Dementia & Alzheimers
A great article on Yahoo states: Although Alzheimer's is now one of the most common diseases of the elderly, the condition barely existed before 1960.
"I looked everywhere. I looked on three continents and in every medical library I could find, including the Library of Congress and the British Museum library," said Alzheimer's specialist Murray Waldman, MD, from St. John's Rehabilitation Hospital in Toronto, Canada.
"No matter where I looked, I couldn't find anything that indicated there was very much Alzheimer's prior to the 1960s."
Epidemiological data collected over a 25-year period shows the incidence of Alzheimer's in the 1960s was 2% in people over the age of 85 years. Today, it's incidence in this population is 50% or more. It's incidence in people over 75 is 20% - and 10% in individuals over the age of 65. Between 1996 and 2000 the incidence of Alzheimer's and other dementias shot up from 1274 to a stunning 21,569 during the same time period.
"This dramatic spike over 40 or so years, he said, cannot be accounted for by an aging population, because what we were looking at was incidence, not prevalence," Dr. Waldman points out.
In another study I found on WebMD.com, there was a link to dementia and low HDL. Although poor memory in middle age has not been directly linked to Alzheimer's disease and other forms of dementia in old age, memory decline is key to the diagnosis of these conditions, lead researcher Archana Singh-Manoux, PhD, tells WebMD.
"Our research does not show a link between HDL and dementia," she says. "We looked at cognitive decline in midlife, but it may turn out that this decline is a risk factor for dementia." Researchers have attempted to study HDL and other lipids like low-density lipoprotein (LDL), total cholesterol, and triglycerides in patients with Alzheimer's and other age-related dementias, but these studies have proven problematic, Singh-Manoux says.
"By the time people are diagnosed they have usually had the disease for many years, and the disease itself may have modified these lipid profiles," she says.
Type 3 Diabetes (yes there is a type 3)
In this research, Alzheimer's Disease Is Type 3 Diabetes–Evidence Reviewed "Even before the initial study had been published, it was realized that if brain insulin/IGF (Insulin-like Growth Factor) resistance and insulin/IGF deficiency were causal in the pathogenesis of Alzheimer's Disease (AD), the related abnormalities should be detectable in the early stages of disease and possibly worsen as disease progresses."
"Altogether, the results from these studies provide strong evidence in support of the hypothesis that AD represents a form of diabetes mellitus that selectively afflicts the brain. Positive data stemmed from (3) direct analysis of postmortem human brains with documented AD; (4) an experimental animal model in which brain diabetes with cognitive impairment and molecular and pathological features that mimic AD was produced by intracerebral administration of a drug that is commonly used to produce Type 2 Diabetes Mellitus (TDM) and (5) a study showing that PPAR (peroxisome proliferator-activated receptors) T1DM (Type 1 Diabetes Mellitus) or T2DM; and (5) a study showing that PPAR agonists, which are used to treat T2DM, prevent many of the AD-associated neurodegenerative effects of ic-STZ. (Which is basically the clinical word for Type-3 Diabetes) The data are supported by abundant in vitro experiments that demonstrated essentially the same or similar effects of STZ or oxidative stress treatments of neuronal cells."
A study on rats by experts from Brown University suggest that a similar process could affect the brain, which relies on insulin to regulate nerve signals related to memory and learning and to produce energy from glucose.
Researchers found that blocking insulin from rats' brains made them disoriented and unable to find their way out of a maze because they could not remember where they were.
Examination of their brains showed the same pattern of deterioration seen in Alzheimer's patients, including increased levels of the amyloid plaque which is a key hallmark of the condition.
So, what they are basically stating is that in clinical trials, there were able to isolate the cause and reverse some of the effects of Alzheimer's Disease if viewed as a form of insulin resistance. Since the brain primarily runs on glucose as a fuel source, the brain is primarily made of fats, insulin resistance could be very problematic for brain tissues. "Altogether, the data provide strong evidence that AD is intrinsically a neuroendocrine disease caused by selective impairments in insulin and IGF signaling mechanisms, including deficiencies in local insulin and IGF production." However, if you are not running on the glucose fuel system by being in nutritional-ketosis, you can prevent and reverse the destructive effects of sugar on the brain.
3. Jalbert JJ, Daiello LA, Lapane KL. Dementia of the Alzheimer Type. Epidemiol Rev. 2008. [Epub ahead of print.]
4. Jellinger KA. Neuropathological aspects of Alzheimer disease, Parkinson disease and frontotemporal dementia. Neurodegener Dis. 2008;5(3-4):118–21.
5. Wang XP, Ding HL. Alzheimer’s disease: epidemiology, genetics, and beyond. Neurosci Bull. 2008;24(2):105–9.
Tim & Lynette Jenné are learners first and foremost. We love to ask "why?" We question the status quo. We also love to research and find answers for ourselves. As parents of four adult children, we've learned a few things along the way that may be helpful to others. We love to live & eat clean, simple lives.