Despite evidence that non-smoking, normal BMI, regular exercise, high fruit/vegetable intake and low/moderate alcohol intake, less than 1% of men change lifestyle. Translation: many don't want health even when presented with evidence of its benefits and the means to achieve it.
This study found a decrease in cognitive decline in individuals undergoing these lifestyle changes.
increased estradiol and estrone levels in men associated with cognitive decline. This was distinct from age, CVD, and APOE genotype. This points to a clear association between increased aromatase activity and inflammation that contributes to cognitive decline in men.
adherence to a MedDiet pattern is associated with less cognitive decline, dementia, or AD
higher adherence to a MedDiet was related to either slowing the rate of cognitive decline, minimizing the conversion to AD or improving the cognitive function
The more specific cognitive domains that improved with MedDietS were memory, delayed recognition, executive function, long-term working memory, and visual constructs
insulin resistance shown to play a role in cognitive impairment. Rising Insulin resistance is not just associated with obesity, but also brain dysfunction similar to that in strokes. This indicates a vascular component in the cognitive function. The same rise in obesity will likely result in a rise in neurodegenerative disorders.
Study finds suggestion of cognitive protection by enduring estrogen exposure. Interesting, that estrogen seems to protect against cognitive decline in women, yet increases cognitive decline in men.
This study points to an association between a low-normal TSH and cognitive decline in the elderly. An association is not causative, but functional hypothyroidism does result in cognitive impairment, so the association would logically fit. The results of this study do as well.
Huperzine A, a natural acetylcholinesterase inhibitor, provides neuroprotection through increase mitochondrial function and decrease in accumulated amyloid Beta protein.
a deficit in CoQ10 status has been determined in a number of neuromuscular and neurodegenerative disorders
A secondary loss of CoQ10 status following HMG-Coa reductase inhibitor (statins) treatment has be implicated in the pathophysiology of the myotoxicity associated with this pharmacotherapy