First things first, Alzheimer’s Disease is not ‘rampant’. It is not an epidemic, and most people will not contract it. It effects NO MORE than 2% of the population. That is not an epidemic. It is barely a blip on the list of major diseases. In the United states only 5.3 million people are suffering from the disease.
Once again Ari LeVaux is trying to stir up trouble. He now writes that sugar is destroying a person’s memory. Oh right. Sugar destroys brain cells? His chemistry is that sugar destroys the liver like alcohol does due to body chemistry. He then becomes hysterical about Nonalcoholic fatty liver disease. Too bad he didn’t read the fine print, nor pay much attention to the study he quoted. There are some who think it is worse because of obesity, yet it occurs most often in people of a normal weight. It supposedly effects or could effect up to 25% of the population. It is also one of those diseases which has a strong genetic predisposition, especially among the Hispanic population. It is a leading cause of cirrhosis in adults. Interestingly, in 2009 the percentage of the population effected was 2-5%. In 2012 it was 10-20%. The new hysterical numbers have been put out by the American Liver Foundation. BUT – if you read the fine print, evidently acetaminophen could also be leading cause of the disease. Of course, they say obesity is a leading cause, but the numbers don’t crunch on that one. Seriously, if you read the fine print, even thought Type 2 diabetes is a factor, the disease is associated with hepatitis.
Ah, yes, the author of this interesting and completely inaccurate article yet again spins a weave of scare mongering. He’s basing it on a study by David Perlmutter, that has merit but also has numerous critics. One of his articles has been completely discredited by a little tabloid called Scientific American.
Having just emerged from 5 years in the trenches of the war on Alzheimer’s, dealing with my father, I think once again, LeVaux is acting like a hysterical fool. One of the greatest tools in the arsenal of any family battling AD, and trying to keep their loved one at home, and as viable as possible is sugar, white, refined, evil, horrible sugar. It is like a miracle drug. Sugar is fuel for the brain. You add it to a double expresso and a few minutes later the AD brain begins working again.
We experimented on my father, following numerous studies dealing with diet. The worst thing we ever did was put him on several AD medications, which literally did nothing but drug him to keep him quiet. Once I learned they were starting to experiment on the same meds, for hyperactive kids, we took him off them. The change was remarkable. B-12 injections, every three weeks can almost stop the progress of the disease, if given early enough.
Almost every morning for nearly 4 years, my mother made him a breakfast of oatmeal (non processed), 2 tbs of coconut oil, a tsp of cinnamon, and 1 tbs of white sugar. He put whole milk on it, and covered it with strawberries which had been sliced and soaked in white sugar. He was allowed to put more sugar on top of the cereal, if he wanted it. And – he was Type 2 diabetic. His physician told her to go ahead, and see what would happen. We kept cookies, ice cream, and desserts for him. The days he did not have sugar – and we experimented – saw a serious decrease in the capacity to function.
I remember, a few years ago, eggs were the worst food on earth. Then it was coconut oil. We’re dealing with some of the problems of oils now because of the move to take almost ban coconut oil. Then salt was the personification of all that was evil. High carbs were the ideal diet food. I wonder how long it is going to be before sugar is rehabilitated? I give it 5 years at the most.
The best part of this is we may be right. In a study that attempts to link AD as a third type of diabetes, the following was presented.
“…Using the previously mentioned approaches, we demonstrated progressive AD Braak stage-dependent reductions in insulin, IGF-1, and IGF-2 receptor expression, with more pronounced deterioration in insulin and IGF-1 compared with IGF-2 receptors, and the lowest levels of gene expression in brains with AD Braak Stage 6 (Figure 2). Therefore, loss of insulin and IGF-1 receptor-bearing neurons begins early and progresses with disease such that, in the advanced stages, the deficits are severe and global. These results provided further evidence that the abnormalities in AD are not restricted to insulin signaling pathways, as they also involve IGF-1 and IGF-2 stimulated mechanisms. Analysis of growth-factor polypeptide genes also revealed AD Braak stage-dependent impairments in insulin, IGF-1, and IGF-2 polypeptide expression, corresponding with progressive trophic factor withdrawal (Figure 2). Again, the results support the hypothesis that abnormalities in insulin and IGF signaling mechanisms begin early in the course of AD and are therefore likely have an important role in its pathogenesis…”
In other words, my family took the right approach. When the brain is deprived of insulin – sugar – it does not function as well. Interestingly, one of the reasons for the new hysteria about Non-alcoholic fatty liver disease is that – ta da – big pharma appears to have new medication on the way, to treat a disease which is basically not fatal, and may not be as prevalent as they say it is.
“...deficiency in the protein responsible for moving glucose across the brain’s protective blood-brain barrier appears to intensify the neurodegenerative effects of Alzheimer’s disease, according to a new mouse study from the Keck School of Medicine of the University of Southern California (USC).
The research suggests that targeting the protein called GLUT1 could help prevent or slow the effects of Alzheimer’s, especially among those at risk for the disease. The study, “GLUT1 reductions exacerbate Alzheimer’s disease vasculo-neuronal dysfunction and degeneration,” appears in the journal Nature Neuroscience.
“Our results suggest that GLUT1 deficiencies at the blood-brain barrier are not just symptoms of Alzheimer’s but, in fact, lead to a series of vascular injuries that worsen the effects of the disease,” said Berislav V. Zlokovic, M.D., Ph.D., director of the Zilkha Neurogenetic Institute (ZNI) at the Keck School of Medicine, the Mary Hayley and Selim Zilkha Chair for Alzheimer’s Disease Research and the study’s principal investigator. “We do not know yet whether medicine can restore GLUT1 expression, but we believe that targeting the protein may help prevent Alzheimer’s from getting worse among individuals predisposed to develop the disease.”
According to the Alzheimer’s Association, roughly 5.2 million people of all ages in the United States today have Alzheimer’s disease, an irreversible, progressive brain disease that causes problems with memory, thinking and behavior. It is the most common type of dementia, a general term for loss of memory and other mental abilities, and is projected to affect 16 million Americans over age 65 by 2050.
Glucose is the brain’s main energy source, and GLUT1 helps move it across the blood-brain barrier, a cellular layer that prevents entry of blood and pathogens into the brain. Previous research has shown diminished glucose uptake in the brain among individuals at genetic risk for Alzheimer’s disease, with a positive family history, and/or who develop the disease but show mild or no cognitive impairment.
In this new study, Zlokovic’s team used transgenic mice to show that GLUT1 is necessary to maintain proper brain capillary networks, blood flow and blood-brain barrier integrity. They found that GLUT1 deficiency led to diminished glucose uptake into the brain as early as two weeks of age and, by six months of age, neuronal dysfunction, behavioral deficits, elevated levels of amyloid-beta peptide, behavioral changes and neurodegenerative changes. The team also found that GLUT1 deficiency in the endothelium — the inner lining of blood vessels — initiated breakdown of the blood-brain barrier. Alzheimer’s disease pathogenesis is widely believed to be driven by amyloid-beta peptide build-up in the brain, facilitated by breakdown of the blood-brain barrier.
Areas of future research may include identification of the metabolic pathways through which GLUT1 deficiencies in the blood-brain barrier influence brain metabolism as well as an examination of whether early embryonic GLUT1 loss affects the central nervous system differently than a deficiency incurred later during development….”
Those of us who have lived in the trenches of AD know what sugar does for someone who has the disease. If you read up on the articles damning sugar as creating AD, they are written by the food police and quacks. Viable studies point to just the opposite. When a person has low blood sugar, their brain doesn’t work properly. Brains need sugar to function.
“…The mammalian brain depends upon glucose as its main source of energy, and tight regulation of glucose metabolism is critical for brain physiology. Consistent with its critical role for physiological brain function, disruption of normal glucose metabolism as well as its interdependence with cell death pathways forms the pathophysiological basis for many brain disorders. Here, we review recent advances in understanding how glucose metabolism sustains basic brain physiology. We synthesize these findings to form a comprehensive picture of the cooperation required between different systems and cell types, and the specific breakdowns in this cooperation that lead to disease….”
So much of this is what we found. One of the worst things you can do with someone dealing with AD is those ‘good’ complex carbs. They drain the brain. We just thought it was my father, but there is scientific basis in it. It is so fascinating how the hard core science says one thing, that the brain must have certain amounts of sugar, yet the food police say another. Caffeine is the other important component when it comes to treating AD.
One of these days the food police will move on to another sacred cow, and sugar can once again be consumed without guilt.