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alzheimer_s [2018/02/26 18:10] (current)
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 +======= Alzheimer'​s and Dementia =======
 +
 +Currently, more than 4 million people in the United States suffer from [[wp>​Alzheimer’s disease]] (AD) or other [[wp>​dementia]]s. AD affects 47% of people over the age of 85. In AD, in addition to [[degenerative change]]s and [[atrophy]],​ individual [[wp>​brain cell]]s begin to produce a sticky proteinous substances which swell the interior of the cell ([[wp>​neurofibrillary tangle]]s) and "gum up" the exterior ([[wp>​amyloid plaque]]s). In essence, the brain petrifies.
 +
 +Causes of dementias include [[hardening of the arteries]] and [[wp>​mini-stroke]]s. ​ [[Inflammation]] is a major contributor to neuronal damage in [[wp>​neuro-degenerative disorder]]s such as AD, [[Parkinson'​s]] disease, [[multiple sclerosis]] ([[MS]]), and [[amyotrophic lateral sclerosis]] ([[ALS]]) (Torreilles F et al.  1999). ​
 +
 +[[wp>​Nitric oxide]] [[wp>​inflammation]] has been shown to play a specific role in [[wp>​neuro-degeneration]] (Strijbos 1998). Blood flow to neural tissue is another important consideration.
 +
 +The historical use of herbal medicines to treat dementia diseases like Alzheimer’s varies according to the different traditions. ​ According to [[TAM]] and [[TCM]] theories, dementias result from multi-systemic decline and brain destruction due to [[aging]], and thus can be prevented or slowed by maintaining overall health and using [[tonic]]s. Consequently,​ our preventive and treatment goals are the reduction of [[wp>​oxidative damage]], reduction of cellular [[toxins]] and inflammation,​ and improvement of cerebral circulation and [[wp>​oxygen transport]] and [[wp>​glucose transport]].
 +
 +• Neural circulation can be improved with [[blood moving herbs]], especially [[corydalis rhizome]] ([[yan hu suo]]), which slows the breakdown of [[wp>​choline]]. ​ (Kim 1999)
 +
 +• According to studies of the pharmacological properties of [[gingko leaf]], [[wp>​gingkolide]]s exhibit [[wp>​anti-oxidant]],​ neuro-protective and [[wp>​cholinergic]] activities relevant to Alzheimer'​s disease mechanisms (DeFeudis, 1991).
 +
 +• In numerous well-controlled clinical studies in Europe and the US, extracts of [[wp>​ginkgo leaf]] have proven "​effective therapy for a wide variety of disturbances of cerebral function, including multi-infarct dementia, early cognitive decline, and mild-to-moderate cases of the more severe types of senile dementia including Alzheimer'​s disease (Clostre 1999). ​
 +
 +• Tonics that can prevent mental and neurological decline include [[flaxseed oil]], DHA ([[wp>​Docosahexanoic acid]] from [[fish oil]]s - more info http://​www.amazon.com/​exec/​obidos/​ASIN/​1591200016/​qid=1113672184/​sr=2-5/​ref=pd_bbs_b_2_5/​104-4860128-2187122),​ [[guggul gum]], [[rehmannia]] root, [[amla fruit]] ([[amalaki]]),​ [[American ginseng]] root, [[ginseng]] root, [[ashwaghanda]] root, [[dang gui]] root, [[garlic]] bulb, [[gotu kola]] ([[brahmi]]),​ [[guduchi]] stem, [[shou wu root]], [[maitake]] [[mushroom]],​ [[milk thistle]] seed, [[ganoderma]] [[mushroom]],​ [[shilajatu]] ([[shilajit]]),​ and [[Siberian eleuthero]] root bark.
 +
 +• Anti-oxidant protection comes from eating lots of fresh [[fruit]]s and [[vegetable]]s,​ and using herbs like [[amla fruit]], [[triphala]] and [[wheat sprouts]].
 +
 +• Because [[wp>​neurotransmitter]]s and other [[wp>​brain chemicals]] are formed from [[wp>​amino acid]]s, and [[digestion]] ([[agni]]) declines with age, digestion-strengthening herbs like [[bromelain]] or [[trikatu]] can be used to ensure proper [[wp>​protein]] and nutrient assimilation.
 +
 +Learning Therapy and Alzheimers:
 +http://​www.globalaging.org/​health/​world/​2004/​hope.htm
 +
 +
 +cannabis may help Alzheimers:
 +http://​www.guardian.co.uk/​medicine/​story/​0,​11381,​1424017,​00.html
 +
 +
 +excellent article on Alzheimers prevention:
 +http://​redflagsweekly.com/​articles/​2005_jan28.php
 +
 +
 +[[Fair Use]] Source: http://​oneearthherbs.squarespace.com/​diseases/​alzheimers-and-dementia.html
 +
 +----
 +
 +Alzheimer'​s disease (AD) is a degenerative condition of the brain that destroys memory, disrupts personality and accelerates death. The disease was first described in 1907 by Dr. Alios Alzheimer, who had a 51-year-old female patient suffering from a severe form of dementia. Upon autopsy, he noticed the deposition "of a peculiar substance in the cerebral cortex,"​ which has since been determined to be a 40 amino acid long protein fragment called amyloid beta-protein. Alzheimer'​s disease affects more than 4 million people in the US, with an estimated 250,000 new cases every year. (Rubin 2001, 742-43; Berkow 1992, 1403; Roberts 1996)
 +
 +The tendency to develop AD is probably multifactoral rather than a case of simple genetics or infection: in the case of familial prevalence, this may or may not be genetic, but rather, evidence of similar predisposing factors. Above all, AD appears to be a 20th century disease, resulting from the combined effect of dietary and environmental changes with genetic and immunological factors. The clinical features of AD include dementia, disturbances in comprehension and language, as well as several other behavioral clues. Dementia refers to an impaired ability to pursue one's occupation and social activities. This may include confusion, difficulty in memory recall, difficult speech, altered judgment and impaired abstract thinking. There may also be a feeling of "not being oneself,"​ a loss of interest in favourite pastimes, diminished creativity and a diminished ability to express affection. Language disturbances include the inability to find the correct word or the use of "​filler"​ words in conversation,​ circumlocation (talking around the subject), an inability to express one's thoughts in a written form or comprehend the written word, and difficulties in performing everyday physical tasks such as dialing the telephone or unlocking the door. Concomitant behaviours may include a deterioration of personal hygiene, inappropriate dress, a loss of social graces, losing and misplacing items, repeated traffic accidents, irritability,​ stubbornness,​ suspiciousness,​ a short attention span, an inability to perform simple instructions and an obsessive attention to trivial matters. The diagnosis of probable Alzheimer'​s disease (PAD) occurs when other possible causes of the above clinical features have been ruled out. This includes multi-infarct disease, Parkinson'​s,​ depression, alcoholic dementia, hypothyroidism,​ adverse reactions to pharmaceuticals,​ vitamin B12 deficiency, hydrocephalus (increased CSF in the brain'​s ventricles) and infections such as syphilis. (Rubin 2001, 742-43; Berkow 1992, 1403; Roberts 1996)
 +
 +There are characteristic changes to the morphology of selective brain structures in AD, specifically of the hippocampus and cerebral cortex, which can be detected by MRI (multiple resonance imaging). The characteristic findings in AD are amyloid plaques, neurofibrillary tangles and the loss of nerve cells and synapses. Amyloid plaques are spherical structures that have a central core of beta-amyloid and varying degrees of inorganic aluminum. The number of these plaques directly corresponds with the severity of the disease. Beta-amyloid is cleaved from a much larger protein called amyloid precursor protein (APP), which is encoded on the 21st human chromosome, which in Down's syndrome is triplicated (trisomy 21). The production of beta-amyloid is not limited to the brain however, but also occurs in the walls of peripheral blood vessels. Thus, the gradual production and accumulation of amyloid plaques may occur well before neuronal degeneration in the brain: thus, AD may begin in early adulthood. The enzyme which cleaves APP has a genetic determinant and current research is focused on finding substances that block the activity of this enzyme. Neurofibrillary tangles are the twisted ends of dead nerve cells, and although not specific to AD, large quantities of them have been correlated with severe dementia. These tangles slow down nerve transmission and impair cellular function. There is a significant loss of brain cells and nerve synapses in AD, within the cerebral cortex and subcortical structures, the major suppliers of acetylcholine,​ norepinepherine and serotonin that serve the higher cortical centres. (Rubin 2001, 742-43; Berkow 1992, 1403; Roberts 1996)
 +
 +In cases of AD a marked depletion of acetylcholine has been noted in an area of the brain called the nucleus basalis of Meynert, in contrast to other neurotransmitters such as dopamine and GABA which remain normal. This has lead to the theory that AD is a degenerative nerve cell disorder that targets cholinergic neurons. Acetylcholine is a neurotransmitter that binds with M-1 muscarinic receptors to evoke changes in that tissue, and is quickly broken down by acetyl cholinesterase. It has been suggested that there may be a deficiency of acetyl-L-carnitine,​ which provides acetyl groups for the production of acetylcholine. (Rubin 2001, 742-43; Berkow 1992, 1403; Roberts 1996; Mitchell 1996)
 +
 +The average adult brain requires 112 grams of glucose to maintain proper brain function and impaired glucose levels can alter brain cells, initiate the induction of a neurotoxin called glutamate and cause dramatic alterations in the synthesis and metabolism of acetylcholine. The areas of the brain that seem to be highly vulnerable to glucose deprivation are the same regions of the brain that are affected by AD. Reactive hypoglycemia,​ caused by the overconsumption of refined carbohydrates,​ the usage of exogenous insulin in the absence of dietary precautions,​ calorie restriction,​ as well as the chronic usage of caffeine, alcohol and tobacco, are all possible cause of impaired glucose metabolism in the brain. (Roberts 1996; Mitchell 1996)
 +
 +Reduction in the levels of brain oxygen, necessary for the production of ATP in oxidative phosphorylation,​ may affect various neurotransmitters,​ acetylcholine and nerve growth factor and is another possible contributing factor in AD. Factors that limit brain oxygen include smoking, lung and heart disease, anesthesia, air travel, excessive sleep, poor breathing habits, migraine related brain blood vessel spasm and cerebral atherosclerosis. The latter of these factors may be caused by chronic states of hyperinsulinemia. (Roberts 1996; Mitchell 1996)
 +
 +Certain food additives have been implicated in the development of AD, such as MSG and aspartame (NutraSweet®). Increased concentrations of glutamate and aspartate have been found in the CSF of AD patients. When MSG was tested on young experimental animals it lead to the rapid destruction of brain cells, leading it to be banned in baby foods. Aspartame consists of 50% phenylalanine,​ 40% aspartic acid and 10% methyl ester. Upon entering the stomach the methyl ester is transformed in free methyl alcohol, which in small amounts can cause blindness, permanent neurological damage and even death. There is increasing evidence that mutation involving a single amino acid may be the cause of the production of amyloid precursor protein (APP). In a family with three generations of early onset autosomal dominant AD, DNA sequencing revealed the substitution of phenylalanine for valine in the transmembrane domain of APP. Excessive amounts of D-aspartate and other stereoisomers have been found in the neurofibrillar tangles of AD patients, as well as in the amyloid plaques. (Roberts 1996)
 +
 +A substantial amount of evidence has indicated that aluminum plays a role in Alzheimer'​s disease. As much as four times the amount of aluminum as normal has been found in the brain of AD patients. Aluminum is known to interfere with essential enzymes needed to metabolize glucose for ATP production, cause the destruction of the blood brain barrier and transform L-aspartic acid into the neurotoxic D-aspartic acid. (Roberts 1996)
 +
 +Demographic studies have found a greater preponderance of AD in women, possibly due to a higher incidence of excessive sugar consumption,​ fad dieting (causing reactive hypoglycemia),​ and greater longevity. On average, men have a higher metabolic activity in the temporal and limbic regions of the brain than women, which may confer a preventative benefit. (Roberts 1996)
 +Holistic treatment of AD
 +
 +The treatment of AD disease is similar in scope to other neurodegenerative conditions such as PD. As AD is likely a condition that progresses slowly from repeated insult and damage to the brain, preventative measures based in eating a healthy diet and following a healthy lifestyle are highly recommended for anyone with a family history of AD.
 +
 +Botanicals
 +
 +    Cerebrovascular stimulants: Rosmarinus, Vaccinium, Ginkgo, Vinca, Crataegus, Capsicum, Zingiber, Zanthoxylum
 +    Nervine trophorestoratives,​ to protect neurons: Centella, Bacopa, Acorus, Withania, Rosmarinus, Avena Hypericum, Ganoderma, Eleuthrococcus,​ Turnera, Sida cordifolia, Phyllanthus emblica, Panax spp., Polygonum, Angelica sinensis, Cordyceps, Grifolia, Coriolus
 +    Antioxidant botanicals: Curcuma, Boswellia, Commiphora, Crataegus, Phyllanthus emblica, Bacopa, Tinospora, Shilajitu, Ginkgo, Rosmarinus, Centella, Silybum, Buplerum, Astragalus, Spirulina, Ganoderma
 +    M1-mimetics,​ to provide cholinergic stimulus in the nucleus basalis of Meynert: Pilocarpus, 10-30 gtt b.i.d.
 +    Acetyl cholinesterase inhibitors, to inhibit the enzymatic degradation of acetylcholine:​ Physostigma venenosa, 5 gtt b.i.d.
 +
 +Supplements
 +
 +    vitamin A, 20,000 IU daily
 +    vitamin B complex, 100 mg b.i.d.
 +    vitamin C, to bowel tolerance
 +    vitamin E, 800-1200 IU daily
 +    EPA/DHA, 1000 mg each daily
 +    phosphotidylserine,​ to support biosynthesis of acetylcholine,​ 100 mg t.i.d.
 +    L-acetylcarnatine,​ to support biosynthesis of acetylcholine,​ 500 mg t.i.d.
 +    iron, 20 mg b.i.d.
 +    calcium/​magnesium,​ 1:1, 800 mg each b.i.d.
 +    chromium, 200 mcg t.i.d.
 +    selenium, 200 mcg b.i.d.
 +    zinc, 50 mg daily
 +    CoQ10, 50 mg t.i.d.
 +    grapeseed extract, 50 mg t.i.d.
 +    superoxide dismutase, 100 mg b.i.d.
 +    bioflavonoids,​ 3-5 g daily
 +
 +Diet
 +
 +    Paleolithic diet, low carbohydrate diet to prevent CVD
 +    emphasize antioxidant foods, e.g. garlic, onions, cruciferous vegetables; foods rich in anthocyanidins,​ e.g. blueberries,​ huckleberries,​ elderberries,​ red and black grapes
 +    emphasize foods rich in the biochemical building blocks of acetylcholine,​ e.g. free-range eggs, lecithin
 +    avoid transfatty and hydrogenated fats
 +    avoid all aluminum containing foods or foods packaged in aluminum (e.g. various antacids, dolomite; aluminum cans, foil and cookware),
 +    emphasize artichokes to enhance liver metabolism
 +
 +Topical
 +
 +    Brahmi taila abhyanga, Brahmi or Vacha nasya
 +
 +[[Fair Use]] Source: http://​www.toddcaldecott.com/​index.php/​healing/​conditions/​177-alzheimers-disease
 +
 +
 +http://​www.ayurveda-california.com/​distance_learning/​index.php/​diseases-treatment-with-ayurveda-chinese-medicine/​alzheimers-and-dementia
  
alzheimer_s.txt · Last modified: 2018/02/26 18:10 (external edit)