Alzheimer’s disease is now the third leading cause of death in the United States, following only cardiovascular disease and cancer. There are approximately 5.2 million Americans with AD, but this estimate ignores the many young Americans destined to develop AD during their lifetime:
What to look for on your blood work:
- Amyloid-B a toxic 42 amino acid peptide that aggregates and forms plaques in the brain with age. Amyloid-beta is associated with Alzheimer’s disease, a progressive neurodegenerative disease that can occur in middle or old age. AD is the most common cause of dementia.
- Apolipoprotein E (ApoE): a lipoprotein produced in the liver and brain. In the brain, ApoE transports fatty acids and cholesterol to neurons. In the bloodstream, it binds and transports cholesterol, bringing it to tissues and recycling it back to the liver. Approximately 25% of people carrying a genetic variant of this lipoprotein called ApoE4, which is associated with higher circulating levels of LDL cholesterol and a 2-to-3-fold increased risk of developing Alzheimer’s disease.
- The importance of insulin sensitivity: if your fasting insulin is over 4.5 milli-international units per liter, your hemoglobin A1c over 5.5 percent, or your fasting glucose over 93 milligrams per deciliter, you likely have insulin resistance, arguably the single most important metabolic contributor to Alzheimer’s disease development progression.
- Keeping inflammation low and monitoring C reactive protein: CRP is produced by the liver in response to any type of inflammation. Specifically, you want to know your hs-CRP (high-sensitivity CRP), since the standard CRP test is often too insensitive to distinguish optimal from mildly abnormal. Your hs-CRP should be below 0.9mg/L. if it is higher, you want to determine the source of the inflammation. This may be from too much sugar and other simple carbohydrates, or bad fats (for example, trans fats), a leaky gut, gluten sensitivity, poor oral hygiene, specific toxins, or any of many other sources. When the source is located. It should be removed, and the hs-CRP rechecked.
- Prevalence and causes of zinc deficiency: zinc deficiency is relatively common (1billion) and may be associated with poor absorption due to reduced gastric acidity (e.g., due to H. Pylori and or the use of proton pump inhibitors), a zinc deficient diet (e.g., due to vegetarianism without supplementation), adrenal stress, diabetes, alcohol use, toxic exposure, intestinal parasites, or aging.
Zinc deficiency, which is common in aging individuals, affects many functions that are directly or indirectly related to cognitive performance and Alzheimer’s disease. For example, zinc deficiency induces insulin resistance, a known risk factor of AD. Zinc deficiency also increases inflammation and reduces the finely tuned nature of the immune response, resulting in a reduced specific response (and thus loss of resistance to infectious agents) and a greater autoimmune response. Zinc is also involved in wound healing, DNA repair, and oxidative damage. Zinc deficiency is associated with increased aging, increased susceptibility to toxins, increased susceptibility to infection, increased production of reactive oxygen species, reduced hormonal function, reduced adrenal support, increased susceptibility to copper toxicity, and gastrointestinal hyperpermeability. Furthermore, treatment has been shown to mitigate cognitive decline. Therefore, zinc deficiency is a concern as a potential contributor to cognitive decline.
- Slower rates of decline in APOE e4 carriers consuming larger amount of dietary omega 3 from seafood: consumption of seafood was associated with slower decline in semantic memory and perceptual speed in separate models adjusted for age, sex, education, participation in cognitive activities, physical activity, alcohol consumption, smoking, and total energy intake. In secondary analyses, APOE e4 carriers demonstrated slower rates of decline in global cognition and in multiple cognitive domains with weekly seafood consumption and with moderate to high long-chain n-3 fatty acid intake from food. These associations were not present in APOE e4 noncarriers.
- A cyclical ketogenic diet beneficial for aging and memory: It’s been shown that long-term exposure to a ketogenic diet (KD) fed every other week starting in middle age, reduces midlife mortality and preserves memory in aging male mice. In health span testing, a striking effect of cyclic KD on memory as well as more modest effects on a broader range of measures. A consistent memory improvement in two distinct tasks over 6 months.
- Detecting fungi where there should not be any: it is noteworthy that a recent report described the direct detection of fungi in the brains of patients who had died with Alzheimer’s disease, contrasting with a lack of detection of fungi in control brains. The increasing number of reports of various pathogens identified in the brains of patients with Alzheimer’s disease-from viruses such as Herpes simplex to oral bacteria such as P. gingivalis to fungi such as C. glabratus-raises the possibility what is referred to as Alzheimer’s disease may be the result of a protective response to various brain perturbations.
- Environmental Relative Moldiness index (ERMI) associated with childhood asthma in high scoring homes: the average ERMI in the homes of asthmatic children in Kansas City was nearly 3 times higher than in the randomly selected homes from the state of Kansas. People may not even realize that they are living in this chronic mold exposure that is causing continuous low levels of inflammation within the body.