensitizers could be utilized to treat at different stages of neurodegeneration.
- Alzheimer’s disease should be regarded as an insulin-resistance-mediated neurodegenerative disorder that has the same fundamental abnormalities that occur in diabetes mellitus, metabolic syndrome, and non-alcoholic fatty liver disease.
- Contrary to popular perception, Alzheimer’s disease is associated with a number of major abnormalities in the brain which are not attended to by diagnostic and therapeutic approaches that specifically target amyloid-beta and phospho-tau accumulation.
- Disease remediation for Alzheimer’s and probably many other neurodegenerative diseases should be approached by attacking underlying impairments in the actions of insulin and insulin-like growth factors. Orchestrating the repertoire of drugs that support their multifaceted functions in the brain by efficiently and safely delivering insulins (short-, long- and ultralong-acting forms), incretins, and insulin sensitizers for disease-stage intervention could slow or halt progression of neurodegeneration.