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The Novus Research Electronic Newsletter and Information Bulletin periodically informs subscribers of new scientific information on anti-aging, the brain and related matters. Subscribers also become aware of the development or status of new products, and special product values as they become available. A sample newsletter from Sept 2001 can be viewed below.
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Sample Novus E-Bulletin:
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NOVUS ELECTRONIC NEWSLETTER
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CONTENTS OF THIS E-NEWSLETTER:
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NEW PRODUCTS FROM NOVUS RESEARCH - In-Sight Eye Nutrition and Anti-Aging Drops.
GENERAL PRODUCT NEWS - Brain Lightning elements further upgraded.
WEBSITE NEWS - New menu system being implemented on the website.
DATA:METHYLCOBALAMIN and the New Story of Vitamin B12
DATA:New Macular Degeneration and Nutrition Study - Harvard University
FEEDBACK: More customer comments on the effectiveness of Brain Lightning
ARTICLE: Memory Starts To Decline In Our 20s, Researcher Finds
ARTICLE: Snack Foods Seem To Hike Risk Of Macular Degeneration
ARTICLE: For Aging Brains, Two Hemispheres Are Better Than One
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NEW PRODUCTS FROM NOVUS RESEARCH
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Novus Research is proud to bring you a brand new product, In-Sight, a new ocular anti-aging product. Now, you can give your eyes the ultimate in nutrition and stave off the effects of macular degeneration, problems with eye capillaries which occur at middle age, and other nutritional problems which contribute heaviliy to loss of quality of sight as the body ages. An absolutely incredible formula!
See http://www.futuredynamicadvantage.com/products/in-sight.html for further developments on this fantastic ocular formula. At some point the main listing for this product will be under the Phoenix Longevity page, although the mail page will be as listed above. Among the components of this exciting product are Lutein, Cryptoxanthin, Zeaxanthin, Bilberry, Chromium, Lycopene, Quercetin, Vitamin E, B-3, B-6, B-12, Zinc, Alpha and Beta Carotene, Manganese, Magnesium, and Cysteine.
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GENERAL PRODUCT NEWS
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The general formula for BRAIN LIGHTING was recently upgraded by changing the source of Vitamin B-12 from cyanocobalamin to methylcobalamin, a much more bio-available formula. The Selenium component was upgraded to Selenomethionine. Both of these changes, although increasing the cost of some of the ingredients, have been done without the intention of raising the cost of Brain Lightning. An even more effective and synergistic product at the same cost!
Check it out at http://www.brainlightning.com
For Specifics on the formula upgrade: http://www.futuredynamicadvantage.com/products/details.html
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WEBSITE NEWS
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Web site menu systems have been recently upgraded, with the new FX side menu being extended throughout the website gradually. This new menu systems allows rapid upgrading for site page listings and categories, especially when new products are added.
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METHYLCOBALAMIN and the New Story of Vitamin B12
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The 50th anniversary of the discovery of vitamin B12 came and went and nobody noticed. There were no conferences to mark the occasion, no fanfares, no speeches, not a mention in the press, not even in the nutritional media. "Vitamin B12 isn't sexy" was the way a friend, a sports nutrition consultant, put it. "Just for old people to keep them from getting anemic." Oh, yeah? Welcome to the new story of vitamin B12.
There's a buzz over B12 these days for two reasons, one scientific and the other economic. First, the science: Over the last decade or so, researchers have strongly implicated the toxic amino acid homocysteine in a variety of disease states. Homocysteine tends to accumulate in the body whenever B12 gets deficient, and this accumulation has been linked with increased risk of Alzheimer's disease [1,2], cardiovascular disease [3], chronic fatigue syndrome/fibromyalgia [4] and multiple sclerosis [5] among other conditions.
Folic acid deficiency can also lead to increased homocysteine levels - that's because folate and B12, in their active "coenzyme" forms, are both necessary cofactors for the enzymatic conversion of homocysteine to methionine. Until recently it's been thought that the availability of folate was the most important determinant of the body's ability to remethylate homocysteine. New research has revealed that vitamin B12 is more important for homocysteine disposal than once believed [3,6,7]. In particular, a study conducted among dialysis patients with kidney failure showed that a monthly shot of B12 plus conventional oral folate was more effective than high-dose folate without B12 in lowering elevated homocysteine [6].
The coenzyme form of vitamin B12 is known as METHYLCOBALAMIN or METHYL B12. It's the only form of vitamin B12 which can directly participate in homocysteine metabolism. In addition, converting homocysteine to methionine via methyl B12 generates an increased supply of SAMe (S-adenosyl methionine), the body's most important methyl donor. Indeed, some of the benefits of methyl B12, such as protection from neurotoxicity, appear to derive from increased production of SAMe [8,9]. Methyl B12 has also been reported to be neurotrophic, or growth-promoting, for nerve cells [10,11], a property which may help regenerate central and peripheral nervous tissues damaged in disorders such as amyotrophic lateral sclerosis [12] and diabetic peripheral neuropathy [13].
All of this scientific news is hot stuff, but it's still only half the story. The other half is that starting around 1998, methylcobalamin first became widely available in this country at an affordable price, thus offering new options for treating B12 deficiencies and lowering elevated homocysteine. Before then, methyl B12 had been enormously expensive and widely available only in Japan, where it still remains a prescription medication. Today any health-conscious American consumer can easily access the most powerful known form of vitamin B12.
When most of us think of vitamin B12, the molecule we really have in mind is cyanocobalamin or cyano B12. As its name suggests, cyano B12 has a cyanide group (CN) attached, whereas methyl B12 carries a methyl group (CH3) instead. Very little of the body's natural B12 is in the cyano form under normal circumstances; exceptions are in cases of cyanide poisoning or chronic smoking, both of which can raise cyanocobalamin levels. The fact that most of our vitamin pills contain cyano rather than methyl B12 is largely an accident of history, the result of using charcoal to filter extracts during the isolation of B12. Unknown to the early researchers who first isolated B12, the traces of cyanide present in such charcoal rapidly convert all natural forms of B12, including methyl B12, into the more stable cyano form. As a result, the discovery of the B12 coenzymes and their metabolic role was delayed for years.
Whenever we swallow a conventional vitamin pill, any cyano B12 present gets carried along and absorbed by an intricate "bucket brigade" of B12-binding proteins. Operating in the stomach and small intestine, this transport system provides a very efficient mechanism for absorbing a few micrograms of B12, yet is quickly swamped by anything larger. As a result, only about 1% of a large oral dose of any form of B12 usually makes it into the bloodstream. Fortunately, we can bypass intestinal absorption entirely by giving B12 by injection or sublingually. In particular, sublingual administration is a simple and effective way of substantially raising blood levels by absorbing B12 through the oral mucosa. It's also unquestionably the most convenient way to take B12, especially for people taking supplements on a daily basis.
So let's say we've taken a sublingual tablet and a significant amount of B12 shows up in the bloodstream. End of story? Not if it's cyano B12. Most of the B12 naturally circulating in the blood is in the methyl form. Before cyano B12 can join this metabolic pool and be properly utilized by the body, it must be stripped of its cyano group and "reduced" (i.e., made to gain electrons) in a time-consuming, multi-step process [1,4]. The result of all this processing is a B12 molecule with its cobalt ion reduced from the +3 to the +1 oxidation state, ready to take on a methyl group and be distributed throughout the body as methyl B12.
It should be obvious there are certain advantages inherent in taking methyl B12 as a supplement, versus "ordinary" B12. For one thing, methyl B12 needn't engage the body's resources to convert it into coenzyme form - it's already there. Even more important is the fact methylcobalamin is the most highly reduced form of vitamin B12 possible; this makes methyl B12 a very potent reducing agent (antioxidant) indeed. In a body undergoing oxidative stress, for example, from a disease process or from a diet deficient in antioxidants, it's possible methyl B12 production can become impaired. A similar derangement in the cellular synthesis of adenosyl B12 (another reduced coenzyme form of B12, into which methyl B12 can be converted) is already known to occur in association with vitamin E deficiency [15]. So it makes sense to consume B12 in a form in which it's already metabolically active and maximally reduced, and thereby put less of a strain on our bodies' antioxidative capacity.
How much methyl B12 should be taken for optimal health? In some studies on animals and humans, big doses (equivalent to 25-40 mg per day for an adult human) were found to halt or improve neural degeneration [10,12]. The problem is, nobody knows the long-term effects of such huge doses. A more prudent approach would be to take about a tenth as much - say, 3 mg per day - as a maintenance dose, with the dose increased as needed in cases of increased stress, oxidative or otherwise. (1 mg = 1000 mcg)
So here's a belated "Happy 50th Birthday" to B12. With all the health and pro-longevity benefits of methyl B12 now becoming evident - including warding off such age-related diseases as Alzheimer's [1,2], atherosclerosis [3], rheumatoid arthritis [16] and possibly even cancer [17,18], it seems the old vitamin has some new life in it. May it and we continue in partnership for many birthdays yet to come.
REFERENCES
[1] McCaddon A, Davies G, Hudson P, Tandy S, Cattell H. Total serum homocysteine in senile dementia of Alzheimer type. Int J Geriatric Psychiatry 1998;13(4):235-239.
[2] Clarke R, Smith AD, Jobst KA, Refsum H, Sutton L, Ueland PM. Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 1998;55(11):1449-55.
[3] Araki A, Sako Y, Ito H. Plasma homocysteine concentrations in Japanese patients with non-insulin-dependent diabetes mellitus: effect of parenteral methylcobalamin treatment. Atherosclerosis 1993;103(2):149-57.
[4] Regland B, Andersson M, Abrahamsson L, Bagby J, Dyrehag LE, Gottfries CG. Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome. Scand J Rheumatol 1997;26(4):301-7.
[5] Baig SM, Qureshi GA. Homocysteine and vitamin B12 in multiple sclerosis. Biogenic Amines 1995;11(6):479-485.
[6] Hoffer LJ, Bank I, Hongsprabhas P, Shrier I, Saboohi F, Davidman M, Bercovitch DD, Barre PE. A tale of two homocysteines - and two hemodialysis units. Metabolism 2000;49(2):215-9
[7] D'Angelo A, Coppola A, Madonna P, Fermo I, Pagano A, Mazzola G, Galli L, Cerbone AM. The role of vitamin B12 in fasting hyperhomocysteinemia and its interaction with the homozygous C677T mutation of the methylenetetrahydrofolate reductase (MTHFR) gene. A case-control study of patients with early-onset thrombotic events. Thromb Haemost 2000;83(4):563-70.
[8] Akaike A, Tamura Y, Sato Y, Yokota T. Protective effects of a vitamin B12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons. Eur J Pharmacol 1993;241(1):1-6.
[9] Kikuchi M, Kashii S, Honda Y, Tamura Y, Kaneda K, Akaike A. Protective effects of methylcobalamin, a vitamin B12 analog, against glutamate-induced neurotoxicity in retinal cell culture. Invest Ophthalmol Vis Sci 1997;38(5):848-54.
[10] Yamatsu K, Kaneko T, Kitahara A, Ohkawa I. Pharmacological studies on degeneration and regeneration of peripheral nerves. (1) Effects of methylcobalamin and cobamide on EMG patterns and loss of muscle weight in rats with crushed sciatic nerve. Folia Pharmacol Japan 1976;72(2):259-68. [Japanese]
[11] Watanabe T, Kaji R, Oka N, Bara W, Kimura J. Ultra-high dose methylcobalamin promotes nerve regeneration in experimental acrylamide neuropathy. J Neurol Sci 1994;122(2):140-3.
[12] Kaji R, Kodama M, Imamura A, Hashida T, Kohara N, Ishizu M, Inui K, Kimura J. Effect of ultrahigh-dose methylcobalamin on compound muscle action potentials in amyotrophic lateral sclerosis: a double-blind controlled study. Muscle Nerve 1998;21(12):1775-8.
[13] Kuwabara S, Nakazawa R, Azuma N, Suzuki M, Miyajima K, Fukutake T, Hattori T. Intravenous methylcobalamin treatment for uremic and diabetic neuropathy in chronic hemodialysis patients. Intern Med 1999;38(6):472-5.
[14] Pezacka E, Green R, Jacobsen DW. Glutathionylcobalamin as an intermediate in the formation of cobalamin coenzymes. Biochem Biophys Res Commun 1990;169(2):443-50.
[15] Turley CP, Brewster MA. Alpha-tocopherol protects against a reduction in adenosylcobalamin in oxidatively stressed human cells. J Nutr 1993;123(7):1305-12.
[16] Yamashiki M, Nishimura A, Kosaka Y. Effects of methylcobalamin (methyl B12) on in vitro cytokine production of peripheral blood mononuclear cells. J Clin Lab Immunol 1992;37(4):173-182.
[17] Shimizu N, Hamazoe R, Kanayama H, Maeta M, Koga S. Experimental study of antitumor effect of methyl B12. Oncology 1987;44(3):169-73.
[18] Choi SW. Vitamin B12 deficiency: a new risk factor for breast cancer? Nutr Rev 1999; 57(8):250-253.
Ed Sharpe, 1999
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MACULAR DEGENERATION AND NUTRITION
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1. Non-smokers with early macular degeneration (ARMD) who consumed at least 6 mg of lutein (equiv. to 2-4 oz spinach) each day were 57% less likely to develop advanced macular degeneration than those who consumed the lowest levels of that nutrient. Seddon, et al. JAMA 1994 Nov 9;272(18):1413-20
2. Smokers with early macular degeneration who consumed the lowest amounts of carotenoids were nearly 600% as likely to develop advanced macular degeneration than those consuming the highest amounts. Seddon, et al. J. Amer Med Assoc; 1994.
3. In a clinical trial 60% of subjects with ARMD or diabetic macular edema receiving 500 mg of vitamin C, 400 IU of vitamin E, 15,000 IU of beta carotene and selenium showed either improvement or no further progression of their disease. So Med J, 1987.
4. The evidence suggests that carotenoids and antioxidant vitamins may help to retard some of the destructive processes in the retina and the retinal pigment epithelium that lead to age-related degeneration of the macula. Am J Clin Nutr 1995 Dec;62(6 Suppl):1448S-1461S
5. The minerals copper and zinc are required to synthesize superoxide dismutase and other enzymes in the retina which scavenge free radicals, preventing oxidative damage which plays a role in the development of drusen, an early sign of Age-Related Macular Degeneration. Olin, et al: Proc Soc Exp Biol Med 1995 Apr;208(4):370-7
6. Glutathione and its related enzyme precursor amino acids (N-Acetyl-Cysteine, L-glycine, and glutamine and selenium are protective against damage to human retinal pigment epithelium cells. Sternberg, Davidson, Jones, et al. Invest Ophthalmol Vis Sci 1993 Dec;34(13):3661-8
7. Quercetin protected bovine retinas in vitro from induced lipid peroxidation, especially when combined with vitamin E, suggesting a potential protective effect in ARMD. Ophthalmic Res 1996;28(3):184-92.
8. The ARMD population manifested decreased intake of nutrients vital to cardiovascular health: vitamin E, magnesium, zinc, vitamin B6 and folic acid. Patients with advanced ARMD taking antioxidants twice daily maintained vision in their better functioning eyes significantly better than those taking a placebo. Richer, J Am Optom Assoc 1996 Jan;67(1):12-29
9. Patients with confluent soft drusen, or "pre-wet" ARMD, were found to have evidence of vitamin B6 deficiency. B. Lane, Ann Mtg Amer Coll of Nutrition, 1991.
10. Dietary lutein and zeaxanthin consumption was shown to increase macular pigment density, likely reducing the risk for developing macular degeneration and cataracts. Hammond, et al. Invest Ophthalmol Vis Sci 1997 Aug;38(9):1795-801. Landrum, et al. Exp Eye Res 1997 Jul;65(1):57-62
11. Taurine, an amino acid, has been used with varying degrees of success to treat and stabilize macular degeneration. Altern Med Rev 1998 Apr;3(2):128-36. Oftalmol Zh 1989;(8):463-5
12. After 18 months, subjects with macular degeneration who took antioxidants on a consistent basis were 2.5X more likely to improve on visual acuity testing, and four times less likely to deteriorate in their worst eye, compared to those who took them less consistently. J. Cat Refr Surg, Mar 1991.
13. Persons with levels of lycopene, the most abundant carotenoid in the serum, in the lowest quintile were twice as likely to have ARMD as those in the highest quintile. Arch Ophthalmol, Dec. 1995
14. General measures for prevention and remediation of macular degeneration would include improving metabolic and vascular functions through a combination of supplementation with trace elements, antioxidants and other vitamins, ozone therapy, increasing physical fitness, improving nutrition (e.g. avoiding hydrogenated oils), abstaining from smoking, and protection from excessive light exposure. Eur J Med Res 1997 Oct 30;2(10):445-54
15. There was a borderline association between age-related macular degeneration and both serum selenium levels and current smoking status. Doc Ophthalmol 1992;81(4):387-400
16. There was an inverse relationship between dietary pro-vitamin A carotenoid and vitamin E consumption and the incidence of large macular drusen, and between zinc and the incidence of pigmentary abnormalities. Am J Epidemiol 1998 Jul 15;148(2):204-14
17. Subnormal zinc and vitamin E serum levels may be associated with the development of age-related macular degeneration. Ishihara, et al. Nippon Ganka Gakkai Zasshi 1997 Mar;101(3):248-51
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MORE FEEDBACK ON BRAIN LIGHTNING
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Taking Brain Lightning for 2 weeks I have noticed -- reduced left hand tremor of 11 years For past MD consultations -- its very common and live with it basically. So, I've lived OK with it but kept an eye out for "solutions". The tremor is task related -- cups, soup spoons, can't handwrite, do anything miniature, put on lipstick, draw, must use two hands, or other hand, stressful and slow. Picture Framing is my home business and I am trying to reestablish. In spite of "handicap". The hand work takes me longer with a "difficulty" I don't know exactly how to describe. I have done OK with it now looking for the creative energy I seemed to have lost and the Brain Lightning has been a boost. New project schedule to finish 11 botanical prints with special mat designs and it's been going so smoothly with pleasing perfect results. And bonus -- better nutrition, being back in the kitchen with improved knife, measuring, cooking skills. What a pleasure to eat soup with my left hand -- I have been super with chopsticks though these years, better than fork so CS most used. And I am surely more relaxed about all this. Never really uptight, got rid of self consciousness using two hands for the simple task of writing in front of people. I've devised ways to deal with it. Glad to share feedback. I do not write well. There were Neurologist exams and prescriptions (stopped 3 yrs ago) on the downward side and then there is Brain Lightning, the best treatment. I am very exited about this. I noticed a difference in a few days. I was with my parents last night and told my father about the Brain Lightning, his response to the reduced tremor was great without expected skepticism since the proof was in the soup and spoon at dinner. Has known about it but not as a big concern -- he has referred me to good practitioners/specialists, and as an MD asked what was in it. I could remember [another plus for BL] the majority of the ingredients and will give him more information. I'm gladly paying more attention to this new development!
Thank you.
Donna Walter, 56
I have been using Brain Lightning for about eight months now, using about three each day. I seem to get a real boost in concentration during the day that really assists me in my work. It seems to extend my ability to maintain mental clarity for longer periods, which is something that any physician would value highly.
H. Limmer, M.D.
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Memory Starts To Decline In Our 20s, Researcher Finds
UNIVERSITY OF MICHIGAN
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http://www.umich.edu/~newsinfo/Releases/2001/Aug01/r081301a.html
People in their 20s don't usually complain about forgetting names or phone numbers or having trouble learning something new. But that's when memory and mental energy first start to decline, according to psychologist Denise Park. Park directs the Center for Aging and Cognition at the University of Michigan Institute for Social Research (ISR).
In studies of more than 350 men and women between the ages of 20 and 90, to be presented Aug. 24 in San Francisco at the annual meeting of the American Psychological Association, Park found that mental aging is a slippery slope, with continuous declines in processing power starting as soon as our 20s.
This gradual reduction in cognitive capital is not really noticeable until the loss is substantial enough to affect everyday activities.
"Younger adults in their 20s and 30s notice no losses at all, even though they are declining at the same rate as people in their 60s and 70s, because they have more capital than they need," says Park, who appears in "The Secret Life of the Brain," a new PBS series funded by the National Science Foundation.
By the time people are in their mid-60s, Park says, the continuous decreases in cognitive abilities may become noticeable. Just when most people are becoming more frequent consumers of medical services, they begin to notice that they are having more trouble remembering and learning new information.
Older people are also much more susceptible to memory distortions such as the "illusion of truth" and the "paradox of repeated denial." Older men and women are more likely to recall false information as being true, Park explains, and the more warnings they hear about a bogus medical claim -- that shark cartilage cures arthritis, for example -- the more likely they are to believe that the claim is true. The bogus information feels familiar if it has been heard often, and thus it seems true.
Younger adults can remember that the information is familiar, but they also remember hearing that it is false.
But there is good news, too. An increase in experience and general knowledge, as measured by vocabulary, compensates for many of the losses, Park has found, with the crossroads coming around the age of 50 -- traditionally considered the beginning of wisdom.
With a grant from the National Institute on Aging, Park is now using neuroimaging techniques such as functional magnetic resonance imaging (fMRI) to study what goes on in the brains of younger and older minds at work.
By linking behavioral testing and neuroscience, she is studying what parts of the brain older adults use for different types of mental tasks compared to younger adults, and what patterns of brain activation high-performing older adults show compared to their lower-performing peers.
"Cognitive performance is a direct result of brain activity and brain structure," she says, "much like cardiovascular fitness relates to our ability to exercise and perform physical tasks.
Only 40 years ago, we had little understanding of how smoking and cholesterol levels were related to cardiovascular health," Park says. "It's likely that just as diet and exercise help to keep our bodies fit and healthy, we'll find ways to improve the functioning of our aging minds."
Established in 1948, the Institute for Social Research (ISR) is among the world's oldest survey research organizations and a world leader in the development and application of social science methodology.
ISR conducts some of the most widely-cited studies in the nation, including the Survey of Consumer Attitudes, the National Election Studies, the Monitoring the Future Study, the Panel Study of Income Dynamics, the Health and Retirement Study and the National Survey of Black Americans.
ISR researchers also collaborate with social scientists in more than 60 nations on the World Values Surveys and other projects, and the Institute has established formal ties with universities in Poland, China, and South Africa.
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Snack Foods Seem To Hike Risk Of Macular Degeneration
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Higher consumption of specific types of dietary fat commonly found in snack foods may be associated with an increased risk of advanced age-related macular degeneration, according to a paper in the August issue of the Archives of Ophthalmology.
Age-related macular degeneration is the leading cause of blindness and vision impairment in the United States.
Johanna M. Seddon, M.D., lead author and associate professor, Ophthalmology, Harvard Medical School, and Director Epidemiology at the Massachusetts Eye and Ear Infirmary, and co-authors found that a higher intake of specific types of fat, including vegetable, monounsaturated and polyunsaturated fats and linoleic acid may be associated with a greater risk for advanced AMD. Foods with higher levels of these fats overall tend to be highly processed, store-bought snack foods.
On the other hand, diets high in omega-3 fatty acids, which are primarily found in certain types of fish such as albacore tuna and salmon, were inversely associated with the risk for AMD when intake of linoleic acid (found in processed food and margarine), was low, said Seddon.
"Since the impact of AMD on our growing elderly population is rising, finding means of prevention is of utmost importance. Thus far only cigarette smoking is a well-established, modifiable risk factor. Additional studies of dietary factors might lead to nutritional means to reduce the risk for development of this important disease among susceptible individuals," Seddon said.
Based on the results of this study, the recommendations are to avoid highly processed snack foods and to consume two or more servings of fish high in omega-3 fatty acids per week to lower the risk of developing AMD.
The multi-center study took place at the Massachusetts Eye and Ear Infirmary, Manhattan Eye, Ear and Throat Hospital in New York, the Wilmer Eye Institute in Maryland and the University of Illinois at Chicago.
Founded in 1824, the Massachusetts Eye and Ear Infirmary is an international center for treatment and research and a teaching hospital of Harvard Medical School.
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For Aging Brains, Two Hemispheres Are Better Than One
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Source: University Of Michigan (http://www.umich.edu)
Date: Posted 8/20/2001
ANN ARBOR --- Older adults actually use different regions of the brain than younger adults to perform the same memory and information processing tasks, according to University of Michigan research to be presented Aug. 24 at the annual meeting of the American Psychological Association in San Francisco.
The research, conducted by U-M cognitive neuroscientist Patricia Reuter-Lorenz and colleagues and funded by the National Institute on Aging, provides intriguing clues about how older adults compensate for some of the age-related declines in short-term memory and mental speed that plague so many older Americans.
"Older adults activate both hemispheres of the brain to remember what younger adults can remember using just one hemisphere," says Reuter-Lorenz, who has just received a new grant from the NIA to continue her research.
In the APA presentation, and in a series of recent publications in the Journal of Cognitive Neuroscience and the Proceedings of the National Academy of Science, Reuter-Lorenz and colleagues report on the findings of a series of studies that use functional positron emission tomography (PET) images to elucidate how the aging brain works. Not only have they found that as we age, two hemispheres are better than one, they have also discovered that in older adults, unexpected regions of the brain are activated for verbal and spatial memory tasks.
When younger adults hold information in short-term memory, like rehearsing a phone number, they activate a network of brain regions involved in speech and short-term verbal storage. Older adults activate these areas also, but show additional activation of a frontal cortex region that young adults use only when performing complex short-term memory tasks.
In one study, older and younger subjects were shown four letters, then asked to determine if a letter presented a few seconds later matched any of the initial four. As expected, Reuter-Lorenz found that seniors made more errors and were slower at the task than young subjects. And PET scans of the subjects' brains while they were being tested showed that older subjects activated more areas of the brain in both hemispheres than young subjects, who showed activity mainly in the left hemisphere.
In another study of spatial memory, subjects were shown a group of marked locations on a screen, then presented a few seconds later with a single mark and asked to determine whether its position matched any in the earlier group. Reuter-Lorenz again found different activation patterns for younger and older subjects. Younger subjects showed greater right hemisphere activation, while older subjects activated both left and right hemispheres.
"Recruiting additional regions of the brain seems to assist older adults in basic memory storage tasks," Reuter-Lorenz says. "But when it comes to more complex processing tasks, this strategy isn't as successful."
When seniors and young subjects were asked to determine the accuracy of a math calculation ((10x9) + 8 = 98), their performance was equivalent. But when subjects were presented with a word in addition to the math problem, and asked to remember it, the performance of seniors dropped dramatically.
Because regions at the front of the brain, in the area known as the dorsolateral prefrontal cortex (DLPFC), were "recruited" by the seniors for the simple short-term memory task, Reuter-Lorenz believes that these regions may have been preoccupied and less available for the more complex tasks.
Overall, though, Reuter-Lorenz believes that older adults benefit from bi-hemispheric processing. Using two hemispheres instead of one, and more of the brain overall, may allow seniors to compensate for some of the mental declines that come with age, she suggests. Moreover, by identifying precisely which areas of the brain seniors are using to remember and process information, she hopes that scientists and physicians will be able to develop more effective interventions to help seniors maintain and improve brain function well into old age.
Editor's Note: The original news release can be found at http://www.umich.edu/~newsinfo/Releases/2001/Aug01/r081501a.html
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