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Obesity, Weight Loss, and Low Back Pain: An Overview for Primary Care Providers—Part 2

Obesity, Weight Loss, and Low Back Pain: An Overview for Primary Care Providers—Part 2

Members of the College of Family Physicians of Canada may claim MAINPRO-M2 Credits for this unaccredited educational program.

www.cfpc.ca/Mainpro_M2
Teaser: 

1,2Darren M. Roffey PhD; 1Simon Dagenais DC, PhD, MSc; 3Ted Findlay DO, CCFP; 4,5Travis E. Marion MD, MSc; 6Greg McIntosh MSc; 7,8Mohammed F. Shamji MD, PhD, FRCSC; 1,2,4,5Eugene K. Wai MD, MSc, FRCSC

1University of Ottawa Spine Program, The Ottawa Hospital, Ottawa, ON, 2Clinical Epidemiology Program, Ottawa Hospital Research Institute, Ottawa, ON,

3
Department of Family Medicine, University of Calgary, Calgary, AB, 4Division of Orthopaedic Surgery, The Ottawa Hospital, Ottawa, ON, 5Department of Surgery, Faculty of Medicine, University of Ottawa, ON, 6CBI Health Group, Toronto, ON, 7Division of Neurosurgery, Toronto Western Hospital, Toronto, ON,

8Department of Surgery, University of Toronto, Toronto, ON.

Abstract

Obesity and low back pain are equally complex medical conditions with multi-factorial etiologies. Their clinical practice guidelines both include recommendations for screening and examination that can be easily implemented. There is sufficient information to compile a framework for the primary care provider, partnering with the patient and appropriate specialists, to manage obesity and low back pain in a structured fashion. Weight loss and exercise are paramount and should be recommended as the first options. Cognitive behavioural therapy, pharmacological treatment and bariatric surgery may then be implemented sequentially depending upon the effectiveness of the initial interventions.

Key Words: Obesity, low back pain, exercise, nutrition, cognitive behavioural therapy, bariatric surgery, weight loss, pharmacological, evidence-based guideline.

Nutrition and Dementia: A Clinical Update

Nutrition and Dementia: A Clinical Update

Members of the College of Family Physicians of Canada may claim MAINPRO-M2 Credits for this unaccredited educational program.

www.cfpc.ca/Mainpro_M2
Teaser: 

Guylaine Ferland, PhD,Département de Nutrition, Université de Montréal; Centre de recherche, Institut universitaire de gériatrie de Montréal, Montréal, QC.
Carol E. Greenwood, PhD,Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, and Kunin-Lunenfeld Applied Research Unit, Baycrest, Toronto, ON.
Bryna Shatenstein, PhD, PDt, Département de Nutrition, Université de Montréal; Centre de recherche, Institut universitaire de gériatrie de Montréal, Montréal, QC.

Abstract
While prospective epidemiologic studies have provided strong evidence linking higher intakes of many nutrients with slower rates of cognitive decline and reduced dementia risk, randomized controlled trials on supplementation with individual nutrients have largely been disappointing. In contrast, recent research points to substantial benefits for brain aging and cognition from consumption of a varied diet centred on plant-source foods, whole grains and fish, and avoidance of foods rich in saturated and trans fats. An unhealthy dietary pattern, in conjunction with obesity, low physical activity, and smoking, could contribute to a pro-inflammatory state and oxidative stress which could exacerbate risk for development of cognitive decline the metabolic syndrome, diabetes, and cardiovascular disease.
Keywords: nutrition, dementia, Alzheimer's disease, nutrients, dietary patterns.

Nutrition Guidelines for Cancer Prevention: More Than Just Food for Thought

Nutrition Guidelines for Cancer Prevention: More Than Just Food for Thought

Teaser: 


Kristen L. Currie, MA, CCRP, Department of Surgical Oncology, Division of Urology, Princess Margaret Hospital, University Health Network (UHN), Toronto, ON.
Sheri Stillman, RD, Clinical Nutrition, Allied Health, Princess Margaret Hospital, UHN, Toronto, ON.
Susan Haines, RD, Clinical Nutrition, Allied Health, Princess Margaret Hospital, UHN, Toronto, ON.
John Trachtenberg, MD, FRCSC, FACS, Department of Surgical Oncology, Division of Urology, Princess Margaret Hospital, UHN, Toronto, ON.

Older adults represent the highest percentage of new cancer diagnoses each year. This, combined with the increasing age of the population, underscores the importance of identifying methods for risk reduction. The World Cancer Research Fund, together with the American Institute for Cancer Research, has published recommendations for cancer prevention through diet and physical activity. These guidelines should be considered when counselling patients in cancer prevention. In this article, colorectal, breast, and prostate cancers are highlighted, and nutritional recommendations for these cancers are presented.
Key words: nutrition, prevention, colorectal cancer, breast cancer, prostate cancer.

Nutrition et démence chez les personnes âgées

Nutrition et démence chez les personnes âgées

Teaser: 


Nutrition et démence chez les personnes âgées

Conférencière : Carol Greenwood, Ph. D., professeure, département des sciences de la nutrition, Université de Toronto; chercheuse titulaire, unité de recherche appliquée Kunin-Lunenfeld, Baycrest Centre, Toronto (Ontario).

La Dre Greenwood a placé le thème de sa discussion sur la nutrition et la démence dans le contexte des considérations sur les influences environnementales constituant un risque de déclin cognitif et de démence. Même si la démence a d’importantes racines génétiques, les facteurs environnementaux jouent un rôle important dans son étiologie. Selon certaines études, ces facteurs sont associés à environ 60 % des cas de démence survenant après l’âge de 80 ans.

Habitudes alimentaires augmentant le risque de déclin cognitif
Pour bien comprendre le risque posé par les facteurs environnementaux, la Dre Greenwood a recommandé à ses auditeurs de porter attention au régime alimentaire sur une longue durée plutôt qu’à des cas particuliers d’apports alimentaires, bons ou mauvais. La connexion entre nutrition et démence repose sur l’idée sous-jacente que les neurones ont besoin d’apports nutritifs. Des changements nutritionnels entraînent des modifications du métabolisme neuronal. Une alimentation saine garantit la signalisation de l’insuline dans le cerveau, nécessaire à l’apprentissage et à la mémoire. Les cliniciens doivent encourager des habitudes alimentaires propres à maintenir les concentrations cérébrales de neurotrophines nécessaires à la plasticité synaptique impliquée dans la consolidation de la mémoire; de plus, une bonne alimentation et des apports nutritifs appropriés peuvent réduire l’inflammation et le stress oxydatif, et maintenir la capacité de la circulation cérébrale à fournir les nutriments essentiels au cerveau.

Des progrès dans ce domaine de recherche permettraient de contrer l‘isolationnisme qui marque parfois la perception des maladies chroniques. Le cerveau est fortement subordonné à la santé de l’organisme tout entier et une modification de l’alimentation peut exercer une influence directe sur des mala- dies liées au régime alimentaire, comme les maladies cardiovasculaires (MCV), le diabète de type 2 et la dépression.

De nombreuses études épidé-miologiques sur l’alimentation sont disponibles et indiquent qu’un apport calorique excessif engendre un stress oxydatif. La Dre Greenwood et ses collègues se sont penchés sur le rôle des apports en graisses. Un apport élevé en graisses, surtout saturées et polyinsaturées, accompagné d’un déficit en graisses oméga, est typique de l’alimentation nord-américaine. Des études ont montré que les régimes alimentaires faibles en fruits, en légumes, en céréales complètes et en huiles de poisson sont associés à un risque plus élevé de démence. Ce régime est également associé aux MCV, au diabète, à la dépression et à d’autres états pathologiques inflammatoires et chroniques. Les effets indésirables sur le cerveau ne sont pas simples, et il est probable que des mécanismes multiples sont impliqués; dissocier le rôle de la maladie chronique d’un impact direct sur la fonction cérébrale risque de donner une fausse idée de ces effets.

Les huiles de poisson constituent un bon exemple de la façon dont un nutriment particulier peut intervenir sur des voies neuronales multiples. Les études portant sur les huiles de poisson et le risque de démence ont eu du mal à isoler le rôle propre de ces huiles parce que, comme tous les nutriments, celles-ci ont de multiples effets sur l’organisme. Comme les graisses oméga font partie des recommandations alimentaires, la distinction entre le rôle soi-disant phy-siologique du nutriment et son rôle pharmacologique s’estompe. L’incorporation de graisses oméga dans un régime alimentaire holistique est une bonne approche, qui « stimule » le système. L’autre approche compte sur un impact pharmacologique important avec une stratégie de type « cibler et isoler » grâce à des suppléments alimentaires et un enrichissement nutritionnel (comme les œufs). Mais une telle approche néglige d’autres propriétés très précieuses des protéines de poisson.

De la même façon, des recherches sur les avantages cliniques associés à une exposition altérée aux antioxydants ont isolé des micronutriments et les ont fournis sous forme de suppléments alimentaires, ce qui a abouti à des données ambiguës. Cependant, on ne peut pas extrapoler les effets de cette consommation à ceux d’un régime alimentaire incorporant des micronutriments sur la base d’un apport nutritif mesuré en grammes par jour. L’approche ciblée oublie également que le cocktail nutritif complet est plus important (p. ex. : aspect synergique) que la consommation de chaque composé séparément. Les constituants alimentaires fonctionnent en bloc.

Il existe des enjeux pressants étant donnés les changements des marqueurs de santé à l’échelle de la population tout entière. Les personnes présentant une adiposité centrale (associée au développement du syndrome métabolique) sont des « bombes à retardement » de comorbidités. Les résultats de nouvelles études indiquent que l’obésité centrale autour de la cinquantaine augmente le risque de démence, indépendamment des comorbidités diabétiques et cardiovasculaires; les sujets présentant le degré le plus important d’obésité centrale triplent leur risque de déclin cognitif1.

Le régime alimentaire méditerranéen

L’approche clinique de tels patients doit inclure un changement d’habitudes alimentaires, et les données probantes proviennent principalement du régime méditerranéen (Figure 1). Les effets bénéfiques sont directement liés à l’augmentation des apports en fruits, en légumes et en poisson, et à la réduction de la consommation de viande rouge. De récentes données en faveur de cette approche ont été fournies par une étude prospective de 2 258 sujets non atteints de démence en milieu communautaire à New York; mieux le régime méditerranéen était suivi, plus le risque de maladie d’Alzheimer (MA) était faible2.

Le rôle du contrôle glycémique et du diabète de type 2
De plus en plus de données scientifiques laissent entendre que le diabète est en soi un facteur de risque de déclin cognitif, ce qui nécessite un contrôle glycémique draconien chez les patients hyperglycémiques.

Des études animales ont apporté des preuves de l’interrelation entre contrôle glycémique et démence, et la Dre Greenwood et ses collègues ont examiné l’effet des habitudes alimentaires typiquement nord-américaines sur la performance cognitive du rat, particulièrement sur l’apprentissage et la mémoire. Les bais-ses de performance étaient clairement associées à une consommation riche en graisses saturées : les rats soumis à ce régime étaient plus susceptibles d’avoir des performances aléatoires lors des tests.

Il reste à identifier quels aspects du régime riche en graisses saturées nuisent à la fonction cognitive, et à démêler ces effets de ceux du diabète. La Dre Greenwood a mentionné des études présentant les résultats d’une évaluation neuropsychiatrique habituelle de personnes âgées hyperglycémiques, qui examinait plus particulièrement la mémoire immédiate et différée (cette dernière faisant appel à la fonction hippocampique). Les résultats montrent que les personnes les plus insensibles à l’insuline réalisent la moins bonne performance. Avec l’âge, la perte de sensibilité à l’insuline est liée à une détérioration de la mémoire.

Maladie chronique et risque accru de démence
Les recherches actuelles indiquent de plus que la résistance à l’insuline peut excéder les effets de la consommation de graisses sur le déclin cognitif. Des études récentes s’appuyant sur l’imagerie structurelle éclairent la relation entre diabète et cognition. Une étude examinant la perte de la fonction hippocampique chez des sujets âgés non encore diagnostiqués pour un diabète de type 2, mais dont le contrôle glycémique est défaillant, a trouvé qu’un très mauvais contrôle glycémique était fortement associé à une atrophie hippocampique. De tels effets sont évidents chez les personnes dont le diabète est bien maîtrisé; à mesure que le diabète perdure et que les sujets perdent le contrôle métabolique et développent une hyper-cholestérolémie et une hypertension, l’atrophie se propage dans le cerveau et des lésions de la substance blanche se manifestent. Ce sont les composantes vasculaires du diabète, qui apparaissent plus tard au cours de l’évolution de la maladie.

La voie de signalisation de l’insuline est nécessaire à la mémorisation

La Dre Greenwood a fait observer que, bien que le cerveau ne soit généralement pas considéré comme un organe sensible à l’insuline, la densité cérébrale de récepteurs de l’insuline est élevée, et les voies de signalisation de l’insuline jouent un rôle intégral dans la consolidation de la mémoire. Ces voies sont perturbées chez les diabétiques. De telles associations avec les voies de signalisation de l’insuline sont importantes et peuvent expliquer les mauvaises performances de mémoire des personnes diabétiques par rapport à des non-diabétiques d’âge apparié, mais ce n’est pas une preuve irréfutable d’une contribution du diabète à la pathologie de la démence.

La Dre Greenwood a suggéré qu’une perturbation des voies de signalisation de l’insuline contribue sûrement à cette pathologie. L’enzyme de dégradation de l’insuline est l’enzyme clé impliquée dans la dégradation du peptide Ab, qui favorise le développement des plaques de la ma-ladie d’Alzheimer. Cette enzyme est régulée à la baisse dans le cerveau des diabétiques, ce qui ralentit la dégradation du peptide Ab. De plus, de fortes concentrations périphériques d’Ab entravent l’exportation d’Ab, et constituent donc un risque élevé d’accumulation du peptide Ab. Les diabétiques présentent également des niveaux élevés de cytokines inflammatoires, engendrant une accumulation pathologique du peptide Ab et des réponses inflammatoires correspondantes. La cascade inflammatoire du peptide Ab favorise la formation de plaques.

Des études portant sur des sujets au diabète bien maîtrisé, mais porteurs d’un polymorphisme génétique au niveau du gène codant pour le facteur de nécrose des tumeurs (TNFa), corroborent cette idée. Ces individus sont moins à même de fabriquer le TNFa et de déclencher des réponses inflammatoires. Les porteurs de SNP (polymorphisme nucléotidique) obtenaient de meilleurs résultats aux tests et leur baisse de performance était moindre. Le rôle des cytokines inflammatoires en terrain diabétique fait selon toute vraisemblance partie intégrante de l’entretien de la santé cérébrale, a déclaré la Dre Greenwood.

Des perturbations de la voie de signali-sation de l’insuline peuvent également contribuer à la formation des enchevêtrements neurofibrillaires. En particulier, le taux de GSK-3, une enzyme atténuée par la voie de signalisation de l’insuline, peut augmenter chez les diabétiques. La GSK-3 est importante, car elle augmente la phosphorylation de la protéine tau associée à la formation des enchevêtrements neurofibrillaires, et ces derniers sont plus nombreux en terrain diabétique ou obèse. L’accumulation d’enchevêtrements signale le passage d’une perte normale de fonction à une pathologie. En conséquence, certains ont avancé que la MA est la séquelle cérébrale du diabète, ce que réfute la Dre Greenwood, bien qu’elle pense que la maladie se manifeste plus rapidement dans ce contexte.

Habitudes alimentaires favorisant le bien-être cognitif

La principale recommandation alimentaire au patient diabétique doit être de consommer des aliments à faible indice glycémique. Les études portant sur la performance cognitive postprandiale ont constaté que les fonctions de mémorisation et de remémoration étaient altérées après une consommation d’aliments à glucides simples. Il semble que ce soit la sécrétion de cortisol induite par l’insuline, et non les modifications de la glycémie, qui est la clé de cette réponse. L’augmentation du cortisol entraîne des effets problématiques sur l’hippocampe, dont certains sont liés au stress oxydatif. En outre, les diabétiques bénéficiant d’un bon apport en antioxydants souffrent de baisses cognitives moindres. La clé réside dans un contrôle glycémique minutieux afin de minimiser l’agression diabétique répétée au cours de la journée.

Conclusion
La Dre Greenwood a fait observer que les modifications du régime alimentaire des personnes âgées peuvent s’interpréter comme une recommandation de perte de poids, et ce risque est souvent avancé comme objection aux modifications alimentaires. Aucune ligne directrice claire ne permet au médecin de décider quand cesser d’encourager la perte de poids, qui est corrélée à un risque de fragilité chez la personne âgée. La meilleure approche pour minimiser la fragilité, a-t-elle conseillé, c’est d’améliorer les apports nutritifs tout en faisant plus d’exercice physique. Une approche plus ferme des habitudes alimentaires est nécessaire, étant donné que l’incidence du diabète et du syndrome métabolique évolue, notamment en raison du vieillissement de la génération du baby-boom. La Dre Greenwood a averti son auditoire que les forces contribuant à l’augmentation de la démence sont largement sous-estimées, et qu’il est grand temps d’instaurer des modifications du mode de vie.

Bibliographie

  1. Whitmer RA, Gustafson DR, Barrett-Connor E, et al. Central obesity and increased risk of dementia three decades later. Neurology 2008;71:1057-64.
  2. Scarmeas N, Stern Y, Tang MX, et al. Mediterranean diet and risk for Alzheimer’s disease. Ann Neurol 2006;59:912-21.

Nutrition and Dementia among Older Adults

Nutrition and Dementia among Older Adults

Teaser: 

Click here to view the entire report from the 28th Annual Scientific Meeting of the Canadian Geriatrics Society

Nutrition and Dementia among Older Adults

Speaker: Carol Greenwood, PhD, Professor, Department of Nutritional Sciences, University of Toronto; Senior Scientist, Kunin-Lunenfeld Applied Research Unit, Baycrest Centre, Toronto, ON.

Dr. Carol Greenwood contextualized her discussion’s theme of nutrition and dementia as contributing to considerations of the environmental influences posing risk for cognitive decline and dementia. While dementia has important genetic roots, a large causative factor is environmental exposure. In cases of disease onset at >80 years of age, studies have suggested that ~60% relates to this factor.

Dietary Patterns that Increase Risk of Cognitive Decline

To understand the risk mediated by environmental exposure, she recommended that listeners focus on chronic diet rather than on instances of good or poor intake. The connection between nutrition and dementia relates to the underlying idea that neurons require nutritional support; altered nutrition equates to altered neuronal metabolism. Sound nutrition maintains brain insulin signaling, needed for learning and memory. Clinicians should aim to promote dietary habits that maintain brain neurotrophin levels, which support synaptic plasticity needed for memory consolidation; further, good diet and appropriate nutrient intake can reduce inflammation and oxidative damage, and maintain the cerebrovasculature’s capacity to supply essential nutrients to the brain.

Advances in this area of research could help to remediate an isolationist philosophy that can pervade viewpoints on chronic disease. The brain is highly sensitive to the health of the body, and through dietary modification it is possible to exert direct impact on diet-associated conditions such as cardiovascular disease (CVD), type 2 diabetes, and depression.

Many epidemiologic studies on diet are available, indicating that excess caloric intake leads to oxidative stress. Dr. Greenwood and colleagues have examined the role of fat intake. High fat intake, particularly of saturated and polyunsaturated fats, along with a dearth of Omega fats, are typical of the North American diet. Studies have shown that diets low in fruits, vegetables, whole cereal grains, and low in fish oils are associated with higher risk of dementia. This diet profile also associates with CVD, diabetes, depression, and other inflammatory and chronic disease states. The adverse effects on the brain are not simple, and multiple mechanisms are likely involved; separating the role of chronic disease from a direct impact on brain function would distort the effects.

Fish oils exemplify how individual nutrients can modulate multiple neuronal pathways. Studies involving fish oils and dementia risk have found the individual role hard to isolate because they, as all nutrients, have multiple effects in the body. As the Omega fats are incorporated into dietary recommendations the so-called physiologic role of the nutrient versus the pharmacologic role blurs. Incorporating the Omega fats on a wholistic nutritional basis is the sound approach, one that “nudges” the system. The other seeks to exert a large pharmacological impact with a “targeting and isolating” approach through supplements or food enrichment (e.g., eggs). Such an approach overlooks other aspects of fish protein that are valuable.

Similarly, investigations of health outcomes associated with altered antioxidant exposure have isolated micronutrients and supplied them in supplemental form, producing equivocal data. However, measuring the effects of this consumption should not be extrapolated to the effects of a dietary pattern that incorporates micronutrients on a grams per day nutritional intake. The targeted approach also overlooks that the full nutritional cocktail is more important (e.g., the synergistic aspect) than consuming any one individual compound. Food constituents work together.
These are pressing issues given the population-wide changes in health markers. Individuals with central adiposity (associated with development of the metabolic syndrome) are a “time bomb” of comorbidities, she stated. New study results suggest that central obesity in midlife increases dementia risk independent of diabetes and cardiovascular comorbidities; individuals with the greatest degree of central obesity bear a threefold increase of cognitive decline.1

The Mediterranean Diet
The needed clinical approach for such patients supports changing eating patterns, and the burden of evidence points toward the Mediterranean diet (Figure 1). The beneficial effects relate directly to increased fruit, vegetable and fish intake and reduced red meat consumption. Recent evidence for the approach was provided by a prospective study of 2,258 community-based nondemented individuals in New York; those with higher adherence to the Mediterranean diet had lower risk for Alzheimer’s disease (AD).2

The Role of Type 2 Diabetes and Glycemic Control
Increasing evidence suggests that diabetes per se appears to be a risk factor for cognitive decline, necessitating aggressive glycemic control in hyperglycemic patients.

Evidence for the interrelationship of glycemic control and dementing illness has been drawn from animal studies, and Dr. Greenwood and colleagues have investigated the effect of typical North American dietary patterns on cognitive performance in rats, specifically on learning and memory. Performance decrements were clearly associated with high saturated fat consumption; rats fed this diet were most likely to show random/chance performance in testing.

The task is to identify which qualities of the high saturated fat diet compromise cognitive function, and to disentangle these effects from diabetes’ effects. Dr. Greenwood cited studies with standard neuropsychiatric assessment results of hyperglycemic older adults, looking specifically at immediate and delayed recall (the latter calls on hippocampal function). Results show those more insensitive to insulin exhibit worse performance. With age, lost insulin sensitivity relates to impaired memory function.

Chronic Disease and Enhanced Dementia Risk

Current research further suggests that insulin resistance may outweigh the effects of fat consumption on cognitive decline. Recent studies using structural imaging have cast light on the relationship between diabetes and cognition. One study investigating loss of hippocampal function in older individuals not yet diagnostic of type 2 diabetes but with compromised glucose control found that worse control strongly associated with hippocampal atrophy. Such effects are evident among well-controlled diabetic individuals; as diabetes endures, and individuals lose metabolic control and develop hypercholesterolemia and hypertension, atrophy disperses throughout the brain, and the presence of white matter lesions becomes evident. These are the vascular components of diabetes appearing later in its course.

Insulin Signaling Is Needed for Memory Processing

Dr. Greenwood observed that while the brain is not often considered an insulin-sensitive organ, it has a high density of insulin receptors, and insulin signaling pathways play an integral role in memory consolidation. These insulin signaling pathways become disrupted in the setting of diabetes. These associations with the insulin pathway are important and may explain why the diabetic individual has poor memory performance relative to an age-matched nondiabetic, but it is not clear indication that diabetes contributes to dementia pathology.

It likely does both, Dr. Greenwood argued. The key enzyme involved in degradation of Ab protein promoting development of AD plaques is the insulin degrading enzyme, which is down-regulated in the brains of those with diabetes, slowing Ab degradation. In addition, the Ab export is impaired due to high levels of Ab in the periphery, leaving them at high risk of Ab accumulation. Diabetics also have higher levels of inflammatory cytokines, producing a disease state of Ab accumulation and corresponding inflammatory responses. The Ab inflammatory cycle facilitates plaque formation.

Studies featuring individuals with well-controlled diabetes but carrying a genetic polymorphism to tumour necrosis factor (TNF)a support this view. Such individuals are less able to manufacture TNFa and launch inflammatory responses. Those carrying the single nucleotide polymorphism (SNP) have performed better on testing and showed fewer decrements in performance. The role of inflammatory cytokines in the context of diabetes is likely integral to the maintenance of brain health, Dr. Greenwood stated.

Disturbances to the insulin signaling pathway may also contribute to the development of neurofibrillary tangles. Specifically, GSK-3, an enzyme dampened by the insulin signaling pathway, may be increased in those with diabetes. GSK-3 is important because it increases phosphorylation of the tau protein associated with development of neurofibrillary tangles, which appear in greater levels in the diabetic/obese state. The accumulation of tangles signals the move from normal loss of function into pathology. Correspondingly, some have argued that AD is the brain sequelae of diabetes, and while Dr. Greenwood expressed her disagreement, she thinks the disease occurs more rapidly in this setting.

Dietary Patterns that Promote Cognitive Well-Being
The focus of dietary recommendations for the diabetic patient should be on low-glycemic index food intake. Studies that have investigated postprandial cognitive performance found that after consuming simple carbohydrate foods, degraded processing and recall function results. It appears that insulin-induced cortisol secretion, and not changes in blood glucose, are key to this response. Increased cortisol exerts problematic effects in the hippocampus, some of which relate to oxidative stress. Further, diabetic individuals with sound antioxidant intake experience fewer decrements in cognition. The key is careful glycemic control to minimize the diabetic insult occurring repeatedly throughout the day.

Conclusion
Dr. Greenwood observed that the risk of appearing to recommend weight loss to an older population is often raised as an objection to dietary modification. There are no clear guidelines as to when physicians should stop encouraging weight loss, which is correlated with frailty risk with advancing age. The best approach to minimizing frailty, she advised, is improved nutritional intake combined with increased exercise. A more aggressive approach to dietary patterns is required, given that the incidence of diabetes and the metabolic syndrome are changing, especially as baby boomers age. Dr. Greenwood advised listeners that the pressures driving dementia upward are vastly underestimated, and now is the time to implement lifestyle modifications.

References

  1. Whitmer RA, Gustafson DR, Barrett-Connor E, et al. Central obesity and increased risk of dementia three decades later. Neurology 2008;71:1057-64.
  2. Scarmeas N, Stern Y, Tang MX, et al. Mediterranean diet and risk for Alzheimer’s disease. Ann Neurol 2006;59:912-21.

The Role of Nutrition in the Prevention and Management of Pressure Ulcers

The Role of Nutrition in the Prevention and Management of Pressure Ulcers

Teaser: 

Zena Moore, RGN, MSc, FFNMRCSI, Health Research Board of Ireland, Clinical Nursing and Midwifery Research Fellow, Royal College of Surgeons in Ireland, Dublin, Ireland.
Seamus Cowman, PhD, MSc, FFNMRCSI, P.G Cert Ed (Adults), Dip N (London), RNT, RGN, RPN, Professor and Head of Department, Faculty of Nursing and Midwifery, Royal College of Surgeons in Ireland, Dublin, Ireland.

Pressure ulcers are common, costly, and adversely affect quality of life. Nutritional status is one risk factor that predisposes individuals to the development of a pressure ulcer. The impact of nutritional supplementation is reflected in the reduced incidence of pressure ulcers; however, the evidence is limited. The precise role of nutritional supplementation in pressure ulcer healing is less clear, yet a trend towards healing has been suggested. Patients should have their nutritional status monitored carefully. If difficulties arise, these should be detected early, and if it is not possible to increase the intake of normal food and fluids, then advice should be sought from the dietitian.
Key words: pressure ulcers, risk, prevention, treatment, nutrition.

Nutritional Guidelines in Canada and the US: Differences between Younger and Older Adults

Nutritional Guidelines in Canada and the US: Differences between Younger and Older Adults

Teaser: 

Joan Pleuss, RD, MS, CDE, CD, Director, Bionutrion & Body Composition Units, Clinical & Translational Research Institute, Medical College of Wisconsin, Milwaukee, WI.

The requirement for some nutrients changes as adults age. The Dietary Reference Intakes, the 2007 Canada Food Guide, and the 2005 Dietary Guidelines for Americans (MyPyramid.gov) provide guidance for the consumer and the professional for nutritional needs throughout the life span. The Guidelines provide recommendations in user-friendly messages. MyPyramid.gov and the Food Guide allow the public to access information on the internet that is individualized for age, gender, and physical activity. The Dietary Reference Intakes provide the health professional with nutrition requirements for gender and specific age groupings through the entire lifespan. This article will address those nutrients whose requirements significantly change with adult aging.
Key words: Dietary Reference Intakes, Canada Food Guide, Dietary Guidelines of America, MyPyramid, aging, nutrition.

Popular Diets and Coronary Artery Disease

Popular Diets and Coronary Artery Disease

Teaser: 


C. Tissa Kappagoda, MBBS, PhD, Professor of Medicine, Department of Internal Medicine, University of California, CA, USA.
Dianne A. Hyson, RD, PhD, Assistant Professor, Department of Consumer Sciences, California State University of Sacramento, CA, USA.

This paper examines the potential impact of some popular diets on cardiovascular risk factors in aging populations. The compositions of these diets are compared against the broader recommendations of the Food and Nutrition Board and the American Heart Association. The Atkins and South Beach diets have been advanced as components of weight loss programs, while the Mediterranean type of diet has been promoted as being especially beneficial to those who are at risk of developing cardiovascular disease. When viewed against the recommendations of the Food and Nutrition Board, it is apparent that these diets are unlikely to meet the special nutritional needs of the older population.
Key words: Atkins, South Beach, Mediterranean diet, nutrition, coronary artery disease.

Identification of Nutrition Problems in Older Patients

Identification of Nutrition Problems in Older Patients

Teaser: 

Heather H. Keller, RD, PhD, Associate Professor, Dept. Family Relations and Applied Nutrition, University of Guelph, Guelph, ON.

Although the prevalence of malnutrition and, specifically, undernutrition are unknown among Canadian seniors, nutritional risk has been identified as a common problem. As nutritional risk can lead to malnutrition and all of its sequelae, efforts are needed to identify nutrition problems early in their course to improve the quality of life of seniors. The following article provides a variety of approaches for identifying nutritional problems, from simple indicators to a simplified and standardized nutritional assessment. Suggestions also are provided on how the practitioner can seek assistance with intervening and helping the senior to overcome these problems.
Key words: nutrition, older adults, screening, intervention, risk, weight.

Nutrition in the Elderly: Food for Thought

Nutrition in the Elderly: Food for Thought

Teaser: 

Taking a 'stroll' through a geriatric unit, either in acute care or rehabilitation, one is struck by how many of the patients seem undernourished. This highlights the need for clinical dietitians as part of the multidisciplinary team required for effective geriatric care. Thankfully, most elderly people are not admitted to a geriatric unit, and their dietary issues are more similar to those facing the population at large.

Clearly, it is much better to eat in a healthy manner to prevent functional decline than it is to engage in heroic 'salvage' operations when catastrophic illness strikes (see the article 'Supporting seniors to age well with healthy eating' in this edition). However, the biggest issue facing most Western populations is not under nutrition, but rather excess weight. Should the same guidelines for overweight apply to those over 65 as have been developed in middle-aged populations? I am somewhat comforted, as I note my expanding waistline, by an article in last year's Archives of Internal Medicine1 that suggests modest degrees of overweight (BMI 25-27) in the elderly do not increase cardiac and all cause mortality (although frank obesity does).

Even more interesting than total energy intake, is the content of the diet. Clearly elderly patients can suffer from specific nutritional deficiencies, such as Vitamin D or zinc (see article in this issue 'Zinc Deficiency in older adults' by AlAteequi and Allard). However, healthy people of all ages are thinking beyond simple dietary deficiency and wondering about the optimal dietary intake. In the current jargon, you are what you eat. This edition contains an article on diet and prostate disease and, of interest to both men and women, one on the relationship of Vitamin E to dementia (see article by Basran and Hogan in this edition). We usually think of vitamin E as a possible treatment of Alzheimer disease, but the antioxidant actions of vitamin E have long been postulated to be of benefit to the aging brain even before dementia occurs. Two recent studies in the Journal of the American Medical Association provide some evidence for the protective effects of vitamin E (and perhaps vitamin C).2,3 Of course, epidemiological studies do not prove cause and effect; rather, they suggest appropriate directions for future treatment studies. What I found interesting is that while in both of these studies the relative risk of dementia was decreased by high dietary vitamin E (and in the first study, but not the second, high dietary vitamin C), supplements of vitamin E seemed to have no benefit.

Why might this be? The most obvious answer is that those who take Vitamin E supplements are different from those who do not; specifically, they might choose to take vitamin E when they detect early memory problems that predict future dementia. As well, vitamin E has only become popular as a supplement recently; thus, those who take their vitamin E as a supplement might not have had as long an exposure to its benefits as have those with a life-long, high dietary intake. It might also be that vitamin E is simply a surrogate for another dietary constituent that is actually of benefit. The fact that the two studies are discordant in their results with vitamin C is also cause for concern.

Regardless of the true relationship between vitamin E and dementia, there is no doubt that this edition of Geriatrics and Aging will provide a great deal of 'food for thought'.

References

  1. Heiat A, Vaccarino V, Krumholz HM. Arch Intern Med. 2001;161:1194-203.
  2. Englehart MJ, Geerlings MI, et al. JAMA 2002;287: 3223-9.
  3. Morris MC, Evans DA, et al. JAMA 2002;287:3230-7.