So you had to go down to the eighth most prevalent cause of death to come up with one that you believe is genetic? That is not the beginning of a strong case for genetics being more important than diet in disease modalities, is it? It sounds like your argument is sort of desperate.
There is an early-onset version of Alzheimer’s that does seem to have a genetic component. In older people, the research is not so conclusive. There is definitely a correlation between poor vascular health in general and Alzheimer’s, and of course we know that poor vascular health is related to eating a lot of meat protein--eggs, animals and dairy products. There is an Algerian study tying Alzheimer’s to a fatty diet, the kind we eat in North America. There is some new research indicating an Alzheimer’s EPIDEMIC in America that may not be Alzheimer’s at all—it might be mad cow disease. Why would there be an epidemic at all if it is an inherited disease? And new research correlates India’s extremely low incidence of Alzheimer’s with the heavy rate of ingestion of curry—turmeric, more specifically. Very complicated, not much conclusively known, etc. Not specifically genetic!
So trying to denigrate Dr. Campbell’s research based on your argument seems to be specious at best, bordering on absurdity, really.
I’ve included a lot of article excerpts in case anyone is interested:
What causes Alzheimer’s
Nerve signals travel across the synapses with the help of chemicals known as "neurotransmitters", including one called acetylcholine. Doctors believe that nerve cell destruction causes a reduction in acetylcholine, leading to impaired transmission of nerve signals.
Other explanations of Alzheimer’s disease focus on areas of abnormal protein in the brain called "plaques" and "tangles", the names reflecting what these abnormalities in the brain look like under the microscope.
The underlying cause of Alzheimer's – what actually triggers the changes in the brain – is still not known. It is likely that no single factor is responsible, but rather that it is due to a variety of factors, which may differ from person to person. People whose parents or brothers and sisters develop the disease appear to be at greater risk of developing it themselves, so there may be a genetic component. However, no straightforward pattern of inheritance has been found.
It is known that head injury is a risk factor, and also that Alzheimer’s disease often affects people with Down’s syndrome.
Some researchers have suggested that people who exercise their brains (for example, doing crosswords and other mental agility exercises) are less likely to develop the disease. And Omega 3 fatty acids, contained in oily fish such as mackerel and salmon may, also help to prevent dementia. But there is no completely solid evidence to show how environmental factors influence the chance of getting Alzheimer’s.
What Causes AD?
Scientists do not yet fully understand what causes AD. There probably is not one single cause, but several factors that affect each person differently. Age is the most important known risk factor for AD. The number of people with the disease doubles every 5 years beyond age 65.
Family history is another risk factor. Scientists believe that genetics may play a role in many AD cases. For example, familial AD, a rare form of AD that usually occurs between the ages of 30 and 60, is inherited. The more common form of AD is known as late-onset. It occurs later in life, and no obvious inheritance pattern is seen. However, several risk factor genes may interact with each other to cause the disease. The only risk factor gene identified so far for late-onset AD, is a gene that makes one form of a protein called apolipoprotein E (apoE). Everyone has apoE, which helps carry cholesterol in the blood. It is likely that other genes also may increase the risk of AD or protect against AD, but they remain to be discovered. The National Institute on Aging (NIA), part of the National Institutes of Health, is sponsoring the AD Genetics Initiative to recruit families with AD to learn more about risk factor genes. To participate in this study, families should contact the National Cell Repository for AD toll-free at 1-800-526-2839 or send an e-mail to: alzstudy@iupui.edu.
Scientists still need to learn a lot more about what causes AD. In addition to genetics and apoE, they are studying education, diet, and environment to learn what role they might play in the development of this disease. Scientists are finding increasing evidence that some of the risk factors for heart disease and stroke, such as high blood pressure, high cholesterol, and low levels of the vitamin folate, may predispose people to AD. Evidence for physical, mental, and social activities as protective factors against AD is also increasing.
alzheimers.org
Alzheimer's risk linked to diet
James Meek
Saturday February 17, 2001
The Guardian
Evidence that diet plays a major role in causing Alzheimer's disease was released yesterday after scientists found that African Americans were more than twice as likely to suffer from the condition as people of similar age in Nigeria.
US and Nigerian scientists have spent more than eight years studying thousands of elderly people in two communities - Indianapolis, in Indiana, and Ibadan, in Nigeria.
In a paper published in the Journal of the American Medical Association, researchers said that the incidence of Alzheimer's in the 65-plus age group among African Americans was 2.5%. Among the Yoruba people of Ibadan of that age, it was 1.15%. When the scientists looked at all types of dementia, they found an even sharper difference - 3.24% in the US and 1.35% in Nigeria.
One possible conclusion is that the mainly vegetarian diet of the Yoruba, compared with the fatty diet of many Americans, offers protection against Alzheimer's as well as against cardiovascular disease, the biggest killer in the rich world.
Hugh Henrie, who led the research at Indiana University, said: "To our knowledge, this is the first report of incidence rate differences for Alzheimer's and dementia between populations in developed and developing countries in studies that used identical methods and groups of investigators."
One possible explanation, they said, was the major difference in risk factors for cardiovascular disease between African Americans and Yoruba. The Nigerians, on average, are leaner, have lower cholesterol levels, and suffer less from high blood pressure and diabetes.
"Vascular disease may contribute both to dementia and to the development, progression, and clinical severity of Alzheimer's," the report said.
Other studies have already hinted at a link between cardiovascular illness and Alzheimer's. However, there has never been enough evidence before to bracket Alzheimer's disease together with heart disease in public warnings about unhealthy eating.
guardian.co.uk
The most frequent misdiagnosis of CJD among the elderly is Alzheimer's disease.[55] Neither CJD nor Alzheimer's can be conclusively diagnosed without a brain biopsy,[56] and the symptoms and pathology of both diseases overlap. There can be spongy changes in Alzheimer's, for example, and senile Alzheimer's plaques in CJD.[57] Stanley Prusiner, the scientist who won the Nobel Prize for his discovery of prions, speculates that Alzheimer's may even turn out to be a prion disease as well.[58] In younger victims, CJD is more often misdiagnosed as multiple sclerosis or as a severe viral infection.[59]
Over the last 20 years the rates of Alzheimer's disease in the United States have skyrocketed.[60] According to the CDC, Alzheimer's Disease is now the eighth leading cause of death in the United States,[61] afflicting an estimated 4 million Americans.[62] Twenty percent or more of people clinically diagnosed with Alzheimer's disease, though, are found at autopsy not to have had Alzheimer's at all.[63] A number of autopsy studies have shown that a few percent of Alzheimer's deaths may in fact be CJD. Given the new research showing that infected beef may be responsible for some sporadic CJD, thousands of Americans may already be dying because of Mad Cow disease every year.[64]
Nobel Laureate Gajdusek, for example, estimates that 1% of people showing up in Alzheimer clinics actually have CJD.[65] At Yale, out of a series of 46 patients clinically diagnosed with Alzheimer's, six were proven to have CJD at autopsy.[66] In another study of brain biopsies, out of a dozen patients diagnosed with Alzheimer's according to established criteria, three of them were actually dying from CJD.[67] An informal survey of neuropathologists registered a suspicion that CJD accounts for 2-12% of all dementias in general.[68] Two autopsy studies showed a CJD rate among dementia deaths of about 3%.[69,70] A third study, at the University of Pennsylvania, showed that 5% of patients diagnosed with dementia had CJD.[71] Although only a few hundred cases of sporadic CJD are officially reported in the U.S. annually,[72] hundreds of thousands of Americans die with dementia every year.[73] Thousands of these deaths may actually be from CJD caused by eating infected meat.
The incubation period for human spongiform encephalopathies such as CJD can be decades.[74] This means it can be years between eating infected meat and getting diagnosed with the death sentence of CJD. Although only about 150 people have so far been diagnosed with variant CJD worldwide, it will be many years before the final death toll is known. In the United States, an unknown number of animals are infected with Mad Cow disease, causing an unknown number of human deaths from CJD. The U.S. should immediately begin testing all cows destined for human consumption, as is done in Japan, should stop feeding slaughterhouse waste to all farm animals (see organicconsumers.org, and should immediately enact an active national surveillance program for CJD.[75]
Five years ago this week, the Center for Food Safety, the Humane Farming Association, the Center for Media & Democracy, and ten families of CJD victims petitioned the FDA and the CDC to immediately enact a national CJD monitoring system, including the mandatory reporting of CJD in all 50 states.[76] The petition was denied.[77] The CDC argued that their passive surveillance system tracking death certificate diagnoses was adequate. Their analysis of death certificates in three states and two cities, for example, showed an overall stable and typical one in a million CJD incidence rate from 1979 to 1993.[78] But CJD is so often misdiagnosed, and autopsies are so infrequently done, that this system may not provide an accurate assessment.[79]
In 1997, the CDC set up the National Prion Disease Pathology Surveillance Center at Case Western Reserve University to analyze brain tissue from CJD victims in the U.S. in hopes of tracking any new developments. In Europe, surveillance centers have been seeing most, if not all, cases of CJD. The U.S. center sees less than half. "I'm very unhappy with the numbers," laments Pierluigi Gambetti , the director of the Center. "The British and Germans politely smile when they see we examine 30% or 40% of the cases," he says. "They know unless you examine 80% or more, you are not in touch."[80] "The chance of losing an important case is high."[81]
vegsource.com
Curry ‘may slow Alzheimer’s’
Publication: BBC News
Date: November 21, 2001
A spicy ingredient of many curries may be an effective treatment for Alzheimer's disease, say researchers.
A team from the University of California at Los Angeles believes that turmeric may play a role in slowing down the progression of the neurodegenerative disease.
The finding may help to explain why rates of Alzheimer's are much lower among the elderly in India than in their Western peers.
Previous studies have found that Alzheimer's affects just 1% of people over the age of 65 living in some Indian villages.
Vindaloos.
Turmeric is found in everything from mild Kormas to the hottest Vindaloos. The crucial chemical is curcumin, a compound found in the spice.
Alzheimer's is linked to the build up of knots in the brain called amyloid plaques.
Turmeric reduced the number of these plaques by a half.
The researchers also found that turmeric had other health benefits.
It aids digestion, helps fight infection and guards against heart attacks.
In the study, middle aged and aged rats were fed a diet rich in curcumin.
All the rats received brain injections of amyloid to mimic progressive Alzheimer's disease.
Not only was there less evidence of plaque build up in the curcumin-fed rats, they also outperformed rats on normal diets when carrying out maze-based memory tests.
Curcumin also appeared to reduce Alzheimer's-related inflammation in the brain tissue.
Researcher Dr Sally Frautschy said the compound had potential as a treatment for the prevention of Alzheimer's disease - particularly in tandem with anti-inflammatory drugs such as ibuprofen.
Dr Richard Harvey, director of research at the Alzheimer's Society, said: "Curcumin has both anti-oxidant and anti-inflammatory properties.
"Drugs with similar properties could potentially be used as preventative treatments for Alzheimer's disease."
However, Dr Harvey warned that it could be many years before such drugs were made widely available.
hvk.org |
