Posts Tagged ‘dementia’

Vitamin D for cognitive decline and Parkinson’s Disease

Sunday, July 25th, 2010

Archives of Internal MedicineTwo studies have just been published linking Vitamin D status to brain health. The authors of one paper appearing in Archives of Internal Medicine observe:

“To our knowledge, no prospective study has examined the association between vitamin D and cognitive decline or dementia.”

They examined the correlation between low levels of serum 25-hydroxyvitamin D (25[OH]D) and the risk of serious loss of cognitive function in 858 adults over 8 years. What did the data show?

“…substantial cognitive decline on the MMSE [Mini-Mental State Examination] in participants who were severely serum 25(OH)D deficient (levels <25 nmol/L) in comparison with those with sufficient levels of 25(OH)D (≥75 nmol/L)…the scores of participants who were severely 25(OH)D deficient declined by an additional 0.3 MMSE points per year more than those with sufficient levels of 25(OH)D.”

Thus their conclusion:

Low levels of vitamin D were associated with substantial cognitive decline in the elderly population studied over a 6-year period, which raises important new possibilities for treatment and prevention.”

Archives of NeurologyThe same week a study was published in Archives of Neurology that examines the relation between Vitamin D and Parkinson Disease. The authors set out to:

“…investigate whether serum vitamin D level predicts the risk of Parkinson disease.”

They crunched the numbers for 3,173 men and women who were followed up over 29 years (the baseline serum 25-hydroxyvitamin D level was determined from frozen samples) for the relationship between serum vitamin D concentration and Parkinson disease. The data showed that:

Individuals with higher serum vitamin D concentrations showed a reduced risk of Parkinson disease. The relative risk between the highest and lowest quartiles was 0.33 [about a third less] after adjustment for sex, age, marital status, education, alcohol consumption, leisure-time physical activity, smoking, body mass index, and month of blood draw.”

Thus their conclusion:

“The results are consistent with the suggestion that high vitamin D status provides protection against Parkinson disease.”

The results of these studies are not surprising considering that Vitamin D is necessary for regulating the immune inflammatory response and both dementia and Parkinson’s involve chronic brain inflammation. By the way, as stated in Science Insider:

“Most Alzheimer’s disease (AD) researchers agree that the disease starts ravaging the brain years, if not decades, before the first symptoms of forgetfulness appear.”

New diagnostic criteria were just proposed at the International Conference on Alzheimer’s Disease in Honolulu.

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Inflammation and insulin resistance genes are activated by surgery

Monday, June 28th, 2010

Journal of Clinical Endocrinology & MetabolismThis interesting paper recently published in the Journal of Clinical Endocrinology & Metabolism describes one of the reasons why support when undergoing a surgical procedure is so important (and links to the risks for delirium and accelerated dementia after surgery in the elderly). The authors set out to investigate the…

“…mechanisms behind postoperative insulin resistance and impaired glucose utilization…”

They shrewdly analyzed the expression of 21 target genes in abdominal adipose (fat) tissue from samples taken at the beginning and end of patients undergoing abdominal surgery. What did the data show?

“After surgery, both sc [subcutaneous] and omental adipose tissue mRNA levels of genes involved in the IL6 and nicotinamide phosphoribosyltransferase pathways were increased, whereas mRNA levels of insulin receptor substrate 1 and adiponectin were reduced. TNF pathway genes were differently regulated between sc and omental adipose tissue, and glucose transporter 4 mRNA levels were decreased only in omental adipose tissue.”

In other words, surgery elicits a shift in genetic expression that favors insulin resistance and inflammation. The authors conclude:

“The transcriptional output of pivotal inflammatory and insulin signaling pathway genes is altered after surgery…This could be of importance for the metabolic aberrations associated to postsurgical complications…”

This helps to understand why patients who are lucky enough to receive adjunctive support for the insulin and inflammatory signaling pathways and receptors recover faster and with less complications.

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The common danger of delirium and dementia after surgery, and pre-existing neurodegeneration

Tuesday, June 22nd, 2010

British Journal of SurgeryPerhaps you saw the recent New York Times article about the devastating experience of delirium in the hospitalized elderly. This is an important topic because it is associated with persistent diminished cognitive function, dementia and earlier death; and it is surprisingly common. As a number of studies point out, it is evidence of pre-existing neurodegeneration that puts brains ‘on the edge’. In a recent study published in the British Journal of Surgery the authors…

“…evaluated the incidence of postoperative delirium (POD) in elderly patients undergoing general surgery, the risk factors associated with POD, and its impact on hospital stay and mortality.”

Their data showed a huge difference between the study subjects with post-operative delirium and those without. The average length of hospital stay was 21 days with POD versus 8 days without. Moreover the mortality rate was 19% versus 8.4% respectively. Their conclusion is very important for both doctors and patients to bear in mind:

The incidence of POD is high in elderly patients for both emergency and elective surgery, leading to an increase in hospital stay and perioperative mortality. To minimize POD, associated risk factors of co-morbidity, cognitive impairment, psychopathology and abnormal glycaemic control must be identified and treated.

Note the comment on glycemic control—this will be expanded in a subsequent post.

British Journal of AnaesthesiaAlthough the danger is more marked in the elderly because there has been more time for neurodegeneration, it is not limited to the geriatric population. A recent paper in the British Journal of Anaesthesia warns that postoperative cognitive dysfunction (POCD, impaired cognition long after the surgery) must not be overlooked:

Postoperative delirium and cognitive dysfunction (POCD)…although not limited to geriatric patients, the incidence and impact of both are more profound in geriatric patients. Delirium has been shown to be associated with longer and more costly hospital course and higher likelihood of death within 6 months or postoperative institutionalization. POCD has been associated with increased mortality, risk of leaving the labour market prematurely, and dependency on social transfer payments.”

Practitioners take note:

“Delirium as a behavioural manifestation of cortical dysfunction is associated with characteristic signs. The EEG may show diffuse slowing of background activity. A wide variety of disturbances in neurotransmitter systems has been described. Serum anticholingeric activity has been associated with delirium and may be especially important, and also other mediators such as melatonin, norepinephrine, and lymphokinespostoperative chemokines have been found to be more elevated in patients who became delirious than in matched controls.”

Regarding postoperative cognitive dysfunction:

Increased inflammatory activity may play a role in early POCD. Elevated C-reactive protein is associated with impaired mental status in elderly hip fracture patients.”

How could we argue with what the authors assert in their conclusion:

Good basic care demands identification of at-risk patients, awareness of common perioperative aggravating factors, simple prevention interventions, recognition of the disease states, and basic treatments for patients with severe hyperactive manifestations.”

American Journal of Geriatric PsychiatryIt’s not just our British colleagues who are diligently investigating this devastating phenomenon. A fascinating study published recently in the American Journal of Geriatric Psychiatry reveals evidence that pre-existing white matter lesions are a risk factor for postoperative delirium:

“Delirium is a common and critical clinical syndrome in older persons. The authors examined whether any abnormalities in the white matter (WM) assessed by diffusion tensor imaging (DTI) predisposes patients to develop delirium…”

Their data clearly showed that damage to the white matter by accelerated neurodegeneration is an important risk factor:

“The abnormalities in the deep WMs and thalamus that were mainly accelerated by aging may account for the vulnerability to postoperative delirium…”

In other words, these are brains already ‘on the edge’ and predisposed to delirium and postoperative cognitive dysfunction from neurodegeneration that has been occurring for years. Now is the time, before more damage is done, to understand what you personally need to prevent unnecessary loss of brain function with age. Another paper published around the same time in the same journal focuses on the critical point of brain reserve. The authors provide…

“…a review of original articles on cognitive and brain reserve across many conditions affecting the central nervous system, with a focus on delirium…Reserve may be a potentially modifiable characteristic. Studying the role of reserve in delirium can advance prevention strategies for delirium and may advance knowledge of reserve and its role in aging and neuropsychiatric disease generally.”

I don’t think I can overemphasize this point. It is the brains that are low on reserve due to pre-existing neurodegeneration that are prone to delirium and postoperative cognitive dysfunction with all their depredations when challenged. How is your brain reserve? How easily do you experience cognitive (memory, focus, attention) or emotional (rage, irritability, depression, etc) dysfunction when stressed? There are objective, evidence-based ways to find out the contributing underlying causes and treat them from a functional perspective if we don’t wait too long.

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Mechanisms of cognitive decline, one of the greatest threats of aging

Sunday, April 11th, 2010

Nature Vol 464There is a lot being written about the ability of the brain to compensate for age-related changes with enhanced connectivity and efficiency that makes for better judgment and emotional maturity. The sad truth is that the brains of at least 50% of us will have sustained too much damage for this to come to fruition. The authors of an extensive review just published in the journal Nature begin with a statement important for anyone reading this:

Cognitive frailty is emerging as one of the greatest health threats of the twenty-first century. As the life expectancy of the population has increased, so too has the prevalence of cognitive decline and dementia, largely in the form of Alzheimer’s disease, which now affects almost 50% of adults over the age of 85 in the United States1. This startling figure can only grow as the average age of the population rises, so understanding the basis of cognitive decline during ageing is critical.”

They proceed to describe some of the major categories that define the process of molecular aging as it pertains to cognitive decline, noting that:

“…altered regulation of fundamental mechanisms of ageing may contribute to the pathogenesis of neurodegenerative disorders.”

It is this kind of attention to fundamental mechanisms with a systems biology perspective that is inherent to the functional medicine approach. The authors identify these major factors:

  1. Mitochondrial dysfunction (the ability of brain cells to produce energy to function and repair)
  2. Oxidative damage
  3. Epigenetic changes (changes in genes due to environmental stimuli)
  4. Autophagy and protein turnover (housecleaning)
  5. Insulin signalling

Additionally, they describe the role of the brain as the master regulator of aging throughout the body.

Their list is not complete—there are additional factors that we attend to including neurotransmitter metabolism and receptor sensitivity, fatty acid cell membrane integrity, the role of steroid hormones in the brain, autoimmune inflammation, excess cortisol (stress hormone) production, etc. If you want to be realistic about a strategy for preventing cognitive decline and Alzheimer’s disease, these are the kinds of things that you have to ask you doctor about and make sure they are being attended to.

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Acute or critical care hospitilization damages cognitive function in older adults

Monday, March 15th, 2010

JAMA 022410This is something to take to heart if you or someone you know require hospital care for an acute or critical illness. This paper just published in The Journal of the American Medical Association presents a study that set out to…

“To determine whether decline in cognitive function was greater among older individuals who experienced acute care or critical illness hospitalizations relative to those not hospitalized and to determine whether the risk for incident dementia differed by these exposures.”

If you have experience with this their conclusion will not surprise you:

“Among a cohort of older adults without dementia at baseline, those who experienced acute care hospitalization and critical illness hospitalization had a greater likelihood of cognitive decline compared with those who had no hospitalization. Noncritical illness hospitalization was significantly associated with the development of dementia.”

Note the last sentence: even noncritical illness hospitalization was associated with dementia. You too may have been distressed to see older folks decline in cognitive function following hospitalization due to depletion of critical internal resources that were already suboptimal, oxidative stress, etc.—and nothing was done to help it (even though functional medicine resources are available). Considering the central role of the brain in regulating all bodily functions, this must be kept  in mind when evaluating subsequent health complaints of any kind.

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Does your brain seem like it isn’t working as well? This predicts further decline.

Wednesday, January 27th, 2010

Alzheimer's & Dementia 0110A study just published in the journal Alzheimer’s & Dementia is a ‘heads-up’ for those who want to avoid cognitive impairment and dementia down the road. The researchers observed 213 subjects over an average of 7 years and documented that those with subjective cognitive impairment (SCI) declined significantly more rapidly to poor brain health and dementia than those with no experience of cognitive impairment. They concluded: “These results indicate that SCI in subjects with normal cognition is a harbinger of further decline in most subjects during a 7-year mean follow-up interval.” Having a little trouble remembering names, where you put your keys, what you came into the room for? Are you learning new things as easily as you did 5 years ago? Don’t wait, determine your brain health strategy now.

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Anti-inflammatory diets slow brain aging

Thursday, January 14th, 2010

Journal of NeuroscienceHere we have important evidence that what we eat has a big effect on how our brain ages. A review of recent studies was published in The Journal of Neuroscience that highlights the importance of slowing down the “age-related neurodegenerative diseases superimposed on a declining nervous system [that] could enhance the motor and cognitive behavioral deficits that normally occur in senescence.” The authors note that drugs are not available, so “it is important to determine what methods can be used today to increase healthy aging [and] forestall the onset of these diseases.” They emphasize the benefit of “diets rich in antioxidants and anti-inflammatory components such as those found in fruits, nuts, vegetables, and spices” to “lower age-related cognitive declines and the risk of developing neurodegenerative disease.” Are you getting what you need to slow the pace of neurodegeneration? The right tests can tell.

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Insulin resistance and dementia or Alzheimer’s disease

Sunday, November 29th, 2009

No doubt about it, you have to take care of your blood sugar and insulin to prevent your brain from degenerating. Here are several papers published in prestigious journals that show the strong connection between insulin resistance and dementia or Alzheimer’s disease:

  1. Insulin resistance and cognitive impairment in Archives of Neurology
  2. Hyperinsulinemia and risk of Alzheimer’s disease in Neurology
  3. Insulin resistance and executive dysfunction in the Journal of the American Geriatrics Society
  4. Hyperinsulinemia and Alzheimer’s disease in the journal Age and Ageing
  5. Body mass index, cardiovascular risk factors, and dementia in Archives of Internal Medicine

Testing your levels of hemoglobin A1C,  glucose, insulin and triglycerides along with measuring your waist-to-hip ratio are among the ways we can see how you’re doing.

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Waist-to-hip ratio in midlife linked to later dementia

Tuesday, November 24th, 2009

Factors that place fat around the waist (insulin resistance) and the activity of that fat tissue (production of signaling molecules that promote inflammation) are both at play behind the connection documented recently in this paper published in the journal Neurology. The authors found that “…a midlife WHR [waist hip ratio] greater than 0.80 increased risk for dementia approximately twofold…,” and conclude: “There are midlife and late-life implications for dementia prevention, and analytical considerations related to identifying risk factors for dementia.” Here are a few more papers related to the same finding:

  1. Research on diabetes, hyperinsulinemia and dementia in Dementia and Geriatric Disorders
  2. A paper on abdominal obesity and Alzheimer Disease published in the same journal
  3. A study in Archives of Neurology that concludes: “A larger WHR may be related to neurodegenerative, vascular, or metabolic processes that affect brain structures underlying cognitive decline and dementia.”


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Advanced dementia is a terminal condition

Thursday, October 29th, 2009

This paper in the New England Journal of Medicine details the clinical course of advanced dementia. It is a terminal condition. Whatever your age, now is the time to have a sound, evidence-based strategy for taking care of your brain.

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