Neurodegenerative

To be completed

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Reminder: Not medical advice, consult doctor before, etc.

What is the general understanding of neurodegeneration?

Complications for the person, their family, and the public perception

How to think about recovery, management, and responsibility without distributing blame (the emotionally charged aspect of this topic makes it hard to work on recovery without divisiveness). 

Each condition to address:

•  What is it?
• What may cause it and what are the commonalities between sufferers?
  • Endocrine
  • Anatomy/physiology
  • Environmental
  • Evolution/anthropology
  • Fetal development
  • Maternal/paternal health before conception
  • Genetics/epigenetics
  • Immune system
  • Nervous system
  • Psychology
• What are some potential ways of managing symptoms?
  • Breathwork
  • Sleep and Circadian Rhythm
  • Nutrition
  • Trauma recovery
  • Social/Communal integration
  • Exercise
  • Purpose
  • Environment tailored
  • Tools: eustress

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Amyotrophic Lateral Sclerosis (ALS)

(Gabor – When the Body Says No)

In ALS motor neurons gradually die. Without electrical discharges from the nerves, the muscles wither. When a muscle has no nourishment, it ‘atrophies’ or wastes away. ‘Lateral’ identifies the areas in a person’s spinal cord where portions of the nerve cells that nourish the muscles are located. As this area degenerates it leads to scarring or hardening (‘sclerosis’) in the region.

Initial symptoms depend on the area of the spinal cord or the brain stem where the disease first strikes: people may experience muscle twitching or cramps, loss of normal speech or difficulties swallowing. Mobility and limb movement are eventually lost, as is speech, swallowing and the capacity to move air in and out of the lungs. About 50 per cent of patients succumb within five years, although some may survive much longer.

There is some evidence there may be immune system involvement, including a dysfunction of the cells in the nervous system that have an immune role. Microglia serve a protective role in the brain, but when hyperstimulated they may become destructive.

The patient in this example seemed to have frozen emotional expression. She was given up by her birth parents and could never make a connection with her birth mother no matter how she tried. She felt there was a huge cavern where her sense of self should be. She also grew up believing she needed to take care of everyone.

Characteristic of other ALS patients, they attempt to avoid asking for help. Rigidly competent behavior, inability to ask for or receive help, and the chronic exclusion of so-called negative feelings.

“Habitual denial, suppression or isolation of … fear, anxiety, and sadness…. Most expressed the necessity to be cheerful…. [Some] spoke casually of their deterioration or did so with engaging smiles.” Emotional repression—in most cases expressed as niceness.

Characterizing the personalities of ALS patients are relentless self-drive, reluctance to acknowledge the need for help and the denial of pain whether physical or emotional. All these behaviors and psychological coping mechanisms predate the onset of illness. The conspicuous niceness of most persons with ALS is an expression of a self-imposed image that needs to conform to the individual’s (and the world’s) expectations. The individual seems trapped in a role, even when the role causes further harm. It is adopted where a strong sense of self should be—a strong sense of self that could not develop under early childhood conditions of emotional barrenness. In people with a weak sense of self, there is often an unhealthy fusion with others.

One of the only traits ALSers seem to share is an energetic past. In almost every case, victims were either classic over-achievers or chronic workaholics.

For the child it is no relief to feel sadness or anger if no one is there to receive those emotions and to provide some comfort and containment. Everything had to be held in rigidly. The physical rigidity of ALS may well be a consequence. There is perhaps only so much energy the nervous system can expend pushing down powerful emotions that cry out for expression. At some point in particularly susceptible individuals, it seems reasonable to suppose, nerves may lose the ability to renew themselves. Could ALS be a result of an exhausted nervous system no longer being capable of replenishing itself?

Rage and anguish exist underneath the veneer of niceness, no matter how sincerely a person mistakes the facade for her true self.

Strong convictions do not necessarily signal a powerful sense of self: very often quite the opposite. Intensely held beliefs may be no more than a person’s unconscious effort to build a sense of self to fill what, underneath, is experienced as a vacuum.

Given the nature of ALS as a disease that destroys the body while leaving the intellect intact, an abstract thinker is in an ideal position to “live a life of the mind.” Prior to Stephen Hawking’s diagnosis and its attendant debility, he had been somewhat aimless, his shining intellectual gifts notwithstanding.

The young Stephen, it appears, was the chosen bearer of the frustrated ambitions of his father who was evidently determined that his son would succeed at educational and social goals he, the father, had never quite attained.

Stephen engaged in a fair bit of indolence and alcohol consumption, with avoidance of classes or studying—those classic forms of passive resistance in college. It was only after his diagnosis that he began to focus his phenomenal intelligence on his work: elucidating the nature of the cosmos, bridging the theoretical gaps between Einsteinian relativity theory and quantum mechanics.

Without the subordination of Jane’s life and independent strivings to his, Stephen likely would not have survived, let alone succeeded to such a spectacular degree. She was the ever-available, unspeaking and compliant mother/nanny figure whose services are expected, taken for granted and noticed only in their absence.

Hawking’s vocation and the unstinting support of his wife were accompanied by the liberation of his aggression by his illness. The “niceness” of most ALS patients represents more than the innate goodness and sweetness of some human beings; it is an emotion in extremis. It is magnified out of healthy proportion by a powerful suppression of assertiveness.

According to Dr. Northrup, her friend healed through the conscious daily practice of emotional self-inventory and of self-love that, little by little, “unfroze” each part of her body.

Alzheimer’s

Nutrient Power Notes

Stages of Alzheimer’s Disease

1. Early warning signs: Many patients exhibit subtle symptoms of AD several years prior to diagnosis. The most common indications are loss of interest in events and activities along with a decline in mental sharpness. Mild cognitive impairment.
2. Mild Alzheimer’s disease: A formal diagnosis of AD usually is made when there is a striking loss of recent memories, while older memories are still retained. Another diagnostic symptom is a shrinking vocabulary and loss of communication skills. In this stage of the disease, most persons still enjoy life and can accomplish basic tasks but require supervision for activities requiring complex thought or logic.
3. Moderate Alzheimer’s disease: The deterioration of neurons eventually spreads throughout the brain and the patient loses the ability to perform many common activities of daily living. Memory continues to deteriorate, and the patient may no longer recognize his own grandchildren or recent friends. Reading and writing skills gradually disappear, and irritability, wandering, falling, and physical aggression symptoms can be very challenging for the family. About one-third of AD victims develop delusions and urinary incontinence. Most families are forced to move their loved one to a long-term care facility when they can no longer cope with the worsening symptoms. This step frequently does not seem to bother the patient.
4. Advanced Alzheimer’s disease: During this final stage, the patient becomes completely dependent on caregivers. As the disease progresses, many develop a wooden expression, lose the ability to speak, and fail to respond to visitors. In the final stages, they become bedridden, totally incontinent, and unable to feed themselves. Death usually results from an infection, respiratory problems, etc. and not directly from AD itself.

Role of Genetics

Familial AD typically develops between the ages of 40 and 55 and represents about 5% of cases. This condition is caused by mutations to genes that produce presenilin 1, presenilin 2, or amyloid precursor protein (APP). The late-onset form of AD represents about 95% of cases, usually developing after age 70. In 1993, researchers at Duke University reported that an apolipoprotein E (ApoE) abnormality represents a powerful risk factor in late-onset AD. ApoE is a protein containing 299 amino acids that can exist in three isoforms: E2, E3, and E4. Isoform E3 is identical to that of E2 except that a cysteine in the amino acid chain is replaced by arginine. In isoform E4, two cysteines are replaced by arginine. The risk of developing AD is lowest in ApoE2, intermediate in ApoE3, and highest in ApoE4. Persons born with an E4 allele from both parents are between 10 and 30 times more likely to develop AD by age 75 when compared with persons without an E4 allele. However, many persons with both E4 alleles live to a ripe old age without developing memory loss or other symptoms of dementia. Moreover, 40% of AD victims do not have the E4 gene.

Risk Factors

• Age: The likelihood of this disease increases sharply with age, and about one-third of persons reaching age 85 are in some stage of the disorder. Surprisingly, there is evidence that the risk of AD declines after age 90.
• Head Injury: Boxers have an increased risk for AD, and some acquire the disorder before age 40.
• Education Level: Higher education delays the onset of AD but that the disease progresses more rapidly once AD has begun in these persons.
• Mental Activity: Mentally stimulating activities such as playing bridge, doing puzzles, or learning a new language reduce the risk of AD.
• Physical Activity: Persons engaging in regular physical activity were found to have reduced AD risk. However, it’s possible this is due to better cardiovascular health or reduced obesity rather that a direct result of physical exercise.
• Vascular Factors: The first brain areas damaged are close to blood vessels. A variety of cardiovascular problems increase AD risk. Examples include strokes, hypertension, hypotension, atrial fibrillation, atherosclerosis, and elevated serum homocysteine.
• Alcohol Use: Mentions drinking red wine. Not likely.
• Physical Illness: Persons with a history of diabetes or other autoimmune diseases appear to have a higher risk of AD. The strongest data are for type 2 diabetes and insulin resistance.
• Toxic Metals: Mercury exposure causes increased oxidative stress and this factor is elevated in AD.
• Poor Nutrition: Inadequate nutrition is a common problem in elderly populations, and low levels of zinc and vitamins A, C, and E result in increased oxidative stress. Several studies indicate that oxidative stress plays an important role in the development of AD. In addition, elevated serum homocysteine is a known AD risk factor that can result from deficiencies of folic acid and vitamin B12. A high-quality diet may represent an important protective factor against AD.

Alzheimer’s Disease Theories

Cholinergic Theory:

This theory states that AD begins with the depletion of acetylcholine activity in the brain. Acetylcholine is a major neurotransmitter important for memory processes and is seriously depleted in AD brains. This has been attributed to a shortage of enzymes (choline acetyltransferase and acetylcholine esterase) necessary for production and regulation of acetylcholine. However, these low enzyme levels only tend to appear in the late stages.

Amyloid Plaque Hypothesis:

Aβ is formed when APP is cut into small sections by enzymes called secretases. The factors that cause the disintegration of APP into Aβ fragments are a subject of active research. The Aβ plaques tend to clump together and form a mass outside brain cells. Advocates of the amyloid theory believe production and aggregation of Aβ to be the key event in the brain cell destruction process. Aβ plaques may be a result and not a cause of AD.

The Tau Hypothesis:

Tau and other proteins assist in keeping the delicate tubules intact and in the proper place. However, in AD patients, tau proteins become chemically modified and clump together, resulting in microtubule disintegration and disabling tangles. The net result is loss of nutrient transport and death of the brain cell.

Inflammation Theory:

The Scripps theory suggests that amyloid proteins are modified during inflammation, causing them to misfold and accumulate into the characteristic plaques found in AD brains.

Oxidative Stress Theories:

Oxidative free radicals perform several useful functions in the body, such as killing bacteria and burning glucose to produce energy. However, a chronic excess of free radicals can lead to death of brain cells. Sources of free radicals include physical injury, bacteria, viruses, inflammation, heavy metals, and nuclear radiation. The body has a supply of antioxidant molecules that have the job of keeping free radicals from reaching concentrations lethal to brain cells. A healthy brain requires (a) a competent blood-brain barrier to reduce influx of toxics, and (b) enough antioxidant protection within the brain to cope with the number of free radicals present. 

Metal Metabolism Theories:

Bush, MD, and colleagues reported that copper overloads cause increased Aβ in the brain. Copper and iron are major sources of free radicals in the human brain, and elevated copper levels have been found in Aβ. Metallothionein and Cu/Zn SOD protect against copper free radicals, but both are depleted in AD brains. This theory suggests that excess copper prevents the natural removal of Aβ from AD brains. Interestingly, two 2009 studies have reported a protective role for copper in AD. It’s possible that either deficiency or excess of copper can be harmful to the brain and that homeostatic regulation of copper levels is essential.

Advanced Photon Source Measurements

Large calcium-rich circular areas were observed in the AD samples and very small calcium-rich zones in the controls. In both cases, the calcium concentrations were 15 times higher in the calcium-rich areas when compared with adjacent tissues. Another interesting finding was the presence of very elevated Cu/Zn ratios in parts of the AD samples but not in the controls.

The Case for Metallothionein

Two separate autopsy studies have reported severe deficiency of MT protein levels in deceased AD patients. MT proteins have several protective functions in the brain including the following:

• Preventing toxic metals from passing the blood-brain barrier
• Regulation of copper levels
• Powerful antioxidant action against free radicals

The protective properties of MT depend on ample amounts of glutathione and selenium. Gene expression of MT is zinc dependent, and most AD patients are depleted in zinc. MT proteins are far more powerful than selenium, coenzyme Q10, vitamins C and E, and other antioxidants that have been used in experimental AD therapies.

Alzheimer’s disease patients have low levels of sulfur and selenium. These reductions are implicated in the lower glutathione levels seen in these patients and the increased oxidative stress and neuroinflammation, which promote neurodegeneration. Sulfur is also a potent aluminum antagonist that can reduce aluminum accumulation. Aluminum is a neurotoxin and considered a causative factor in Alzheimer’s disease. High amounts of aluminum in the brain tissue are associated with familial Alzheimer’s disease and other neurological disorders.

Dementia drug: https://news.berkeley.edu/2019/12/04/drugs-that-quell-brain-inflammation-reverse-dementia/

Brain rhythm impact on AD: https://picower.mit.edu/news/scientists-eager-explain-brain-rhythm-boosts-broad-impact-alzheimers-models

BCG therapy lowered incidence of AD and bladder cancer: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0224433

Hyperbaric oxygen therapy for AD: https://www.sciencedaily.com/releases/2019/01/190124124742.htm

Sleep deprivation increase AD: https://www.eurekalert.org/news-releases/749967

Glucose metabolism and AD: https://jamanetwork.com/journals/jama/article-abstract/2758712

Common herpes virus causes signs of AD: https://www.newscientist.com/article/2242749-common-herpes-virus-causes-signs-of-alzheimers-disease-in-brain-cells/

Lower risk with long-term flavonoid intake: https://academic.oup.com/ajcn/article/112/2/343/5823790

Anticholinergic drugs make lead to AD: https://www.sciencedaily.com/releases/2020/09/200904125116.htm

Parkinson’s is two diseases: https://www.sciencedaily.com/releases/2020/09/200922092156.htm

Polyphenols, TCM, and Mediterranean: https://pubs.rsc.org/en/content/articlelanding/2022/fo/d1fo02147h/unauth

When the Body Says No

One of the first structures to deteriorate in Alzheimer’s is the hippocampus. The hippocampus is active in memory formation and has an important function in stress regulation. It is well known that chronically high levels of the stress hormone cortisol can shrink the hippocampus.

• Non-handled rats are more likely to suffer shrinkage of the hippocampus and also exhibit greater memory impairment in old age.
• In humans, the widely reported Nun Study found that low linguistic ability in early life had a strong association with dementia and premature death in late life.
• The author of the world classic Gulliver’s Travels hardly appears to have been deprived of linguistic capacity. On a closer look, Jonathan Swift’s life and writing both manifest a poverty of felt emotional experience and of direct emotional expression. His skillsets were largely confined to intellectual ideas and to an acerbic wit so dry that his humor often escaped less sophisticated readers.
• Swift’s lifelong abhorrence of intimacy and his underlying fear of emotional contact or vulnerability are the defensive responses of a child deprived of emotional nurturing, a child who had to learn quickly to fend for himself. “There was, it seems, no one adult who particularly cared for Jonathan, or for whom he particularly cared.”

From diagnosis to death, life expectancy in Alzheimer’s averages eight years, regardless of the age when the disease first strikes. In rare instances, that may be as early as the sixth decade.

An international scientific consensus is steadily gaining ground that points to Alzheimer’s as one of the diseases on the spectrum of autoimmune conditions, along with multiple sclerosis, asthma, rheumatoid arthritis, ulcerative colitis and many others.

The autoimmune diseases all entail imbalances in the body’s physiological stress-regulation system, in particular the hormonal cascade set of by the hypothalamus. This surge of hormones culminates in the release of cortisol and adrenalin by the adrenal glands. Many studies have shown dysregulated physiological stress responses in Alzheimer’s, including abnormal production of hypothalamic and pituitary hormones and cortisol. In human beings with Alzheimer’s and in animal models of dementia, there is excessive production of cortisol, which is paralleled by the degree of damage to the hippocampus.

A typical warning sign of Alzheimer’s, as with Swift’s case, is the lack of genuine emotion. If the shutting-down of emotion occurs early enough, during the critical phases of brain development, the capacity to recognize reality may become permanently impaired.

• Reagan would often confuse fact from fiction and his memory was quite selective. He was also “sheathed in a strange calm.” His mother was emotionally unavailable and his father was a raging alcoholic. The result was a child that could feel no resentment and rage that was buried deep beneath his consciousness.

Such instances do not indicate that the person has no emotions; someone truly lacking attachment could at least pretend to possess some fellow feeling. On the contrary, the emotions can be too overwhelming to be experienced consciously—but they are physiologically all the more active. Once more we witness that avoiding the experience of emotion in fact exposes people to greater and longer-lasting physiological stress. Because they are unaware of their own internal states, they are less able to protect themselves from the consequences of stress. Furthermore, the healthy expression of emotion is itself stress-reducing. Stress-induced chronic hormonal and immune changes prepare the physiologic ground for diseases like Alzheimer’s.