Alzheimer's disease

Alzheimer’s Disease, a Nutritional Therapy Approach

1. What is Alzheimer’s Disease

Alzheimer’s disease (AD) is a leading cause of dementia in people between the ages of 60 and 70 years. According to the World Health Organisation, 70% of the 50 million people worldwide, who are living with dementia, have AD.

Although the terms are sometimes used interchangeably, dementia and Alzheimer’s are not the same thing. There are different types of dementia, like AD, vascular, with Lewy bodies, Parkinson’s, fronto-temporal and others. Term dementia isn’t a specific disease, but rather a general name to describe any decline in brain function. This affects memory, focus, judgment, language or visual perception, and is serious enough to interfere with daily life functions.

Symptoms

Alzheimer’s disease develops when nerve cells (neurons) in the brain stop working properly and ultimately die. It is a progressive, irreversible (at least according to Western Medicine) disorder of the brain. It affects the parts involved in thinking, remembering, using language, problem-solving and other cognitive abilities.

People affected may become confused, suspicious, depressed, anxious, angry or withdrawn. As the disease becomes more severe, fundamental bodily functions, like talking and walking start to deteriorate too. Eventually people with AD become bed bound and require constant help with activities like eating and drinking. Unfortunately AD can shorten people’s life span dramatically.

Diagnosis

A complete examination covers a thorough medical and family health history. This aims to identify relatives with a history of AD, which indicates higher increased risk of AD onset. In addition, doctor should order blood and urine tests to rule out other conditions with symptoms resembling those of AD.

Few short, basic cognitive skills tests, involving remembering a short list of words or doing some simple calculations, may also be used.

Neurological exams, that test for reflexes, coordination, eye movement, sensation, speech, muscle tone and strength can rule out other illnesses. For example a stroke may cause AD-like symptoms.

After the above preliminary investigations, doctors may decide to test for the presence of two proteins in patients’ cerebral-spinal fluid. The first protein is “amyloid beta 42”, which has the ability to increase brain formation of amyloid plaques. These plaques are sticky clumps of protein, which will eventually engulf surrounding dying nerve cells. The second protein is “tau”, and is very important for normal brain function. In in AD parts of its structure become twisted and called neurofibrillary tangles, which may damage and kill neurons. Neurofibrillary tangles and amyloid plaques are the main diagnostic features of AD.

A new study found that blood tests can detect brain beta amyloid protein build up long before AD onset (1). As of writing this article this diagnostic tool is not available yet.

2. Possible Causes of Alzheimer’s Disease

Although there is not one cause to AD, scientists believe that it develops due to genetic, environmental, and lifestyle factors.

One certain fact is that AD is not part of normal ageing as there are so many people entering their nineties with their cognitive skills intact.

So, let’s investigate possible causing factors:

Genetics

Scientists have identified over 20 genes that seem to raise the chances. While 25% of patients have a family history of AD, only 1% inherit the gene mutation that causes it (2).

Scientists found a group of genes called APOE that can raise chances of developing the late onset type of AD. For instance, the APOE4 gene, present in 10-15% of people, having one copy of E4 (E3/E4) increases the risk 3 times. While two copies (E4/E4) can increase the risk by 12 times (3).

However, having these genetic variants does NOT mean a person will develop the condition. Various epigenetic mechanisms can switch genes on and off and up or down regulate their expression. Factors such as lifestyle, including stress levels and diet, as well as environmental, play a critical role in gene activity.

Methylation

Methylation is important for mitochondrial function and energy production. Low mitochondrial function and poor methylation can lead to low energy, poor thyroid function, decreased memory and heart disease. Cancer, chronic fatigue, mood disorders, diabetes, infertility, and ageing are also related to mitochondrial dysfunction.

Research shows that at least 45% of people have an MTHFR mutation gene. This may consequently impact on our body’s ability to turn folic acid into methylfolate (the active form). When the body is less able to use folate in the methylation cycle, it won’t get the benefit of the B vitamins cycle to work properly. This may negatively affect formation of healthy new cells and neurotransmitters. It may also impact on liver and kidney function, impairing detoxification, immune system activity and decrease anti-oxidant activity.

During physical, psychological or environmental stress, our methylation cycle requires more B vitamins to work effectively.

In 2009 a study of identical twins separated the effect of genetics from environmental factors. The study analysed DNA methylation in both twins, one on which had a diagnosed of AD (4). They found that DNA methylation was significantly decreased in the twin with AD compared with the healthy twin. Interestingly, even though both twins were chemical engineers with similar levels of education, the AD twin worked broadly with pesticides, where the non-demented twin did not. This observation suggests that work-related pesticide exposure could have contributed to the development of AD (more about toxin exposure below). The results of this study show that, not only genetic mutations, but also environmental influences can trigger AD.

Heavy metals toxicity

There is a growing evidence for a link between aluminium toxicity and AD, and between other metals and AD too. The link between aluminium and Alzheimer’s disease has been the subject of scientific debate for several decades. Aluminium (Al) is a mineral that is not essential for human body. It, though, a well established neurotoxin, which may also cause other neuro-degenerative diseases.

In 1965 scientists discovered a link between Al and AD during an animal study. They administered intracerebral aluminum, which caused neurofibrillary degeneration and the appearance of tangle-like structures. These are the landmarks of AD in humans (5).

Another study in 1973 reported an increased level of Al found in the brains of AD patients (6).

More on Aluminium

Other recent studies have demonstrated that considerable amount of Al crosses the blood brain barrier, enters the brain, and accumulates there in a semi permanent way (7, 8). Therefore, Al may cause severe health problems, including cognitive deficiency and dementia, in vulnerable age groups like infants, giving autism like symptoms, elderly people and those with impaired renal functions.

Aluminium is unfortunately all around us. You can find it in cookware and in pharmacological agents including antacids. Numerous foods and products intended for human consumption contain aluminium and its compounds. In addition, aluminium ions can, under certain conditions, leach into food from food packaging and tableware. As well as food sources, cosmetic products, such as aluminium containing antiperspirants and toothpastes with whitening effect, can be a significant source of Al intake. Skin care manufactures use aluminium in lipsticks as colour pigments, or as coating of nanoparticles in sun creams.

”Type 3 diabetes”

Diabetes is also a significant risk factor for AD, doubling the chances of developing it (9). While insulin majorly plays a role in sugar metabolism, it also takes part in brain signaling. So, it’s becoming understood, that the same pathological process that leads to insulin resistance and Type 2 diabetes, may also happen to our brain. As we overindulge on processed grains and sugar, the brain becomes consistently disrupted by high insulin levels, leading to cognitive and memory impairments.

In one study, when researchers disrupted the proper signaling of insulin in the brain, they were able to induce many of the characteristic brain changes seen in AD (10).

This connection between high sugar diets and Alzheimer’s disease was again challenged in a study published in 2018 (11). Based on various assessments completed during the 10-year follow-up period, researchers noted, the higher a person’s blood sugar, the faster their rate of cognitive decline.

The association between high blood sugar and AD is why the disease has sometime been called “Type 3 diabetes.”

Disrupted neurotransmitters and neuroinflammation

Our brain has billions of nerve cells called neurons, whose job is to pass electrical and chemical signals back and forth to process information or tell other cells in the body what to do. The chemicals that carry those signals are called neurotransmitters. Glutamate is an excitatory neurotransmitter, which means it increases neurons action potential. Glutamatergic mechanisms are involved in fast nerve cells communication as well as in learning and memory processes.

Under certain conditions, glutamate may become a neurotoxin leading to slowly progressive neuronal cell loss. There is good evidence for an involvement of the glutamatergic system in functional brain changes of people with dementia (12, 13).

When a disruption in the homeostasis (biological balance) of anti-inflammatory and pro-inflammatory signaling occurs, as seen in AD, it results in chronic neuro inflammation (14). The binding of damaged proteins to receptors found in central nervous system may trigger an immune response, setting off an inflammatory cascade in the brain that contributes to AD progression. Highly sugary, processed food diet, stress and toxin exposure will contribute to this inflammatory cascade even more.

This chronic neuroinflammation has only been identified recently as an important component.

Sun exposure

Most of us know vitamin D as the sunshine vitamin. It is synthesised in the skin from exposure to UVB rays from the sun or obtained through diet. The amount of vitamin D we can synthesise from sun exposure depends on our age, skin type, location and time of year. The elderly and those with darker skin produce less of it. While vitamin D undeniably plays a role in building and maintaining strong bones, healthy mood and immune system, scientists have recently found a link between vitamin D and AD.

Vitamin D is a steroid hormone that exhibits neurosteroid actions in the central nervous system. Its anti-inflammatory, anti-oxidant and nerve protecting properties may partially explain why neuronal degeneration occurs in vitamin D deficient AD diagnosed patients.

The Scottish Dementia Research Centre has noted that there is a very strong link between vitamin D deficiency and dementia.

In a 2014 study, researchers discovered that those who were severely deficient in vitamin D had a 125 percent higher risk of developing some form of dementia versus those with normal levels (15). The findings also imply there is a threshold level of circulating vitamin D, below which the risk of dementia increases (around 50 nanomoles per litre (nmol/L) or 20 nanograms per millilitre (ng/ml)). Higher levels were associated with better brain health.

3. Conventional Alzheimer’s Treatment

While there is currently no cure for AD, there are treatments that can improve symptoms, at least temporarily.

Alzheimer’s drugs focus on a chemical messenger known as acetylcholine, another neurotransmitter. These drugs (acetylcholinesterase or AChE inhibitors) have the function to keep acetylcholine levels high to keep nerve cells firing and slow the progress of the disease.

Memantine is another available drug, that is not an AChE inhibitor and it is a glutamate receptor antagonist. Dr’s may use this drug when a person can’t tolerate AChE inhibitors or both used together in more advanced cases. The combination has shown modest benefits in patients with moderate to severe Alzheimer’s disease, but may not work well for everyone. Dizziness is the most common side effect, but patients may also experience headaches, constipation and less often, confusion.

Antidepressants are sometimes given if the patient has some form of depression.

4. Holistic Approach

Diet

After looking into possible links to AD, it is important to know that eating sugar and refined carbohydrates may cause pre-dementia and dementia. However, cutting out the sugar and refined carbs along with adding good quality mono- and polyunsaturated (omega 3 and 6), and even saturated fat (mainly plant based like coconut oil) may prevent pre-dementia and early dementia.

Research from the Mayo Clinic reveals that diets rich in refined carbohydrates may increase by 89% the risk of developing dementia. Whereas high-fat diets may reduce by 44% the risks of getting AD (16). It is worth exploring plant based ketogenic diet as it may also contribute to blood sugar and insulin management.

Gluten/wheat sensitivity is very common these days due to the nature of this protein as well as pesticide and herbicide use, with an often addition of genetically modified grains. Research shows that gluten negatively affect the blood-brain barrier, which may allow heavy metals to accumulate in the brain. Gluten may also contribute to hyper-permeability of our gut lining, which may allow food particles and microbes to enter the bloodstream. This condition, known as “leaky gut”, may trigger our immune system and promote inflammation, which may be responsible for the development of auto-immune conditions, but also AD.

One of the easiest ways to optimise our diets is to make sure we are eating real food, avoiding processed foods, including refined sugar, MSG, gluten containing grains, dairies, GMO foods sprayed with pesticides (such as Round-up/ glyphosate). Cooking from scratch (on aluminium free cookware), reading labels and opting for organic produce will help us avoid pro-inflammatory anti nutrients. Including green, bitter, leafy greens (like kale, watercress) and herbs (like coriander and parsley), as well as superfoods (like wheatgrass and CHLORELLA), may help our bodies cleanse from heavy metals.

Exercise

Exercise may also help in the prevention and treatment of AD.

In a study, patients diagnosed with mild to moderate AD who took part in a four month long supervised exercise program, had undoubtedly fewer neuropsychiatric symptoms associated with AD than the control group that did not exercise (17).

Cognitive function and memory may be improved through regular exercise (18), and this effect is in part related to the effect exercise has on neurons formation (neurogenesis) and the regrowth of brain cells, by targeting a gene pathway called brain-derived neurotrophic factor (BDNF). Exercise can trigger a change in the amyloid precursor protein metabolism, in effect slowing the onset and progression of AD (19).

Herbs and supplements 

Natural substances, like plants and herbs extracts, have multiple times shown to have potential to prevent much of the damage seen in AD and to promote central nervous system repair.

Studies have shown that CURCUMIN (from turmeric), due to its anti-inflammatory and anti-oxidant properties, as well as its effects on cell signaling, may strongly suppress abnormal amyloid beta proteins processing and damaged tau proteins formation (20).

Tests have shown that brains of AD patients may have lower levels of DHA fatty acids, normally found in wild fish and algae. In 2015 it was reported, that high DHA fish oil supplementation reduces markers of inflammation (21).

It is worth checking homocysteine in the blood, as raised levels mainly come from vitamin B6, B9 and B12 deficiency, which takes us back to poor methylation. When people have high homocysteine, they have a dramatically higher risk of developing Alzheimer’s. If homocysteine is high, I strongly recommend Methylated B-COMPLEX supplementation.

Traditionally used as Ayurvedic brain tonic medicine, the plant GOTU KOLA native to Southeast Asia, shows various neuroprotective effects. Reducing oxidative stress, inhibiting enzymes, and preventing the formation of amyloid plaques in AD (22).

Good practice is also checking vitamin d levels. Importance of sun exposure and healthy vitamin D levels is very important, so in case of deficiency, according supplementation is much advised. Bear in mind that you may be potentially deficient in vitamin D during winter months or if you live in the Northern hemisphere, have dark skin pigmentation, suffer with stress or mental health problems, follow a vegan diet or have an auto-immune condition.

More on Vitamin D3

I personally recommend aiming for vitamin D blood levels between 70 to 90 nmol/L. If you come under any of the categories named above a possible good entry level may be 1000IU daily. If your condition is very severe you may want to consider taking 5000IU or even 10000IU daily. Never supplement high doses of vitamin D for more than three months. Always get tested for optimal dosage and speak to a health care professional to assess your individual health case.  

It was also found that MAGNESIUM may be useful in improving cognitive function and other symptoms in AD patients (23). In both humans and animals, low magnesium levels can trigger inflammation in various of tissues, including brain.

One of the vital functions for magnesium in central nervous system, is modulation of the glutamate receptors. Low levels of magnesium significantly enhance excitotoxic sensitivity and may be why often magnesium depletion causes seizures in otherwise healthy people (24).

Oxidative stress, which is particularly high in the aged brain, is also correlated with magnesium deficiency (25). Low levels cause a significant fall in cellular GLUTATHIONE (master anti-oxidant) and in turn a dramatic increase in free radical formation. A powerful antioxidants complex can be found here.

Magnesium also aids in sleep, with help of a melatonin, which is a sleep hormone and a powerful anti-oxidant too.

Optimal sleep

What is very important to know is that most of the repair and clean-up in our brain happens while we sleep. Disrupted sleep is associated with mitochondrial dysfunction and neuron degeneration. While sleep problems are common in AD patients, we can improve the amount and quality of our sleep, so it will help our brains function more efficiently. By avoiding any stimulants before bedtime (like alcohol, sugar, caffeine, blue light, late work and workout) we can adjust our circadian rhythm by getting the right length and quality of sleep we need. If sleep is an issue, I will invite you to visit this dedicated page.

5. Final words

Alzheimer’s disease is the leading cause of dementia and it affects people mainly between 60 and 70 years of age. It impairs memory and other cognitive functions, as disease progresses causing symptoms to worsen over time. No one knows the ultimate cause of AD, as there are multiple factors that contribute to its onset. Genetics, heavy metals toxicity, insulin resistance, and chronic systemic inflammation are all possible causes. Western medicine treatment is limited, with drugs available to slow down progression of disease.

Dietary and other lifestyle changes should be implemented without a doubt. Multiple studies demonstrated that exercise, sun exposure, low-sugar/high-fat diet as well as use of certain herbs and supplements, may drastically improve or even reverse one’s AD symptoms.

Author: Sylwia Wyrębek, Naturopathic Nutritionist

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References:

  1. https://www.nia.nih.gov/health/biomarkers-dementia-detection-and-research.
  2. https://www.ncbi.nlm.nih.gov/pubmed/203013403.
  3. https://www.ncbi.nlm.nih.gov/pubmed/203013404.
  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719870/?report=reader5.
  5. https://insights.ovid.com/jnexn/196504000/00005072-196504000-000026.
  6. https://www.ncbi.nlm.nih.gov/pubmed/47355957.
  7. https://www.ncbi.nlm.nih.gov/pubmed/145074728.
  8. https://www.ncbi.nlm.nih.gov/pubmed/151523069.
  9. https://care.diabetesjournals.org/content/39/2/30010.
  10. https://www.nejm.org/doi/full/10.1056/NEJMoa1215740
  11. https://link.springer.com/article/10.1007/s00125-017-4541-7
  12. https://www.cambridge.org/core/journals/cns-spectrums/article/interplay-of-neurotransmitters-in-alzheimers-disease/EC8E3F7482585743AE24EE66A10ECF63
  13. https://www.ingentaconnect.com/content/ben/car/2004/00000001/00000001/art00003
  14. https://www.sciencedirect.com/science/article/pii/S2352873718300490#bib58
  15. https://n.neurology.org/content/83/10/920.short
  16. https://www.ncbi.nlm.nih.gov/pubmed/22810099
  17. https://www.medicalnewstoday.com/articles/297287.php#1
  18. https://www.pnas.org/content/108/7/3017.full
  19. https://www.jneurosci.org/content/25/17/4217
  20. https://www.ncbi.nlm.nih.gov/pubmed/15590663
  21. https://new.hindawi.com/journals/bmri/2015/172801/
  22. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4342646/
  23. https://www.ncbi.nlm.nih.gov/pubmed/16790324
  24. https://www.ncbi.nlm.nih.gov/pubmed/11990449
  25. https://www.ncbi.nlm.nih.gov/pubmed/22119986

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