Causes of memory loss

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Some researchers have attributed the causes of memory loss to incorrect nutrition, pollution, oxidation and atherosclerosis, leading to a lack of vital anti-oxidants to the brain, which in turn suffers from free radical damage. This results in a lower level of vital neurotransmitters in the brain, in particular serotonin and acetyl-choline. 

Some definitions...

  • Memory... the faculty by which the mind stores and remembers information
  • Dementia... a chronic or persistent disorder of the mental processes caused by brain disease or injury and marked by memory disorders, personality changes, and impaired reasoning
  • Alzheimer's... progressive mental deterioration that can occur in middle or old age, due to generalised degeneration of the brain. It is the commonest cause of premature senility
  • Amnesia... a partial or total loss of memory

The hippocampus is a major component of the brain of humans and other vertebrates. It belongs to the limbic system, and forms elongated ridges on the floor of each lateral ventricle of the brain. It's thought to be the centre of emotion, memory, and the autonomic nervous system. It plays important roles in the consolidation of information from short-term memory, to long-term memory and spatial navigation.

Severe memory loss afflicts one in ten people over sixty-five and one in two over eighty-five. The first indications are associated with confusion, depression, and irritability.

Memory loss is abnormal forgetfulness. It can be sudden due to trauma, or gradual. It can be transitory or permanent. Ageing brings some form of memory loss, but it's not significant unless accompanied by disease or trauma.

Dementia is not specific, it's a term used to denote a decline in memory sufficient to impair a person's ability to perform normal activities.

The following are some of the symptoms, which must be significantly impaired to be classified as severe memory loss or dementia...

  • inability to focus and pay attention
  • problems with communication and language
  • memory loss
  • inability to reason
  • lack of judgment
  • problems with visual perception

Other terms used are cognitive dysfunction or cognitive impairment.

Alzheimer's disease is the commonest form of dementia, accounting for 60 to 80 percent of cases. 50% of individuals who reach 85 have it. The second commonest form is vascular dementia, which often occurs after a stroke.

The following can be causes of memory loss...

  • oxidative stress
  • stress, which increases inflammatory cytokines
  • epigenetic alterations in gene expression caused either by early-life psychological stress and/or toxins/lack of vital nutrients while a foetus. It causes late-onset, selective deterioration of both complex behaviour and synaptic plasticity.
  • a lack of nutrients
  • plasma vitamin B-12 less than 258 pmol/L, with plasma folate concentration greater than 20.2 nmol/L, predicts especially rapid cognitive decline
  • excess sugars which cause glycation, this occurs when a sugar molecule binds to a protein or lipid molecule without the control of an enzyme. This impairs the function of the molecule, leading to...
  • advanced glycation endproducts or AGEs, resulting in many of our inflammatory diseases. AGE's are particularly high in diabetes
  • diabetes that is poorly controlled
  • a lack of blood flow to the brain
  • damage to blood vessels
  • homocysteine
  • surgery-induced cognitive decline
  • multi-infarct dementia caused by multiple strokes
  • depression, depression is also a side effect of memory loss
  • drug side effects, particularly the anti-cholinergic drugs. They inhibit the neurotransmitter acetylcholine, vital for memory and cognitive function
  • statins increase the risk for high blood glucose. Labels now show memory loss and confusion can occur
  • excessive use of alcohol
  • thyroid problems
  • high and prolonged levels of cortisol in the blood may cause memory loss
  • lack of exercise, the brain relies on a good supply of blood carrying oxygen, exercise increases blood flow

All impact on the ability of the brain to function normally.

One paper says...

"There is also growing evidence that neurodegenerative diseases such as Alzheimer's and Parkinson's may be caused by detrimental environmental and dietary factors that alter gene expression by means of DNA methylation and histone modification... Inflammation and oxidative damage due to the overproduction of proinflammatory cytokines play an important role in the development of AD and other neurodegenerative conditions... The brain's high metabolic activity results in elevated oxygen consumption and constant production of reactive oxygen species (ROS) in mitochondria. At the same time, the brain tissue is rich in unsaturated fatty acids and transition metal ions yet has relatively fewer antioxidants comparing to other organs creating favorable conditions for oxidative damage. Since the blood-brain barrier prevents many dietary antioxidants from entering the brain, it largely relies on endogenous antioxidants such as Cu- and Zn-dependent superoxide dismutase... Among compounds that have a protective effect and can reduce oxidative damage are some neurotrophic factors such as brain-derived neurotrophic factor (BDNF)... Epigenetic silencing of certain genes is currently considered the main reason for age-associated increase in tumorogenesis, oxidative stress, and inflammation."

Epigenetic changes in gene expression has now given rise to the term "The foetal origin of adult disease". Where insults to the foetus from environmental factors like toxins, or a lack of certain nutrients like vitamin D, not only affect the foetus, but give rise to adult diseases such as obesity, diabetes, cardiovascular disease, cancer, Parkinson's disease, Alzheimer's and more.

Another paper says...

"In addition, a correlation between an accumulation of oxidative stress and aging has also been established. Thus, it is important to clarify the detailed relationship between oxidative stress and cellular damage in neurodegenerative diseases and the aging process. In the cellular and molecular mechanisms underlying oxidative stress-induced cell death, it is well known that excitotoxicity, Ca2+ overload, mitochondrial dysfunction, and the stimulation of intracellular signaling cascades play a role. As expected, antioxidants including many phytochemicals and vitamins have been found to support the survival of neurons under oxidative stress."

Progesterone prevents excitotoxicity, whether from excess glutamate or Ca2+ (calcium ions). Excess glutamate causes excess Ca2+ ions to enter the cell, leading to cell death. Both glutamate and Ca2+ are needed by not only the brain, but by other systems. But if in excess they do great damage. The neurotransmitter dopamine also prevents glutamate and Ca2+ cell death.

Excess oestrogen increases glutamate output, which in turn causes excess Ca2+. Oestrogen also increases free radicals, plus destroying beta-endorphin neurons in the brain, these produce endorphins which promote a feeling of well being and relaxation. Beta-endorphins also appear to boost the immune system, protecting against cancer.

Hormonal dysregulation can play havoc if there's an excess of catabolic hormones to anabolic hormones. The catabolic hormones are the thyroid hormones, cortisol and oestrogen. The anabolic are dehydroepiandrosterone sulphate (DHEAS), testosterone, insulin like growth factor 1 (IGF-1) and progesterone.

Anabolic hormones play a role in neuroprotection and neuroregeneration. They facilitate recovery after Traumatic Brain Injury, particularly progesterone, and attenuate neuronal loss.

One study in older men found elevated thyroid hormones may increase oxidative stress and apoptosis, leading to neuronal damage or death, finally leading to a decline in cognitive function. But as men get older their testosterone levels drop and their oestrogen rises, which probably accounts for some of the decline.

It appears that an increased ratio of serum copper to serum iron prior to dementia has potential as a biomarker for cognitive decline.

Higher levels of plasma malondialdehyde (MDA), a marker for Inflammation, are related to severity of depression, impairment of visual-spatial and auditory-verbal memory, plus short-term memory.

High AGE's (advanced glycation end products) is associated with greater cognitive decline in older adults with and without diabetes. Chronic hyperglycaemia and hyperinsulinaemia stimulates the production of AGE's, which leads to the production of free radicals, or reactive oxygen species (ROS). Plus accelerating brain ageing by inducing tau hyperphosphorylation and amyloid production.

Some believe Alzheimer's patients have diabetes of the brain, and are giving insulin nasal sprays to enhance glucose metabolism. Using a nasal spray the insulin enters the brain immediately, without disturbing blood glucose in the body. Insulin certainly helps enhance mental clarity in diabetes patients.

But the problem is not one of insulin, but of sensitising the cells to glucose, the brain's primary fuel. Oxidative stress and Insulin Resistance play a large role in this insensitivity. Reverse these, better still prevent them in the first instance, and the problem is solved.

People with Lupus or fibromyalgia can suffer from cognitive dysfunction or cognitive impairment, leading to the common term 'brain fog'.

Depression is a common finding. Brain-derived neurotrophic factor (BDNF) plays an important role in maintaining neurons. Evidence suggests that BDNF is decreased in depressed patients.

HRT impairs cognition and nearly doubles the risk of dementia. If women have two ovaries removed before the age of forty six there is a 70% increased risk of dementia. But if women have only one ovary removed before the age of thirty eight there is a 260% increase in dementia.

Understandably, the doctors believe it is due to the decline in oestrogen, and giving oestrogen would correct this. But the studies on HRT disprove this point. Progesterone is the forgotten hormone, remove the ovaries and you remove progesterone production too.

Many toxins interfere with the release of acetylcholine (ACh) and prevent it's secretion. One characteristic of Alzheimer's is a markedly decreased concentration of ACh in the cerebral cortex and caudate nucleus.

There are only a few drugs officially classified as anti-cholinergic drugs or antispasmodics. Those that are, are used to prevent intestinal cramps or bladder irritability. But many OTC drugs have anti-cholenergic properties too, such as antihistamines, acid blockers and antidepressants. Very few people know these also block the affect of acetylcholine, and therefore cause memory loss.

Elevated diabetes risk was found in a 2008 study on statins of nearly 18,000 patients. A separate study published in the Lancet medical journal in 2010 found that statins can raise the risk of diabetes by 9 percent. The FDA now requires a warning label to be added to statins that states diabetes and memory loss is a risk factor.

Alluminium is capable of triggering amyloid precursor and tau181 protein overproduction leading to Alzheimer's.

Natural treatment of memory loss

As with most western diseases, oxidative stress appears to be behind the causes of memory loss and the dementias including Alzheimer's. High doses of antioxidants and anti-inflammatories should be considered.

Progesterone increases BDNF and protects against glutamate excitotoxicity. It also promotes myelination of nerves. As an anti-inflammatory in inhibits lipid perioxidation. The progesterone metabolite, allopregnanolone (THP), is significantly lower in demented patients. It shows promise as a bio-marker, and one can only assume a potential treatment if raised, as it reverses cognitive decline in a mouse model of Alzheimer's disease. Progesterone and its metabolites (DHP and THP) resulted in a significant decrease in the expression of tau. Progesterone significantly reduces tau hyperphosphorylation.

A study on oestradiol, progesterone, and it's two metabolites, dihydroprogesterone and allopregnanolone, was assessed in medial prefrontal cortex and hippocampus, while corticosterone was assessed in plasma. It was found neither oestradiol nor corticosterone contributed to cognitive performance. Whereas higher levels of progesterone in medial prefrontal cortex and hippocampus was associated with better cognitive performance in ageing.

Women should use between 100-200mg/day progesterone

Men should use between 10-100mg/day progesterone

Depending on the severity of the symptoms, more might be required.

For more information on how to use progesterone see...

Before using progesterone, please see the page on...

Vitamin D is both a vitamin and a hormone, and the most potent antioxidant. It's needed by every cell to function normally. Stress reduces levels dramatically. It counters the action of angiotensin, prevents the constriction of blood vessels, and a rise in blood pressure. A lack can lead to depression and countless diseases caused by oxidative stress.

Many studies are finding a link between higher vitamin D levels and a lower risk of developing Alzheimer's. A study published in 2013 found lower levels of sun exposure were associated with increased risk of cognitive impairment. Low vitamin D levels are associated with all-cause dementia, Alzheimer disease, stroke (with and without dementia symptoms), and cerebrovascular disease

One study says...

"The observational evidence includes that low serum 25-hydroxyvitamin D [25(OH)D] has been associated with increased risk for cardiovascular diseases, diabetes mellitus, depression, dental caries, osteoporosis, and periodontal disease, all of which are either considered risk factors for dementia or have preceded incidence of dementia."

The similarities between Progesterone and Vitamin D are almost endless.

Both are made from cholesterol. Progesterone in various organs and cells, and vitamin D3 by the action of UVB sunlight as it strikes the cholesterol covering our bare skin.

Both progesterone and vitamin D regulate gene expression, have a positive fundamental effect on cell differentiation and growth, with anti-oxidative and autoimmune anti-inflammatory mechanisms. Both positively effect the nervous system by stimulating neurotrophic factors, quenching oxidative hyperactivity and regulating autoimmune responses.

Choline is most important, being an integral part of acetylcholine (ACh) which is vital for memory. The rate limiting step in ACh synthesis is choline and acetyl-CoA. Unfortunately increasing choline, or phosphatidylcholine, a phospholipid, in the diet has not been successful, possibly because insufficient was used in the studies. A better source appears to be choline alfoscerate. Studies in rats have shown that high choline intake during pregnancy improves cognitive function in adulthood and prevents memory decline associated with old age.

Cysteine is a sulphur amino acid, a potent antioxidant. In fact some believe a shortage leads to ageing, as it counters the effect AGE's have on cells. It's also the major precursor to glutathione, which is possibly the most important antioxidant in cells, apart from vitamin D. Levels are low in oxidative stress.

Taurine is another sulphur amino acid, with powerful antioxidant properties. Any stress, in particular trauma, reduces levels sharply. It's also a powerful anxiolytic.

Glutamine, although a non-essential amino acid, becomes essential when stressed, as levels drop sharply, so it's of great importance in trauma and surgery. It's also one of the precursors to glutathione.

Glycine, another amino acid, is also one of the precursors to glutathione. Although normally abundant in food, particularly animal protein, stress slows digestion. This compromises the availability of glycine and therefore glutathione. Glycine is a calming amino acid.

GABA is another anxiolytic, the most calming amino acid found in the brain.

Tyrosine is essential for any stressful situation. It's the precursor to the stress hormones adrenaline and noradrenaline, so any stress depletes tyrosine levels. It's also the precursor to dopamine, which is essential for increasing mood. Stress drops dopamine levels, consequently mood drops. But with a drop in dopamine, prolactin rises. Although known as the hormone of lactogenesis, it's also an inflammatory hormone, inflammation stresses the body.

Chromium is crucial in maintaining a stable blood sugar level. A diet high in sugar causes a loss from the body. Chromium levels drop with increasing age. It plays a vital role in the dopamine pathway.

Selenium is a potent antioxidant, preventing the formation of free radicals within cells and the mitochondria. It's also a co-factor for glutathione synthesis. Low selenium is a risk factor for cognitive decline.

Zinc is another antioxidant, a constituent of insulin, making it extremely important for blood sugar control.

All the B vitamins drop when stressed. In particular vitamin B5 (pantothenic acid), the anti-stress vitamin.

Inositol increases the action of insulin and decreases insulin resistance. It has a calming affect, helps in combating depression, panic attacks, mood swings, obsessive-compulsive disorder, bipolar disorder and anxiety.

Vitamin E has beneficial effects against neurodegenerative diseases.

Folate deficiency is a risk factor for neural tube defects during foetal growth. A deficiency also increases the risk in elderly people for cognitive decline and Alzheimer's. It causes oxidative stress, Ca influx into cells, and accumulation of hyperphosphorylated tau and -amyloid.

Vitamin K, one of the co-factors for vitamin D, has important actions in the nervous system, including the brain where it is involved in the synthesis of sphingolipids. These lipids have important roles in the brain. A lack of vitamin K prevents the synthesis of sphingolipids leading to age-related cognitive decline and neurodegenerative diseases such as Alzheimer's disease.

A complex developed at MIT called Souvenaid appears to stimulate growth of new synapses. It comprises choline, uridine and the omega-3 fatty acid DHA. Uridine is a nucleoside, one of the four basic components of ribonucleic acid (RNA). It's found in sugarcane extract, tomatoes, brewer's yeast, beer, broccoli and offal.

There is some evidence that DHA induces a Th-1-like immune response, significantly increasing the IFN-gamma/IL-10 ratio. And should therefore be avoided if depression is present.

D-ribose, a pentose sugar, shows some promise in increasing mental clarity. D-ribose is a component of RNA.

Significant improvements in geriatric patients with cognitive impairment were found after giving phosphatidylserine, both in terms of behavioural and cognitive parameters.

There is some evidence that the Indian medicinal herb Bacopa monnieri, is effective against cognitive impairment.

Medical treatment of memory loss

The following drugs are cholinesterase inhibitors, i.e. they prevent the breakdown of ACh. They only work for a limited time, as the don't prevent the damage...

  • Donepezil (Aricept)
  • Rivastigmine (Exelon)
  • Galantamine (Razadyne)

Side effects are...

  • nausea
  • vomiting
  • loss of appetite
  • increased frequency of bowel movements

Useful websites on the causes of memory loss

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