The Okinawan diet refers to the traditional eating habits of the people of the Japanese island of Okinawa (population 1.3 million).
It is based on whole grains, legumes, fruits, vegetables, fish, tofu, seaweed, nuts, seeds, and herbs.
The islanders eat very little meat and avoid processed foods. They drink green tea instead of coffee. They do not smoke and rarely use alcohol. They exercise regularly and maintain a healthy weight.
Okinawa Island hosts more than 40 centenarians per 100,000 inhabitants, 3 times more than in all of Japan.
This longevity is not only the consequence of a favorable genetic background but would above all be the conjunction of a protected environment, good eating habits, regular physical activity and a strong social fabric.
Life expectancy on this island is 82 years with only 2.6 years of disability after 100 years. The difference between men and women is clear, with a woman/man ratio of 5 female centenarians for 1 male centenarian.
Diabetes is rare on the island of Okinawa, while cancers (colon, breast, prostate, etc.) are nearly 80% less numerous than in Western countries.
The diet of centenarians on the island of Okinawa
The inhabitants of the island of Okinawa consume a wide variety of foods, and their calorie consumption is about 300 calories less when in industrialized countries.
The use of soybeans and rice is very high, as is that of fish, unlike that of meat and dairy products.
The intakes of vitamins A, B, C and proteins are also very high, unlike those of carbohydrates and salt.
The following nutrients, known to fight against inflammation and aging, thanks in particular to their antioxidant properties, are also widely consumed:
Polyphenols from green tea, certain vegetables, fruits (berries)
Omega 3 fatty acids
Magnesium (soya, tofu, green vegetables)
Soy is an excellent source of alpha-linolenic acid, protein and phytoestrogens. These compounds are known to have beneficial effects for the cardiovascular system and have anti-cancer properties.
Caloric intake has been estimated at just over 1000 calories per day, thanks to the consumption of foods with low energy density which allow the absorption of fewer calories, due to their high content of water, fiber and proteins.
Physical activity and social life
The centenarians of the island of Okinawa practice gardening, walking, martial arts and dance, a physical activity which is accompanied by an active social life (third age clubs, parties).
Genetic factors
Environmental factors do not explain everything, and it would seem that the frequency of certain alleles is more frequent among the inhabitants of Okinawa.
Les neurotransmetteurs, souvent appelés messagers chimiques, sont des molécules utilisées par le système nerveux pour transmettre des messages entre les neurones ou des neurones aux muscles.
Plus d’une cinquantaine de neurotransmetteurs ont été identifiés à ce jour.
La communication entre deux neurones se produit dans la fente synaptique (le petit espace situé entre les synapses des neurones).
Puis les signaux électriques qui ont voyagé le long de l’axone sont convertis en signaux chimiques par la libération de neurotransmetteurs, provoquant une réponse spécifique dans le neurone situé en aval.
Pour provoquer cette réponse, le neurotransmetteur doit se fixer sur le récepteur situé sur le neurone en aval.
Les neurotransmetteurs libérés à la terminaison du neurone en amont (1) se retrouvent dans la fente synaptique entre les deux neurones puis se fixent sur les récepteurs situés sur le neurone en aval (2).
Les neuromodulateurs sont un peu différents, car ils ne sont pas limités à la fente synaptique entre deux neurones et peuvent donc affecter un grand nombre de neurones en même temps.
La plupart des neurotransmetteurs sont des petites molécules d’amines, des acides aminés ou des neuropeptides.
Il existe à ce jour une douzaine de neurotransmetteurs à petites molécules connus et plus de 100 neuropeptides différents.
Ces produits chimiques et leurs interactions sont impliqués dans d’innombrables fonctions du système nerveux ainsi que dans le contrôle des fonctions corporelles.
Un neurone et sa terminaison synaptique sont identifiés par le neurotransmetteur qu’ils produisent et libèrent.
Par exemple, un neurone cholinergique est un neurone qui libère le neurotransmetteur acétylcholine à hauteur de ses synapses.
Les principaux neurotransmetteurs
Voici les principaux neurotransmetteurs, avec entre parenthèses leurs abréviations et le qualificatif correspondant :
Un neurotransmetteur influence un neurone de trois manières : excitatrice, inhibitrice ou modulatrice.
Un neurotransmetteur excitateur favorise la génération d’un signal électrique appelé potentiel d’action dans le neurone en aval, tandis qu’un neurotransmetteur inhibiteur l’empêche. Le fait qu’un neurotransmetteur soit excitateur ou inhibiteur dépend du récepteur auquel il se lie.
Exemples de neurotransmetteurs excitateurs ou inhibiteurs
Neurotransmetteur
Acétylcholine
Excitateur
Dopamine
Excitateur
Noradrénaline
Excitateur
Sérotonine
Excitateur
Glutamate
Excitateur
GABA
Inhibiteur
Les neurotransmetteurs exercent diverses fonctions dans le cerveau lorsqu’ils sont libérés ; en voici les principales :
Neurotransmetteur
Fonctions
Acétylcholine
Favorise l’attention, la mémoire et l’apprentissage
Stimule la contraction des muscles squelettiques
Dilatation des vaisseaux
Contraction des bronches, de la pupille, des intestins
Bradycardie (coeur)
Stimule l’excrétion de certaines hormones
Dopamine
Contrôle la motricité et la posture
Coordonne certains processus cognitifs et émotionnels
Favorise l’attention
Module l’humeur
Joue un rôle dans la dépendance
Noradrénaline
Contrôle la vigilance
Favorise l’attention
Ajuste certains comportements tels que le stress, l’émotion
Agit comme une hormone dans le sang en stimulant la contraction des vaisseaux sanguins et augmentant la fréquence cardiaque.
Sérotonine
Régule l’humeur
Régule le cycle circadien
Contrôle de la douleur
Régule la température
Régule l’appétit
Glutamate
Favorise l’apprentissage et la mémorisation des informations à long-terme, la plasticité des synapses du cerveau
GABA
Diminue l’excitabilité des neurones
Il est surtout présent dans les neurones du cortex.
Contribue au contrôle moteur et à la vision.
Une altération de leur fonction provoque des dérèglements dans le cerveau, à l’origine de troubles – cognitifs, psychologiques et comportementaux – suivant le neurotransmetteur impliqué.
Voici quelques exemples de neurotransmetteurs dont la baisse ou l’augmentation est associée à des troubles ou maladies.
Les neurotransmetteurs libérés par les vésicules vont diffuser dans la fente synaptique dans laquelle :
Ils sont dégradés par des enzymes, des protéines que l’on peut comparer à des ciseaux coupants en deux un neurotransmetteur pour l’inactiver.
Ils sont recapturés par des molécules (appelés transporteurs) situées sur la membrane du neurone présynaptique. Ces transporteurs ‘pompent’ les neurotransmetteurs afin qu’ils soient réutilisés. Le neurone économise ainsi la synthèse de neurotransmetteur. D’une manière générale, plus la libération de neurotransmetteur est importante, plus l’activité des transporteurs l’est.
Ils se lient à des protéines (appelées récepteurs) situées sur la membrane du neurone présynaptique et postsynaptique.
Les récepteurs situés sur la membrane du neurone présynaptique (appelés récepteurs présynaptiques) contrôlent la libération, la synthèse et la recapture du neurotransmetteur.
Par la suite, la quantité restante de neurotransmetteur (c’est-à-dire la quantité qui n’aura été ni dégradée ni recapturée) se liera aux récepteurs situés sur la membrane du neurone postsynaptique (on parle de récepteur post-synaptique).
Enfin, la liaison du neurotransmetteur avec son récepteur conduira à un effet physiologique (par exemple, à une contraction du muscle si le neurotransmetteur libéré est l’acétylcholine.
Où et comment les neurotransmetteurs sont-ils synthétisés ?
Ils sont synthétisés par les neurones dans la terminaison nerveuse et/ou le corps cellulaire. Dans ce dernier cas, le messager chimique migre librement ou est transporté grâce aux vésicules jusqu’à la terminaison synaptique.
Cette synthèse se fait à partir d’autres molécules (dites précurseurs) appelées substrats et met en jeu des enzymes (de synthèse) qui accélèrent ces réactions.
Voici en résumé le devenir d’un neurotransmetteur au niveau de la terminaison nerveuse :
Image de droite : à l’arrivée de l’influx nerveux sur la terminaison du neurone (1), les vésicules (2) libèrent les neurotransmetteurs (3) dans la fente synaptique. Ces neurotransmetteurs vont se fixer sur les récepteurs (4) situés sur l’autre neurone, induisant un courant électrique (5).
Le dernier neurotransmetteur découvert
En 2025, des chercheurs ont émis une hypothèse que la créatine fonctionnait comme un neurotransmetteur dans le système nerveux central, du moins chez la souris. Ils ont détecté la créatine dans les vésicules synaptiques et ont observé sa libération lors d’une stimulation neuronale.
Antioxidants are nutrients found naturally in foods that help protect against free radicals.
Free radicals are molecules that cause cell damage and can contribute to aging and disease.
There are two main categories of antioxidants: vitamins and minerals. Vitamins A, C, E, and K are called fat-soluble vitamins because they need fat to be absorbed into the body. These vitamins are found in fruits, vegetables, nuts, seeds, and whole grains. Minerals such as zinc, iron, copper, manganese, calcium, magnesium, selenium, and iodine are water-soluble vitamins. These vitamins are found mostly in lean meats, fish, beans, and dairy products.
What are flavonoids?
Flavonoids are important molecules in herbal medicine that come from plant metabolism, they are found in different parts of the plant at the level of fruits, flowers or leaves. Scientists have already identified more than 8,000 different flavonoids, these molecules belong to the large family of phenolic compounds. They have antioxidant properties. Foods enriched in flavonoids are tea (particularly green tea), red fruits, olive oil, garlic, dark chocolate, grapes and vines, spinash, broccoli and onion.
Antioxidant flavonoids can prevent memory decline
Researchers at Rush University Medical Center in Chicago studied more than 960 people with an average age of 81 and found that those who ate foods containing antioxidant flavonoids, found in plant pigments, were healthier.
Specifically, participants who consumed the most kaempferol, found in kale, beans, tea, spinach and broccoli, had a 0.4 unit slower rate of cognitive decline per decade compared to those in the lowest group.
And those who consumed the most quercetin, from sources such as tomatoes, kale, apples and tea, had a slower rate of cognitive decline of 0.2 units per decade.
Consuming wine, kale, oranges, and tomatoes has also been shown to be beneficial.
These results were confirmed by other previous studies
The researchers studied 1,924 people aged 65 and older who were enrolled in the Rush Memory and Aging Project. They looked at how many times each person ate or drank fruit and vegetable servings per day and whether they had high blood levels of antioxidants. After about four years, the participants took tests to measure their cognitive function. Those who ate or drank more fruit and vegetables had better memory than those who didn’t.
The researchers analyzed data on 2,977 people aged 65 and older who were enrolled in the Health ABC Study. They looked at how much fruit and vegetable intake participants had over the course of five years. Participants who ate the most antioxidants were about half as likely to develop dementia compared to those who ate the least amount of these nutrients.
The study looked at data on 2,000 people over age 65 who were followed for four years. They found that those who ate or drank more antioxidants had better cognitive function than those who didn’t.
It’s not uncommon for people who undergo general anesthesia during surgery to experience some degree of memory impairment afterwards. This is because anesthetics work by blocking certain parts of the brain responsible for memory formation.
Memory problems are even more common in people over the age of 70 following anesthesia. Symptoms persist for months or years in some patients. Patients with Alzheimer’s disease appear to be particularly at risk of impaired cognition following anesthesia, and some studies suggest that exposure to anesthetics may increase the risk of Alzheimer’s disease.
People over 70 are more at risk
In adults over the age of 70, exposure to general anesthesia and surgery is associated with a subtle decline in memory and thinking skills, according to a new study published in 2018. The study analyzed nearly of 2,000 people and found that exposure to anesthesia after age 70 was linked to long-term changes in brain function.
Although the decline in brain function was small, it may be more pronounced in people with already low cognitive function or pre-existing mild cognitive impairment. In older people whose cognitive impairment is not yet clinically recognized, exposure to anesthesia and surgery may highlight underlying problems with memory and thinking.
We need to be sure that patients considering surgery, and their families, are properly informed that the risk of cognitive dysfunction is possible,” explains the study’s lead author. Additionally, alternative strategies should be discussed with patients before surgery is performed for those deemed to be at high risk. This study provides further reasons for clinicians to begin performing routine cognitive assessments prior to surgery. operation to further assess the risk of exposure.
The authors emphasized that it is not possible to determine whether anesthesia, surgery, or underlying conditions requiring surgery caused the decline.
Source : Schulte PJ et coll. Association between exposure to anaesthesia and surgery and long-term cognitive trajectories in older adults: report from the Mayo Clinic Study of Aging. British Journal of Anaesthesia, 2018.
Anesthesia around the age of 40 does not increase the risk of memory loss
There is no significant link between being exposed to general anesthesia after age 40 and the development of mild cognitive impairment years later, according to an epidemiological study.
The potential link between on the one hand exposure to anesthesia following surgery and on the other hand cognitive decline and dementia has recently been a matter of debate, with previous findings contradicting those recently published. This new study found no link between exposure to anesthesia and cognitive decline when taking into account the number of exposures or the total cumulative duration of exposure.
« It is reassuring for the majority of older people who may need surgery to learn that anesthesia and surgery are unlikely to be associated with long-term cognitive decline, » says the lead author of study (David O. Warner, Mayo Clinic, Rochester, Minnesota, USA).
The researchers looked at Mayo Clinic data from 1,731 residents between the ages of 70 and 89 whose cognitive functions were assessed every 15 months. Medical records (including surgeries with anesthesia) were obtained for each participant after the age of 40. Of these, 536 (31%) developed mild cognitive decline over a period of 4.8 years. No adverse effects of anesthesia were reported in the study.
Although the current results are « comforting », it is quite possible that people at risk are more vulnerable to anesthesia, in particular the elderly with vascular disorders and who are undergoing vascular surgery. Researchers believe that anesthesia produces an inflammatory state in the brain – called neuroinflammation – which would trigger cognitive impairment in people at risk.
Source : Juraj Sprung et coll. Association of Mild Cognitive Impairment With Exposure to General Anesthesia for Surgical and Nonsurgical Procedures. Mayo Clinic Proceedings, 2016.
Age-dependent effect
A study published in the journal Anaesthesia confirmed that anesthesia can cause long-term damage to brain cells and impair memory. It’s important to note that these results only apply to older adults. Younger people tend to recover faster after anesthesia because their brains are better able to adapt to the effects of drugs.
However, older adults often have weaker immune systems and are more susceptible to infections, which could make them more vulnerable to complications following surgery. One limitation of this study is that it relied on self-reported information about whether participants had undergone surgery.
Anesthesia and risk of dementia
In 2016, American researchers reported that exposure to anesthesia was not associated with an increased risk of dementia, and Alzheimer’s disease in particular. This prospective study included nearly 4,000 participants aged 65 and older. This result contradicts that published by the European Society of Anaesthesiology (ESA) in June 2013 which reported a 35% increase in the risk of dementia.
In order to justify these results, the researchers indicated that some anesthetics would promote the inflammation of neural tissues, resulting in lesions characteristic of Alzheimer’s disease (accumulation of amyloid and tau protein). In this study, the average age of the participants was 75 years old and 62% were women. 632 participants (9%) developed dementia 8 years after follow-up.
However, there have been no clinical trials to establish a link between anesthetic exposure and the development of Alzheimer’s disease. Therefore, before drawing firm conclusions, it is necessary to conduct additional studies. However, one should be aware of the potential risks and take precautions with vulnerable elderly patients.
Source: Mother G et coll. Alzheimer’s disease and anesthesia. Turk J Med Sci 2015;45(5):1026-33).
Le neurone fonctionne en émettant des signaux électriques (on parle également d’influx nerveux). C’est ce qui le différencie des autres cellules.
Chaque neurone possède un axone qui agit comme un fil électrique, en conduisant l’influx nerveux (sous la forme d’un potentiel d’action) vers le neurone voisin, assurant ainsi l’activité fonctionnelle du cerveau.
La transmission de l’influx nerveux se fait grâce à la présence, dans la membrane entourant le neurone (cette membrane est une fine couche d’un centième de millième de millimètre d’épaisseur), de canaux ioniques. Ces canaux sont des sortes de vannes laissant passer des ions positifs tels que le calcium et le potassium.
Pas d’influx nerveux: le neurone est au repos
Lorsque aucun influx n’existe, le neurone est au repos et sa membrane plasmique est normalement polarisée: on parle de potentiel de repos. A ce moment, l’extérieur du neurone est positif par rapport à l’intérieur, car les ions sodium (qui sont des ions positifs) sont plus importants à l’extérieur qu’à l’intérieur.
Un influx nerveux arrive: le neurone s’excite
Lorsqu’un influx nerveux arrive, les canaux ioniques s’activent et laissent entrer, en quelques millièmes de seconde, des ions sodium (des ions potassium sortent peu de temps après): la face interne de la membrane devient alors chargée positivement. Un influx nerveux est généré et se propage du corps cellulaire vers la terminaison de l’axone à une vitesse de 1 à 150 mètres par seconde. Son amplitude est d’environ 100 millivolts et sa durée d’environ 1 à 2 millièmes de seconde.
Par où le neurone reçoit l’influx nerveux ?
La réception se fait essentiellement sur la membrane des dendrites (sortes de minces filaments agissant comme des antennes) et du soma (le soma est aussi appelé corps cellulaire) du neurone. Un neurone peut recevoir une information d’environ un millier de neurones. L’axone peut également recevoir des influx.
Où est généré l’influx nerveux ?
Le neurone intègre le message et génère, en réponse à ce message, un potentiel d’action qui prend naissance dans la région où l’axone quitte le soma (région appelée segment initial).
Comment se propage l’influx nerveux ?
L’ouverture de canaux à sodium en une région donnée (que nous appellerons A) stimule la membrane de la région adjacente qui devient à son tour excitable…et ainsi de suite. C’est de cette manière que l’influx nerveux se propage. Il est à noter que la membrane située dans la région A de l’axone revient à l’état de repos: en effet les canaux à sodium se referment tandis que les canaux à potassium s’ouvrent, laissant sortir les ions potassium.
L’influx nerveux est transmis) à un autre neurone ou à un autre type de cellule (par exemple une cellule musculaire) par l’intermédiaire de la synapse.
Le neurone à l’état de repos
Le neurone est à l’état de repos si aucun influx nerveux n’est transmis. Les canaux à sodium et potassium sont fermés et une pompe maintient en l’état ce déséquilibre ionique (les ions sodium sont majoritairement à l’extérieur du neurone tandis que les ions potassium sont plus concentrés à l’intérieur qu’à l’extérieur) : le potentiel d’action est en phase de repos.
Le neurone à l’état excité
Le neurone est à l’état excité. Lorsqu’un influx nerveux arrive sur les dendrites et le soma du neurone (flèche verte), un nouvel influx prend naissance dans la région où l’axone quitte le corps cellulaire (A), provoquant l’ouverture de canaux sodiques et l’entrée rapide (quelques millisecondes) d’ions sodium (1); puis s’ouvrent les canaux potassiques, laissant sortir les ions potassium (2): la membrane revient à son état de repos. L’entrée d’ions sodium change les propriétés électriques du point voisin (B) de l’axone et provoque à son tour une entrée d’ions sodium, puis une sortie de potassium qui ramène la partie B de l’axone à son état de repos. Et de fil en aiguille, l’influx nerveux se propage sur toute la longueur de l’axone jusqu’à ses terminaisons (flèche rouge).
La myéline
Les gaines de myéline sont des membranes formées de tissu adipeux qui protègent les cellules nerveuses Ces membranes sont enroulées en spirale autour de certains axones. La myéline est fabriquée par deux types différents de cellules de soutien. Dans le système nerveux central (SNC) – le cerveau et la moelle épinière – des cellules appelées oligodendrocytes s’enroulent autour des axones pour créer une gaine de myéline. Dans les nerfs à l’extérieur de la moelle épinière, les cellules de Schwann produisent de la myéline.
Peu importe où elle se trouve dans le système nerveux, cette gaine de myéline assure une propagation plus rapide des signaux: la vitesse de conduction de l’influx sur un axone myélinisé (c’est-à-dire un axone avec myéline) est jusqu’à 200 fois plus rapide (100 mètres par seconde) que celle d’un axone sans myéline.
Les myélines sont séparées (tous les 1 à 3 millimètres) par des espaces appelés noeud de Ranvier (L.-A. Ranvier: histologiste français du XXème siècle). Ces espaces (d’une longueur de quelques millièmes de millimètre) sont très excitables car ils contiennent la majorité des canaux ioniques.
Conduction saltatoire
L’influx nerveux ne se propage pas uniformément mais saute de part en part sur les noeuds de Ranvier : on parle de conduction saltatoire.
Légende: A – Axone D – Dentrites M – Gaine de myéline R – Noeud de Ranvier S – Soma et son noyau (N)
La structure et la composition de la membrane neuronale et de la gaine de myéline se modifient lors du vieillissement cérébral « normal », entraînant une diminution de la vitesse de l’influx nerveux. Cette modification serait à l’origine du déclin cognitif observé lors du vieillissement normal.
Deux nouvelles études mettent en évidence une augmentation des effets secondaires d’analgésiques opioïdes couramment prescrits chez les personnes atteintes de la maladie d’Alzheimer. Les chercheurs ont également identifié un mécanisme qui pourrait causer le problème.
Dans un essai contrôlé randomisé mené auprès de 162 résidents de foyers de soins norvégiens, des chercheurs de l’Université d’Exeter, du King’s College de Londres et de l’Université de Bergen ont constaté une augmentation significative des effets secondaires tels que les changements de personnalité, la confusion et la sédation, qui peuvent avoir de graves répercussions sur la vie des personnes atteintes de démence.
L’équipe souhaite que des études soient menées pour examiner la posologie appropriée d’analgésiques (ex. buprénorphine) pour les personnes atteintes de démence.
Environ la moitié des personnes atteintes de démence qui vivent dans des foyers éprouvent une douleur.
Des recherches antérieures ont reconnu que la douleur est souvent sous-diagnostiquée et mal prise en charge chez les personnes atteintes de démence, ce qui a un impact sur la qualité de vie.
Après le paracétamol, les analgésiques à base d’opioïdes sont fréquemment le second choix de traitement pour les cliniciens chez les personnes atteintes de démence et sont prescrits à près de 40 % des personnes atteintes de démence vivant dans des foyers de soins.
Ils soulagent efficacement la douleur, mais les recommandations actuelles ne tiennent pas compte du fait que les personnes atteintes de démence obtiennent un soulagement notable de la douleur à partir de doses plus faibles que celles habituellement prescrites, et sont particulièrement sensibles aux effets indésirables.
L’équipe a étudié 162 personnes de 47 foyers de soins norvégiens qui souffraient de démence et de dépression. Chez ceux à qui la buprénorphine a été attribuée dans le cadre de leur traitement, les effets secondaires nocifs ont plus que triplé. Les chercheurs ont également constaté que ceux qui prenaient de la buprénorphine étaient significativement moins actifs pendant la journée.
Selon Clive Ballard, professeur à l’Université d’Exeter Medical School :
La douleur est un symptôme qui peut causer une énorme détresse et il est important que nous puissions soulager les personnes atteintes de démence. Lorsque nous essayons de soulager leur douleur, nous avons besoin de plus de recherches dans ce domaine, et nous devons trouver le bon traitement. Nous devons établir la meilleure voie de traitement et examiner la posologie appropriée pour les personnes atteintes de démence.
Il est important de noter que les recherches menées par l’équipe du professeur Ballard et présentées lors de la conférence internationale sur la maladie d’Alzheimer 2018 (AAIC) permettent de mieux comprendre pourquoi les personnes atteintes de démence sont plus sensibles aux analgésiques opioïdes, ce qui suggère qu’elles surproduisent les opioïdes naturels du corps.
Une seconde étude portant sur un modèle de souris Alzheimer a révélé une sensibilité accrue à la morphine (analgésique opioïde) par rapport aux souris saines. Les personnes atteintes de la maladie d’Alzheimer ont répondu à une dose beaucoup plus faible pour soulager la douleur et ont éprouvé plus d’effets indésirables lorsque la dose a été augmentée à un niveau normal. En regardant plus loin, l’étude a révélé que les souris Alzheimer produisaient plus d’endorphines (opioïdes endogènes naturels du corps).
Leisure activities can be defined as activities done by people in their free time.
It has been hypothesized that leisure activities improve cognitive function, physical function, and mental health, at least in a western elderly population.
Leisure activities include things like reading, watching TV, playing games, going out to eat, etc. These activities help older adults stay active and engaged in life. They also provide opportunities to socialize with others.
The possible protective effects related to the slowing of age-related decline have therefore been the subject of research over the past two decades.
Leisure activities such as painting are important for older people. They can help delay the signs of aging and maintain good physical, cognitive and mental health.
Two main explanations have been proposed for the beneficial effects of activities on cognitive function and memory in particular: 1) individuals with higher cognitive function may be more likely to perform cognitively demanding leisure activities; 2) People engaging in intellectually demanding leisure activities may slow cognitive decline.
A study examined the impact of leisure activities on cognitive function, physical function, and mental health in a group of Japanese elderly people.
Since most field studies are based on samples from Western countries (e.g., the United States and Germany), little is known about this relationship in Far Eastern countries, including Japan.
The study included a total of 809 Japanese participants (381 men and 428 women). The age range was from 72 to 74 years old.
The study aims 1) to verify the previous hypothesis that there is a relationship between the practice of leisure activity and successful aging by using a more robust and comprehensive methodological approach; 2) extend the current empirical evidence – which focuses primarily on cognitive function – by examining the impact of activities on less studied dimensions of successful aging such as physical function and mental health and 3) verify that these effects are also present in eastern populations.
Overall, the results published by the researchers support the idea that leisure activities help improve or preserve cognitive function, physical function and mental health, three indicators of successful aging.
The results are in line with the hypothesis suggesting that intellectually demanding activities (e.g. music, board games, video games, and other form of internet-based brain training) preserve cognitive abilities of the elderly and that conversely, the lack of cognitive stimulation is accompanied by a greater risk of their cognitive abilities.
Thus, the results of the present study support the idea that leading an active lifestyle, assessed here by engagement in leisure activities, is a means contributing to successful aging, regardless of country and culture.
This study, thanks to its rigorous methodological approach, provides a more reliable estimate of the positive impact of leisure activities on cognitive function, including memory, but also on the link that exists between these activities and the preservation of good physical and mental health in the elderly.
Source: Sala G, Jopp D, Gobet F et al. The impact of leisure activities on older adults’ cognitive function, physical function, and mental health. PLoS One. 2019; 14 (11): e0225006. Published November 8, 2019. Doi: 10.1371/journal.pone.0225006
Alzheimer’s: beneficial leisure activities for caregivers
Recreational activities benefit the heart health of caregivers caring for people with Alzheimer’s disease.
Take a walk outside, read, listen to music…These activities and many others can reduce the blood pressure of relatives caring for people with Alzheimer’s disease.
“Greater engagement in pleasurable leisure activities was associated with lower blood pressure in caregivers over time, according to the study’s lead author. Participation in leisure activities may have benefits for the cardiovascular system of caregivers. »
The study included 126 caregivers enrolled in the UCSD Alzheimer’s Caregiver Study, a follow-up study evaluating associations between stress, coping, and cardiovascular risk among caregivers. Of the 126 caregivers, 89 were female and 37 were male, with an average age of 74, providing home care for a spouse with Alzheimer’s disease.
In annual interviews over five years, caregivers provided information on the frequency with which they engaged in various leisure activities that they found enjoyable. These ratings were analyzed in association with blood pressure over time.
Caregivers reported high levels of enjoyable activities. Most of them said they spent time outdoors, watched television, listened to music, and read or listened to stories. About half of caregivers reported exercising frequently.
Caregivers who engaged in pleasurable leisure activities more often had lower average blood pressure, compared to those who engaged in fewer leisure activities. In follow-up analyses, these activities were associated with a significant reduction in diastolic pressure (the second number in blood pressure), but not systolic pressure (the largest number).
As expected, caregivers who engaged in physical activity more frequently had lower blood pressure. However, other types of « more sedentary » activities (reading, listening to music, shopping) also led to a reduction in blood pressure.
Blood pressure also decreased following placement in a nursing home or death of the person with Alzheimer’s disease. This was consistent with previous studies that showed caregivers’ health improved when their caregiving duties ended.
“Being a caregiver for a loved one with a disability is a very stressful experience, associated with an increased risk of cardiovascular disease and death. Stress can contribute to high blood pressure, which is the most important risk factor for cardiovascular disease. The new results suggest that leisure activities can prevent the development of arterial hypertension in relatives caring for Alzheimer’s patients,” continues the researcher.
« Although the study cannot determine how many activities caregivers should do, we believe that three to four weekly activities that are enjoyed could have a positive impact on an individual’s blood pressure. »
“We recognize that caregivers may find it difficult to engage in enjoyable leisure activities because they are busy with their caregiving duties,” Dr. Mausbach said. So we work with caregivers to find activities they can participate in with more confidence, even when their spouse is present, and we help them use their schedule well so that they know the times of the day when they are the most able to do activities. If caregivers use respite centers, they are in an ideal position to use some of that time to engage in these activities. »
Source: Brent T. Mausbach et al. Engagement in pleasant leisure activities and blood pressure. Psychosomatic Medicine, 2017; 1.
Almonds may improve your appetite-regulating hormones when you snack on them. However, almonds do not appear to be more effective than a high-carbohydrate option in promoting satiety.
Nuts are a great source of protein and healthy fats. They can be eaten raw or roasted, ground into flour, or made into milk products like yogurt. They’re also a good source of vitamin E, magnesium, copper, manganese, phosphorus, potassium, iron, zinc, selenium, and folate.Nuts are also a good source of fiber, antioxidants, and phytochemicals.
A review of more than 100 studies published in 2018 concluded that eating nuts regularly can reduce the risk of heart disease, Type 2 diabetes, and some cancers. People who eat nuts regularly tend to weigh less and have healthier blood pressure and cholesterol levels. Eating nuts regularly also reduces inflammation and improves sleep quality.
Almonds are a great source of protein, fibre, vitamins B6, E, K and magnesium. They contain monounsaturated fats, polyunsaturated fats, antioxidants, phytosterols and vitamin E. They are also rich in potassium, copper, manganese, phosphorus, zinc, iron, calcium, sodium, selenium, iodine, thiamin, riboflavin, niacin, pantothenic acid, folic acid, biotin, choline, lysine, methionine, tryptophan, tyrosine, phenylalanine, histidine, arginine, proline, glycine, glutamic acid, alanine, valine, leucine, cysteine, serine, threonine, aspartic acid, glutamine, arginine, lysine, proline, valine, methionine and isoleucine.
A new study finds that eating almonds can lead to changes in appetite-regulating hormones that could potentially help people lose weight. These hormones play a role in regulating how much food you eat and how quickly your digestive system breaks down foods.
The researchers recruited 20 healthy adults who were overweight or obese and randomly assigned them to either eat almonds or a high-carbohydrate snack bar. They measured the subjects’ blood sugar, hunger hormones, and feelings of fullness before and after eating each snack. After eating the almonds, the participants reported feeling less hungry than when they ate the snack bar.
Blood sugar levels remained stable throughout the experiment, while the high-carbohydrate snack caused spikes in blood sugar. The researchers also noted that the almond snack lowered the levels of two hormones associated with hunger and fullness.
Participants who ate almonds experienced a reduction in C-peptide, a hormone that reflects the level of insulin produced by the pancrease. Lower levels of C-peptide are associated with a decreased risk of developing diabetes and cardiovascular disease.
In addition, the almond snack raised the levels of three hormones associated with satiety and fullness, including pancreatic polypeptide, glucose-dependent insulinotropic peptide, and glucagon-like peptide.
A 2021 meta-analysis including 86 randomized-controlled trials reported that nut consumption is unlikely to promote weight gain.
Vos dents jaunissent et vous pensez qu’il est temps de commencer un blanchiment dentaire? Vous ne supportez peut-être pas de vous voir dans le miroir à cause de la coloration de vos dents. Tout cela vous indique qu’il est temps d’entreprendre un traitement de blanchiment ? Vous avez probablement un bon œil. Blanchir vos dents peut faire des merveilles pour votre apparence et votre estime de soi. Mais avant de prendre rendez-vous avec votre dentiste, il y a des choses que vous devez d’abord considérer. Dans cet article, nous allons vous en dire plus sur les éléments que vous devez prendre en compte.
Recherchez et trouvez un dentiste de bonne réputation
Si vous vous lancez dans le blanchiment des dents, vous devez d’abord savoir à quoi vous avez affaire. Le blanchiment dentaire doit être opéré par un dentiste. Non seulement vous obtiendrez les meilleurs résultats de cette manière, mais c’est aussi le moyen le plus sûr. Cela signifie que vous devez trouver un dentiste de bonne réputation qui pourra vous guider tout au long du processus. C’est lui qui évaluera votre état et vous fera savoir si vous êtes un bon candidat pour le blanchiment. Le mieux est de demander des recommandations à votre dentiste de famille. Le plus important est que vous recherchez un dentiste de qualité.
Décidez du type de blanchiment que vous voulez faire
Lorsque vous devez choisir le type de blanchiment que vous souhaitez effectuer, vous avez l’embarras du choix. Vous pouvez choisir entre le blanchiment en cabinet et le blanchiment à domicile. Le blanchiment en cabinet est le type de blanchiment le plus populaire. Il s’agit d’un processus réalisé dans le cabinet du dentiste où des matériaux blanchissants sont placés sur vos dents. Il s’agit d’un processus rapide qui peut prendre entre 30 minutes et 2 heures. Le blanchiment à domicile se fait à l’aide d’une gouttière que vous portez sur vos dents. Il peut s’écouler jusqu’à 3 semaines avant que vous puissiez constater le résultat souhaité. Comme nous l’avons déjà dit, nous vous recommandons d’aller chez le dentiste, mais vous pouvez aussi le faire vous-même à la maison.
Renseignez-vous sur les coûts associés à la procédure
Quel que soit le type de procédure de blanchiment que vous choisissez, vous devez tenir compte des coûts qui y sont associés. Si vous disposez d’une assurance dentaire, vous pourrez peut-être bénéficier d’une prise en charge partielle de ces coûts. Vérifiez si votre assurance dentaire couvre le traitement ou non. De cette façon, vous saurez exactement combien vous devez dépenser. Car cela peut être coûteux.
The risk of cardiovascular disease would increase in people with symptoms of depression.
The researchers studied more than 7,300 elderly people in France with no history of heart disease, stroke or dementia at the start of the study period. About 30% of women and 15% of men had high levels of depressive symptoms.
Participants were reassessed two, four and seven years later. At each follow-up visit, about 40% of depressed people no longer showed symptoms of depression, while the same percentage had instead developed symptoms.
Less than 10 percent of participants were taking antidepressant medication .
Those who had high levels of depressive symptoms at each visit had an increased risk of heart disease or stroke within 10 years. This risk increased by 75% for individuals who presented with symptoms of depression at each of the four visits.
The results suggest that depression could be a risk factor for cardiovascular disease. However, they do not allow us to conclude that there is a cause and effect relationship.
The authors of the study (Dr Renaud Pequignot, INSERM, Paris) suggest that doctors should closely monitor people aged 65 and over with depression.
According to the World Health Organization, depression and cardiovascular disease are the leading causes of disability and death, respectively. Depression increases the likelihood of having cardiovascular disease and vice versa.
A link also exists between depression and stroke
Australian researchers have found that women with depression have a 2.4 times greater risk of stroke than those withoutdepression. « When physicians care for their patients, they need to determine the severity of their mood disorders and the long-term adverse effects they may have, » said Caroline Jackson, Ph.D., the first author of the study and epidemiologist at the University of Queensland in Australia. “Current stroke prevention guidelines tend to overlook the potential role of depression. »
This large-scale study examined the association between depression and stroke in 10,547 middle-aged women (47-52 years old) who had to answer questionnaires about their physical and mental health. About 24% of the participants said they were depressed.
A previous study reported a 30% increased risk in participants who were on average 14 years older. Although depression is associated with an increased risk of stroke, the absolute risk of stroke remains low (2%) for this age group.
The researcher does not know the reason for the association between depression and stroke.
“Inflammatory and immune mechanisms with adverse effects on blood vessels could be the cause,” says Dr. Jackson.
Source: Depression linked to almost doubled stroke risk in middle-aged women (source: Stroke, mai 2013).
In 2012, a meta-analysis published in the journal Stroke and listing 17 articles confirmed the existence of a link between the presence of depression and an increased risk (+34%) of stroke, taking into account the body mass index, smoking, high blood pressure, and diabetes. This correlation is similar for both men and women, although the prevalence of depression is higher in women. However, this study does not show that depression is the cause.
Another study confirms that symptoms of depression are causally linked to an increased risk of cardiovascular disease, suggesting that depression is a modifiable risk factor for heart disease.
The study involved over 10,000 English individuals whose mental state was assessed 6 times over a 20-year period.
The risk of coronary heart disease doubles when these people report depressive symptoms during at least 3 assessments.
However, no association between depression and stroke has been reported. According to the author of the study, depression is not a cause of stroke, but rather a consequence of the presence of a vascular disease.
Source: Depressive disorder, coronary heart disease, and stroke: dose-response and reverse causation effects in the Whitehall II cohort study. European Journal of Preventive Cardiology, février 2014.
According to a meta-analysis of 68,000 English people, subjects with symptoms of psychological distress (anxiety, depression, social problems or loss of confidence) have an increased risk of death ranging from 16% (if symptoms of psychological distress are mild) to 67% (if symptoms are high).
These deaths are caused by a heart attack or stroke (and in the case of high symptoms, cancer). Researchers have hypothesized that acute stress can reduce blood flow to the heart or that depression can lead to increased levels of inflammation (source: British Medical Journal, July 2012).
The risk of heart attacks and strokes can be halved if depressive symptoms are treated before signs of cardiovascular disease appear.
The results of this study confirm that depression increases the risk of cardiovascular disease, and emphasize the need to treat depression before the onset of these diseases, in order to reduce the consequences on the heart (heart attack) and the brain (stroke).
The researchers followed 235 depressive patients for 8 years. The risk of heart attack and stroke was reduced by 48% in those who received both psychotherapy and antidepressant medication, compared to those who did not.
Source: Effect of Collaborative Care for Depression on Risk of Cardiovascular Events: Data From the IMPACT Randomized Controlled Trial. Psychosomatic Medicine, 2013; 76 (1): 29.
The risk of cardiovascular disease would increase in people with symptoms of depression.
The researchers studied more than 7,300 elderly people in France with no history of heart disease, stroke or dementia at the start of the study period. About 30% of women and 15% of men had high levels of depressive symptoms.
Participants were reassessed two, four and seven years later. At each follow-up visit, about 40% of depressed people no longer showed symptoms of depression , while the same percentage had instead developed symptoms.
Less than 10 percent of participants were taking antidepressant medication .
Those who had high levels of depressive symptoms at each visit had an increased risk of heart disease or stroke within 10 years. This risk increased by 75% for individuals who presented with symptoms of depression at each of the four visits.
https://googleads.g.doubleclick.net/pagead/ads?client=ca-pub-6418418722285643&output=html&h=280&adk=4050653018&adf=1406710629&pi=t.aa~a.1319766153~i.13~rp.4&w=620&fwrn=4&fwrnh=100&lmt=1669589474&num_ads=1&rafmt=1&armr=3&sem=mc&pwprc=2836906431&ad_type=text_image&format=620×280&url=https%3A%2F%2Fwww.neuromedia.ca%2Fdepression-et-maladie-cardiovasculaire%2F&fwr=0&pra=3&rh=155&rw=619&rpe=1&resp_fmts=3&wgl=1&fa=27&uach=WyJXaW5kb3dzIiwiMTUuMC4wIiwieDg2IiwiIiwiMTA3LjAuNTMwNC4xMDciLFtdLGZhbHNlLG51bGwsIjY0IixbWyJHb29nbGUgQ2hyb21lIiwiMTA3LjAuNTMwNC4xMDciXSxbIkNocm9taXVtIiwiMTA3LjAuNTMwNC4xMDciXSxbIk5vdD1BP0JyYW5kIiwiMjQuMC4wLjAiXV0sZmFsc2Vd&dt=1669589474528&bpp=1&bdt=2194&idt=-M&shv=r20221110&mjsv=m202211100101&ptt=9&saldr=aa&abxe=1&cookie=ID%3D01b0c5a39770ecfb-22b2fab8fcd60093%3AT%3D1669036290%3ART%3D1669036290%3AS%3DALNI_MatZdN1a7l4Z79FbtLnVUmomwvcyg&gpic=UID%3D0000090044eb23b0%3AT%3D1669036290%3ART%3D1669588868%3AS%3DALNI_MYhSB2OGW_At8xnwXBIb344FORBjg&prev_fmts=300×600%2C0x0%2C620x280&nras=3&correlator=163436190768&frm=20&pv=1&ga_vid=614835833.1660652538&ga_sid=1669588869&ga_hid=1077856911&ga_fc=1&u_tz=-300&u_his=17&u_h=622&u_w=1106&u_ah=588&u_aw=1106&u_cd=24&u_sd=1.737&dmc=8&adx=75&ady=1336&biw=1089&bih=517&scr_x=0&scr_y=0&eid=44759875%2C44759926%2C44759837%2C44777877%2C42531706%2C31070762%2C44774605&oid=2&psts=AMjMPc2vjxKE-nSS-cijoN60Ip3iHoxilDeVug9YUCG13w8m0dDEDGHrSrXs4Pj9YLj7pIz_EQZJYWf-CfI_cw&pvsid=45713807817310&tmod=1802249955&uas=0&nvt=1&ref=https%3A%2F%2Fwww.neuromedia.ca%2Fwp-admin%2Fpost.php%3Fpost%3D2739%26action%3Dedit&eae=0&fc=384&brdim=0%2C0%2C0%2C0%2C1106%2C0%2C1106%2C588%2C1106%2C517&vis=1&rsz=%7C%7Cs%7C&abl=NS&cms=2&fu=128&bc=31&ifi=4&uci=a!4&btvi=2&fsb=1&xpc=j2OzmWXoxA&p=https%3A//www.neuromedia.ca&dtd=26 The results suggest that depression could be a risk factor for cardiovascular disease. However, they do not allow us to conclude that there is a cause and effect relationship.
The authors of the study (Dr Renaud Pequignot, INSERM, Paris) suggest that doctors should closely monitor people aged 65 and over with depression.
According to the World Health Organization, depression and cardiovascular disease are the leading causes of disability and death, respectively. Depression increases the likelihood of having cardiovascular disease and vice versa.
https://googleads.g.doubleclick.net/pagead/ads?client=ca-pub-6418418722285643&output=html&h=280&adk=4050653018&adf=1394324155&pi=t.aa~a.1319766153~i.19~rp.4&w=620&fwrn=4&fwrnh=100&lmt=1669589474&num_ads=1&rafmt=1&armr=3&sem=mc&pwprc=2836906431&ad_type=text_image&format=620×280&url=https%3A%2F%2Fwww.neuromedia.ca%2Fdepression-et-maladie-cardiovasculaire%2F&fwr=0&pra=3&rh=155&rw=619&rpe=1&resp_fmts=3&wgl=1&fa=27&uach=WyJXaW5kb3dzIiwiMTUuMC4wIiwieDg2IiwiIiwiMTA3LjAuNTMwNC4xMDciLFtdLGZhbHNlLG51bGwsIjY0IixbWyJHb29nbGUgQ2hyb21lIiwiMTA3LjAuNTMwNC4xMDciXSxbIkNocm9taXVtIiwiMTA3LjAuNTMwNC4xMDciXSxbIk5vdD1BP0JyYW5kIiwiMjQuMC4wLjAiXV0sZmFsc2Vd&dt=1669589474528&bpp=1&bdt=2195&idt=1&shv=r20221110&mjsv=m202211100101&ptt=9&saldr=aa&abxe=1&cookie=ID%3D01b0c5a39770ecfb-22b2fab8fcd60093%3AT%3D1669036290%3ART%3D1669036290%3AS%3DALNI_MatZdN1a7l4Z79FbtLnVUmomwvcyg&gpic=UID%3D0000090044eb23b0%3AT%3D1669036290%3ART%3D1669588868%3AS%3DALNI_MYhSB2OGW_At8xnwXBIb344FORBjg&prev_fmts=300×600%2C0x0%2C620x280%2C620x280&nras=4&correlator=163436190768&frm=20&pv=1&ga_vid=614835833.1660652538&ga_sid=1669588869&ga_hid=1077856911&ga_fc=1&u_tz=-300&u_his=17&u_h=622&u_w=1106&u_ah=588&u_aw=1106&u_cd=24&u_sd=1.737&dmc=8&adx=75&ady=1988&biw=1089&bih=517&scr_x=0&scr_y=0&eid=44759875%2C44759926%2C44759837%2C44777877%2C42531706%2C31070762%2C44774605&oid=2&psts=AMjMPc2vjxKE-nSS-cijoN60Ip3iHoxilDeVug9YUCG13w8m0dDEDGHrSrXs4Pj9YLj7pIz_EQZJYWf-CfI_cw&pvsid=45713807817310&tmod=1802249955&uas=0&nvt=1&ref=https%3A%2F%2Fwww.neuromedia.ca%2Fwp-admin%2Fpost.php%3Fpost%3D2739%26action%3Dedit&eae=0&fc=384&brdim=0%2C0%2C0%2C0%2C1106%2C0%2C1106%2C588%2C1106%2C517&vis=1&rsz=%7C%7Cs%7C&abl=NS&fu=128&bc=31&ifi=5&uci=a!5&btvi=3&fsb=1&xpc=e97WPeqDTZ&p=https%3A//www.neuromedia.ca&dtd=32 Source : Péquignot R. et coll. High Level of Depressive Symptoms at Repeated Study Visits and Risk of Coronary Heart Disease and Stroke over 10 Years in Older Adults: The Three-City Study. Journal of the American Geriatrics Society, 2016; 64 (1): 118.
A link also exists in depression and stroke
Australian researchers have found that women with depression have a 2.4 times greater risk of stroke than those without . « When physicians care for their patients, they need to determine the severity of their mood disorders and the long-term adverse effects they may have, » said Caroline Jackson, Ph.D., study author. and epidemiologist at the University of Queensland in Australia. “Current stroke prevention guidelines tend to overlook the potential role of depression. »
This large-scale study examined the association between depression and stroke in 10,547 middle-aged women (47-52 years old) who had to answer questionnaires about their physical and mental health. About 24% of the participants said they were depressed.
A previous study reported a 30% increased risk in participants who were on average 14 years older. Although depression is associated with an increased risk of stroke, the absolute risk of stroke remains low (2%) for this age group.
The researcher does not know the reason for the association between depression and stroke.
“Inflammatory and immune mechanisms with adverse effects on blood vessels could be the cause,” says Dr. Jackson.
Source: Depression linked to almost doubled stroke risk in middle-aged women (source: Stroke, mai 2013).
In 2012, a meta-analysis published in the journal Stroke and listing 17 articles confirmed the existence of a link between the presence of depression and an increased risk (+34%) of stroke, taking into account the body mass index, smoking, high blood pressure, and diabetes. This correlation is similar for both men and women, although the prevalence of depression is higher in women. However, this study does not show that depression is the cause.
Another study confirms that symptoms of depression are causally linked to an increased risk of cardiovascular disease, suggesting that depression is a modifiable risk factor for heart disease.
The study involved over 10,000 English individuals whose mental state was assessed 6 times over a 20-year period.
The risk of coronary heart disease doubles when these people report depressive symptoms during at least 3 assessments.
However, no association between depression and stroke has been reported. According to the author of the study, depression is not a cause of stroke, but rather a consequence of the presence of a vascular disease.
Source: Depressive disorder, coronary heart disease, and stroke: dose-response and reverse causation effects in the Whitehall II cohort study. European Journal of Preventive Cardiology, février 2014.
According to a meta-analysis of 68,000 English people, subjects with symptoms of psychological distress (anxiety, depression, social problems or loss of confidence) have an increased risk of death ranging from 16% (if symptoms of psychological distress are mild) to 67% (if symptoms are high).
These deaths are caused by a heart attack or stroke (and in the case of high symptoms, cancer). Researchers have hypothesized that acute stress can reduce blood flow to the heart or that depression can lead to increased levels of inflammation (source: British Medical Journal, July 2012).
The risk of heart attacks and strokes can be halved if depressive symptoms are treated before signs of cardiovascular disease appear.
The results of this study confirm that depression increases the risk of cardiovascular disease, and emphasize the need to treat depression before the onset of these diseases, in order to reduce the consequences on the heart (heart attack) and the brain (stroke).
The researchers followed 235 depressive patients for 8 years. The risk of heart attack and stroke was reduced by 48% in those who received both psychotherapy and antidepressant medication, compared to those who did not.
Source: Effect of Collaborative Care for Depression on Risk of Cardiovascular Events: Data From the IMPACT Randomized Controlled Trial. Psychosomatic Medicine, 2013; 76 (1): 29.
