Anti-Inflammatory Foods and Drugs for Alzheimer’s Dementia
The “inflammation hypothesis” is one of the more than a dozen published theories on the cause of Alzheimer’s disease. In my video on anti-inflammatory foods, I discussed the dietary inflammatory index, a composite net scoring of all the anti-inflammatory foods versus pro-inflammatory foods people eat. A systematic review of the association between dietary inflammatory index scores and cognition noted that pro-inflammatory diets have been linked to worse memory and up to six times the odds of suffering cognitive impairment. However, the one MRI study assessing brain volumes found no evidence of structural differences between the extremes of dietary inflammation scores.
There have been some two dozen observational studies suggesting that taking anti-inflammatory drugs like aspirin may protect against Alzheimer’s disease. The use of anti-inflammatories could potentially explain why Alzheimer’s rates in those suffering from arthritis are nearly half that of the general population. One study published in the New England Journal of Medicine followed about 7,000 men and women 55 years and older found that those prescribed NSAID drugs for a total of 24 months or more had only 20 percent of the risk of developing Alzheimer’s disease within the subsequent seven years. Might taking low-dose aspirin help prevent or treat dementia? Randomized controlled trials involving literally tens of thousands of people have tried putting those very questions to the test.
Compared to placebo, aspirin did not appear to affect the decline in brain function among older adults, did not prevent dementia, and did not improve the cognition of those already with Alzheimer’s. What it did do was quadruple the risk of being hospitalized with major bleeding, (and 2 percent of those in the aspirin group died of brain hemorrhaging). No evidence of benefit for cognitive decline, dementia, or cognition: just more adverse events, like ten times the rate of gastrointestinal side effects.
How can we reconcile the observational data with the interventional data? One possibility is the randomized trials caught people too late. One of the advantages of observational studies is that it’s easier to collect data over decades. For example, those with higher levels had three times the risk of developing dementia 25 years later. So, inflammation may play a role, but you may have to catch it early.
Alzheimer’s manifests as a disease of the elderly, but it’s a disease that may take decades to develop. Most Alzheimer’s sufferers aren’t diagnosed until they’re in their seventies, but we now know that their brains began deteriorating long before that. Based on thousands of autopsies, pathologists seemed to detect the first silent stages of Alzheimer’s disease—what appear to be tangles in the brain—in about half of people by age fifty and even 10 percent of those in their twenties. Though Alzheimer’s is incurable, it may be preventable.
The “inflammation hypothesis” is one of the more than a dozen published theories on the cause of Alzheimer’s disease. In my video on anti-inflammatory foods, I discussed the dietary inflammatory index, a composite net scoring of all the anti-inflammatory foods versus pro-inflammatory foods people eat. A systematic review of the association between dietary inflammatory index scores and cognition noted that pro-inflammatory diets have been linked to worse memory and up to six times the odds of suffering cognitive impairment. However, the one MRI study assessing brain volumes found no evidence of structural differences between the extremes of dietary inflammation scores.
There have been some two dozen observational studies suggesting that taking anti-inflammatory drugs like aspirin may protect against Alzheimer’s disease. The use of anti-inflammatories could potentially explain why Alzheimer’s rates in those suffering from arthritis are nearly half that of the general population. One study published in the New England Journal of Medicine followed about 7,000 men and women 55 years and older found that those prescribed NSAID drugs for a total of 24 months or more had only 20 percent of the risk of developing Alzheimer’s disease within the subsequent seven years. Might taking low-dose aspirin help prevent or treat dementia? Randomized controlled trials involving literally tens of thousands of people have tried putting those very questions to the test.
Compared to placebo, aspirin did not appear to affect the decline in brain function among older adults, did not prevent dementia, and did not improve the cognition of those already with Alzheimer’s. What it did do was quadruple the risk of being hospitalized with major bleeding, (and 2 percent of those in the aspirin group died of brain hemorrhaging). No evidence of benefit for cognitive decline, dementia, or cognition: just more adverse events, like ten times the rate of gastrointestinal side effects.
How can we reconcile the observational data with the interventional data? One possibility is the randomized trials caught people too late. One of the advantages of observational studies is that it’s easier to collect data over decades. For example, those with higher levels had three times the risk of developing dementia 25 years later. So, inflammation may play a role, but you may have to catch it early.
Alzheimer’s manifests as a disease of the elderly, but it’s a disease that may take decades to develop. Most Alzheimer’s sufferers aren’t diagnosed until they’re in their seventies, but we now know that their brains began deteriorating long before that. Based on thousands of autopsies, pathologists seemed to detect the first silent stages of Alzheimer’s disease—what appear to be tangles in the brain—in about half of people by age fifty and even 10 percent of those in their twenties. Though Alzheimer’s is incurable, it may be preventable.
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