GENETIC AND NON-GENETIC RISK FACTORS IN AD: A SUMMARY OF SOME RECENT STUDIES
(with interpretations by Jo Danna)
Any research findings reported here should not be used to diagnose or treat someone with AD or a related dementia. A health professional should be consulted for that purpose.
Nor should the research findings mentioned in this report be interpreted as " proof" in a particular area of investigation. They are only tentative evidence awaiting more studies that support these findings. That's the way research works, bit by bit until an overwhelming case is made..
The overall conclusions drawn from the research findings are mine only. I am responsible for any mis-interpretations and errors in reporting the studies. I am not a neurologist, chemist, geneticist, physiologist or in any way connected to research on AD and related dementias. I took a few courses in neurology and physiology many years ago which merely helps me to understand some terminology, nothing more. It's possible that I've put the wrong emphasis on, or even misinterpreted, some research results, especially when these involve complicated genetic factors which I have to admit I don't fully understand. I welcome corrections from those on the List who know more than I do. However, I have done (anthropological-psychological) research on cognition and am familiar with the hidden traps of research methodology on human behavior, especially mental behavior.
I should have meticulously included all sources of the studies mentioned. The problem is, some of these sources are buried within my mountains of data and so I carelessly go ahead without them. If any of you are interested, I will try to locate the original sources. They must be here, somewhere.
PURPOSE OF THIS REPORT
Many list members have reported a family history of AD or a related dementia. (See excerpts below.) Many of you are worried about the inheritability of AD for yourselves and your children. I share your concern, and this is why I researched the topic and wrote this report. The results should allay your fears. You are all good people, giving much of yourselves to care for an afflicted LO. You certainly don't need the added stress of worrying about the dreaded " G" word (genetics).
1) " . . . . Several on my father's side of the family had either diagnosed Alzheimer's or a decidedly peculiar behavior in their seventies. It makes me count each day and stop and smell the roses. I sincerely hope I never get the illness. However it is a thought in the back of my mind when I write a durable power of attorney or drive on long car trips with the kids.. . . . caregivers have so much stress and are so tired. That is the most likely explanation for their forgetfulness. They may worry about " coming down" with Alzheimer's but I think it's a natural, baseless anxiety in most cases. No one wants to watch this progression up close and then undergo it himself/herself. "
2) " . . . . It has struck five members (that we know of) in my Dad's family and they have all gone."
ARGUMENT: THE FOCUS OF CURRENT RESEARCH IS TOO NARROW |
Because I believe that not enough research is done on environmental and lifestyle risk factors, I sifted through the results of many studies hoping to make sense of the different strands of research findings coming from many directions and at breakneck speed. In fact, some or even much of the findings cited below may already be outdated..
I did this as a concerned lay person whose mother and father both had dementia. My mother has AD and my father most likely had vascular dementia. Although cardiovascular disease runs in his side of the family, he is the only one to have developed dementia! My parents were the only ones to emigrate from a remote Italian mountain village. As far as I was told and observed ( having lived there a year to do research on cognition) , no other member of each side of my family developed AD, although people in that village lived to a great old age.
So the current focus on genetics seems one-sided to me. Instead of searching for non-genetic risk factors so that they can be eliminated or avoided and thus preventing, or delaying till great old age, AD from occurring in the first place, the current apporach is too mechanistic. The human body is viewed as a machine; something goes wrong, so let's tinker with it until we find the part (gene) that's broken. Very few studies take an " ecological" approach which includes investigating environmental and lifestyle factors as possible influences, either as the sole cause of dementia or as triggering a genetic predisposition..
A number of studies show an increased incidence of cancer, heart, even AD and other forms of dementia among migrants who come to urban, developed countries from various developing parts of the world.. Clearly, something in addition to/or other than genetics is involved. What this is, is still a mystery, although some clues have been uncovered. These will be discussed later on.
Several astute List members have also suspected a common, non-genetic thread running throughout the lives of relatives who had AD; e.g.,
1) " - - - It's scary. In my dad's side of my family the following had AD: my dad, two of his brothers, a cousin (only one we know of) and this same cousin's mother. . . . I think there is a common gene running through the family or it's environmental. Most of these people had occupations involving agriculture and or farming. None had early onset AD (which is known to be hereditary). I'm trying to do everything I can just in case I am at risk."
2) " . . . . My mother in-law is the first one with a family history. Her mother and father both died with apparent Alzheimers and now her older sister has been diagnosed with apparent Alzheimers. This history leaves me with a lot of questions!!!! She was born in Hazzard Co., Kentucky in a small coal mining town . . . . Her father worked in and around the mines and their home was built on the side of the mountain close to the mines.. . . Her mother had several babies die at birth. So far she has only one sister who has not been diagnosed with Alzheimer. . .. This is a large percentage of her family with Alzheimer's and I most likely will not be able to find out if there are any aunts or uncles with this disease because her family will deny this disease. I am interested in finding out if there is a larger percentage of Alzheimer's in mining areas or like, if there is a connection with environmental issues (mine gasses etc.) or is this just a freakly high genetic chance with this family."
3) " Hi listmates, Dad, who is 83 and in stage 6, was first noticed to have a problem 12 or 13 years ago. He lived in a coal mining town in Wilkes-Barre, PA until he was 16. He had worked in the coal mines 1 or 2 years. His older sister lived her entire life in Wilkes-Barre, and died of Alz at age 83. All other aunts and uncles died earlier of something else, and my cousins in PA are still too young to show signs of ALZ. I wonderd if there is a correlation."
GENERAL SUPPORT FOR MY ARGUMENT |
(This is just a general introduction. Specific research findings that support this argument will come in later sections.)
NOTE 1: All following excerpts are paraphrased from research studies and/or media articles.
NOTE 2: Human, especially mental, behavior is so complex, it seems reasonable to assume that the thesis of the following excerpt about cancer also applies to AD and related dementias.
. . . (There are) suspected environmental links to the disease even though such connections have not been proved. . . . (The) usual medical approaches to fighting breast cancer in recent years have emphasized genetics and life style (such as smoking and a high cholesterol diet). . . . (There is) concern that researchers might be playing down environmenal factors because of pressure from business. . . Delegates from developing nations were told of breast cancer rates rising in close relation to the degree of modernization in their countries. . . . Mentioned are toxic substances that have caused problems in the developed countries all in the name of progress. . . . Already there is a suspected link between electromagnetic fields and cancer. . .
(NOTE: Surprise, surprise! Similar concerns have been raised in AD. More on this later.)
The link between the environment and cancer need not be proved conclusively before governments act to ban potential substances.
World Breast Cancer Forum Blames Environmental Ills by Anthony DePalma. The New York Times 7/20/97.
Much progress has been made in identifying genes and mutations involved in AD and other dementias, especially those linked to the rare early-onset familial AD. However, even researchers admit that additional genetic and environmental factors need to be identified. This is, especially true of late-onset AD. (I lost the source of this excerpt, but eventually I'll find it.)
Dr. Rudolph Tanzi wrote " . . . in all other cases where a faulty gene is suspected, environmental risk factors appear to loom large. In fact, in some cases of AD there does not appear to be a genetic influence." (However, in a recent report he sent to me, the focus is on searching for as yet unidentified additional genetic factors.)
The following is from Dementia: Not Just a Search for the Gene. by Gatz, M.; et al. Gerontologist. 34(2): 251-255. April 1994.
.... Aging is marked by a decline in organ function that reduces each organ's reserve capacity. . . . genetic explanations for AD are not adequate.. . . non-genetic or environmental factors warrant consideration as well. As with chronic illnesses, the interaction of multiple risk factors for dementia is described in terms of a clinical threshold. As the number of risk factors increases, the probability of observing symptoms also increases; and the point at which the threshold is crossed is influenced jointly by the person's genetic predispositions to dementia and his or her level of environmental risk factor exposure. . . . . The health policy implication of this study is to target resources toward identifying and modifying environmental risk factors that might delay or prevent dementia.
The following excerpts come from Build a Better Brain., by Beth Livermore. Psychology Today (I can't find the date of this issue.)
Neuroscientists know that, along with genetic inheritance, experience alters the brain circuits. Animal research shows the brain is extraordinarily plastic, responding actively to a novel environment by growing new connections. Although the brain lacks the ability for cell-body renewal, nerve cells do generate new connections, or synapses, the points at which signals are transmitted-forging new and enhanced pathways for the flow of information. . . . . The vast majority of them are in the cerebral cortex . . . . Using ... technological advances . . . neuroscientists are providing an unprecedented understanding of our brains.
Researchers believe that, from birth to adolescence, we are laying down the basic circuitry of the brain.. . . Exposure to novel tasks and novel stimuli generates the development of new circuits and synapses for handling all of them. From then on, continued stimulation throughout life further strengthens these pathways and enhances their interconnections. Sometime around 18 years, networks stop forming. We are hard-wired by the end of adolescence. However, connections between neurons proliferate and shrink depending upon use.. . . . the more synapses between cells, the more avenues for information transmission (brain reserve) . . .. Perhaps that explains why rats raised in enriched environments later learn faster than counterparts kept in barren cages.
And perhaps it will help researchers to understand a recent controversial study showing a significant correlation between low levels of education and the incidence of Alzheimer's disease. Individuals who lack formal education may develop fewer synapses, or junctures between neurons, than individuals who have routinely stretched their minds. Then, when disease occurs, there is less brain reserve to call on.
(Years ago, a psychologist from Jean Piaget's Institute Rousseau in Geneva who collaborated in my research on cognition in a Sicilian mountain village, used the term, " atrophy," to explain the poor test results shown by inhabitants of the most isolated hamlet (no electricity, roads, radio, TV, newspapers, etc.) I didn't understand what this meant then, but I do now.)
Many scientists now believe the majority of AD cases result from the interaction between a genetic predisposition and non-genetic factors most of which have not been identified. In other words, if you have one or more relatives with late onset, or even early onset AD, you are not doomed.
Overall, the results of several studies suggest (to me) that your chances of getting AD are greatly reduced if you avoid known environmental risk factors, things like excessive intake of tofu, even zinc (which the brain needs for normal communication between neurons), aluminum based deodorant, and certain toxins in the environment which I report below. However, it's not so easy to avoid occupations which appear to carry a high risk, like fishing in shallow bay waters along the East Coast that are polluted with sewage and farm runoff, working or living near electromagnetic fields, printers, sewing machines, and other occupations.
Earlier, I quoted the expression, " in all other cases where a gene is suspected, environmental risk factors APPEAR to loom large." This and similar mushy words (like seem, suggest, indicate, possible) are almost always used in the interpretation of research results. This is because there usually are other, yet-to-be-discovered factors that interact with the ones revealed by a particular study. In other words, there isn't just one risk factor involved, there are probably multiple, hidden risk factors.
For example, they used to say that a blow to the head which knocks a person out cold can cause AD years later. Now they've discovered that only persons who carry a particular gene are ten times more likely to get Alzheimer's disease than persons with neither risk factor. A head injury alone, without the gene, does not raise the risk. Such studies add more evidence of a close collaboration between genes and environment in AD. ( Dr. Richard Mayeux of Columbia University is quoted in a study described in Neurology and reported in Nation Briefs, by Glenn Kessler. Newsday, 3-29-1995, pp A17.)
" It's a puzzlement," says the King of Siam in the musical, " The King and I." This is a gross understatement when applied to the tangled skein of genetic and environmental risk factors in AD. Not only are there hidden environmental risk factors, researchers now believe there may be even more genes involved in AD than the ones already discovered.
Often in the research reports, the expression " mutated gene" is seen. This makes the respective contributions of heredity and environment even murkier. A benign gene can mysteriously turn deadly as a result of spontaneous internal change or from external environmental assaults such as radiation and noxious chemicals. Maybe the following studies explain why my mother (and maybe, though less-likely, my father) has AD whereas no one among their extended families in Italy had it, as far as I could learn in the many months I lived there.
Some of the most fascinating research on risk factors involves comparing two matched groups of people who come from the same gene pool but have lived in different environments and cultures. These are called cross-cultural studies. In at least one of these studies, " stress" is suggested as a risk factor to explain the greater incidence of AD among the first generation hyphenated-Americans studied than among a matched peer group still living in the " old country." The stress of adapting to a new physical and cultural environment (and the social isolation encountered which has been mentioned as another possible risk factor) may have turned a " good" gene, a Dr. Jekyll gene, into a Mr. Hyde gene. But more evidence is needed to support the hypothesis that either factor alone, or in combination with others, is a risk factor.
However, the more I read, the more it seems to me that our highly industrialized, chemically polluted, densely populated, urban, electro-magnetized environment is speeding up the Darwinian process of evolution of our species. In other words, humankind is rapidly evolving to adapt to this man-made environment. Those who have the adaptable genes survive and propagate whereas those who do not wither on the vine. Unfortunately, it also suggests that even though you have the genes of a superman or woman, environmental assaults can cause a good gene to mutate and give you AD anyway, which is then passed on to the next generation.
One thing seems certain, however, and that is both lifestyle and environment exert a powerful influence on the risk of developing AD. In other words, if the first-generation Japanese-Americans studied (more below) have a significantly higher risk of AD than their matched peers in Japan, why is it that not every one of them developed AD? Or only some workers near electromagnetic fields? Or only some sewing machine operators? Or some tofu eaters? Is it because those with an inherited bad gene or a spontaneously mutated good gene are especially sensitive to one or more of the environmental risks implicated?
Until scientists discover exactly which genes are the mainsprings of AD and then learn how to use gene therapy to make them benign, I suppose the only thing we can do is to go easy with or avoid entirely the environmental risk factors so far uncovered. That doesn't mean you should be fanatical about it. For example, Dr. Rudolph Tanzi, is a Harvard medical researcher who discovered that just a tiny excess of zinc added to a test tube containing A-beta (a normal brain protein) turned it into a deadly form that caused beta amelyoid plaques. Yet, he still takes vitamin supplements containing zinc. Without sufficient zinc, the brain just couldn't do its job.
So, keeping the above issues in mind, the following is what I've teased out from my readings on genetics and environment in AD.
A BRIEF REVIEW OF GENES THAT ARE " CAUSATIVE" AND GENES THAT ARE (MERELY) " RISK" FACTORS.
(The following excerpts are paraphrased.)
1) In 1995, scientists found a gene which, when it mutates into a Dr. Hyde gene, causes a severe form of Alzheimer's disease. People who inherit the defective gene can develop what is now called Early Onset Familial Disease as young as in their 30s. Fortunately, this type of AD is very rare, with only about 400 families worldwide known at this time. Although rare, its symptoms and brain abnormalities look the same as in the more common AD forms. Scientists Find Aggressive Form Of Alzheimer's Disease., by Malcolm Ritter. Th e New York Beacon,, 7-12-1995.
2) (The following excerpts are from recent messages by Dr. Rudolph Tanzi to this List. Dr. Tanzi is a researcher and associate professor of neurology at Harvard Medical School. )
By 1996, about 40 known gene mutations had been identified in three different genes involved in the majority of " Early-onset Familial AD" : Amyloid beta protein precursor (APP) on chromosome 21; Presenilin 1 on chromosome 14; and Presenilin 2 on chromosome 19. The chances of inheriting a mutation from a parent who carries it are 50-50.
IF (my emphasis) inherited, the odds are nearly 100% that the child will get AD at about the same age the parent got it, with the average age of onset between 40 and 50. Some people even develop it in their 20's and 30's. Luckily these mutations are rare, accounting for only 5-10% of all forms of AD.
Confounding the picture is the possibility that not all cases of Early Onset Familial AD have been traced to these rogue genes. About 40% to 30% of cases are due to unknown causes.
NOTE: " Early-onset Familial AD" should not be confused with " Early-onset AD" (onset under age 60, with most cases between ages 50 to 60) which MAY OR MAY NOT BE genetic. These cases account for about 5-10 % of AD. It's possible that in such early onset cases, the known gene defects are NOT involved. " We do not yet know what mutation they possess or even if it's in one of the three 'causative' Early Onset Familial AD genes mentioned above. "
It's also possible that a person can have early-onset AD which is NOT familial and DOES NOT involve one of the rogue genes or even any genes at all. (In a recent report, Dr. Tanzi says that additional genes, as yet unidentified, may be involved.)
(However, IMHO, it's also possible that non-genetic risk factors are involved.)
Risk Factor Genes:
1) According to Dr. Tanzi, these AD-related genes can be compared to genes that predispose some smokers, but not all, to contracting lung cancer. They have a genetically heightened risk of coming down with the disease which is " triggered" by an environmental toxin, in this case, nicotine. Thus, " Risk Factor Genes," only predispose (do not guarantee) that a person will develop AD. (The following is another excerpt about this.)
2) Researchers have found the first genetic risk factor for the type of AD that begins after age 60. The gene is a specific version of apolipoprotein E (ApoE), a protein that carries cholesterol through the bloodstream. . . . inheritance of a specific form of ApoE raises the odds of having AD to a level comparable to that associated with smoking, getting lung cancer, or having high blood pressure that leads to a stroke..., people with two ApoE4 alleles (one of three ApoE versions) are much more likely to develop AD than those who have none or only one copy.
Apolipoprotein E4: A Genetic Risk Factor for Late-Onset Alzheimer's Disease, b y Saunders, A.M.; Roses, A.D. Caring. 13(8): 24-28. August 1994.}
3) (Back to Tanzi) In most cases of AD where there is a family history , " Risk Factor Genes," NOT " Causative" gene defects, are involved. The most well known, confirmed genetic " risk factor" is the APOE gene on chromosome 19. A version of this gene, called APOE4, is present in at least one copy in roughly 30-35 % of the population at-large. Inheritance of the APOE4 gene has been associated with increased risk for AD but does not guarantee its onset. In fact, Tanzi's studies indicate that you can inherit two copies of the APOE4 gene and not develop later AD.
For this reason, Dr. Tanzi cautions about genetic testing. He says the most common genetic risk factor, APOE4, should NOT be used as a predictor for the disease since it is very possible to inherit one or two copies of APOE4 and not get AD.
List members who have reported one or more family members with AD (and there are many of you), with average age of onset over 50, can breathe easier now that you know that the more severe and rare causative gene defects are most likely not involved.
PART 3: GENETIC AND NON-GENETIC FACTORS IN AD |
NOTE: Some of the following research results may unduly frighten readers. The reason I include them is to provide enough support for my argument that not enough funds are going into research for non-genetic risk factors for AD and other dementias.
The good news is that a cure for AD will come in about five to four years, says Dr.Zaven Khachaturian, director of the Ronald and Nancy Reagan Research Institute of Alzheimer's in Chicago. (Plundered Memories, The Sciences, July/August 1997)
The bad news is that the number of people coming down with AD will grow proportionate to the population of aging baby boomers -- a real time bomb -- unless ways to PREVENT AD and other dementias are found. We need preventative measures as well as a cure.
I mentioned at the beginning that I decided to do this report because of worried messages by List members who have several members of their families with AD. I forgot to mention that my many nieces and nephews, whom I love dearly, are scared witless because they have 3 out of 4 grandparents who died of AD or a related dementia. This situation is not unusual. We are sitting on a time bomb!!!
STUDIES INDIRECTLY RELEVANT TO GENETIC/NON-GENETIC FACTORS |
1) The ApoE- E4 allele, an important genetic risk factor, may account for a small fraction of the disease in the general population. (Yet,) Denis A. Evans, of the Rush Alzheimer's Disease Center, and his colleagues found an approximately two-fold increased risk of developing Alzheimer's disease associated with ApoE- E4 in an East-Boston, Mass. population.
(NOTE: Is this an epidemiological phenomenon, something in the lifestyle and/or environment that needs to be studied? I can't find the source of this study, but it's buried somewhere, not lost.)
2) F. Lopera, M.D., of Antioquia University, Medellin, Colombia studied a large, early-onset family in Antioquia, Colombia. All affected members of the family share the same mutation in the presenilin 1 gene and show similar disease symptoms and progression. Age of onset, however, varied widely, ranging from 34 to 62 years. (NOTE: This, too, points a finger at environmental/lifestyle factors.)
3) Faulty Repair Response to Environmentally Damaged DNA. The National Cancer Institute reports that all Alzheimer' s patients in a recent study showed a faulty repair response to damaged DNA. The results came from studying a skin disorder, xeroderma pigmentosum (or XP), a disease characterized by ultra-sensitivity to sunlight. XP patients, who are prone to skin cancer, also suffer from neurological problems resulting from the inability of their nerve cells to repair damage which occurs normally in all people.
Researchers suspected that Alzheimer's patients, who also suffer neurological degeneration like many XP patients, also might have a cell-damage-repair problem. Sure enough, they found that the cells of Alzheimer's patients react differently than cells from people without the disease after the cells were exposed to HIGH concentrations of fluorescent light (which under laboratory conditions can damage DNA). The normal cells repaired damaged DNA, whereas the Alzheimer cells did not. This finding suggests that a DNA repair defect may underlie nerve cell death, the primary deficit in Alzheimer' s disease. The Alzheimer's Association cautions that this is a very small study that needs to be confirmed.
Study Suggests Strong Link Between Alzheimer's, DNA ,1996 National Public Radio, Morning Edition. (Also in an issue of The Proceedings of the National Academy of Sciences,)
CROSS-CULTURAL STUDIES |
1) Many studies find that other diseases - e.g., heart disease and bowel cancer - increase in populations as they migrate West. Recent studies suggest that a neurological disease can also increase with a change in lifestyle, culture and/or environment. For example, Alzheimer's disease is more common in the Western world than in the East.
(Alzheimer's and Lifestyles; Social activity may be a factor, study in AMA Journal suggests, by Alex Abrams. Home Edition., Los Angeles Times, 9-30-1996, pp B-4.)
2) Japanese-American Study: Dr. Lon White, chief of the National Institute of Aging's Asia-Pacific Office., and his colleagues have been collecting information since 1965 on 3,734 first- and second-generation Japanese-American men living in Oahu who were born between 1900 and 1919. They found that Japanese men who migrated to Hawaii decades ago have higher rates of Alzheimer's disease than men living in Japan. (5.4 percent among the Japanese-American men compared to 1.5 percent in Japan.). The rate among the Japanese-American men is similar to that seen among men in the United States and Europe.
(The study is reported in JAMA, Journal of the American Medical Association. I have the title and date buried somewhere.)
Among the risk factors implicated are the following:
a) Social Isolation and Brain Stimulation:
One of the " lifestyle alterations that result from such migrations" is the relative social isolation of the immigrants which can leave the brain under-stimulated, leading to a smaller reserve of functioning brain cells. (Other studies also show a link between low level of education and higher risk of Alzheimer's. Researchers wonder whether this finding adds to evidence that the brain needs to be exercised to remain fit.)
Furthermore, men in the study who showed strong use of two languages were better protected than men with only marginal use of the languages. This factor is also under investigation.
A study of Japanese-Americans living in Seattle who led a more Japanese lifestyle indicates that something in this lifestyle gives more protection against cognitive decline. Among the lifestyle factors pointed to were social support groups and low-fat diet. ( reported in Newsday, Lifestyle May Prompt Alzheimer's, by Jamie Talan 9-25-1996, pp A38.)
Other studies have pointed to America's high-fat diet as a risk factor. (Japanese immigrants to the United States have higher rates of heart disease.)
A surprising result was that the Japanese immigrant men who ate the largest amount of soy tofu had the most severe form of Alzheimer's. Researchers suspect that the plant estrogens in tofu block the body's naturally occurring estrogens from protecting the brain. They are also accumulating evidence that tofu may speed the aging process.
c) Environmental Pollution
Many of the Japanese men, after immigrating to Hawaii, worked in agricultural fields where pesticides may have led to neurological impairment (See next section on Environmental Risk Factors for more on this.)
3) Low Rates of Alzheimer's Disease Found in Cherokee Indians: The purpose of the study was to determine the degree of Cherokee ancestry among a group of Cherokee Indians in Northeastern Oklahoma. The ApoE gene type in 26 people with symptoms of Alzheimer's disease and in 26 controls without AD was investigated..
Results showed that those with AD were more likely to be one-fourth Cherokee or less (38 percent versus 4 percent for the control population). The researchers suggest there exists some form of genetic protection from Alzheimer's in those with mainly Cherokee ancestry. They also suggest that, based on DNA evidence, there may be a connection to studies showing a lower incidence of Alzheimer's in Chinese men.
However, Dr. Creighton Phelps, head of the Alzheimer Disease Center program for the National Institute on Aging,, says, " In other studies, we're looking at lower rates of Alzheimer's disease in Japanese, Chinese, Cree Indians, and other peoples, compared to Caucasians. Recent findings make it likely that several different genes, as well as environmental factors, influence the development of Alzheimer's disease in different ethnic groups. (Reported in the October, 1996 issue of the Archives of Neurology (pages 997-1000)
(IMHO, this study supports the findings of Japanese-American longitudinal study which showed that changes in lifestyle and environment play an important role in predisposing a person to Alzheimer's disease. Considering the enormous cultural and environmental differences between the groups referred to above and our own more " advanced," highly urbanized culture, more studies on non-genetic risk factors should be done.)
4) Nigerian Study: Residents of Ibadan, Nigeria, are mostly poor and 85 percent are illiterate. Yet, although poverty and lack of education are risk factors for Alzheimer' s, the disease is only a fourth as common in Nigeria as it is among " genetically similar blacks living in Indianapolis, Indiana." Researchers still don't know whether Nigerians consume a more brain-friendly diet than Americans, or whether some other aspect of African life wards off mental deterioration.
(Note: What puzzles me is how they determined " genetic similarity" of the African-Americans.)
Staying Sharp, by Karin Vergot, Psychology Today, 1-1-1996, pp 9.(The study is reported more fully in the American Journal of Psychiatry (Vol. 152, No. 10).
Part 4: ENVIRONMENTAL AND LIFESTYLE RISK FACTORS|
Evidence is growing that our lifestyle (and environment) can affect the onset of AD. For example, the Japanese study mentioned earlier showed double or triple the rates of Alzheimer's in the sample of men who migrated to Hawaii decades ago compared to a control group in Japan. The rate of Alzheimer's in the Japanese immigrant men was similar to that seen among men in the United States and Europe.
(Alzheimer's and Lifestyles; Social Activity May Be a Factor, Study in AMA Journal Suggests; Home Edition ( Los Angeles Times ) September 30, 1996 )
1) Electromagnetic Fields (EMF) and Occupations
Two studies -- one by researchers at the University of Southern California and the other at the Universities of Kuopio and Helsinki-- found that people with high occupational exposure to EMFs are at least three times as likely to develop Alzheimer's disease as those without significant exposure.
Another study found that dressmakers and tailors were over-represented among Alzheimer's victims. Industrial and home sewing machines produce much larger EMFs than other appliances, and people who use sewing machines regularly have the greatest exposure of any occupation--as much as three times that of electric power line and cable workers. The relative risks were consistent in the three studies: 2.9, 3.1, and 3 times higher than the low exposure group.
Women were more susceptible to the effects of EMFs: In one of the Finnish studies, women with the highest exposure were 7.3 times as likely as women in the low exposure group to develop Alzheimer's; in the other two studies, the relative risks were 3.3 and 4.2 times as great.
Some animal studies also suggest that EMFs might damage the brain. In the mid-1980s, Henry Kues and Sam Koslov of Johns Hopkins University's Applied Physics Laboratory in Laurel, Md., studied the effects of low levels of microwave radiation on the eyes of monkeys. Persistent exposure to radiation, at levels well below safety guidelines, damaged the cornea, apparently by opening the blood-brain barrier in the eyes. The monkeys' brain tissue contained neurofibrillary tangles and other changes characteristic of Alzheimer's disease. Koslov believes that opening the blood-brain barrier in the affected cells allowed toxic chemicals to leak in, eventually killing the cells and producing the tangles.
THE RESEARCH WAS LATER ABANDONED FOR LACK OF FUNDING, [my emphasis!!!] (Studies Link EMF Exposure to Higher Risk of Alzheimer's; Health, by Thomas H. Maugh. Los Angeles Times, 7-31-1994. )|
2) Printing Industry
Archives of The University of Washington studies on memory loss in older adults shows some interesting statistics about former profession and Alzheimer's. In one study, a " noticeable" number of participants had worked in the printing industry.
The following message was sent by a List member.
1. Dad, who is 83 and is in stage 6, was first noticed to have a problem 12 or 13 years ago. He lived in a coal mining town in Wilkes-Barre PA until he was 16. He had worked in the coal mines 1 or 2 years. His older sister lived her entire life in Wilkes-Barre, and died of AD at age 83. All other aunts and uncles died earlier of something else, and my cousins in PA are still too young to show signs of AD. I wonderd if there is a correlation.
2. My mother in-law is the first one with a family history. Her mother and father both died with apparent Alzheimers and now her older sister has been diagnosed with apparent Alzheimers. She was born in Hazzard Co. Kentucky in a small coal mining town. Her father worked in and around the mines, and their home was built on the side of the mountain close to the mines. Her mother had several babies die at birth. So far she has only one sister who has not been diagnosed with Alzheimer. I most likely will not be able to find out if there are any aunts or uncles with this disease because her family will deny it. I am interested in finding out if there is a larger percentage of Alzheimer's in mining area, if there is a connection with environmental issues (mine gasses etc.) or is this just a freaky high genetic chance with this family.
4) Farming - Pesticides
The Japanese-American study reported above, also implicates this as a risk factor. Many men, after emigrating to Hawaii, worked in agricultural fields " where pesticides may have led to neurological impairment."
From a List member:
It's scary. In my dad's side of my family the following had AD: my dad, two of his brothers, a cousin (only one we know of) and this same cousin's mother. Most of these people had occupations involving agriculture and or farming. None had early onset AD.
5) Traumatic Brain Injury
A blow to the head that knocks you out can raise your chance of getting Alzheimer's disease someday, but only if you carry a particular gene, a study reported in the journal Neurology suggests. Elderly people who had a severe blow to the head and carried the gene were 10 times as likely to have Alzheimer's as people with neither risk factor. A head injury alone, without the gene, did not raise the risk.
( Newsday, 3-29-1995, pp A17. )
(Punch-drunk Boxers Have Alzheimer's Gene - Study., Reuters, 5-15-1997)
A version of the ApoE gene, linked with Alzheimer's, was more likely to turn up in boxers with more brain damage, claims Barry Jordan, a neurologist at the University of California at San Francisco. Between 10 and 50 percent of boxers eventually develop punch-drunk syndrome, which causes them to have slurred speech, trouble walking and memory lapses. The DNA and brain scans of 30 boxers were examined. All the boxers had some brain damage, but the one-third who had the Alzheimer's-type ApoE gene had more damage. One boxer had two copies of the gene. " His condition was noticeably more severe,"
. . . . Other experts urge tests on athletes such as football and soccer players, who are also known to suffer some brain damage in their high- contact sports. (reported in New Scientist Magazine. )
Neurological studies show that AD brains have between 10 and 50 times higher concentrations of aluminum in neuron tangles than normal neurons. Epidemiological studies on exposure to airborne particles of aluminium indicate this appears to raise the risk of developing AD. One study reported " a higher than average incidence in people who use antiperspirant sprays that contain aluminium."
For a time, it was thought that excess aluminum exposure was, in itself, a cause of AD tangles. Many researchers are now skeptical since aluminum is the third most common element in the earth's crust and humans ingest it constantly in food and water. Furthermore, the kidneys normally excrete any aluminum absorbed through the intestines and the brain has a protective barrier against it in blood.
(IMHO, like the early theory that a blow to the head that knocks you out cold is enough to cause AD, this may happen only where there's a genetic factor which interferes with the body's processing of excess aluminum. It could still be an environmental-genetic thing.)
There's evidence that zinc is involved in the damage that occurs in some parts of the brain after a heart attack during which insufficient blood and oxygen reaches the brain. Until now, researchers did not know why only some parts of the brain show damage even though the whole brain runs short of blood. Now they believe it's due to toxic amounts of zinc. Zinc is needed by cells in these specific parts of the brain to communicate with other cells. Unfortunately, these are the ones involved in learning and memory (hippocampus), the emotions ( amygdala), and conscious thought (part of the cortex).
(Zinc may be key to heart patients' brain damage. by Jackie Frank. Reuters, 5/16/96) Zinc is necessary for normal communication between brain cells. But just a slight increase above normal level appears to be implicated in AD. Taking vitamin supplements containing zinc for ailments like acne, impotence, and low energy won't do any harm, says Dr. Rudolph Tanzi of Harvard Medical School. But taking megadoses is another matter. He demonstrated this in a simple experiment in which he put some A-beta, which is normally found in cerebrospinal fluid, brain, and blood, in a test tube. Then he added just a trace of zinc, raising the normal level slightly. Within two minutes, the solution turned into a sticky glob similar to the plaques that form in Alzheimer's victims' brains. This dramatic discovery indicates that excess zinc converts normal A-beta into beta amyloid, which makes up the plaque of Alzheimer's disease.
(Zinc levels may offer new theory on Alzheimer's, by Tim Friend. USA TODAY, 9/2/94)
Now researchers are trying to solve the mystery of how AD patients' brains metabolize zinc. Once they know that, they're on the road to prevention and treatments.
After reading a research report that megadoses of zinc made Alzheimer's patients dramatically worse, Dr. Rudolph Tanzi, of Harvard University, mixed some zinc with normal brain protein in a test tube, and immediately ameloid-like clumps formed. He did the same test with other metals, including aluminum, but only zinc formed the clumps. What's scary is that he used levels of zinc that are only slightly higher than is normally found in the human brain.
But this is not yet considered proof that excess zinc is a direct cause of Alzheimer's disease. More research involving Alzheimer's patients is needed. Remember the aluminum scare of a few years ago in which no link with Alzheimer's has been proven so far? Zinc may be a similar situation. Until then, there's no need to cut out zinc containing foods like seafood. Dr.Tanzi still takes a multivitamin pill every morning, which contains the recommended daily dose of 15 milligrams of zinc.
For more details, see the September 1st 1994 week's issue of Science.
(The above is a summary of a National Public Radio Morning Edition broadcast on 9-2-1994 - Zinc May Play a Role in Alzheimer's Disease.)
SLOW ACTING VIRUS/INFECTION |
1) Herpes Virus
According to British researchers, the herpes virus that causes cold sores may be teaming up with a genetic mutation of apolipoprotein-E (APOE) to cause damage that leads to Alzheimer's disease. Herpes is found in the same areas of the brain that are affected in Alzheimer's. The herpes family of viruses causes cold sores, chicken pox, shingles and other diseases. Once a herpes virus infects someone it stays in the nerve cells forever. Almost everyone is infected with HSV-1, although not everyone gets cold sores and there is no indication that herpes infection of the brain is common.
The researchers analyzed DNA from the brains of 90 people with and without Alzheimer's. They found 52.% percent of Alzheimer's patients who had the herpes virus in their brains also had the APOE-epsilon 4 mutation. Only 10 percent of Alzheimer's patients without the virus in their brains had the mutation, and only a very few of the non-Alzheimer' s patients had it. Whereas a combination of HSV-1 in the brain and APOE-epsilon 4 (gene) is a strong risk factor for Alzheimer's disease, either of these features alone does NOT increase the risk of Alzheimer's, states a report in the Lancet medical journal. (1977 is the only date I have)
Involvement of herpes could explain why anti-inflammatory drugs can prevent or delay onset of Alzheimer' s symptoms, because inflammation can reactivate herpes episodes.
Younger volunteers did not have herpes in their brains, which suggests that as the immune system weakens with age, the virus can spread to the central nervous system.
New treatments for Alzheimer' s, especially antivirals or anti-inflammatories, may result from these findings.
(Loss of smell may offer clues about Parkinson's., Reuters, 5-12-1997 )
Most Parkinson's Disease victims have trouble smelling. British researchers Christopher Hawkes and colleagues at Leeds General Infirmary said tests showed damage to the olfactory bulb, which links the nasal passages and the brain. (reported in the British Medical Association's Journal of Neurology, Neurosurgery and Psychiatry.)
Alzheimer's is also known to affect smell. " One possibility is that Parkinson's Disease and perhaps Alzheimer' s Disease might be caused by a virus or chemical agent that gains entry to the central nervous system via the nose," say the researchers. They cite reports that showed the herpes virus could get into the brain through the nose.
2) Mad Cow Disease and Creutzfeldt-Jakob Disease
Experiments with human Creutzfeldt Jackob Disease support the existence of a slow acting infectious pathogen. Many latent or persistent viruses can cause neurodegenerative disease and may have a role in late onset dementias. There are reasons to believe that CJD infections may share properties with some of these latent viruses in causing dementia.
Human-rodent transmission studies suggest that CJD, or a CJD-like variant can be a common but latent infection of humans, with relatively infrequent expression of neurological disease. Although susceptibility to the disease involve the individual's makeup and possibly age-related factors, viral principles are also operative.
Worldwide, Creutzfeldt-Jakob Disease normally affects about 1 person in a million each year. Although it usually affects older people, a cluster of 10 recent cases in Britain had victims younger than 42, some in their teens. " The most likely" explanation is that they were exposed to mad cow disease. The Mad Cow epidemic peaked in early 1990's, and presumably arose from cattle that were infected.
In humans, Creutzfeldt-Jakob Disease resembles AD. It produces progressive apathy, irritability, dementia, balance problems, severe muscle spasms, and behavioral and emotional changes. Early symptoms included personality changes, difficulty sleeping, withdrawal, fearfulness and paranoia, difficulty maintaining balance.
(Dementias, Neurodegeneration, and Viral Mechanisms of Disease from the Perspective of Human Transmissible Encephalopathies. A review by Manuelidis L. Annals of the New York Academy of Sciences 1994; 724:259-81. )
3) Glasgow's Syndrome
(And the Waters Turned to Blood: The Ultimate Biological Threat, by Rodney Barker
The following is paraphrased from a book review, Wet and Nasty by Charles C. Mann, which appeared in The New York Times Book Review 4/27/97. It sounds like a Stephen King horror story but it's true. )
A one-celled organism, Pfiesteria piscicida, is apparently one of the dinoflagellates which are free-swimming creatures with characteristics of both plants and animals. It spends most of its life in a dormant state on the river floor. Some dinoflagellates are the cause of " red tide," the poisonous blooms that increasingly afflict coastal areas, responsible for some of the extensive fish kills that were plaguing rivers in North Carolina and elsewhere in the South. They are dangerous to humans. After exposure to the toxin, people are affllicted with sores, nausea, mood swings, memory loss and a host of Alzheimer-like symptoms.
SPECIAL INTERESTS REJECTED THE SCIENTIST'S CLAIM THAT THE RED TIDE WAS IN LARGE PART CAUSED BY RUNOFF FROM SOME OF THE STATE'S GIGANTIC HOG FARMS, AS WELL AS FROM OTHER AGRICULTURAL RESIDUE. (my emphasis !!!)
In Durham, N.C., a 37-year-old scientist's mental collapse began one night when he woke his wife and flew into a rage about how she had left the vacuum cleaner cord draped loosely over the handle. The next morning, he couldn't remember his outburst. A few days later, he got lost on his way home from work. When he tried to call his wife for help, he couldn't remember his phone number. At work, he started missing appointments and then insisted he never made them. He had long conversations with co-workers he instantly forgot. In time, he couldn't complete a short sentence without losing his train of thought.
Physicians and marine scientists suspect that a toxic marine algae had slowly poisoned the young scientist while he worked in the laboratory. The culprit, the dinoflagellate--a half-plant, half-animal microorganism--thrives in shallow bay waters along the East Coast that are polluted with phosphates, a widely dispersed nutrient in sewage and farm runoff.
For two years, the young scientist had studied this one-celled creature, next to rows of fish tanks containing water from a coastal bay inhabited by the organism. The creatures apparently excreted a powerful toxin into the aquarium water and eventually the laboratory air, jumbling his brain. After taking two months off to recover, he seems nearly normal and has returned to work. Apparently, the damage to his brain was gradually reversed once he distanced himself from the organism.
Although some marine algae, including red tides, are known to be toxic to fish and contaminate shellfish, this is the first known instance of a human poisoned directly by them. The dinoflagellate is found in large concentrations from Delaware to Florida in bay waters that are popular with millions of swimmers, fishermen and boaters. No one knows yet if the organism inhabits estuaries along the Pacific coast.
Some scientists who are studying what is now known as Glasgow's syndrome, caution that more studies are needed to prove the organism was to blame. But one scientist is " dead certain."
Poisonous algae blooms have been found in increasing numbers around the world. Worried about public health, North Carolina environmental officials began exploring whether shrimpers and other fishermen who frequent Pamlico Estuary are suffering unusual neurological symptoms and other ailments. Some fishermen have experienced periodic memory lapses and sores that don't heal. " I don't think people need to be scared, but they need to be made aware that there is a potential for human health problems as far as the estuary goes," the afflicted scientist said. Researchers suspect that the surge in toxic algae is related to nitrogen and phosphorus, nutrients in sewage and farm runoff. The organism is probably expanding in scope because nutrient contamination that feeds algae blooms is worsening due to population growth along the shoreline. The highest algae concentrations are found near sewage outfalls, and laboratory tests show the algae grow rapidly in waters containing phosphates but not other pollutants.
(Another full report on this is Scientist Learns Toxic Algae Health Threat Firsthand, by Marla Cone. Home Edition., Los Angeles Times, 5/20/94. )
4) Lyme Disease:
The organism involved can invade the brain and spinal cord and cause memory problems, hallucinations, panic attacks, paranoia, manic depression, seizures and even dementia. Memory problems are the most common signs of a brain infection. Victims often receive the wrong diagnosis or treatment..
(Reported in an article by Jane Brody, The New York Times, 2-15-95)
STRESS, DIET AND CARDIOVASCULAR PROBLEMS |
Several studies implicate America's high-fat diet for the higher rates of heart disease seen among Japanese immigrate to the United States.
William B. Grant, author of Dietary Links to Alzheimer's Disease, says there is evidence that diet is a factor in preventing AD. Grant collected data on the prevalence of AD and national diets for eleven countries. His statistical analysis shows strong correlation between high-fat national diets and high rates of AD. For example, the incidence of Alzheimer's disease in the age 65-plus population in the United States is 5 percent; only 1 percent in Nigeria and China; and among Japanese who live in united States more than twice that of native Japanese. He attributes this to their low-fat diets.
Grant points to another study showing increasing consumption of fish reduces the risk of developing AD. This is because " fat leads to inflammation," and fish oils reduce inflammation. Furthermore, he claims support in the finding that Vitamin E delays the onset of Alzheimer's disease. Vitamin E is an antioxidant that fights free radicals produced from eating excess fat. He believes other antioxidants such as vitamin C and selenium might also be effective in reducing the risk of developing AD.
Alzheimer's Disease Review is published by the University of Kentucky, and is available on line at http://www.coa.uky.edu/ADReview/
(Study Links High-fat Diet to Alzheimer Disease., US Newswire, 06-19-1997)
3) Vascular Risk Factors
Dutch and Belgian researchers have found evidence linking Alzheimer's disease with clogged arteries. Alzheimer's patients were more likely to have atherosclerosis, fat clogged arteries. A blood protein , known as apolipoprotein-E (APO-E), which is associated with the transport of fat in the blood, played a strong role. The worse the atherosclerosis, the more cases there were of dementia. This is not surprising, as atherosclerosis can reduce blood flow to the brain. Patients who suffered dementia were more likely to carry a certain gene controlling production of apolipoprotein-E.
(Clogged Arteries Linked with Alzheimer's, Reuters, 1-16-1997 )
Geri Hall wrote on Wed, 16 Apr 1997: So far, high cholesterol levels and AD are not linked as causative, but there is one link for a small group of people. Those people who are homozygous (who have 2 such genes - one from each parent) for APOE-4 genes are at very high risk for both late onset AD and early onset cardiovascular disease. During cardiovascular studies, the APOE-4 homozygotes had high rates of cognitive decline.
NOTE: Most of us know that a high-fat diet, chronic stress, and overweight increase the risks of having a stroke. The following studies show the correlation between strokes and AD.
1) The relationship between stroke and Alzheimer's disease may be " extremely important," say researchers at Erasmus University Medical School in Rotterdam and Richard Mayeux, at Columbia University. They looked at ApoE in dementia patients with stroke and found ApoE-E4 is a genetic risk factor for dementia with stroke, with up to a seven-fold increase in risk. This association " should be investigated further."
Small strokes increase the risk of developing Alzheimer's, as well as the severity of symptoms, according to several studies reported in the Journal of the American Medical Association [date?]
" If we can identify individuals who have risk factors for cerebral vascular disease and treat those risk factors, we may be able to postpone the manifestations of Alzheimer's disease," said Dr. G. Webster Ross. The study suggests that people may be able to lower their risk for Alzheimer's by not smoking and controlling high blood pressure and diabetes.
(Health Watch for Women 1997, The Atlanta Journal and Constitution, )
The Nun Study
David Snowdon and colleagues at the University of Kentucky examined the prevalence of dementia among a group of nuns. Autopsies performed on the nuns' brains revealed that among nuns with abundant Alzheimer's disease lesions, those who had strokes in strategic regions had significantly poorer cognitive function and more dementia than those without strokes. Their findings show the influence of cerebrovascular disease on severity of clinical symptoms in AD. They also suggest that treatment of vascular disease could delay or diminish the development of symptoms in many alzheimer's disease patients."
( reported in a March 12 (year?) special issue of the Journal ofthe American Medical Association (JAMA)
Stress has been linked to high blood pressure and cardiovascular disease. The Japanese study also raises the risk factor of stress resulting from culture shock and social isolation among the immigrants. The researchers wonder, " Is it the stress of adapting to a new culture that puts people at greater risk? Or is it something in our western environment?"
(NOTE: Or, is it a combination of these and other factors already mentioned, such as hopelessness and depression?)
Middle-aged men who feel hopeless or think of themselves as failures may develop atherosclerosis, the narrowing of the arteries that leads to heart attacks and strokes, faster than their more optimistic counterparts. People who expressed high levels of despair had a 20 percent greater increase in atherosclerosis over four years, according to a report in the August issue of the journal Arteriosclerosis, Thrombosis and Vascular Biology. The lead author is Susan Everson. Earlier studies have associated hopelessness with heart disease, heart attack and death from heart disease. " I'm not surprised that we have not demonstrated that psychosocial factors may play a role," said Dr. Marty Sullivan, associate professor of medicine at Duke University Medical Center.
Atherosclerosis is a progressive disease in which fat, cholesterol, cellular waste products and calcium collect in the blood vessels, reducing their ability to deliver oxygen and nutrients. Depression, anxiety and other types of psychological stress can affect the body's central nervous system, influencing the production of stress hormones.
(Despair and Risk of Artery Disease, The New York Times, 9/3/97. )
(NOTE: In the following studies, urban stress caused by congestion, noise, pollution, etc. may be involved, IMHO.)
Of 1,545 subjects recruited into the UK Medical Research Council elderly hypertension treatment trial, 50 cases of dementia were identified, including 31 cases of probable or possible Alzheimer's disease. These persons were compared with 223 unimpaired controls from the same population for exposure to familial, cardiovascular, educational, and geographic risk factors for dementia.
Results confirm the association of family history of dementia with dementia (odds ratio OR = 4.36) , and AD (OR = 4.69), and of advanced age with dementia (OR = 2.81). Rural residence exerted a protective effect for dementia (OR = 0.21) and AD (OR = 0.28). There were near-significant associations between AD and dementia and several cardiovascular risk factors (ECG ischemia, systolic hypertension, and SMOKING) among subjects lacking a family history of dementia.
We postulate the existence of a non-familial form of dementia transcending traditional categories of multi-infarct dementia and AD, MORE COMMON AMONG URBAN RESIDENTS, AND MEDIATED THROUGH VASCULAR PATHOLOGY (my emphasis, having taught in Harlem)
(Risk Factors For Alzheimer's Disease And Dementia: a Case-control Study Based on The MRC Elderly Hypertension Trial. Prince M, Cullen M, Mann A. Neurology 1994; 44(1):97-104)
The frequency of dementia was studied in 251 patients aged 60 years or older who were hospitalized with acute ischemic stroke, based on examinations performed 3 months after stroke onset. Dementia was found in 66 patients (26.3%). In a control sample of 249 stroke-free subjects, dementia was found in only eight subjects (3.2%). Advancing age and fewer years of education were significant, independent correlates of dementia, with a trend evident for race (non-white versus white).
Confining the analysis to subjects residing in the Washington Heights-Inwood community of northern Manhattan, the OR was 10.3, with significant age and race effects.
(NOTE: This is a highly congested, poverty area with many African American residents. - JO). Ischemic stroke significantly increases the risk of dementia, with independent contributions by age, education, and race.
(Dementia after Stroke: Baseline Frequency, Risks, and Clinical Features in a Hospitalized Cohort., Tatemichi TK, Desmond DW, Mayeux R, Paik M, Stern Y, Sano M, Remien RH, Williams JB, Mohr JP, Hauser WA, et al: Neurology1992; 42(6):1185-93. )
Subjects were patients with multiple cerebral infarctions. Predominantly elderly African Americans. There were 61 multi-infarct disease index cases and 86 controls without cognitive impairment.
Index cases were older age (75.5 vs 69), were less well educated (odds ratio, 4.37), had lower annual incomes, more frequently had a family history of dementia.
Advanced age, lower educational attainment, history of myocardial infarction, and recent cigarette smoking were positively associated with case status. Additional well-designed epidemiologic studies are needed to clarify these associations.
(Risk Factors for Dementia Associated with Multiple Cerebral Infarcts. A Case-control Analysis in Predominantly African-American Hospital-based Patients. Gorelick PB, Brody J, Cohen D, Freels S, Levy P, Dollear W, Forman H, Harris Y Neurology 1993; 50(7):714-20. )
A BRAIN STIMULATING ENVIRONMENT APPEARS TO PROTECT AGAINST AD.|
Dr.Zaven Khachaturian, jokingly remarked at a dementia symposium at NYU that being married to a high-I.Q spouse has a protective effect. (He is director of the Ronald and Nancy Reagan Research Institute of Alzheimer's in Chicago.)
Education & Low Skill Occupation
Several studies link a low level of education to a higher risk of Alzheimer's, suggesting that the brain needs to be exercised to remain fit.
1) The more years of education, the lower the risk of dementia, according to researchers at Columbia University College of Physicians and Surgeons. The risk is two to three times greater for those with low-skilled occupations and little education. With education, the onset of dementia is delayed by five years. Others have reported this education boost.
(Staying Sharp, by Karin Vergoth,, Psychology Today, 1-1-1996, pp 9. Vol. 29. )
2) Japanese Study: Low Skilled Farming
Among the other correlations found in the Japanese study was this: Many of them, after emigrating to Hawaii, worked in agricultural fields doing low-skilled labor. (Of course, the risk of pesticides leading to neurological impairment has also been mentioned above.)
(Alzheimer's and Lifestyles; Social activity may be a factor, study in AMA Journal suggests; by Alex Abrams. Home Edition., Los Angeles Times,09-30-1996, pp B-4. )
NOTE: How to account for the many well educated with AD? Is this a genetic + environmental time bomb? There is at least one Nobel Prize winner who died of AD. I don't recall his name.
3) Social Stimulation: Japanese Study
Among the " lifestyle alterations" that result from such migrations is the social isolation experienced by the men. One of the researchers, Dr. Lon White, suggested the Japanese men may have been less socially stimulated in their new environment. , , other studies suggest solitary lifestyles common among elderly Americans can leave brain unstimulated, thus leading to a smaller reserve of functioning brain cells.
(Alzheimer's and Lifestyles; Social Activity May Be a Factor, Study in Ama Journal Suggests; by Alex Abrams. Home Edition., Los Angeles Times, 9-30-1996, pp B-4 )