Natural Treatment for Memory Loss
Dementia is a disorder in which loss of brain cells severely impairs mentation and produces slowness of thought, memory loss, confusion, and disorientation. Advanced dementia can also cause personality changes. Dementia is common among older people -10 of people over the age of 65 have dementia and over 30 of those over 85 are affected. Alzheimer's disease is the most common cause of dementia. It is marked by loss of brain cells that produce acetylcholine, an important neurotransmitter. Another common cause of dementia is decreased blood supply to the brain, termed multi-infarct dementia. This type of dementia is the result of multiple, small strokes, each one damaging a small section of the brain. The strokes occur in an unpredictable, random pattern over months or years and, as more and more brain cells are damaged and lost, dementia develops.
Deficiency in the brain may produce dementia despite normal blood levels.11 Absorption of dietary vitamin B12 is poor in many older people and in younger people with digestive disorders Vitamin B deficiencies can produce dementia, particularly in older people, those with chronic illnesses, and heavy consumers of alcohol9 Fig. 5.27 Supplemental vitamin E and Alzheimer's disease. 341 subjects with Alzheimer's disease of moderate severity were given either 2000 mg day vitamin E or placebo for 2 years. In the treated group there were significant delays in time to death, institutionalization, loss of ability to perform daily functions, or severe dementia a median of 670 days for the vitamin E group, compared with 440 days for the placebo group. Treatment with vitamin E slows progression of moderate-severity Alzheimer's disease. (Adapted from Sano M, et al. N Engl J Med. 1997 336 1216)
Autopsy studies of Alzheimer's patients have consistently demonstrated elevated mercury levels in the affected areas of the brain.85 Likewise, there is a direct correlation between brain levels of mercury and the number of amalgam fillings.86 To better understand the relationship between mercury toxicity and degenerative diseases of the brain, it is necessary to examine the cellular events that occur with these disorders and relate them to the mechanism of toxicity of mercury. Hippocrates described dementias over twenty-four hundred years ago in an historical text, but, it wasn't until 1907 that the pathologist Alois Alzheimer described the changes in the brain associated with dementia occurring before age sixty-five, often referred to as presenile dementia. At the time it was thought to be a different disorder than senile dementia of old age, but since Alzheimer's first studies we have come to realize that these are actually the same disease. These changes include atrophy of several...
One of the most-discussed environmental connections to disease is the relationship between aluminum exposure and Alzheimer's disease. In truth, the connection applies to most neurodegenerative disorders, including Parkinson's and ALS. While no absolute proof of causation currently exists, there is a lot of compelling circumstantial evidence, as well as laboratory evidence, for such a connection. The epidemiological evidence comes from studies that looked at drinking water levels of aluminum and the incidence of Alzheimer's disease for large communities. Several of these studies demonstrated a close correlation. In one such study, eighty-eight counties in England and Wales were examined for incidence of Alzheimer's disease and its relation to aluminum levels in various districts. Researchers found that areas with high aluminum water levels had an Alzheimer's disease incidence 1.5 times higher than areas with low aluminum levels. While this study was criticized because of poor design,...
In the case of dementia, my approach is to see whether there are some nutrients that the person may need. Some people have improved quite a bit on a program in which they received injectable B vitamins and magnesium. Some of these elderly people have difficulty absorbing vitamins and minerals simply because of long-term chronic deficiencies, so an injectable program becomes very, very helpful. There is some research relating aluminum toxicity Alzheimer's disease. Dr. Krapper McCloughlin has done some work in Canada, and we have been doing some work recently too, with patients who suffer from dementia, using another chelating agent called Dephoroximine or Desphoral, which is primarily useful in removing iron and aluminum--and not calcium--from the body. Usually, dementia is a one-way street people tend to get worse and worse. using this chelation process, some patients have at least had their dementia process stopped. Some patients have even improved a little using a combination...
It is estimated that about one-quarter of all dementias are caused by nutritional factors that are, at least partially, reversible.9 Deficiencies of severalB vitamins - niacin, vitamin B12, thiamin, and folate - can cause dementia.9,14,15 Chronic heavy alcohol consumption can also produce dementia - large amounts of alcohol have a direct toxic effect on brain cells. Because multi-infarct dementia is caused by small strokes, the same dietary changes that were recommended for prevention of high blood pressure and stroke (see pp. 180) can decrease risk of this disorder and also slow down progression of the disease in affected individuals by preventing more strokes.16,17 Often, because of their disability and poor dietary habits, demented patients develop nutritional deficiencies that can sharply accelerate their disease.9
On the up side, enough scientific evidence has been collected on a handful ofbotanical supplements to support their limited use. For example, under a doctor's guidance, gingko biloba may be used to help treat the symptoms of age-related memory loss and dementia (including Alzheimer's disease) green tea extract may help reduce cancer risk. A growing body of research evidence is being gathered about their safety and effectiveness, as well as their limitations and dangers. Improves memory in individuals with Alzheimer's disease or dementia Do not take if you have Alzheimer's disease
During the early 1970s, doctors working in the dialysis units of several hospitals noticed that a growing number of their patients were developing rather unusual symptoms, such as jerking muscles, hallucinations, and rapid-onset dementia. Several of these patients died before the culprit was discovered high concentrations of aluminum in the water being used for dialysis. Ironically, this was ordinary tap water. Once aluminum was removed from the water, the dialysis dementia syndrome disappeared and patients improved significantly when chelated with a substance called deferoxamine, a medication that removes aluminum from body tissues. This was the first human demonstration that aluminum could cause dementia, somewhat similar to Alzheimer's dementia. Several studies have shown that aluminum forms a highly absorbable chemical complex with glutamate in the gastrointestinal tract. Not only will the aluminum-glutamate complex enter the blood stream in much higher concentrations than normal,...
While this would seem to settle the controversy, it didn't. The picture was further clouded by yet more accurate analysis using highly sophisticated laser microprobe mass spectrometry (LMMA 500), which can analyze components of the neuron itself. Using this technique, no significant differences in aluminum were found between Alzheimer's brains and normal control brains.189 That is, while the aluminum levels in the Alzheimer's brains were higher than controls, the difference was not statistically significant. Does this throw the whole theory of aluminum's role in Alzheimer's disease into question Not exactly Remember that in the first three chapters we learned that a metal's toxic effects on the brain depend on numerous variables, such as strength of the antioxidant network, general nutrition, genetic weaknesses, enzyme competence, and the presence of other cellular protectors, such as growth factors. The degree of brain damage secondary to aging, primarily through free-radical damage,...
An early hypothesis about the cause of Alzheimer's disease suggested that onset was connected to impairment of the neurotransmitter, acetylcholine. We do know that brain levels of this neurotransmitter, which plays a major role in memory, are severely reduced in Alzheimer's brains. Of the enzymes important to acetylcholine production, attention has centered on choline acetyltransferase (which is also dramatically diminished in Alzheimer's disease), which is inhibited by aluminum. Also decreased is the enzyme acetylcholinesterase, which breaks down acetylcholine.202 In severe cases, these enzymes can be reduced as much as 75-95 percent in selected parts of the brain. While acetylcholine has gotten most of the attention in Alzheimer's dementia, studies have noted that several other neurotransmitters are also diminished, including dopamine, norepinephrine and serotonin.203 all can be affected by the action of aluminum on key enzymes utilized in their production. When aluminum combines...
Projections have been made that within our children's lifetime, 1 in every 45 Americans will be living with Alzheimer's disease (Brookmeyer et al., 1998) since women live longer than men, the majority of these will be women. This will present interesting and serious public health issues, since historically women have been the primary caregivers. Taking into account the current prevalence of AD in the U.S., and everything that is known about the progression of the disease, Brookmeyer et al. (1998) projected that even a modest 1- or 2-year delay in the onset of AD will have a significant impact on the prevalence of the disease in 50 years. These projections underlie the urgent need for continued research to identify the molecular mechanisms that increase one's risk for AD and other dementias, and in turn the mechanisms that underlie potential neuroprotection by factors such as soy isoflavones and other phytochemicals. Adding to the complexity in our understanding of human dementias, and...
Another important finding has been that DNA-repair enzymes can vary as much as 180-300 times among individuals. This is critically important when we consider that our ability to repair free-radical-damaged DNA can mean the difference between developing cancer, degenerative brain diseases, or other devastating disorders and enjoying good health. Recent studies have shown that people who develop certain types of cancer have an impaired ability to repair damaged DNA. Similar defects in DNA-repair enzymes have also been seen in cases of Alzheimer's dementia. Free radicals also damage DNA-repair enzymes, as do several of the toxic metals. Another genetic toss of the coin can play a major role in your risk of developing two particularly devastating diseases. It has been shown that persons carrying the apolipoprotein E4 gene (apoE4) are at a very high risk of developing Alzheimer's disease and heart disease. Even having one copy of the gene increases your risk. One autopsy study found that...
The textbook Aluminum and Alzheimer's Disease An Update presents the relationship between aluminum and mercury poisoning and disease There have been reports of increased aluminum in the bulk of brain tissue in Alzheimer's patients and more recently associations of aluminum with neurofibrillary tangles and neuritic plaques. Aluminum has also been associated with neurofibrillary degeneration in patients with amyotrophic lateral sclerosis and Parkinsonism type dementia.
1 Contrary to popular opinion, a 15-year, 1,700-person heart disease study at the Institute of Preventive Medicine, Kommunehospitalet in Copenhagen, Denmark, showed that older men and women who regularly consumed up to 21 drinks of wine a week were less likely than teetotalers to develop Alzheimer's disease and other forms of dementia. Similarly, a recent 12-year, 1,488-person survey at Johns Hopkins University in Maryland suggests that regular, moderate drinkers score better over time than teetotalers do on the Mini-Mental State Examination (MMSE), a standard test for memory, reasoning, and decision making.
Not infrequently, a person will suffer from numerous small strokes in silent areas of the brain and not even be aware of it. With time, these small strokes (called mini-strokes) accumulate so much damage that the person develops dementia, speech loss, or varying degrees of weakness in the arms and legs. Many such patients are simply labeled Alzheimer's disease, and, as a result, the person is relegated to a life in a total care facility.
One of the arguments given by those who defend the safety of dental amalgams is that there is no clear-cut evidence of mercury poisoning from dental amalgams. Certainly, other than the fellows trying to extract silver from amalgam in a frying pan, that is true, yet we also have abundant evidence that the mercury vapor arising from dental amalgams produces in utero levels in babies which can cause abnormal brain development. We also have considerable data relating the number of dental amalgams to toxic levels of mercury in the tissues, levels known to produce organ and cellular malfunction. Such correlations have been demonstrated in people with Alzheimer's dementia as well.
In Excitotoxins, The Taste That Kills, I made it clear that there was no evidence that the excitotoxins found in foods are themselves the primary cause of neurodegenerative disorders such as Parkinson's and Alzheimer's disease, but one frightening possibility is that there may be a link between the widespread excitotoxic contamination of our food supply and the heretofore-unexplained dramatic increase in neurodegenerative diseases which have also begun to occur on average at an earlier age. While these diseases existed long before the introduction of excitotoxic food additives, this does not mean that certain food additives We know, for example, that people carrying the apoE4 gene have a significant risk of eventually developing Alzheimer's disease. Now if you happen to carry the apoE4 gene and consume foods high in excitotoxins, your risk of developing the disease will, most likely, be much greater than a person who eats unadulterated foods. Why Because having the apoE4 gene...
Earlier, I said that excessive quantities of glutamate and other excitotoxins in the brain can result in neuron death that is associated with everything from Alzheimer's dementia, Parkinson's disease and Lou Gehrig's disease (ALS), to strokes and brain injury. This destructive process depends on calcium entry into the neuron triggered by the excitotoxins. Cadmium, in tissue culture, blocks this toxicity. At first, this might seem to be a good thing, but cadmium, even in low concentrations, has been shown to reduce cell survival. It appears that calcium blockage is so efficient that the cell cannot survive.
There is now good evidence that increases in plasma glucose can enhance learning in rodents and humans ( 69). Many drugs that impair learning and memory (e.g., opiates, g-aminobutyric agonists, cholinergic antagonists) can have their actions reduced by glucose ( 70). Injecting glucose into the medial septum and into the amygdala of the brain in rats attenuates the inhibitory action of morphine in a trained avoidance task ( 6.9). It is suggested that glucose metabolites, such as pyruvate, may contribute to the mechanism by which glucose regulates brain cell function. Glucose has also been shown to enhance the memory of aged rodents and humans. In healthy humans 60 to 80 years old, glucose (50 g) was more effective than saccharin (27 mg) in improving narrative memory test performance (69), but it had no effect on performance of nonmemory tasks, i.e., attention, motor speed, or overall IQ. These actions of glucose showed an inverted U-shaped dose-response curve, the optimal glucose dose...
Electron from body cells to become stable. Over time, that may lead to cell dysfunction and contribute to the onset of health problems such as cancer, artery and heart disease, cataracts, age-related macular degeneration, diabetes, Alzheimer's disease, and some deterioration that goes with aging. Antioxidants in your body counteract the action of free radicals.
One of the first compelling pieces of evidence that postmenopausal estrogen-replacement might protect against Alzheimer's disease in elderly women was the epidemiological study by Mayeux and coworkers (Tang et al.,1996) that showed a high correlation between estrogen use and lowered incidence of AD. Their study, which analyzed a large group of postmenopausal women in the New York City area, determined that if estrogen-replacement was undertaken for even as little as 1 year, a woman was 50 less likely to get AD. Moreover, if estrogen-replacement was undertaken for more than 1 year, a woman's risk for AD was reduced severalfold (Figure 8.4). Figure 8.4 Postmenopausal estrogen replacement lowers risk for Alzheimer's disease. The three different groups of women represented here either undertook no estrogen-replacement therapy (ERT) postmenopausally, undertook ERT for up to 1 year, or undertook ERT for greater than 1 year. (Drawn from Tang, M.X. et al., 1996. Lancet, 348 429-432.
Studies have shown that stress increases the death of specific brain cells, especially those concerned with memory and orientation, the very ones affected by Alzheimer's disease.465 To a large degree this is due to the fact that prolonged stress of any kind dramatically increases free-radical generation and lipid peroxidation in the brain.
In the brain, adenosine acts as a neurotransmitter. It is synthesized in glial cells and neurons, and its release into extracellular space is enhanced during states of fatigue and sleep (Adrien, 2001). The adenosine A2A receptors act, in part, by inhibiting the N-methyl-D-aspartate (NMDA) component of excitatory synaptic currents (Gerevich et al., 2002), and the neural distribution of these receptors suggests some probable sites of action of caffeine in the brain. Included are the striatum and medulla, as well as portions of the basal forebrain, the mesopontine area, and the sleep-regulating preoptic nucleus of the hypthothalamus (Boros et al., 2002). The nucleus acubens (Solinas et al., 2002) and the lateral amygdala (Svenningsson et al., 1999) may also be involved. Caffeine probably produces its stimulatory effect, in part, by blocking the A2A receptors that activate the GABAergic neurons populating the inhibitory tracts to the striatal dopaminergic reward system (Daly and Fredholm,...
Nutrigenomics offers a huge opportunity to customize what people eat for their unique genetic makeup. The goal the potential to slow and even prevent all kinds of diseases-some directly nutrition-related, such as celiac disease, diabetes, obesity, cancer, and heart disease, others not, such as sickle cell disease, cystic fibrosis, and Alzheimer's disease-for those at risk. Understanding functional foods and nutrigenomics goes hand in hand, as science reveals the unique ways that foods' many substances work and interact within body cells.
An interesting topic, still to be investigated in detail, is the relationship of MRPs with products that derive from physiological protein glycation, especially in diabetic patients and that are involved in ageing and act as promoting agents in Alzheimer's disease. However, it has been suggested that dietary restriction of food MRPs may be useful to reduce the burden of AGEs in diabetic patients and possibly improve the prognosis of the disease (Koschinsky et al, 1997).
Be wary of claims about the benefits these products supposedly offer. Some companies claim that at-home genetic tests can measure the risk of developing a particular disease, like heart disease, diabetes, cancer, or Alzheimer's. But the FDA and CDC say they aren't aware of any valid studies that prove these tests give accurate results. Having a particular gene doesn't necessarily mean that a disease will develop not having a particular gene doesn't necessarily mean that the disease will not.
Deficiency in the central nervous system (even with normal blood levels of vitamin B12 and without anemia6) may cause psychosis, depression, and or mania. Dementia with confusion and memory loss, particularly in the elderly, may benefit from vitamin B12.7,8
Dementia The aging population worldwide yields concern for an increased prevalence of dementia. Hypothetical reasons exist for lifelong dietary patterns influencing the most common forms of dementia. Harman has elucidated a theory that free radicals might be involved in the onset of dementia.97 Vegetarian diets high in antioxidants may confer protection against free radicals and thus reduce the risk of senile dementia.98 Multi-infarct dementia may also be related to the consumption of cholesterol and different fatty acids. Giem et al.99 investigated the relationship between animal product consumption and evidence of dementia in two sub groups of the Adventist Health Study cohort. To ensure a wide range of dietary exposure, 272 California residents were matched for age, sex, and zip code, which included one pure vegetarian, one lacto-ovo vegetarian, and two heavy meat eaters in each of 68 quartets. The second sub group included 2984 unmatched subjects who resided within the Loma...
Cognitive Function Phosphatidylserine and cognitive dysfunction and dementia Claim Statement (including disclaimer) Consumption of phosphatidylserine may reduce the risk of dementia in the elderly. Very limited and preliminary scientific research suggests that phosphatidylserine may reduce the risk of dementia in the elderly. The FDA concludes that there is little scientific evidence supporting this claim.
This chapter has dealt with the potential for soy isoflavones to have potential benefit in the primate brain, in particular against brain protein modifications that are linked with AD pathology. Future experiments are important to understand both the molecular basis of human dementia and the protective actions of physiological estrogen and phytochemicals, such as the soy isoflavones, in either mimicking or complementing estrogen action. Recent experiments suggest that soy isoflavones undergo halogenation in inflammatory situations where neutrophils are stimulated to release a respiratory burst of hypochlorous acid (Boersma et al., 1999). This modification may enhance the ability of soy isoflavones to protect against oxidative damage under inflammatory conditions (Boersma et al., 1999).
Reports of aluminum toxicity were published as early as 1972, and many practitioners observed isolated incidences of dialysis-related encephalopathy and dementia (39). Laboratory testing of serum aluminum began to be performed on symptomatic patients and was also used as a screening tool for the dialysis population. Municipal water supplies started to test for aluminum and discontinued use of aluminum as a purifier. Dialysis centers installed filtration systems to remove aluminum from the water used to make the dialysate. Dietitians advised patients not to use pitted aluminum cookware and other potential environmental sources of aluminum toxicity. Increased efforts were made to control dietary phosphate intake so that large doses of binders could be avoided. Reports of desferoxamine, a chelating agent, to diagnose and treat aluminum bone disease were published as early as 1981 (40).
The term metabolic syndrome (occasionally called insulin resistance syndrome) refers to a constellation of clinical findings including obesity, hypertension, hyperlipidemia, and insulin resistance, with increased risk for type 2 diabetes and cardiovascular disease. It has also been linked with chronic kidney disease, liver disease with steatosis, fibrosis, and cirrhosis, and cognitive decline and dementia. Despite recent controversy regarding the concept of a metabolic syndrome, the International Diabetes Federation (IDF) developed a new unifying worldwide definition building upon the World Health Organization (WHO) and ATP III definitions, as will be discussed in later chapters (82).
In my practice, I see a considerable number of elderly people suffering from either age-related memory loss or a major neurological disease, and over the years one thought has haunted me How many of these poor people are suffering needlessly because of some environmental hazard What a tragedy it would be to know that some common treatment a dental filling or flu vaccination could produce or contribute to older people being struck down by horrible diseases. In the brain, mercury quickly attaches itself to proteins, mostly enzymes. One particularly important molecule affected by mercury is glutathione, which is found in every cell in the body, and is especially important in the central nervous system (the brain and spinal cord). Because glutathione contains sulfhydral groups, mercury attaches to it very tightly and can remove glutathione from the cell. As we have seen, one molecule of mercury can inactivate two molecules of glutathione. So why is glutathione so important Because of its...
Informed, prosperous, and health-conscious, the baby boomers are known as a generation that plans to fight vigorously against the encroachments of age. During the 1990s, as the boomers began reaching their fifties, they increasingly turned to supplements to ward off osteoporosis, memory loss, and a host of other ailments. With increased demand, the vitamins, minerals, and herbs they sought migrated from health food stores to mass merchandisers. Between 1997 and 2002 the supplement industry experienced a 34 percent jump in sales, to more than 19 billion annually.
Vitamin B12 also can lead to anemia and high levels of homocysteine. Among mature adults, low levels of vitamins B12 and B6 are linked to memory loss, and low levels of B12, to age-related hearing loss. With coexisting conditions, other symptoms of vitamin B12 deficiency may go unrecognized. Meat, poultry, fish, eggs, and dairy foods are all good sources. To avoid deficiency, mature adults are urged to eat vitamin B12-fortified foods and to take a supplement with vitamin B12. Some health problems impair the body's ability to absorb naturally occurring vitamin B12. If you're over age fifty, the Dietary Guidelines advise Consume vitamin B12 in its crystalline form (from fortified foods or supplements) and meet the recommendation of 2.4 micrograms per day. In older adults, dehydration may cause symptoms that seem like dementia, or impaired mental function, or might worsen existing dementia.
Recall that accumulated attrition of brain cells and their connections accounts for brain aging and degenerative diseases. What this means for chronic users of powerful drugs is an elevated risk for developing Parkinson's or Alzheimer's at forty or even thirty, rather than sixty. Not surprisingly, this is exactly what we are seeing today. The age at which people are developing degenerative diseases of the brain has been sliding steadily toward a younger age group. Also, there has been a dramatic rise in the total incidence of these brain diseases over the last several decades.
For GABA tea, the biological function of blood pressure moderation was even more predominant due to the mutual enhancement of GABA and catechins com-bined.113,114 Until now, research about the biological functions of GABA tea has concentrated more on its blood pressure moderation However, several foods rich in GABA, such as germinated brown rice and GABA-enriched fermented milk product, have gained considerable attention due to their biological functions Besides reducing blood pressure, many other functions were reported, such as reducing anxiety and stress,115 aiding against onset of Alzheimer's,116 helping with sleep and mood problems,116 increasing growth hormone,59,117,118 helping aging persons feel younger, and relieving postmenopausal depression .88,101,119,120 In addition, new techniques using microbial fermentation to produce a high content of GABA in foods have been developed.90,115,116,121,122
For example, doses up to 500 mg a day, when given to autistic children, improve about 50 percent of the children without significant side effects. Doses this high are used to stop seizures in a rare childhood disorder called pyridoxine sensitive seizures, in fact, it is the only thing that will stop the seizures and prevent deterioration to the point of dementia. Higher doses are also used to lower elevated homocysteine levels. Considering that a standard dose is 25-50 mg a day, the possibility of side effects is practically non-existent.
We have good experimental and human pathological evidence that prolonged free-radical injury to neurons and astrocytes precedes most neurodegenerative diseases by decades. We also have overwhelming evidence that neural energy impairment plays a pivotal role in these diseases. Autopsy studies of large numbers of Alzheimer's victims have consistently shown elevations of mercury, as well as other toxic metals, within the parts of the brain characteristically damaged by the disease. So, I think those who dismiss these concerns out of hand are themselves not using good science and certainly are not using common sense.
Yet scientific data are never perfect, and in this relatively new area of research on the effects of soy in the nervous system, the data are both sparse and complex. An epidemiological study that followed the dietary patterns of a group of elderly Japanese men in Hawaii found a link between high tofu consumption and increased incidence of dementia, and reduced brain size at death (White et al., 2000). While the raw data were undeniable, the conclusion that higher tofu consumption was correlated with increased incidence of dementia is difficult to reconcile with the documented health benefits of soy and the lower incidence of dementia in Asian countries. However, until the molecular mechanisms that underlie AD pathology, and the increased risk for dementia caused by estrogen loss, are better understood, the epidemiological data of White et al. (2000) remain poorly understood, yet unchallenged.
Physical Findings Functional Deficits Deficiency Pellagra - 3 D's Dermatitis (190) Reddened skin darkens, vesicles, bullae develop with desquamation Bilateral symmetrical distribution on sun exposed skin (Casal Necklace) Skin thickened, pigmented over joints Palms, soles dry, scaling with rough elbows. Diarrhea (182) Raw, burning from mouth to rectum. Dementia (194) Confusion, confabulation, memory loss, disorientation, and delirium. Oral (182) Scarlet sore tongue, filiform papillae progressing to complete atrophy. Neurological (261) Confusion, Loss of memory, Disorientation, Confabulation, Mania, Depression, Delirium, and Polyneuritis. TOXICITY (256) Vasodilation, Nonspecific gastrointestinal effects, Jaundice with hepatotoxicity. Functional niacin deficits include diarrhea, with and without bleeding, dysphagia, nausea, vomiting, and anorexia (190). Autopsy reports reveal scarlet, exfoliated oral surface, extending throughout the GI tract (191). Diffuse inflammation is also found in...
Vitamin B12 is necessary for the maintenance of myelin, which insulates nerves and affects neurotransmission 79 . Although dietary B12 deficiencies are rare due to efficient recycling, strict vegetarians and individuals with decreased appetite anorexia should consider supplementing their diet. Neurological symptoms associated with deficiency include numbness and tingling, abnormalities in gait, memory loss, and disorientation. Vitamin B12 is found almost exclusively in animal products. Fortified cereal and grain products provide an alternative for those individuals who do not consume animal products. Although vitamin B12 is important to CNS functions, no associations have been reported for vitamin B12 and depression 90 or postpartum depression 88 .
Taining your health, both physical and mental. With age, we gain not only wrinkles and gray hair but also wisdom, an appreciation for our mortality, and the desire to protect our good health. You may know that maintaining fitness into the golden years reduces the inflammation that can lead to heart disease, but you might not know that staying fit likely reduces the risk of Alzheimer's disease by 50 percent (Etnier et al. 2007).
Wolfgang Klein and co-workers demonstrated that cells exposed to 1 ppm fluoride exhibit a 50 percent reduction in DNA-repair-enzyme activity.125 Not only does this increase cancer risk, it also encourages aggravation of degenerative diseases of the nervous system, such as Alzheimer's disease, Parkinson's disease, and Lou Gehrig's disease (ALS), as well as other degenerative diseases of aging. When unrepaired DNA damage occurs in reproductive cells, the damage is passed on to children as well.
In a December 2007 report, the UK Human Genetics Commission (2007, Appendix 2) identified 26 companies based in the USA, UK and Europe that advertise and or sell DTC genetic tests. While not an exhaustive count of the number of firms currently operating in this field, the tests provided by these 26 companies reveal the range of health concerns for which testing is available and the variable models by which services are offered. DTC tests assess genetic predisposition for a range of diseases and conditions, including cancer (mainly breast, ovarian, prostate and colorectal cancer), cardiovascular disease, osteoporosis, diabetes (type 1 and type 2), obesity, celiac disease, inflammatory bowel disease, hemochromato-sis, factor V Leiden, thrombophilia, glaucoma, macular degeneration and Alzheimer's disease. They may test for genetic factors that affect lipid, glucose, caffeine, alcohol and pharmaceutical metabolism. Pregnancy and newborn screening tests are also available. Some tests are...
A fairly recent series of studies found that infant animals treated with MSG have higher cortisone levels than normal mice, and following stress it takes longer for the high levels to normalize.255 This same process occurs in the elderly, and is known to endanger the brain. High levels of cortisone, especially over a long period of time, can destroy neurons in the hippocampus, a part of the brain damaged in Alzheimer's disease. Some have proposed that the elevated levels of Cortisol and slow clearance following stress eventually lead to Alzheimer's dementia. That our children may be constantly exposed to high cortisone levels from early childhood is a frightening prospect.
Some have advocated using intravenous calcium or disodium EDTA intravenously or orally during treatment. Of some concern is the observation by Duhr and colleagues that when mercury complexes with EDTA it forms a compound that, in the brain, can powerfully inhibit a process (tubulin polymerization) that closely resembles a pathological event seen in Alzheimer's brains.105 The experiment was done in isolated human neurons and not in live animals. In humans, EDTA does not pass through the blood-brain barrier very easily and only low concentrations would be expected to enter the brain. In this study, it was found that the presence of EDTA could increase the toxicity of mercury to tubulin tenfold. But, they were using EDTA concentration fifty to five hundred times higher than the mercury. They also found that magnesium offered significant protection against this toxicity. Magnesium has been shown to promote normal microtubule formation in the brain, again emphasizing the importance of...
Fenfluramine acts by raising the level of serotonin (a chemical in the brain) which in essence tricks the brain into believing that the stomach is full. The drug itself does not produce weight loss, but allows it by suppressing appetite. Phentermine is an amphetamine-like drug. Side effects of fen-phen include drowsiness, dry mouth, and short-term memory loss.
This condition may be inherited as an autosomal dominant trait, as it was described in three siblings (two female, one male) and their father.30 The patients developed symptoms during childhood and, in addition to pseud-obstruction, suffered from dysphagia, diarrhea and constipation. They became developmentally delayed, had autonomic dysfunction and ataxia, and developed dementia. A characteristic feature of the condition is the presence of eosinophilic intranuclear inclusions in the neurons of the myenteric plexus and in the central nervous system.3 In some of the patients
All of the comments 1 have made concerning Alzheimer's disease also apply to Parkinson's disease. Like Alzheimer's and ALS, Parkinson's disease is associated with free-radical and lipid-peroxidation damage to a very restricted part of the brain called the substantia nigra and its connections. Like the others, excitotoxicity appears to play a central role in the disease process itself. There is strong evidence that iron toxicity is also critical in this disease. Some feel that the free-radical generation caused by mercury is related to the fact that it causes free iron to be released from its binding protein, ferritin. I again emphasize, all of the neurodegenerative diseases I have discussed can and frequently do overlap, which would indicate a common cause. Why one person would develop Parkinson's disease and another ALS may depend on a multitude of factors such as associated toxins, nutritional factors, associated viral injuries, genetic sensitivities, biochemical differences, and...
The connection between exposure to mercury in its various forms and degenerative diseases of the nervous system is fairly strong. Many of the symptoms of chronic low-level mercury exposure closely resemble the neurobehavioral symptoms seen in many neurodegenerative diseases. For example, the asthetic-vegetative syndrome (micromercurilism) caused by exposure to low levels of mercury, is characterized by decreased productivity, loss of memory, loss of self-confidence, depression, fatigue, and irritability, many of which symptoms are also present in the dementias. Also, the studies done on dentists exposed to mercury vapor demonstrated impaired memory recall. It is also interesting to note that one A more recent study of nine exposed workers from a thermometer plant found symptoms of Parkinson's disease in four, which eventually cleared in all but one. They also experienced loss of muscle power, tremors, and atrophy of muscle mass, all symptoms associated with motor neuron injury, as in...
Mercury is considered by toxicologists to be one of the most poisonous naturally occurring substances on the earth. Because of its tremendous toxicity, it is carefully regulated by the EPA, the Occupational Safety and Health Administration (OSHA) and other regulatory bodies. The amount allowed in the atmosphere is fewer than 50 ug M3, fifty-millionths of a gram per cubic meter of air. In the summer of 1990 the EPA banned the use of mercury-containing interior latex paint after discovering that levels of mercury in the urine of occupants living in recently painted houses could reach 118 micrograms (ug) per gram of creatine, a level associated with human toxicity. Such levels could produce subtle neurological damage such as memory loss, irritability, difficulty concentrating, and tremors.
This is important because there is a strong link between brain aluminum levels and neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Histological examinations of test animals' brains indicated that damage was concentrated in the left hemisphere of the brain, with a significant reduction in neuron density. This loss of brain cells was greater in animals drinking aluminum fluoride water than in those given sodium fluoride or distilled water. The damaged neurons exhibited clumping, enhanced protein staining, and destructive chromosomal changes. Similar damage was seen in the blood vessels supplying this part of the brain as well, a consistent finding in Alzheimer's disease. This type of damage to the brain's blood vessels could lead to the same changes in the blood-brain barrier we see in Alzheimer's disease. Animals exposed to both aluminum fluoride and sodium fluoride showed a buildup of vascular R-amyloid in the lateral posterior thalamus. B-amyloid is a...
Back in 1991, I was injured on the job by some paint fumes and my whole life changed. I developed serious food allergies and sensitivities to everything in my environment. I became allergic to everything in my own home, I reacted to plastics of all kinds, and I couldn't breathe outdoor air. I was literally a captive in my own home for the first year. When I couldn't go out, all the air inside my own home had to be filtered especially for me and I had to wear charcoal face masks to breathe. Also, I began to experience depressions, mood swings, and a lot of confusion and memory loss. I would go into one room and forget why I was there. I know a lot of people have that complaint, but I had it consistently throughout the day. I would lose my memory about what I was doing. I couldn't go out in the car and drive myself to the store because I wouldn't be able to find my way. I lost the ability to read normally. Still now, two years later, I have to read things over and over and give my brain...
As people age, balance, coordination, short-term memory, information retrieval, and other brain tasks are hindered. A lifetime of oxidative stress may induce damages to lipids and proteins that lead to cellular damage. Dementia results from impaired vascular supply, both chronic and acute, and from the formation of amyloid plaques associated with Alzheimer's disease. An animal study recently provided some evidence that dietary antioxidants can protect the brain from oxygen-induced damage (Joseph et al., 1998). Six- to eight-month-old F344 rats were fed a control diet or diets containing antioxidants (500 IU kg vitamin E, 10 g kg dried aqueous blueberry extract, 9.4 g kg dried strawberry extract, or 6.7 g kg dried spinach extract). After 8 weeks of the diet, the rats were subjected to 48 h of 100 O2 to
Phosphatidylserine (PS) is supplement that has been found to hold great promise for people suffering from various pathologies that affect the brain, such as certain forms of dementia, Alzheimer's, and others. Early European studies showed phosphatidylserine could slow and reverse the rate of brain cell aging in laboratory animals. PS also restored mental function in older animals to levels exceeding those found in some younger animals (although studies in humans with Alzheimer's disease were less impressive, PS still produced improvements in cognitive function). Research has shown that in addition to improving neural function, PS appears to enhance energy metabolism in brain cells. In the brain, PS helps maintain cell membrane integrity and may protect brain cells against the functional deterioration that occurs with normal aging.
One area in which good hydration is especially important is in the brain. With aging and progressive atherosclerosis, millions of tiny arteries begin to narrow and lose their elasticity. Periodically, several of these small arterioles will shut down, producing a very tiny stroke that may go completely unnoticed. Gradually, the number of these small strokes begins to accumulate, until we start to lose our ability to think clearly and become forgetful. One form of Alzheimer's disease is associated with these strokes and widespread atherosclerosis. Even in the absence of Alzheimer's disease, people suffering from this process often become demented, a condition called vascular dementia. Staying well-hydrated will help to prevent these small vessels from closing off.
Elderly individuals, patients with Alzheimer's dementia, or Down syndrome showed increased glutamine toxicity in peripheral lymphocytes compared to controls 72 . Aside from these sporadic and somewhat anecdotal reports of toxicity, glutamine appears to be quite safe. Even with high intakes of glutamine, the concentrations of ammonia and glutamate are not greatly increased, and the plasma concentrations of other amino acids, hormones, and electrolytes are not altered 85 .
3.44.3 Alzheimer's disease In Japan, homopantothenate (pantoyl g-aminobutyrate), the next highest homologue of pantothenic acid, is used to enhance cognitive function, especially in Alzheimer's disease. It acts via g-aminobutyrate receptors to increase acetyl choline release and cholinergic function in the cerebral cortex and hippocampus (Bender, 1999). A rare side-effect of the treatment is hepatic encephalopathy and the excretion of a variety of dicarboxylates, both effects being reversed by pan-tothenate, suggesting homopantothenate may cause pantothenate deficiency. If this is verified dicarboxylic aciduria may provide a marker of pantothenate status. However, the alternative theory might be that the adverse effects are due to toxicity of homopantothenate which is antagonised by pantothenate.
With aging we also see a decrease in an important immune chemical called interleukin-2, which affords protection by enhancing T-lymphocyte production and function. Carotenoids improve age-related declines in interleukin-2 production. Another cytokine, interleukin-6, increases with aging519 and is associated with autoimmune diseases, Alzheimer's disease, and cancer.520
Other characteristic features seen with B12 deficiency include paresthe-sia in the limbs, inability to maintain balance when walking, weakness and excessive fatigue, loss of vibration and position sense, and a range of psychiatric disorders including disorientation, depression, mood disturbances, irritability, memory loss, and dementia. The lesions result from the patchy and progressive demyelination in peripheral nerves, the spinal cord, and the brain. Vitamin B12 deficiency is fairly common in the elderly and is associated with impairment in cognitive function or the exacerbation of coexisting dementia in the geriatric population.117
More likely to be deficient in vitamins D and B12. The nutritional status of all elderly, both vegetarians and non-vegetarians, should be individually evaluated, paying special attention to vitamin D, B12, calcium, zinc, and folate. Evaluation of vitamin B12 status is particularly important in geriatric patients due to the increased risk of anemia and dementia from atrophy of the small bowel, lack of intrinsic factor, and achlorhydria. A significant number of elderly persons with dementia have been found to be vitamin B12 deficient.117
Vitamin B-6 is a vital component for chemical reactions involving proteins and amino acids. (Remember those protein-building blocks ) It also participates in the formation of red blood cells, antibodies, and insulin, in addition to maintaining normal brain function. Deficiency causes skin changes, convulsions in infants, dementia, nervous disorders, and anemia.
Pellegra is a disease caused by a dietary deficiency of, or a failure to absorb, niacin (vitamin B3) or the amino acid tryptophan, a precursor of niacin. First reported in 1735 by Don Gasper Casal, a Spanish physician, pellagra means rough skin. Primary symptoms include the 3 Ds dementia (mental symptoms), dermatitis (scaly skin sores), and diarrhea. A pellagra epidemic emerged during the 1900s in the United States, when corn (maize) began to replace other sources of dietary protein among the rural poor. Niacin in corn is tightly bound to protein, and thus poorly absorbed. Niacin enrichment of cereal grains and diets adequate in protein and calories eventually eradicated pellagra from the United States. Seasonal epidemics still occur in parts of Southeast Asia and Africa, however.
Folic acid helps maintain normal levels of serotonin. Deficiencies contribute to depression, dementia, and schizophrenia. In a study of depressed patients taking lithium, those also given folic acid supplements for a year showed dramatic relief of depression, compared to those given no supplements.
Niacin deficiency causes pellagra and occurs in parts of India and the African continent. Pellagra is frequently associated with the 'hungry season', strong sunshine and with diets of mainly maize and millet. The clinical features of pellagra are dermatitis, diarrhoea and dementia. Pellagra is occasionally found in malnourished alcoholic patients and it has been found associated with the intake of mycotoxins from the mould Fusarium. Pellagra occurs in Hartnup's disease, an autosomal recessive disorder with impaired absorption of several amino acids including tryptophan (Thurnham, 2000).
Based on the many roles of niacin in energy processes, poor niacin status can reduce the efficiency of energy systems. Some of the earlier symptoms of a niacin deficiency include a decreased appetite, weight loss, and a general feeling of weakness. More severe niacin deficiency can result in a severe disease syndrome called pellagra, which is characterized by the three D's (dermatitis, diarrhea, dementia) possibly leading to the fourth D (death).
Spinach ranks top of the veggie list because of its strong base content. A spinach salad or some cooked spinach can neutralize nearly any dietary acid-forming food and that's good for the bones and the muscles. Spinach has also got fiber to improve gastrointestinal health and promote fat loss. It's also got folic acid for reducing the risk of heart disease, cancer, and memory loss with aging. Popeye was right you'd better eats your spinach
Although aging does not seem to have an effect on folate absorption or use, it is a crucial nutrient for older adults. Research has found that low folate status is a risk factor for cognitive decline 31 . The mechanism by which this decline occurs seems to be through the methylation pathway of homocysteine metabolism. As a result of folate deficiency, the pathway is disturbed, and S-adenosylhomo-cysteine accumulates. The accumulation of S-adenosylhomocysteine inhibits methylation reactions, possibly resulting in cognitive dysfunction 31 . The RDA for folate for all adults is 400 ig d of Dietary Folate Equivalents 30 .
Consistent exercise programs enhance the health of the elderly.117-118 The concept of a relation of cholesterol and triacylglycerol levels to colorectal carcinoma greatly enhances the elderly vegetarian's or vegan's healthy status.119 The high level of significance of this is shown in Table 11.3. Clearly, the elderly vegan, in particular, can keep low serum lipids levels. Further study is needed to define the relationship between the consistent antioxidant dosage of the elderly vegetarian or vegan relative to the degenerative neuromuscular and neurological diseases, and, in particular, Alzheimer's disease.120
Free radical noun an atom or group of atoms that is highly reactive owing to the presence of an unpaired electron (note Because of the effect they have on cells in the body, free radicals are thought to be a contributory cause of medical conditions such as cancer, atherosclerosis and Alzheimer's.)
Alzheimer's Disease In treating Alzheimer's patients, the following are some of the approaches I've found helpful. 3. Have all of your silver, mercury amalgam dental fillings removed from your teeth. Tom Warren, who wrote Beating Alzheimer's, emphasized the importance of this procedure. 12. Finally, since the brain of an Alzheimer's patient shrinks, we have to rehydrate it with pure water, daily it takes about six months to compensate for the shrinkage. I recommend several books Dr. Michael Weiner's Reducing the Risks of Alzheimer's (Stein and Day, 1987) Dr. Abram Hoffer and Dr. Morton Walker's Nutrients to Age Without Senility (Connecticut Keat's Publishing, 1980) Ross Pelton's MindFoodand Smart Pills, Nutrients and Drugs that Increase Intelligence and Prevent Brain Aging (San Diego T&R Publishers, 1986) and Tom Warren's Beating Alzheimer's The Case for Unlocking Brain Disease, Alzheimer's to Schizophrenia and Other Chronic Diseases (Washington 1988).
Phenylketonuria (fee-nyl-key-ton-uria), or PKU, is an inherited metabolic disease that results in severe developmental delay and neurological problems when treatment is not started very early and maintained throughout life. The disease is caused by the absence of the enzyme phenylalanine hydroxylase, which normally converts the amino acid phenylalanine to another amino acid, tyrosine. This results in a build-up of phenylalanine and a low level of tyrosine, which causes a variety of problems, including cognitive decline, learning disabilities, behavior or neurological problems, and skin disorders.
Role in disease prevention and treatment. In addition to clinical deficiency diseases such as anemia and goiter, research indicates that trace minerals play a role in the development, prevention, and treatment of chronic diseases. A marginal status of several trace minerals has been found to be associated with infectious diseases, disorders of the stomach, intestine, bone, heart, and liver, and cancer, although further research is necessary in many cases to understand the effect of supplementation. Iron, zinc, copper, and selenium have been associated with immune response conditions. Copper, chromium and selenium have been linked to the prevention of cardiovascular disease. Excess iron in the body, on the other hand, can increase the risk of cardiovascular disease, liver and colorectal cancer, and neurodegenerative diseases such as Alzheimer's disease. Chromium supplementation has been found to be beneficial in many studies of impaired glucose tolerance, a metabolic state between...
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