Nurses Role in Promoting Healthy Diet for Elderly with Dementia - Assignment Example

Running hed THE NURSES ROLE IN PROMORTING HELTHY DIET FOR OLDER PEOPLE WITH DEMENTI The nurses role in promoting helthy diet for older people with dementi Nme of the School Nme of the Student Introduction The older dult popultion is expected to more thn double between now nd 2040, tripling the number of people ge 85 yers nd older (Henderson, Jorm, 1998). This trend, combined with the socil nd helth cre needs tht ccompny dvnced ge, poses present nd imminent chllenges to the socil work profession. Of prticulr concern is the growing mgnitude of diseses tht cuse dementi nd ffect lot of people now. lzheimer's disese is the most common form of dementi nd currently ffects over 13 million people worldwide. The direct nd indirect cost of lzheimer cre is over $100 billion ( 81 billion) in the US lone. The direct cost of lzheimer cre in the UK ws estimted t 15 billion ( 22 billion)(Melding, 2005) Helth cre socil workers in community nd institutionl settings serve in the role of strengthening nd supporting fmily members cring for people with dementi. Therefore, it is essentil tht prctitioners understnd the effects nd the dynmic nd chnging nture of cregiving so tht interventions my be tilored ppropritely to meet the needs of those t vrious junctures in the cregiving experience. For exmple, competent nursing home socil workers must be knowledgeble bout the psychosocil effects of plcement on cregivers so they cn develop pproprite nd supportive services for fmily members. To the sme extent nurses should be wre of dieting effects on dementi tht cuse progression of disese if not tken into creful considertion. In the following pper I m going to tke look into the importnce of nursing in promoting helthy diet for older people with dementi. Discussion will be bsed round the disese of dementi of the older popultion since these re the people tht re more reluctnt to this type of mentl disorder. 1. Defining Dementi First, let me clrify few terms. 'Dementi' is term used mediclly to describe syndrome (set of symptoms) tht is cused by mny different diseses. These include lzheimer's disese, vsculr dementi nd dementi with Lewy bodies. n nlogy is the term 'cncer', which is used to describe ny mlignnt tumour but is not itself specific disese. The nswer to the frequently posed question 'Wht is the difference between lzheimer's disese nd dementi' is tht, in sense, there is no difference-lzheimer's disese is one of the mny different types of dementi. (Brodty, 2001) The dementi syndrome is defined s n cquired decline in memory nd thinking (cognition) due to brin disese tht results in significnt impirment of personl, socil or occuptionl function. Other brin functions tht re ffected include orienttion, comprehension, clculting bility, lerning cpcity, lnguge, judgement, resoning nd informtion processing. While there re some notble exceptions, s I discuss lter, dementi is usully of grdul onset nd progressive. The World Helth Orgniztion (WHO) guidelines recommend tht these symptoms nd impirments be evident for t lest six months before confident dignosis cn be mde. While most dementis re currently irreversible, this does not men tht dementi is untretble. Its progression (course) cn often be influenced nd mny symptoms cn be meliorted. s I discuss in lter chpters, mjor dvnces hve occurred over the lst decde in this re. (Brodty, 2001) Most dementing illnesses re progressive, nd erly symptoms nd problems differ mrkedly from those in lter stges. This my simply be mtter of degree-for exmple, mild memory impirment moving to profound memory impirment. Other symptoms nd problems usully develop lter in the course of the illness, urinry incontinence being one exmple. While it is customry to describe dementi in stges, there is overlp between stges nd it my not lwys be esy to stte precisely which stge person hs reched. The first stge is 'pre-dementi' stge, lso nmed by some reserchers 'mild cognitive impirment'. Currently we re unble to identify ccurtely nd relibly wht it constitutes. The next three stges, s commonly described to crers during dignostic ssessment, re 'erly' or 'mild', 'moderte' or 'middle' nd 'lte' or 'severe' dementi, respectively. The finl stge, 'dvnced dementi', is usully found only in nursing home residents. The stges should be regrded s guideline rther thn s scrosnct sttement bout the person's progress (Mthers, Vos, Stevenson, 2004). 2. Connecting diet nd dementi progression. Diet cn ffect person's risk of developing mny types of illness, including dementi. helthy nd blnced diet, which enbles person to mintin norml body weight, is likely to reduce the likelihood of developing high blood pressure or hert disese, both of which put person t greter risk of developing dementi. Too much sturted ft cn cuse nrrowing of the rteries, mking hert ttck or stroke more likely. Hert ttcks, strokes nd vsculr disese increse person's risk of developing vsculr dementi. See the Society's informtion sheet nd its booklet Understnding vsculr dementi for further informtion. Fresh fruit nd vegetbles contin mny vitmins nd nti-oxidnts, which my prevent hert disese nd protect the brin. number of reserch studies hve shown tht the polyunsturted ftty cids found in oily fish might lso help to protect the hert nd blood vessels, nd lower the risk of developing dementi. Some reserch hs suggested tht cffeine nd vrious spices nd herbs, including curcumin, sge, lemon blm nd ginkgo bilob, might hve protective effect on the brin. However, reserch is continuing nd there is no conclusive evidence s yet. Recent studies suggest tht vitmin might be protective for the brin nd tht vitmin E might help to improve the symptoms of dementi Eting Mediterrnen diet could cut the risk of lzheimer's disese by s much s 40 per cent, sys lrge US study. The Med diet, rich in cerels, fruits, legumes nd whole grins, fish nd olive oil, hs been linked to longer life, less hert disese, nd protection ginst some cncers. The diet's min nutritionl components include bet-crotene, vitmin C, tocopherols, polyphenols, nd essentil minerls. The new cohort study, published on-line in the nnls of Neurology, followed 2258 elderly New Yorkers with no dementi for bout four yers. The diets of the subjects were mesured using semi-quntittive food frequency questionnire, nd 'Mediterrnen Diet' score ws determined. (Jorm, 2002) The reserchers lso gthered medicl nd neurologicl histories, performed physicl nd neurologicl exms, nd interviewed ech of the prticipnts in-person. Subjects were ressessed every 18 months. "Higher dherence to the Mediterrnen diet ws ssocited with significntly lower risk of developing lzheimers disese," wrote led uthor Nikolos Scrmes from Columbi University Medicl Center. Scrmes nd his collegues found tht ech incresing point on the Med diet score ws linked with 10 per cent drop in lzheimer's risk. Individuls whose diet closely resembled the Med diet hd 40 per cent lower risk of lzheimer's thn those who dhered the lest to the diet. The ssocition ws still significnt if the scientists djusted the results to tke into ccount fctors like ge, gender, ethnicity, BMI nd smoking, for exmple. The study hs severl limittions, including the use of food frequency questionnires (FFQ) to determine dietry intkes. However, in this instnce the scientists sy tht the FFQ would underestimte the effect. (Jorm, 2002) nother limittion could be tht people chnged dietry hbits throughout the four yers of study. gin, the scientists rgue tht this would not chnge the results significntly since complince to the diet ppered constnt. Professor Clive Bllrd, director of reserch for British Chrity, the lzheimer's Society, sid tht the study mde n importnt contribution to growing body of literture linking dietry lifestyle nd the risk of lzheimer's. There hve been number of studies looking seprtely t the benefits of eting fruit, vegetbles nd oily fish for reducing your risk of lzheimer's disese. This study supports the ide tht eting combined diet of plenty of fruit, vegetbles nd fish might help to prevent dementi. It is likely tht the reson for this is combintion of fctors. It is thought tht fruit nd vegetbles cn help to lower blood pressure nd tht the nti-oxidnts found in them, including vitmins C nd E, could prevent hert disese, lessening the risk of dementi s well s directly ffecting potentilly brin-dmging free rdicls," sid Bllrd. (Check, 2003) Professor Bllrd emphsized tht eting helthy diet, regulr exercise, nd weight wtching could reduce the risk of developing dementi in lter life. 3. Chnges in eting behvior during dementi Eting behviour chnges in vriety of wys in moderte to severe dementi but 'refusl to et' cuses gretest concern, especilly when it is ssocited with weight loss, which tends to hppen in most persons with severe dementi nywy. 'Refusl to et' encompsses rnge of issues nd in mny cses is n inccurte description of wht is hppening. The coordintion required to use knives nd forks to et declines due to the dementing process, nd sometimes food left untouched simply reflects this loss of function. Most persons with severe dementi need to be fed, but some spit out the food, push it wy or won't open their mouths. s dementi becomes more severe, the bility to et flls off. The mstictory process becomes uncoordinted, chewing my be ineffective, tongue movements my fil to prepre the food bolus to be swllowed, nd the swllowing reflex my be incompetent. (Engelhrt et l., 2002) These re ll good resons for pprent food refusl. Other fctors tht my contribute to 'refusl to et' include the qulity of the food, ill-fitting or bsent dentures, inbility to see the food due to poor eyesight nd the lck of socil milieu tht encourges eting. Mny crers become concerned tht food refusl my be due to the dementing person 'giving up' in depressed mood, nd this my occsionlly be the cse. (Engelhrt et l., 2002) Other chnges in eting behviour, which my become pprent in erlier stges of dementi, include predilections for certin food such s sweets nd chocoltes, overeting, eting of inedible objects (pic) nd n ltertion in tste which my be relted to reduced sense of smell. (Engelhrt et l., 2002) 4. Dementi nd the role of ntioxidnts Incresing ge is the most estblished risk fctor for dementi, though there is still debte bout whether the risk continues to increse fter the ge of 90. Some uthorities believe tht there my be reduction of the risk; others suggest tht the rte of dementi in centenrins my be t lest 70 per cent. It lso remins uncler whether the incresed rtes of dementi in old ge re cused by the geing process itself or by other diseses or events tht re themselves ge-relted. Obviously we do not wnt to prevent person from getting older, but better understnding of the geing process nd of fctors tht enhnce its effects my led to some useful prevention strtegies. (Morris et l., 2005) One prticulr strtegy involving the ingestion of ntioxidnts my lredy be informlly in plce. ntioxidnts potentilly hve role in preventing dementi. s the brin ges, its cpcity to remove certin hrmful smll molecules known s 'free rdicls' is reduced, resulting in cell deth nd incresed susceptibility of nerve cells to other fctors tht cuse dmge. The brin cells' nturl defences ginst this dmge include mnufcturing ntioxidnts tht mop up free rdicls, but with ge some of these protective mechnisms decline. Curcumin (from the herb turmeric), lph-lipoic cid, flvonoids, vitmin B 6, vitmin C, vitmin E nd vitmin re just few of the mny ntioxidnts vilble on the shelves in helth food stores. number of these substnces hve been exmined for their bility to prevent lzheimer's disese, vsculr dementi or cognitive impirment, but the results so fr re equivocl. Vitmins C nd E There is modest evidence tht vitmins C nd E my hve protective role ginst dementi. The Honolulu-si ging Study found tht older men who took supplements of vitmins C nd E hd lower rtes of vsculr dementi nd cognitive impirment but not lzheimer's disese. n epidemiologicl study published in the influentil Journl of the mericn Medicl ssocition (JM) in June 2002 suggested tht eting foods rich in ntioxidnts (such s fibres, grins, fish, green vegetbles), especilly vitmin E (but not vitmin E supplements), my help lower the risk of developing lzheimer's disese. 5 second study published in the rchives of Neurology in July 2002 found vitmin E to be protective ginst memory decline. (Foley, White, 2005) n editoril in JM concluded tht while the studies were not conclusive s to whether ntioxidnt vitmins re truly protective ginst lzheimer's disese (becuse of weknesses in their design), they supported the view tht dietry ntioxidnt vitmins my prevent the development of lzheimer's disese. 7 The optiml dose of vitmin E is not known. Mny doctors recommend 500 interntionl units (IU) twice dily; this level is sfe for most individuls nd should hve the ntioxidnt effect desired in the brin. However, people tking nticogulnts such s wrfrin my not be ble to tke vitmin E, nd should be monitored closely by their doctor. t lest five clinicl trils re currently underwy specificlly to exmine the role of vitmins C nd E nd other ntioxidnts in preventing memory decline nd lzheimer's disese; until the results of these trils re vilble, it is unknown whether vitmin supplements will prevent lzheimer's disese. (Foley, White, 2005) lcohol (red wine) It is well estblished tht excessive lcohol intke, usully in combintion with thimine deficiency, cn cuse brin dmge. One well-known type of brin dmge is the Wernicke-Korskoff syndrome, in which profound short-term memory impirment occurs. Unlike dementi, this is not progressive condition but it is irreversible, leving the sufferer severely impired even when lcohol consumption ceses. More controversilly, lcohol hs long been regrded s cuse of dementi, lthough occurs. Unlike dementi, this is not progressive condition but it is irreversible, leving the sufferer severely impired even when lcohol consumption ceses. More controversilly, lcohol hs long been regrded s cuse of dementi, lthough precise brin pthology hs not been estblished. (Ruitenberg, 2002) Epidemiologicl studies hve not demonstrted tht lcohol is risk fctor for dementi. Indeed, s demonstrted in the Rotterdm Study, light to moderte drinking (one to three drinks per dy) ws significntly ssocited with lower risk of ny dementi, nd vsculr dementi in prticulr, in individuls ged 55 yers or older. The effect seemed to be unchnged by the source of lcohol. 8 However, some studies hve suggested tht red wine my hve prticulr benefit. The flvonoids in wine- powerful ntioxidnt substnces lso contined in te, fruits nd vegetbles-hve been thought to offer protection. One study hs found tht the intke of ntioxidnt flvonoids ws inversely relted to the risk of dementi. 9 While these findings my give some encourgement to drink lcohol in old ge, few words of cution re required. For some individuls there my be fine line between potentilly beneficil mount of lcohol nd deleterious mount. Further, women experience the deleterious effects of lcohol t much lower mounts thn men. Until prospective controlled studies of light to moderte lcohol intke re undertken, it remins n unproven preventive strtegy. In those who hve estblished dementi, reltively smll mounts of lcohol cn cuse incresed confusion nd behviourl chnges. The lck of strong evidence for the effectiveness of ntioxidnts in the prevention of dementi should not be viewed too negtively. The lck of evidence does not men tht they re ineffective-it is just tht to determine whether prticulr ntioxidnt my be effective requires very lrge, rndomised, plcebo-controlled studies, such s the trils underwy in the United Sttes involving thousnds of subjects monitored over mny yers. (Foley, White, 2005) 5. Dementi nd brin reserve in older people Low levels of forml eduction hve been found to be ssocited with higher levels of cognitive impirment, dementi in generl nd lzheimer's disese in prticulr. nother wy of looking t it is tht people with higher levels of eduction re less likely to develop dementi. In one Cndin study, people with more thn ten yers of eduction were four nd hlf times less likely to hve dementi thn those with less thn six yers of eduction. Pooled dt from Europen studies, however, hs suggested tht the effects of eduction my only occur in women. (Schofield, 2002) The mechnism of this reltionship between eduction nd dementi is uncler but there re number of possibilities. One possibility is tht low level of eduction my be proxy for deleterious environmentl influences. nother is tht high level of eduction my be proxy for intelligence, s more intelligent people re likely to obtin more forml eduction. The evidence tht low intelligence my be linked with the development of dementi is quite vried. Lower premorbid intelligence hs been found to predict the development of dementi in elderly people. More generlly, lower premorbid intelligence predicts worse cognitive outcome following hed injury. Possibly the most intriguing evidence, however, is the Nun Study, in which cohort of elderly Romn Ctholic nuns were ssessed, with number hving their brins studied post-mortem. Diry entries written in their lte teenge yers were exmined for linguistic bility. Low linguistic bility during the teenge yers ws ssocited with lzheimer's disese brin pthology t utopsy. One interprettion of these findings hs been tht incipient lzheimer's disese ws lredy present in the teenge nuns; certinly, it hs been shown tht the pthologicl chnges of lzheimer's disese my be present for 30 to 50 yers before its clinicl onset. nother interprettion is tht the linguistic bility ws proxy for intelligence. (Schofield, 2002) So how might intelligence reduce the risk of dementi One hypothesis, proposed by Peter Schofield from the University of Newcstle, UK, is tht more intelligent people hve lrger 'brin reserve'. The concept of brin reserve is bsed on the fct tht our brins crry redundnt neurons tht ct s type of bck-up in times of need. In this hypothesis, when the brin is dmged, for exmple by stroke or through the grdul development of lzheimer's disese, the brin reserve comes into ply to replce or cover for the dmged cells. If the brin reserve is indequte to cover for the dmge, the threshold of the disese is reched nd the person becomes symptomtic. Thus the lrger the brin reserve, the greter the dmge tht cn be sustined before symptoms occur. Whether this effect is due to there being 'further to fll' before reching disese threshold, or whether the lrge brin reserve in some wy resists the neuropthologicl chnges, for exmple through greter cognitive flexibility, is uncler. Whtever the model, person with lrge brin reserve my hve incipient lzheimer's disese for mny yers nd be symptomtic. In this sitution, intelligence is delying the onset of dementi. Other importnt fctors contribute to brin reserve. ny physicl dmge to the brin my reduce the reserve. This ties in with the finding tht hed injuries cusing loss of consciousness for t lest fifteen minutes my increse the risk of lzheimer's disese up to twofold, though the studies re inconsistent nd possibly the most methodologiclly sound prospective study hd negtive result. Boxers my develop 'dementi pugilistic' due to repeted blows to the hed nd recently Jeff stle, former Englnd soccer interntionl, ws found to hve died from degenertive brin disese cused by 'heding' the soccer bll, skill for which he ws fmous. Other types of previous brin dmge, including strokes, nd mentl retrdtion my lso increse the likelihood of dementi occurring. Brin size is nother fctor-the lrger the brin, the lrger the brin reserve. This my be linked with intelligence, s more intelligent people tend to hve lrger brins. People with lrger brins, s mesured by CT scns, MRI scns or hed circumference, re less likely to develop the symptoms of lzheimer's disese, even if they hve the fetures of the disese in their brins t utopsy. Mentl ctivity lso influences brin reserve. It is possible tht mentl ctivity enhnces neuronl integrity through the ction of better cerebrl blood flow in reducing levels of stress nd improving DN repir. More tntlisingly, it my lso enhnce brin growth. number of studies hve shown tht engging in vrious forms of intellectul ctivity through life, even in the sixth nd seventh decdes, my protect ginst cognitive decline nd enhnce memory function. In study published in JM in 2002, investigtors from Rush Presbyterin St Luke's Medicl Centre in Chicgo followed 801 older Ctholic nuns, priests nd brothers for lmost five yers, trcking their everydy ctivities: reding the newspper, listening to the rdio, plying gmes such s chess, or wtching television. They found tht those clergy who did three or more of these things t lest severl times week were lmost 50 per cent less likely to develop lzheimer's disese thn those who red, listened to the rdio nd plyed gmes only few times month. It my not just be the quntity of mentl ctivity tht is importnt. Deciding to stimulte your brin through series of repetitive, boring mentl exercises, or putting pressure on yourself by tking on n intellectul pursuit tht is well beyond your cpcity, my both be detrimentl. uthors of memory books often recommend mentl exercises tht include 'pegging' numbers to words for esier recll, visulising pictures with numbers nd words, crossword puzzles, logic nd grph puzzles, nd exercises to improve the recll of word lists. Unless you enjoy doing these things they re unlikely to be of much benefit. Put simply, the mentl ctivity should be fun! The implictions of these findings re tht erly life events my influence the development of dementi nd tht prticipting in vried mentl nd physicl ctivities through life my imprt protective role. 6. Cerebrl blood flow. The Chinese herb Ginkgo bilob is thought to increse circultion to the brin. In Europe nd some sin countries, stndrdised extrcts from ginkgo leves re tken to tret wide rnge of symptoms, including dizziness, inflmmtion nd reduced blood flow to the brin nd other res of impired circultion. It is routinely prescribed in Europe for memory problems nd lthough there is some evidence tht it my be beneficil, the studies re not strong. The US Ntionl Institute on ging helped fund tril in which 2000 older dults t risk of dementi took dily doses of ginkgo or plcebo; the results, relesed in ugust 2002, were negtive. One of the problems with existing studies is tht mny different strengths nd types of ginkgo preprtions hve been used, nd it is uncler if there is n optiml nd sfe dosing regime. However, Germny recently pproved ginkgo extrcts (240 mg dy) to tret lzheimer's disese nd this my give some guide. Too often it is incorrectly presumed tht ll herbl remedies re sfe, nd it should be noted tht ginkgo cn cuse stomch bleeding, especilly when tken with spirin. Physicl exercise cn increse cerebrl blood flow, which my in turn be beneficil for mentl function. There re certinly studies tht demonstrte tht exercise cn improve memory nd mood, though none hve specificlly shown tht exercise prevents dementi. There re mny vlid resons for embrcing physicl exercise; it would not be surprising if it turns out tht dementi prevention is nother benefit. 7. Nutrition Vitmin B 12, Vitmin B 6 nd folte-the role of homocysteine Vitmin B 12 (coblmin), vitmin B 6 (pyridoxine) nd folte ply vitl roles in effective DN synthesis nd norml brin metbolism. These B-group vitmins ct s ctlysts in chemicl rections in which homocysteine is converted to methionine, nd dietry deficiencies cn result in build-up of serum homocysteine. High levels of homocysteine hve been linked with lzheimer's disese, vsculr dementi, cerebrovsculr disese nd cognitive impirment in generl. In ddition, vitmin B 12, vitmin B 6 nd folte deficiencies re known to cuse depression nd other neurologicl syndromes. Wht is uncler t present is whether these ssocitions reflect cusl mechnism between high levels of homocysteine nd dementi. There is some evidence tht high levels my excerbte cognitive impirment fter cute stroke, so there my be n dditive effect. Certinly, homocysteine provides nother link between lzheimer's disese nd cerebrovsculr disese, but the extent to which it my be responsible for either condition is not known. Probbly the most importnt issue is tht there is simple tretment for preventing high levels of homocysteine. diet rich in green lefy vegetbles, low-ft diry products, citrus fruits nd juices, wholewhet bred nd dry bens cn significntly lower levels of homocysteine. Since 1998, the US Food nd Drug dministrtion (FD) hs required the ddition of folic cid to enrich breds, cerels, flours, corn mels, psts, rice nd other grin products, but it is too soon to know whether this will reduce the rte of dementi. In UK, where folte enhncement of grin products does not routinely occur, folte supplements could be considered. In individuls with norml folte levels but elevted homocysteine levels, low dose folte supplementtion (50 microgrms dily) should suffice, while individuls with folte deficiency my require up to 5 milligrms dily until the deficiency is overcome before reverting to lower dose. Of course, vitmin B 12 replcement is required if tht vitmin is deficient. Unfortuntely there hve been no rndomised controlled studies of folte supplementtion for the prevention of dementi. While it is specultive to suggest it s resonble prevention strtegy, it is unlikely to be of hrm nd my hve other crdiovsculr benefits. Folte supplementtion could be regrded s universl preventive mesure suitble for the entire popultion. Fish recent French study hs reported tht the consumption of fish t lest once week reduces the risk of dementi by one-third over seven-yer period. This protective effect my be explined by the omeg-3 polyunsturted ftty cids contined in fish oils, which hve protective effect ginst crdiovsculr disese nd hence on the vsculr risk fctors implied in vsculr dementi nd lzheimer's disese. They could lso hve specific effect on brin development nd neuroprotection, though this is unproven. nother fctor my be eduction; this ws found to exert n independent effect, with more highly educted older people eting more fish. Cffeine Whether or not this is the best plce to del with cffeine is debtble-while for some of us cffeine is mjor nutrient, there my be rgument bout it! There hs long been evidence in the test tube tht cffeine my hve potentil role in treting lzheimer's disese. Cffeine belongs to fmily of chemicls tht includes drugs such s propentofylline, currently in the finl pre-licensing stges by the USFD s tretment for lzheimer's disese. (Hogervorst, 2003) Propentofylline cts by modulting the ctivity of glil cells in the brin. Cffeine itself hs been shown to stimulte nerve cells to tke in more choline, the building block for cetylcholine, the most importnt neurotrnsmitter for memory function. Cffeine lso blocks receptors for denosine, nother neurotrnsmitter, function thought to be of potentil therpeutic benefit in lzheimer's disese. (Hogervorst, 2003) In July 2002, the first clinicl evidence tht cffeine consumption might be ssocited with lower rtes of lzheimer's disese ws published in cse control study. The study hs numerous weknesses but does point to the need for lrger, prospective studies. t this stge, however, there is insufficient evidence to recommend the use of cffeine to prevent lzheimer's disese. It should be remembered tht cffeine cn hve dverse effects on sleep nd on the hert, nd cn increse nxiety. (Hogervorst, 2003) Conclusions Trditionl strtegies to prevent disese hve focused upon disese elimintion. In the cse of dementi, dely in the onset of the disese my hve preventive effect s potentil victims my die of other disorders before they develop dementi. n understnding of risk nd protective fctors for dementi is required before ny preventive strtegies cn be undertken. Universl prevention strtegies re those tht cn be pplied to the whole popultion. Most universl strtegies to preventing dementi re esy to pply, hve wide rnge of helth benefits nd few, if ny, drwbcks. Exmples include dietry chnges to improve ntioxidnts in our food, continuing physicl exercise nd continuing eduction. The extent to which these strtegies my reduce the risk of dementi is uncler, but they re unlikely to hrm. 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