Lecture 6 - Meditation and Aging

aging

well known fear of aging in our society, mostly due to health concerns, invariant aging hypothesis, interested in science based strategies to slow aging, fear of aging is common

aging and cognition

most functions peak at age 20 and decline after with few exceptions like vocab and info, reaction time increases first, especially for complex tasks and effects on accuracy occur later

aging and cognition

in the OSPAN test, education is a sort of moderating factor, those who are educated are more likely to perform at a level that is subpar with young people

aging and the brain

the brain changes with age due to cortical atrophy so losing cells and connections, neurotransmission being the amount of chemicals released or receptors responsive to them, activity imbalances and cellular aging (epigenetics), brain changes could contribute to cognitive changes, cortex changes happen first so either loss of cells or loss of connections between cells then cellular aging occurs after

cortical thinning with age

effects are greater in the frontal, parietal and temporal areas, shows relatively more thinning with age

regions most vulnerable in aging

superior, middle ad inferior frontal gyri, superior and middle temporal gyri, precuneus, inferior and superior parietal cortices and temporo-parietal junction, though thinning of the frontal and parietal regions tends to be greater, thinning of the temporal cortex is especially concerning for cognition

thinning predicts future impairment

accelerated thinning in temporal cortex is associated with future cognitive impairment, cortex thins overtime but some are relatively more predictable than others, at an early stage of studying this association, not a great diagnostic value

brain reserve theory

a certain amount of cortex may be required to maintain performance, excessive thinning may exhaust the reserve and lead to cognitive impairment/disease, in this framework, maintenance of the cortex via meditation may preserve performance with age, doesn’t acknowledge all the things we do to mitigate decline with age

cognitive reserve theory

view performance as the result of cognitive processes so things like education and meditation may grant new cognitive strategies that compensate for aging

meditation and the brain with age

most of the studies are observational, easier to use but conclusions we make are weaker/limited cause so many alternative explanations could be interpreted from our results, meditators do not have larger brains but they may show slower gray matter decline and preservation of white matter tracts with age, when metrics are used to estimate brain age from brain structure, meditators are classified as having younger brains (look younger in terms of their features

glucose metabolism

marker of brain activity, declines with age but decline is less significant in meditators, effects are strongest in the vmPFC, posterior cingulate cortex and the insula

chronic stress

risk factor for cortical thinning, notable in psychiatric disorders, HPC is sensitive as the role of cortisol is speculated, by reducing stress and/or improving mood, meditation might affect brain structure by improving sleep or cardiovascular function, mechanisms almost certainly intact, some evidence that more stressful events we have the more cortical thinning we get, meditation helps mitigate stress so in turn it aids in reducing thinning, effects on the brain are interesting but are most interesting if they are also connected with effects on cognition

meditation, aging and cognition

in controls but not meditators, aging is associated with reduced gray matter, impaired attention and increased reaction time

raven’s progressive matrices

non verbal test of fluid intelligence, often used in IQ assessments, performance normally declines with age, decline is less evident in meditators and yogi, favored cause seen as a non verbal measure of cognitive function, one of the better tests you could use

criticisms of meditation and aging studies

there is a hyper fixation on brain reserve within most studies, less consideration of cognitive reserve (harder to study but critical to explore), even in studies relying on brain reserve theory, few studies correlate brain with behavior so need more evidence of this type, many studies are cross-sectional and observational so you cant make any causal claims, sample sizes are small, effects und are weeak, high risk of bias in some studies, need for large, controlled, high quality randomized control trials

the age well RCT

found no effects on brain structure/perfusion but high global composite score (reflects multiple abilities), age related changes in macro level brain structure are linked to changes in brain cells at the micro level, the study was conducted over 18 months and attrition rate was low

cells of the body

the tissues in our body, including the brain are made of cells, they express a wide range of structures called proteins which are vital to the function of the cell

DNA is within the cell

the instructions for producing proteins are contained in the genetic material (DNA) within the cell’s nucleus, maybe changes in DNA overtime that are relevant to aging may be affected by meditation in some capacity

DNA copying during replication

throughout our lifetime, our cells maintain themselves via replication/mitosis, each time it duplicates, DNA must be copied, copy process malfunction could cause some mutation, cells can only replicate a certain number of times

the problem of cellular aging

enzymes that duplicate DNA during the division process cannot copy the whole DNA strand they have to stop before the end, each time the cell divides, some DNA is lost, cells can only divide a finite number of times

how do we avoid the cellular aging problem?

the ends of the chromosomes are capped by telomeres, when DNA is copied during division, telomeres are lost instead of valuable DNA, these telomeres progressively shorten with cell division, with some maintenance by telomerase (enzyme that manages telomeres

telomere length as a predictor

it is inversely correlated with risk for coronary disease, dementia, psychiatric disorders and cancer prognosis, associated with telomere disease, generally reduced by stress, correlations with mood and cognition are less studied and likely more complicated

effects of meditation on telomeres

meditation may enhance telomerase activity but tends not to affect telomere length, meditation induced stress reduction is thought to be key, relationship between stress and telomeres noted elsewhere, effects seen for many styles (ex; loving kindness, mindfulness and zen), effects are greatest in people with certain personality traits (high neuroticism and low agreeableness)

caveats of meditation effects on DNA

most studies examine white blood cells (leukocytes), it is unknown if telomeres in neurons respond similarly as neurons do not divide, no known direct association between telomeres and neuronal function (speculative), studies may be more relevant to immune function, some studies report increased length (controversial) and sample size is often small, there are also very few studies with quality issues being an issue

methylation of DNA

DNA is packaged in a particular way (tightly coiled, wrapped up and surrounded by other structures), when the packaging changes, access to and protein expression from the DNA changes, this packaging changes with your experiences, including those that come with aging

epigenetics

refers to modifications in DNA function that occur without changes in DNA sequence several epigenetic processes, including methylation (addition of methyl groups) of DNA, as we age, there is increased methylation in the DNA (silencing of info) and changes in protein expression, it is a robust marker of aging, we can use it to predict age (if there’s more methylation this indicates faster aging)

effects of meditation on methylation

in heterogeneous samples from 30 to 60, meditators show a similar change in DNA methylation with aging to controls (no difference), implications of the epigenetic modifications are unclear as specific patterns of gene methylation are not being reported and patterns of protein expression are not being investigated, there are very few studies and aging-related changes may be distinct from other short term changes

aging and disease

thanks to modern medicine, we now live longer than before and have the largest elderly cohort in history, however there are health risks with advanced aging, including dementia

dementia

disorder marked by memory impairment, personality changes and impaired reasoning, the most common form is Alzheimer’s Disease

alzheimer’s disease symptoms

memory loss, language problems, difficulty in doing simple tasks, disorientation in time and space, loss of reasoning capacity, difficulty in having elaborate thoughts, loss of objects, mood changes, behavioral changes and loss of initiative

alzheimer’s disease (AD)

a progressive, incurable disorder, no highly effective treatments, most common form of dementia affecting over 50 million ppl, and in 10-15% of people over the age of 65, care is very costly due to high levels of impairment

neural features of AD

neuronal loss, neurofibrillary tangles, B-amyloid accumulation and reduced cholinergic tone

progression of AD

MCI is an indicator of AD, temporal cortex is the first to change in the disorder then it spreads to widespread brain atrophy

meditation and AD

risk factors include hypertension, blood, perfusion and stress which are all affected by meditation, it may be of some benefit in slowing the progression of AD, effects of meditation in the elderly and those with AD are of interest, meditation may rescue cognitive function lost during aging/neurodegenerative disease, attention in the elderly appears most sensitive to meditation, other effects are less strong, disrupted mood and sleep are major difficulties in AD and may be sensitive to meditation, it may also be worthwhile to examine caregivers of patients with AD

criticism of meditation in AD studies

there are few studies being done on it, the study design is often poor as there is a lack of control groups, biomarkers related to AD like amyloid beta levels and genetic tests are often not recorded, there is a hyperfixation on cognition in AD which may be a mistake and examining only patients with AD may be too narrow