The topic of Alzheimer's disease (AD) is near and dear to my heart and a harrowing one because my father developed dementia. It took his life after a long battle. A sense of fear bubbles to the surface once in a while as I wonder if the same fate awaits me.
According to recent estimates, AD may be ranked as the third leading cause of death, just behind heart disease and cancer. We now understand that AD is a brain disorder and the most common cause of dementia. AD was named after Dr. Alois Alzheimer in 1906, as she observed changes in the brain tissue of a woman who died of an unusual mental illness, exhibiting symptoms of memory loss, language problems, and unpredictable behavior. In this patient's brain tissue, she identified abnormal clumps (amyloid plaques) and tangled bundles of fibers (neurofibrillary, tangles, or tau). These plaques and tangles are considered the main characteristics of AD. Another characteristic is the loss of connections between neurons, leading to challenges in transmitting signals within different parts of the brain as well as from the brain to the rest of the body.
As scientists continue to unravel the various aspects of AD, it’s now understood that changes in the brain may begin a decade or more before symptoms initially manifest. The damage initially occurs in the hippocampus and entorhinal cortex - parts of the brain that are essential in forming memories. As additional neurons die, more areas in the brain are also affected. By the final stage, cell damage is widespread, resulting in significant brain shrinkage.
In recent years, scientists have made tremendous progress but still haven’t completely understood the pathophysiology and etiology of AD. It’s complex! Causes may include a combination of aging, inflammation, insulin resistance, mitochondrial dysfunction, genetics, and epigenetic factors. These factors that may increase or reduce the risk of developing AD vary from person to person.
Genetics – Alone, does it determine fate?
There may be multiple genes involved as risk factors for AD. In particular, one of the APOE genetic variants - APOE ε4 - is infamous and draws special attention. (Thank God, I found out I don't have this variant!) However, it’s crucial to keep in mind that carrying the APOE ε4 does not necessarily mean that a person will develop the disease, and individuals with no APOE ε4 may still develop AD.
Epigenetic Factors – Do they play a role?
Research suggests a host of factors beyond genetics may play a role in the development of AD. There has been a great deal of discussion on the connections between cognitive decline and cardiovascular disease, Type 2 diabetes, and obesity. Moreover, nutrition, physical activity, social engagement, and mental stimulation are all hot topics that are considered more promising modalities for reducing the risk of cognitive decline.
Diet may influence cognitive aging via several inflammatory pathways. Diet plays a crucial role in delivering antioxidants and anti-inflammatory factors, balancing gut microbiomes, and addressing digestive disorders linked to food sensitivities that may alleviate inflammation and slow AD progression. Several dietary approaches have been studied for preventing or managing AD, including the Ketogenic diet, anti-inflammatory diet, Mediterranean diet, DASH diet, Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet, and intermittent fasting. So, the big question: which diet to choose? Here is how to prioritize: Don’t worry about the name of the diet but focus instead on creating a personalized approach by sticking with the principles focused on taming systemic inflammation, reducing oxidative stress, and optimizing mitochondrial function:
Replace processed foods with a whole-food-based diet comprised primarily of plant-based foods with a heavy intake of vegetables and fruits.
Go low on grains: Many people have non-Celiac gluten sensitivity, promoting a chronic inflammatory state, contributing to brain neuroinflammation and AD pathogenesis. Other non-gluten grains contain antinutrients such as lectin and phytates, which can also contribute to inflammation. However, a small intake of pseudo-grains (quinoa, amaranth, and buckwheat) is considered benign.
Reduce glycemic load: Recent studies have shown that a high-glycemic diet is associated with a greater cerebral amyloid burden. Poorly controlled blood sugar may increase the risk of developing AD. Some even call AD “diabetes of the brain” or “Type 3 diabetes”.[6,7] Consuming low glycemic foods and meals with low glycemic loads may lower the risk of AD or slow AD progression. Also, foods rich in omega-3 polyunsaturated fats should be consumed regularly to improve insulin sensitivity.
Special foods for supporting mitochondrial function: That mitochondrial dysfunction promotes AD is a well‐accepted finding. There is evidence to support the notion that abnormal mitochondrial function may trigger neurodegeneration. The Mito Food Plan can be incorporated as an addition. It’s described as the anti-inflammatory, low-glycemic, gluten-free, low-grain, high-quality fats approach (many things listed above). It also emphasizes supporting mitochondria function to improve energy production using therapeutic foods such as DHA from omega-3 polyunsaturated fat and coconut MCT oil.
From the prospective of a healthy diet, cooking methods should also be considered. Improper cooking habits can contribute to the loss of nutrients and the formation of toxins such as advanced glycation end products (AGEs). Studies have shown that the accumulation of AGEs in the body can cause excess oxidative stress and exacerbate neurodegenerative and other chronic diseases. In general, steaming is an excellent way to cook vegetables, and low heat and wet cooking style is recommended for preparing animal meat.
A COUPLE OF SUPPLEMENTAL THERAPIES