because prevention is better than cure.

because prevention is better than cure.

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Dementia & Alzheimer’s (2007)

This study investigated dementia & Alzheimer’s. Over 8000 over-65s were monitored for development of dementia and Alzheimer’s over a 4 year period and details of their dietary habits were analysed. Daily consumption of fruits and vegetables was found to be associated with a decreased risk of all types of dementia. Weekly consumption of fish was also associated with a decreased risk of all dementias and Alzheimer’s Disease but only amongst those people who do not have the genetic variation called ApoE4. The regular use of omega-3 supplements was associated with a slight decreased risk of all dementias. However, the regular use of omega-6 supplements, where it was not balanced with the use of omega-3 supplements or fish, actually doubled the risk developing dementia amongst those who do not have the ApoE4 gene. In summary, frequent consumption of fruits and vegetables, fish, and omega-3 rich oils may decrease the risk of dementia and Alzheimer disease, especially among ApoE4 non-carriers. In addition, balance of the omega 3:6 ratio may also be an integral risk factor, although further research is warranted.

Gateau P et al.,’Dietary patterns and risk of dementia: The Three-City cohort study, Barberger’.  Neurology. 2007 Nov 13;69(20):1921-30

Click here for the abstract

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Homocysteine & Dementia (2002)

This study investigated homocysteine & dementia. A total of 1092 subjects without dementia (667 women and 425 men; average age, 76 years) were followed for an average of 8 years. Their homocysteine levels were monitored. The study used multivariable proportional-hazards regression to adjust for age, sex, apolipoprotein E genotype, vascular risk factors other than homocysteine, and plasma levels of folate and vitamins B12 and B6. Over a median follow-up period of eight years, dementia developed in 111 subjects, including 83 given a diagnosis of Alzheimer’s disease. The multivariable-adjusted relative risk of dementia was 1.4 (95 percent confidence interval, 1.1 to 1.9) for each increase of 1 SD in the log-transformed homocysteine value either at base line or eight years earlier. The relative risk of Alzheimer’s disease was 1.8 (95 percent confidence interval, 1.3 to 2.5) per increase of 1 SD at base line and 1.6 (95 percent confidence interval, 1.2 to 2.1) per increase of 1 SD eight years before base line. With a plasma homocysteine level greater than 14 micromol per liter, the risk of Alzheimer’s disease nearly doubled.

Conclusions: An increased plasma homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer’s disease.

Seshadri S et al, Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease.N Engl J Med., 346(7):476-83, 2002

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Nutrients & Brain Aging (2011)

This study investigated nutrients & brain aging. In this ground-breaking study, 104 healthy elderly people (with an average age of 87) had blood levels of 30 different nutrients measured. Mean age was 87 ± 10 years and 62% of subjects were female. Results suggested that two NBPs associated with more favourable cognitive and MRI measures: one high in plasma vitamins B (B1, B2, B6, folate, and B12), C, D, and E, and another high in plasma marine ω-3 fatty acids. A third pattern characterized by high trans fat was associated with less favourable cognitive function and less total cerebral brain volume. Depression attenuated the relationship between the marine ω-3 pattern and white matter hyperintensity volume.

Conclusion: 

Distinct nutrient biomarker patterns detected in plasma are interpretable and account for a significant degree of variance in both cognitive function and brain volume. Objective and multivariate approaches to the study of nutrition in brain health warrant further study. These findings should be confirmed in a separate population.

Click here for abstract.

Bowman GL, Silbert LC, Howieson D, Dodge HH, Traber MG, Frei B, Kaye JA, Shannon J, Quinn JF (2011) Nutrient biomarker patterns, cognitive function, and MRI measures of brain aging. Neurology Dec 28. [Epub ahead of print]

 

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Early Diagnosis of Alzheimer’s – Amyloid Protein vs Homocysteine Testing

Worldwide 46.8 million people have dementia. In the UK, 1 in 14 people over 65 have Alzheimer’s, the most prevalent form of dementia; and increasingly dementia sufferers are also struggling with other chronic conditions, such as diabetes and depression. Research on new strategies for earlier diagnosis is among the most active areas in Alzheimer’s science. This is as the majority of cases are diagnosed when irreversible brain damage or mental decline has already occurred. 

The amyloid protein test used for earlier diagnosis

Amyloid beta is a protein found in the brain that is involved in the pathophysiology of Alzheimer’s and cognitive decline. This 2019 study found that a blood test to measure amyloid, is 94% accurate in earlier diagnosis of Alzheimer’s disease. This is specifically when in combination with age and genetics (testing positive for the APOE4 gene) as risk factors. Whilst this is a positive development for future considerations in treating Alzheimer’s, there has been no successful amyloid-lowering drug trial to date.

In addition, it is well-known that the damaging clumps of amyloid protein can begin to develop and lead to brain atrophy decades before an individual even begins to experience symptoms of memory loss and cognitive function, so unless testing is given earlier on in life as a preventative measure, an amyloid-lowering drug when the damage has already been caused may not be very effective. 

Amyloid, a protective mechanism?

To date, the majority of research into the treatment of Alzheimer’s has been focused on the “amyloid hypothesis”. In 2018 alone, the US National Institutes of Health spent $1.9 billion on Alzheimer’s research. However, according to this study, there has been a 99% failure rate in the development of drugs that target this disease. Questions about the reliability of the amyloid protein hypothesis are being posed by scientists, after various studies discovering how amyloid plaques actually function as a type of sticky defence against bacterial invasion, lead to a different hypothesis. In one significant study, where mice that were genetically engineered to make Alzheimer’s proteins had bacteria injected into their brains, researchers found that amyloid plaques engulfed bacterial cells overnight, suggesting a protective mechanism.  

Why we cannot ignore the link between high homocysteine levels and Alzheimer’s 

According to a Consensus Statement released by an international panel of experts on dementia: Research has shown, time and time again, that having high homocysteine (Hcy) levels, and low folic acid and B12 levels in the blood correlate with an increased risk for Alzheimer’s disease.

An earlier review written by Professor David Smith in 2008, highlighted that there are a total of ‘seventy-seven cross-sectional studies on more than 34,000 subjects and 33 prospective studies on more than 12,000 subjects’…that…‘have shown associations between cognitive deficit or dementia and homocysteine and/or B vitamins.’ 

In a meta-analysis published in 2014 by BMC Public Health, raised homocysteine was considered to be one of the three strongest risk factors, along with low education and decreased physical activity.

Two further trials have clearly shown that lowering homocysteine, through the supplementation of B vitamins, reduced age-related cognitive decline in normal ageing and also slowed down both brain atrophy and cognitive decline in people with Mild Cognitive Impairment.

The efficacy of B vitamins to prevent the progression of Alzheimer’s.

In one study, 270 people over 70 with Mild Cognitive Impairment were recruited to trial the efficacy of B vitamins to prevent the progression of Alzheimer’s. MRI scans were done at recruitment and half the participants were given high doses of three B vitamins (B6, B9 and B12), half took a placebo tablet.

After 2 years, participants were scanned again and scientists found that the rate of brain atrophy in those treated with the B vitamins was on average 30% slower than those taking placebo. In addition, in those that had the highest homocysteine levels at baseline, the effect of B vitamin treatment was even more potent, helping to slow down brain atrophy by 53%. This result fits all the criteria for a disease-modifying treatment and so is especially important. There is, therefore, ample evidence to propose that lowering homocysteine by giving appropriate supplemental levels of homocysteine lowering nutrients, including B6, B12 and folic acid, would reduce risk.

In a commission published by the Lancet, 9 modifiable risk factors were outlined, clearly excluding homocysteine:  

Mid-life hearing loss – responsible for 9% of the risk Failing to complete secondary education – 8% Smoking – 5% Failing to seek early treatment for depression – 4% Physical inactivity – 3% Social isolation – 2% High blood pressure – 2%Obesity – 1% Type 2 diabetes – 1% 

Ignoring homocysteine is surprising, since a meta-analysis from the National Institute of Aging estimated that about 22% of Alzheimer’s disease may be caused by raised levels of homocysteine.

Integrating homocysteine testing and inexpensive B vitamin-based treatment into the heart of mainstream health strategies on Alzheimer’s could potentially play a vital role in the prevention of dementia, if caught early enough.

Every 3 seconds, someone in the world develops dementia and the International Alzheimer’s Society estimates that by 2050 there will be 131.5 million people living with this disease. This is not something we can ignore.

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